Good morning, everyone. Hi. Thank you for coming so early. I'm Alice Edwards, my PA from RWJ Rutgers in New Jersey, and I'm the PA liaison to the scientific committee meeting here, and Robin is our new nurse practitioner liaison, and she's on all of the things that you'll see, but unfortunately she was not able to make it, so Danielle, one of our PAs and some of our other educational content has agreed to come, so thank you, Danielle. You are going to be seeing a myriad of speakers today. Some of them have changed since the original content, and I apologize, just last-minute changes for people, so CME self-reporting, just a few housekeeping things, and course evaluations will be available on NeuroU, a link in course evaluation and CME self-reporting instructions will be emailed to you as well. Please provide candid evaluation feedback, as it does help us when we go to do this again next year, so knowing what is great for you and what didn't really hit helps us as well. AANS scientific program subcommittee takes your feedback into consideration when selecting futuring offers for us, as well as other content. Download the AANS meeting app if you have not already done so, and you'll have the meeting schedule there, and you'll be able to put on there what you want to go to, and it'll remind you of things as well if you allow those prompts. Audio taping, video taping, and photography is strictly prohibited, so please silence all your cell phones, and you can visit the exhibit hall throughout the meeting to see the latest innovations, technology, and industry partners. Okay, before we get started, you all have cards on your tables, and of course, we're going to have people come in later, if they sit at your table later, please tell them to fill it out when they get in. So we're going to use this in our burning questions later, or burning topics later, so the first question, just put a one, and please everybody answer, it's completely anonymous, is what would you have wanted to learn or know before you went into neurosurgery? The second is what would you have wanted to know, or be aware of, or learn, or be told in whatever capacity about your current job before you took it? And the third is, is there a misconception about APPs in neurosurgery, and what would you like to debunk about it? The fourth is anything else. So first is what would you have wanted to know before going into neurosurgery? The second, maybe your current job, what would you have wanted to know, something you'd like to change about it? The third is if there's like any misconceptions, or the working environment that you're in at work, what would you like to change with your working partners? And then the fourth is, again, anything you'd like for us to know or talk about. Thank you, and let me get my notes, because I totally cannot give Dr. Kellner's bio without the bio. Okay, so Dr. Kellner is here from Mount Sinai, and he specializes in endovascular minimally invasive treatment of different forms of stroke, aneurysms, AVMs, AV fistulas. He is an undergraduate degree from Harvard. He also has a medical degree from the College of Physicians and Surgeons at Columbia, and he is currently at Mount Sinai, and he has authored over 60 peer-reviewed publications and 10 book chapters, among many other things. Thank you so much for being with us today, Dr. Kellner. Thank you so much for inviting me, and for coming in at 8 o'clock to hear this talk. Let me arrange this just so I can see it while I'm talking, a little bit here, there we go. All right, so we're going to talk about the APP in cerebrovascular neurosurgery, and really about cerebrovascular neurosurgery and kind of the new topics, which are really ischemic stroke and hemorrhagic stroke. And I'll just give an update about where we are in both of those fields, and the kinds of things we're doing, the procedures we're doing, that APPs are involved in at our institution. Here are my conflicts of interest. They're mostly research-related around ischemia and hemorrhagic stroke, and then a few things I've invested in. I'm going to avoid talking about any specific devices or techniques or anything like that, kind of keep it general. And I'd also like to acknowledge my son, who's here with me, not in this room, but in L.A. today, and I told him I would give him a shout-out if he let me escape for a few hours. So first I'm going to talk a little bit about Mount Sinai, and how we're all very proud of our APP program. APPs in cerebrovascular, we have many, I'm going to go through the numbers a little bit, but these are the main roles that the APPs do. We basically have an APP paired with every attending, and there are 10 cerebrovascular attendings. The APP runs clinic, they often perform floor procedures, and they sometimes, if they're able to train up effectively, will perform angios independently. They also evaluate consults for acute stroke patients and other cerebrovascular diseases, and they evaluate the acute stroke patient when the acute stroke patient comes in. A little bit of detail about our program, we've got 48 full-time faculty in general in neurosurgery, so it's a very large program, and you can see here we actually have 119 APPs in the neurosurgery department, so it's quite a massive APP army, and they really run the show. Specifically about endovascular, we've got 275 stroke cases last year, and over 2,000 cases each year, so a lot of work to coordinate, and that's over 11 hospitals and 8 biplane angiosuites. And just kind of a general way to think about where APPs are in our system, we've got, as I mentioned, 11 hospitals, these eight core hospitals, and the APPs are involved all throughout inpatient services, outpatient services, and operative procedures. Here are just some of the numbers, and I'll focus on cerebrovascular and then transition into talking about actual cerebrovascular disease, but at Mount Sinai Queens, we set up a stroke center that's entirely run by full-time NPs, and when a patient comes in, they evaluate them first, and then they'll manage the angio and procedure as the nurse and nurse practitioner in the room. And then our core cerebrovascular group has a core set of NPs that, as I mentioned, are paired with each of the attendings, and then we've also got, as you can see, a massive army here with different CVNPs kind of dispersed throughout the system wherever we have cerebrovascular practice occurring. Here are a few pics. We also like to go out and have a lot of fun. So let's get into some of the science, and I'll tell you about thrombectomy, and I'll also talk a little bit about minimally invasive ICH evacuation. Everybody knows stroke is a very common disease process. There are about a million stroke discharges in the U.S. each year. About a quarter of those are second strokes or repeat strokes. Three quarters are new strokes, and in 2020, one in six deaths from cardiovascular disease was due to a stroke. Every 40 seconds, someone in the U.S. has a stroke. Every three and a half minutes, someone dies from a stroke. And about 250, as I mentioned, have had a previous stroke, 87 are ischemic, which is this first half of the talk, and then the other 13% in the U.S. is hemorrhagic, so that'll be the second half. And it's obviously a major problem here, costing the U.S. $53 billion. So just kind of some general background. And then we're really going to focus on neurosurgical stroke cases, which are basically large vessel occlusions makes up the bulk, and this all came around since I've been in attending since 2015. Before that, we weren't broadly doing any treatment for large vessel occlusions, but now we're regularly doing thrombectomy, and I'm going to go through what thrombectomy is in case anyone is interested in doing cerebrovascular APP work. A large vessel occlusion is when a clot blocks one of the major vessels in the brain, and we're talking intracranial vessels, so we're talking about the intracranial ICA, which is this right here, M1, A1, or basilar, which is in the back here. And so any of those vessels counts as a large vessel occlusion if a clot comes from somewhere else and lodges there or if it forms in situ, and this is the disease process that we now know if we act quickly and get the patient to the operating room, we can do a procedure that has a very significant effect and can help them quite significantly. When you get into an angiosuite and you perform an angiogram for a patient with a large vessel occlusion, this is what you see. You've got the artery coming up here. This is the internal carotid artery coming up. It branches into the middle cerebral artery, which is going to supply this side of the brain right here, and you can see those branches are missing, and the anterior cerebral artery, which is this middle part right here. So it's very clear to see where that blockage is. It's right there. It's not always that clear if it's more distal, but when you have an M1, there's no question that's where it is. Here's a 3D recon of that showing you where it is in 3D, and here's a patient where you can see that that vessel seems to be missing there. This must be a post-contrast scan, and so just to talk about large vessel occlusion in general, two out of three will not improve after they get TPA. Seventy-four percent will be dependent at 90 days, so without any treatment, this really is quite a severe disease process. You can imagine with no blood going to a particular side of the brain. There's 20 percent mortality for untreated large vessel occlusion, and there are 24 for every 100,000 people in the U.S., so as cerebrovascular disease goes, it's fairly common. In New York itself, we have about 1,600 calculated potential LVOs on an annual basis, and as I mentioned earlier, you saw that at Mount Sinai, we're doing about 250. We have many hospitals in New York City, and they're each probably getting around that number. So before 2015, we were trying thrombectomy in trials, but it wasn't working out, and this is something that's been really interesting and is also replaying in other disease processes now, where in 2013, these three major trials all came out pretty much exactly 10 years ago. This is March 7, 2013. It was a dark day for endovascular neurosurgery, and those trials failed. They were all negative. Thrombectomy did not seem to work in any of those trials, and looking back and trying to figure out what happened, we now know that the patient selection was not ideal, and we learned from all these points. The devices we were using and the techniques we were using were outdated, and we've improved upon them significantly. We weren't able to get the vessel open frequently enough, and we weren't giving everybody TPA like we are now when they're undergoing this kind of procedure, and we weren't getting there fast enough. So we learned all those things, and then two years later, in 2015, there was this flurry of studies that all came out positive, and this gave us level one evidence that thrombectomy is the right thing to do for patients with large vessel occlusion, as long as you can get to them in time, and in time back then meant six to eight hours. You had to get to them within six to eight hours. Eight hours was the one study, and most of them were six, and if you couldn't get to them in that amount of time, then we thought it probably wasn't worth doing the procedure. So that dramatically changed how we treated this patient population, and now we've developed systems of care around evaluating these patients as quickly as possible, kind of the same things that cardiac intervention saw occur in the late 90s. We saw this occur in the late 2010s, 2015, 16, 17, where we really figured out how to figure out if patients are having a large vessel occlusion and get them to the operating room as fast as possible. And so here's the outcomes of this, and I'm not going to really go through these numbers at all, but just I'm going to boil it down to say all those studies, when you put them together and do a systematic meta-analysis of them, patient-level meta-analysis, you can see that there was an extremely strong favorable result for endovascular treatment over medical management, and the number needed to treat was only 2.6. If you do a lot of clinical research, you know that 2.6 is an extremely strong treatment effect. It's actually one of the most strong treatment effects in all of medicine. So now we've got this extremely effective treatment, and now we know that we have to get these patients to the operating room as quickly as possible to get that clot out. When I say operating room, I mean angiosuite. So what happened with these new trials that made these work and the 2013 trials did not? As I mentioned, it's the technology improved. We figured out how to get patients to the room faster and get a procedure done faster, and then we figured out which patients were the best ones to treat. So let's talk about the technology first, and this is one of the reasons I went into Cerebrovascular is I thought the technology was so cool and the things we could do. This was 2013, where you put in this device called the MERCY device, it was kind of like a corkscrew, and you would get the corkscrew through the clot and you would try to pull it back, kind of like uncorking a bottle of wine here. And this would work pretty well, but it worked only about half the time. So half the time patients were getting the treatment and we weren't able to open the vessel back up. Then over a few years, another technology came out, and this was prominently used in those 2015 studies called a stent treaver, a combination of stent and retrieving. So you're retrieving a clot with a stent, you deploy the stent inside the clot, but you never let go of a stent, like you might if you're doing a carotid stent or a stent somewhere else in the body, you would just place it and leave it. In a stent treaver, you have to do the retrieving part, so you keep connected to the stent, deploy the stent in the blood clot, and then you pull the whole thing back like you're fishing. The other thing we developed, we developed better catheters that we could move right up to the blood clot and we could apply suction forces. So now we're pulling and we're sucking at the same time, and that got the job done frequently enough. Here are a bunch of the stent treavers that we're now using. You can see there's really been a massive explosion in the options, and the technology has continued to advance in the last eight years since this was proven to be a good therapy. Here are a bunch of the catheters, they take on different shapes. You can see people are trying different things. You can see this one kind of has an oval shape and is tapered a little bit there. And we figured out what our goal is in these procedures. We now know what kind of surgical proficiency we need and how we can grade that. And we use this thing called the TICI score, which is modeled after the TIMI score for myocardial reperfusion. This is cerebral reperfusion. And so if you get in there and you see a blockage, and you try to get it out but you can't, and you don't make any progress, that's a zero. If you open up less than 50% of the territory in question, that's a one. And then if you open up 50, if you open up all of it, that's a three. So obviously you're shooting for a three. But from all these studies, we figured out that a 2B or a three is kind of the target. So that's what we started looking at. And this is looking at all those studies from 2015, how frequently we hit that 2B to three outcome target. And then in the studies from 2013, how frequently we hit that target. And so you can see that technology and strategy and maybe even experience improved enough that we started getting the job done. And I'm kind of focusing on this because we're in exactly the same place in intracerebral hemorrhage. And intracerebral hemorrhage evacuation might be at a pivotal moment tomorrow. There's going to be the results of a study called the NRICH study announced at this conference. And if that's positive, it will be the first positive ICH evacuation study. And it was based on using some new technology. So we might be making this jump in hemorrhagic stroke right now. So let's talk about time also. Time is brain. We all know that phrase. And this is the equation for time is brain. We know that in these studies, you had a higher chance of getting a good outcome, which is down here at 90 days, if you took less time from the symptom onset to get that clot out. And so here are the studies that got the clot out really quickly in less than 270 minutes on average. Here are the studies up here that took a while. And you can see the probability of a good outcome went way up if you got it out faster on average. And so that's another thing we learned. And the equation for that basically is every 30-minute delay is a 10% reduction in odds of good outcome. So we know we need now systems of care in place, a massive team to see that patient, evaluate that patient, get them into the procedure room, get the access, and then get the catheters up and do that aspiration. And in our system, that initial frontline assessment in one of our hospitals is entirely run by APPs. And then in many different hospitals, the access is performed by an APP, and then the APP will assist in the rest of the stroke procedure. But what we learned a little bit later is that there are some patient factors at play. Time is relative, and it depends on collaterals. There we go. And so these are two different patients. There's one on the top here, and there's one on the bottom. This is patient one. This patient's called a slow progressor, where over six hours, this is a CAT scan, you don't see really any change. When a patient starts having a stroke and the stroke's progressing, then you see a dark area form. But if a patient's able to hold on over time, it's because they have good collaterals. And so patient one here has good collaterals, patient two, just by their anatomy or what's going on in their brain that day, their collaterals were not able to save that brain. So this is a fast progressor. And so we see these two kinds of patients, where over similar periods of time, one might progress to a stroke, and the other one might be able to hold on even longer and not progress to a stroke. So time is brain, but it's also relative to the patient's anatomy. And it's relative to how good their collateral circulation is. So here's a regular angiogram. I'm just going to show you what collaterals are. You've got the ICA coming up. Here's the MCA going out to the side. Here's the ACA coming up the middle. And here are the ACA to MCA collaterals. So if a clot were to lodge here, it would shut down the blood flow here. But if a patient has good collaterals, they might be able to supply that whole area retrograde from the ACA supply. And also there are other collaterals from the back going to the front. And here's a little graphic that kind of explains that. In the normal state, you've got good flow through all the arteries, and then you've got anastomosis happening where the collaterals link to each other from different aspects of the circulation. Let's say a patient has an infarct and it has a blockage. If collaterals are bad, they're not going to be able to make up this area and supply blood to this area, and you're going to see a large infarct form. But if they're really strong, robust collaterals, then perhaps the collaterals can take over and maybe even completely get blood back to that clot from the other side. And sometimes you see that. We're on a CT angiogram. You can only see the clot because the collaterals are so good that the contrast is getting all the way back. So just to repeat, we know that time is brain, or brain is time. And we also know, though, that there's some relative aspect, and brain is really time dependent on collaterals. And this knowledge led to two more studies coming out in 2018 that even expanded the time window further. If we check the collaterals and we see some patients are surviving, and they have a small core at the time that we greet them, but they have a large penumbra, then we can actually bring them to the procedure room all the way out to 24 hours. And we can do that thrombectomy, and if we just selected the patient correctly, then they actually do better than medical management. And that was dependent on this particular scan called a CT perfusion. And here the CT perfusion shows you how well the collaterals are supplying around a blood clot. Here there is a large penumbra, and here there's a large core. So these are two different patients. This patient is the fast progressor, and they have essentially no blood flow to where the core is, and then they progress to have a complete stroke. Here they have a large penumbra, and they don't progress to have a large stroke. And here's how this looks. Now this is completely automated. A AI algorithm will assess this and text you the answer within minutes. And so this one is showing you that there's a small core and a large penumbra, meaning that there's a large area of brain to save. And so this is a patient that we would take to the procedure room really whatever time they showed up. If they showed up 24 hours later after their symptom onset, we would still take this patient to the procedure room and do a thrombectomy. And that's supported by those studies that came out in 2018. And then we figured out how to choose patients better. We decided, we figured out all these criteria that let us know these patients are going to benefit from a thrombectomy. And we've been expanding that over time. Let me show you two case examples, one in the early time window out to six hours, and then one in the later time window out to 24 hours, depending on CT perfusion. Here's an 80 plus year old. She had hypertension arthritis. She had a modified Rankin score of one, meaning she wasn't completely normal at her baseline, but she was pretty good. She was independent. She was able to do everything on her own, but she had a subtle neurologic deficit. She was at her physician office actually, and while she was with her physician, she suddenly developed onset of aphasia and right hemiplegia. So I guess you couldn't be in a better situation or better place to have those symptoms detected quickly and get you into the hospital quickly. Her last known well, this is the abbreviation we like to use, was 2.45 PM. And she was brought right to Mount Sinai Brooklyn with aphasia, a gaze deviation, right hemiplegia. And at that point, she got pretty bad. She had a stroke scale of 23. With a stroke scale of zero, you're normal, and 23 and higher than 23, you've got some severe deficits. So the higher number here, the worse. She got TPA because she got in there so quickly. It was within four and a half hours, so that's the window for TPA. And then the endovascular team, which is a system-wide team, including the APP team, we were notified at 4.17, so that was less than two hours after her symptom onset. Here's what her CAT scan looked like. You can see that she didn't have any stroke progressing at the time we saw her. And then we were able to get her to one of the hospitals that has a biplane for a thrombectomy. And here's what her angio looked like. You can see right here, that's where that blockage is. You can see this is the internal carotid artery, here's the ACA, and here's the M1. And so you can see that's an M1 occlusion. That's a large vessel occlusion. And then from the lateral, you can see it looks like there's a lot missing here, right? This is an illustration of how the procedure goes. It's a lot more exciting than showing the angiogram, so I'll just walk you through this. You get a microcatheter up to the clot. You actually put it through the clot, and then bring, sorry, microwire, and then you bring a microcatheter over the wire also through the clot. And now you bring up the stent reaver, and then you deploy the stent reaver by pulling the microcatheter back. So there you go. Now you can see it's starting to open up, and as it opens up, it meshes the clot within the stent reaver. And then you activate suction. What we do nowadays, you bring up another catheter, activate suction, so you're sucking and pulling at the same time, and also reversing flow. And then you start pulling it back and pulling it down into that suction catheter, and eventually you get it out. It looks like this little tiny little piece here. And then you do another run. You verify those vessels are open. If you remember, the blockage was right here, and now we can see all those vessels, that candelabra vessel is filling very nicely. Here's how that patient did over time. Her stroke scale was 18 when she got to the procedure room, and the next day it was 7, and then over a few days, she got all the way down to 1, which is essentially back to where she was before. Here's her MRI. Instead of having a huge left MCA stroke, you can see she had a few small infarcts, a few areas where the brain had suffered too much during that short period of time where it was blocked, but most of that tissue was saved. Here is just a few thrombectomies that show you the way different devices can work. Sometimes you can do thrombectomy with an aspiration catheter alone, and that's right here. You can see the clot kind of stuck on there like a cork. And sometimes you use the stent reaver, as I mentioned. Let's go through another case. This is a later time window case. So this is a 65-year-old. She had a history of hypertension and smoking. She works out every day, pretty good for a 65-year-old, and her baseline rank and score was zero, meaning she's in perfect health, taking care of herself, doing all her activities to fill her living, and has no neurologic deficits. She was last known, well, the prior night. So this is a very common phenomenon where someone will go to sleep, and then when they wake up, they have stroke symptoms. That's called a wake-up stroke. And actually, the name of the study that showed that doing thrombectomy for these patients might be helpful was called the DAWN study, referencing all of the wake-up strokes that used to come in that we couldn't treat because we didn't have good evidence for it. But now, after the DAWN study and another study, we really do have good evidence that if we do a CT perfusion and that patient looks like they have brain to save, we can get the procedure done. So her symptoms were discovered at 10 a.m., so that's almost 12 hours after she was last seen well, before she went to bed. And she had aphasia and right hemiplegia, meaning she couldn't move her right side, and she had difficulty speaking to some degree. This was time for a stroke scale of 16. So she was doing better than our stroke scale of 23 patient a few minutes ago, but still pretty significant deficits. She presented to another hospital where the CT and the CT angiogram demonstrated essentially no-progress stroke and large vessel occlusion. Here's exactly what the wording was, and this time, instead of an MCA, it's a little bit more proximal. She had an IC occlusion with good collaterals. After she was outside the six-hour time window, we got a CT perfusion, and the CT perfusion showed that she had a small core and a large penumbra to save. And when we got this angio started, here you can see where the contrast stops, and this is in the neck. Here's the skull in the background here, and you can see this left common carotid, and here's the internal carotid. There's either a blockage here or there's just decreased flow and the blockage is further along. From the CT angiogram, we knew there was further along, so when that happens, you just get all the way up to where we saw it on the CT angiogram and do the thrombectomy from the distal ICA. And then after just one pass using a stent reaver, we're able to reperfuse that, and you can see now, you can see both the ACA and the MCA are both fully recanalized. And then, of course, we always take pictures of the clots and share them around, so I guess like fishing with a big fish, right? Here's her MRI. There's a little bit of a stroke in the basal ganglia here, but actually, and a few small hits up here, but really looking pretty good, especially for having her ICA completely blocked for a period of time. She probably had good flow from collaterals, across the circle of Willis, probably also from the posterior circulation. Here's how she did over time. She was 16, as I mentioned, before the operation, then she was 14 the next day, and then six on day one. So you see often, when you do this right, you do see improvement in the hospital. And there are so many things we can do. So all I showed you so far was that we expanded the time window in the first set of second generation trials, and so that's right here. But even since then, and I'm not going to go through that, and even recently, there have been a lot of other trials that have come out that have expanded the selection of patients we can do this for. We found new thrombolysis trials, now we can give a different medicine called TNK. We figured out that doing this in the posterior circulation, in the basilar artery, is also effective. And then recently, we found out that if a patient comes in, and they already show they have stroke progressed, they still benefit. So some people are even not doing CT perfusion anymore, and we're just doing a CAT scan, right, when someone comes in, and if it looks like they're having a large vessel occlusion, and they still have a low aspect, meaning some stroke progressed, we'll still do it. And then there are lots of ongoing trials to see if someone has a clot more distal in the vasculature, maybe that's a patient who could benefit from this. And maybe also patients who have very few symptoms, if they come in with a large vessel occlusion, even though they're doing pretty well, there's a chance they might decompensate over a day or two. And so people are looking at, do you take them right away, or do you wait for them to decompensate? And so that's a low NIH stroke scale. And there are even other ones that people are expanding this treatment indication for. So we've seen the volume of these procedures increase substantially over the years. As you saw on that slide, we're at about 250 a year, which is kind of one every day to every other day. And it's always an all-hands-on-deck fire drill, you know, with multidisciplinary services engaged, getting the patient to the room as quickly as possible. Let's transition to hemorrhagic stroke in the 10 minutes I've got left, and then we'll have time for some questions. We're talking about ischemic stroke and stroke in general. Now we'll talk specifically about hemorrhagic stroke, and I'm going to talk about the kind of hemorrhagic stroke that's not from an aneurysm or a vascular malformation, but it just occurs spontaneously. So it's a spontaneous intracerebral hemorrhage. We know the global prevalence is high. It was 101.5 million had suffered a stroke in 2019. The prevalence of ischemic stroke was 77.2 million, and the prevalence of intracerebral hemorrhage specifically was 20.7 million. So you saw those ratios earlier when I was saying ischemic stroke was 87% of strokes in the U.S., and hemorrhagic stroke was 13%. Globally intracerebral hemorrhage is a little higher. In Asia, intracerebral hemorrhage is much more common, about twice more common than it is in the United States. And it's also the deadliest and most disabling form of stroke. These patients are severely debilitated. 40 to 50% of patients die in 30 days, and 27% are independent at 90 days. So the inverse is 75% are dependent of survivors, are dependent and living in some kind of nursing facility. And this is recent data. This is from 2022. Just like thrombectomy in 2013, we were talking about how a bunch of trials had occurred and they were all negative. And why were they negative? Patient selection, maybe technique, maybe devices. Now we're looking at the past in ICH and seeing a similar array of negative trials. This is the STICH trial. It was published in 2005. In this trial, craniotomy was compared to medical management, and this trial was negative. And we got a lot of data from that, though. And we tried to run a second-generation trial, looking at only the patients that seemed like there was a signal in STICH1. And those patients were clots that were close to the surface, so you're not going through a lot of brain to get to it, and patients that came in doing pretty well. They were GCS9 or greater, so conscious patients with clot close to the surface. But that second trial also was negative. And then a minimally invasive trial called MISTI that only completed in 2019, and this one was also negative. Doing this technique where you put an EVD catheter into the hematoma, give a little bit of TPA to liquefy the clot, and let it drain out over a few days, that appeared to not work as well. But we did learn a lot from this, and that helped in the design of the current trials and even next-generation trials. And as I mentioned, we're going to hear the results of one of those tomorrow with the NRICH results being presented at the plenary session. So let's kind of break this down, just like we did with ischemic stroke. What are the major questions that we're trying to answer with the ICH trials, intracerebral hemorrhage trials? Should we even take out the clot? If we do it, how should we do it? What devices should we use? In ischemic stroke, it's aspiration catheters and stent reavers. In intracerebral hemorrhage, it's different kinds of ports and endoscopes to get you to the clot, and then different kinds of suction devices and morcellation devices to chop it up. And when should we take it out? Should we do it right away, or should we wait a few days and let it kind of cool down, let the inflammation run its course a little bit, and then get at it? None of these questions are answered at this point, but I'm just going to show you a little bit of the data and where we are, kind of in anticipation of tomorrow's presentation. The guidelines for 2015, right when all those ischemic stroke trials started coming out positive, for surgery, for ICH, really only one little specific byline here. If a patient has a cerebellar hemorrhage and it's causing brainstem compression or hydrocephalus, then you should take it out. And so there have been a lot of studies since 2015, the 2022 guidelines expanded on that a little bit and actually made some space for minimally invasive evacuation. In very specific patients, it does seem like there's a mortality benefit, but functional benefit is still in question. So that's very recently came out. That's from only six months ago. Trials for ICH evacuation have gone all the way back to 1961. Here's the first one here by McKissick. And this one showed, you can see looking at patients who had conservative management with no surgery versus surgery. If you just look at the mortality alone, you can see that patients weren't doing very well with surgery back then. And most of those came from the partial disability group and kind of shifted down to the group of patients who had passed away around the time of the bleed. So then we moved to 2015, I mentioned the STITCH trial. There was essentially no difference between the groups in that. Here's the Kaplan-Meier curve. And then STITCH2, there was a little bit of a signal, but it was also negative. And then a few other studies, and I'll kind of zoom ahead to what we're doing right now with various minimally invasive techniques. So let me go to this slide here. So there have actually been a lot of trials, although each of them have had their own methodological issues. And back in 2018, our group looked at a meta-analysis of all the 17 trials that had been done at that point. And when you look at all the trials together, even though you acknowledge that they have some issues, each of them, you do see a signal in favor of minimally invasive surgery. And so that formed some of the evidence that led to the MISTI trials. And the MISTI trials, I mentioned, they're putting a catheter into the hematoma, giving some TPA, letting it drip out. And by doing that, they're able to get out about 40% of the blood, 60% of the blood and leave 40% of the blood. So here's the treatment group, getting a catheter in, and the blood is draining out over time and over four days at the end of treatment. You can see 40% on average is left there. And then MISTI 3 came along in 2019, and that was overall negative. And so here's that outcome chart. Won't drag you through all the details here, other than to say they were comparing the proportion of patients who got this minimally invasive evacuation treatment to the patients who got medical management, who had an MRS of zero to three at a year. So that means they were able to walk independently, but had some significant neurologic deficits. And so if you look at those proportions, they're essentially similar. There was no difference here. And we learned from this trial that this particular technique did not appear to help patients over time. But we did learn that the more blood you got out, the more likely the patient was to do well over time. And here's the probability of a good outcome at one year. And here's the amount of blood left at the end of treatment. And so what this taught us is, if you can consistently get the blood out and leave no more than 15 milliliters at the end of your treatment, then it does seem like you can improve on medical management here. You can get the probability of a good outcome up pretty high. This was a secondary outcome measure, but it taught us a lot about the physiology of this process. And you may not have seen this before, but if you're proficient in the procedure, you can get enough of the blood out. Just like with ischemic stroke, if you can get that clot out enough of the time, then perhaps you can get to a positive trial. And so this is what we set up in New York to treat these patients. We took, you saw that I was showing you a lot of different hospitals in our healthcare system. If an ICH patient shows up at any one of those hospitals, or any other satellite hospital who refers these patients, then they get centralized to one hospital in our healthcare system. So here's Central Park, here's Mount Sinai Hospital, and here's Mount Sinai West. And Mount Sinai West became our ICH center, where no matter where a patient goes, they're sent there for this treatment. And that's where I live. So just to kind of show you that graphically, and we're using artificial intelligence to identify these patients and automatically calculate the volume of their hematoma, which is one of the criteria for surgery. If a patient shows up in Queens, if they show up in Mount Sinai Hospital, or they show up down here, downtown, Mount Sinai downtown, no matter where they are, they're kind of automatically getting triaged and brought to our ICH center. And by doing that, we're able to centralize the treatment of all these patients, and we're able to learn from them as a system, including the APP team and the NSIC who take care of these patients, the cerebrovascular MPs who take care of these patients, and PAs, and the PTs, and the social workers, and everybody become very adept at dealing with this very sick and neurologically debilitated population. And so we kind of developed a technique that I'm going to talk about to use an endoscope and remove the blood here. And the way this technique works is you stereotactically put a catheter into the hematoma, and then you put an endoscope in, and then you suck out the blood using a suction device. And after you've debulked it and got a lot of the blood out, then you start irrigating. And when you're irrigating, you're really looking for anything bleeding. And this kind of disease process obviously starts from something bleeding. Sometimes it stops before you get to the patient. Sometimes the patient's hematoma expands, and when you're in there and you're evacuating the blood, you can detamponade whatever's bleeding, and then you've got to address that. And so this particular technique, and we called it SCUBA because of the good visibility inside the brain, and I'll show you a picture of that. You can identify bleeding and cauterize it, and that's really the secret there to keep that patient from having bleeding after the operation. So here's how that works. We do it all in the angio suite, and here's where the incision's going to be. Here's the stereotactic navigation that helps us to set our trajectory. Here's the draping that's done in the angio suite and the planned incision on the patient's left upper forehead. And here you can see after the incision, here's a burr hole here. Here's a burr hole ultrasound probe. And this is the introducing sheath that we're going to place. And so you place this sheath, and then you take out this center part, and then you can use that as a portal, as a port to get into the hematoma and put the endoscope through and other instruments. So here that is going into that burr hole. And here's the stereotactic navigation guiding that. This is the endoscope that's going to go into that sheath. Here's the working channel of the endoscope, and here's a channel for fluid to go in for irrigation, and here's a channel for fluid to passively come out. And so that's 6.1 millimeters in diameter. And then this is the working channel. And down that working channel, you'll put a suction device. Here's one option for a suction device. This particular suction device has a spinning bite end in there. So when you press a button here, that will spin and morselate the clot. And if you put your finger over this hole, just like any other neurosurgery suction, that will aspirate and suck the blood clot in. So you're sucking it in while also chopping it up. Here's the aspiration device going down the working channel. Here's the endoscope going into the sheath here. And the sheath is in the head going into the hematoma. And so here's one patient example of a patient who had a large hematoma, and we transferred over from Mount Sinai, Queens, and then ended up doing pretty well after this procedure. This is one of our first patients, so this is from 2016 or so, quite some time ago, and this guy's still doing pretty well. He was 86 at the time that he had this. He was neurologically intact. He was still working as a professional pianist. You can see he's got a little bit of interventricular hemorrhage here, but a very large blood clot. And you can see where it's angled here. And so when you're evaluating a patient with intracerebral hemorrhage, you often talk about the hemphill score, or the ICH score. That predicts how a patient's going to be doing at 30 days, and this gentleman with his criteria actually had a pretty high chance of mortality at 30 days. We always do a CT. Sometimes we'll do an MRI beforehand, but usually after. And so we got this gentleman into the angiosuite, and we were able, in about an hour, to get all that blood out through a burr hole in the right parietal area here. And this is how he did over his hospital stay. He came in at a stroke scale of 17, and you can see that, kind of like what I was showing you with those ischemic stroke patients, he actually did make some recovery. And then by the time he went to rehab, he was at a stroke scale of only four. So doing pretty well. And then at 30 days, I got a text message from his family member showing me that he was back at the piano. And then at 90 days, he was back home. He was self-critical that he needed more practice than he used to on the piano. But he was back to professionally playing. And here he is in the office here. Can't hear what he's saying, but he's saying something very philosophical. So we looked at our first 100 patients, and we've now done about 350 since 2016. But I was showing you some of those metrics about surgical proficiency. You want to hit that target of leaving no more than 15 milliliters. And we were doing that 86% of the time. In that trial that didn't work out, the MISTI trial, they were hitting it 60% of the time. And so it's possible that endoscopic evacuation and or end or endoport evacuation, which was evaluated in the MISTI trial, it's possible that those might, with that technology, you might hit that surgical target more often, and maybe often enough to move the needle to benefit for surgery. So with that, let me jump to where we are with trials. And so this is the trial I was referring to a few times. It's going to be presented tomorrow. It's going to be exciting. It's going to be positive. It's really going to change the way we treat this disease process globally. And then there are a bunch of other trials that have also completed and we're waiting for some results from. And then there are a few other trials really focusing on early evacuation. We were talking about how time matters in ischemic stroke and it also matters in, we think it matters in hemorrhagic stroke, but that's never been proven. And so there are a few ongoing studies looking at early evacuation, and then a few in the planning stage looking at evacuation within 12 hours. And so with that, I'll stop here and take any questions. Thank you. Go for it. Hi Dr. Kalman, how are you? So for your school patients, are you finding, first of all, are you having any issues that are on anti-coagulation? And if yes, are you able to restart your anti-coag sooner than those who've had cardiomyopathy? That's a great suggestion. Our neurologists have suggested, can you get the clot out? Can you address the bleeding? Can you cauterize whatever's going on so we can get this patient back on earlier? That's never really been proven. It does seem like, you know, if your re-bleed rate is at 5% and the expansion rate is at 33%, then it does seem like you're able to decrease the chance of any further expansion or bleeding in the future. But I think that we'll have to prove that. But we are reversing patients if they have a reversible anticoagulant and then bringing those patients after they're reversed for evacuation. All right, thanks so much, everybody. All right, thank you, Dr. Kellner. Up next, we have Dr. Makan. He is the Director of Functional Neurosurgery at Columbia University. He directs the department, I'm sorry, the departmental efforts in epilepsy surgery, low-grade glioma, brain mapping for tumors, and adult hydrocephalus at Columbia University, Irving Medical Center, and New York Presbyterian Hospital. He has over 20 years of experience combining clinical skills and compassionate care to maximize patient outcomes. This morning, he's gonna be talking to us more about speech and motor mapping and the AWAKE Cranny. Okay, good morning, everybody, welcome. So in deciding what to talk about, I actually talked to Jordana, the nurse who works with me every day, and I decided, you know, rather than focus just on speech and motor mapping, that it would be worthwhile if people agree to spend a little bit of time also just talking about surgical anatomy and how we decide which patients need to be mapped, what parts of the brain are relevant, important. I would like, if we could, if you guys have questions as I go along, please interrupt me. You know, I've got a lot of information to get through, but it's not critical we get through all of it. So if there's something you wanna know, just put your hand up, it's a small room, and let's have a conversation if there's anything along the way. So in starters, I've got a bunch of disclosures, but none of them are relevant to this talk. So one of the most important points here is the main areas where we do brain mapping, are brain tumors and epilepsy. And low-grade gliomas are the most prominent example of that, and it's now pretty clear over the last 20 years that for a low-grade glioma surgery, the more tumor we can remove, the better it is for the patient. So the better it is for the patient in terms of survival, extent of resection, malignant degeneration, seizure control, and surgical morbidity. So we wanna try to maximize tumor removal, but at the same time, we have to avoid deficits. Because if you hurt a patient, there's also significant data, more in high-grade, but also in low-grade gliomas, that if you hurt a patient, they do worse. Because now they have to recover, they have to go to rehab, they have deficits, they defer their treatment. So the overall balance in this complicated patient population is that we have to maximally remove tumor or the area of seizure onset while minimizing patient risk. And so that's where brain mapping comes in. And brain mapping is really the critical tool that allows us to do that, to maximize removal while minimizing deficit. So the main points we're gonna focus on, we're gonna spend a bunch of time on anatomy, and then we're gonna talk about what team and tools are necessary, training, experience, and then how we learn from each other, and then a few case examples. So now, as you guys know, in the everyday environment, we've got amazing tools. We're using stereo EEG in the upper left here in epilepsy patients, and even sometimes in tumor patients. We've got great brain imaging. We've got lasers. We've got focused ultrasound. But the reality is, and this is a famous quote from Lars Lexell who developed the gamma knife in terms of technology. Technology is just an instrument. It's only as good as we are in using technology. And one of my primary mentors in neurosurgery in training was a guy named George Ogerman, who I'll get back to. And he used to, you know, people always would say in medical school, one of the problems in medicine is that 50% of what we learn is ultimately gonna be proven to be false. The problem is we just don't know which 50%. But what George used to always say is that anatomy is not part of that 50%. So as a surgeon, you can never know too much anatomy. You can never learn too much anatomy. So it's interesting. Prior to our overall, you know, the applications of frameless stereotactic guidance and everything else now, you know, people would use surface anatomy to know where things are in the brain. And it's a little bit of a lost art. And what I try to do with my residents is after we have the frameless stereotaxy done in the OR and we're ready to navigate, I say, okay, take the pointer and find the tumor. So you get one shot without the navigation to know where on the head it is. And so basically on surface anatomy, if you start at the orbit and you go to the inion in the back, you can divide the head into quarters. And if you go right back to three quarters of the way, that's the typical access of the Sylvian fissure without mass effect. And if you go halfway, and the easy thing that I was taught is you just put a silk stitch and you just mark a line on the patient's head with a silk stitch from the back to the front, halfway along that line is gonna be just in front of where the central sulcus is, where motor and sensory cortex is. So there's a lot of these old school sorts of marks that actually still have relevance when you're figuring out where things are in the office on the head, or like Chris was saying, when you're trying to figure out where are you evacuating a clot from. So on midline, I mean, looking from above, so here's the coronal suture, here's the sagittal suture, here's the sagittal sinus. So in general, the central sulcus, which is our central localization spot for everything in the frontoparietal regions, is gonna be four to five centimeters behind the coronal suture. So back in this region here. So then when you guys are looking at MRI scans, there's a bunch of different ways that you look to find the central sulcus. So you start off that the frontal lobe has three gyri, has a superior frontal gyrus, a middle frontal gyrus, and inferior frontal gyrus. And these all run front to back. And then when you come back on the brain, you see the gyri start to run side to side. So where these run side to side, the front one's pre-central motor, the back one's post-central sensory. It's that simple. And then when you get back to these two gyri, you see that one of them is always thicker than the other one. The thicker one in front is pre-central motor, the thinner one behind is post-central sensory. And then when you look at the pre-central motor to sensory, you see there's this omega shape right here. So that omega shape is exactly that. It's called the omega sign, which that's the hand motor. Yeah, question. Oh, I have a cursor. That's weird. Let's see. Do we have a pointer? That's strange because it's showing on my screen. Can you guys make the cursor show up here? Thank you for bringing that up. Okay, great, now we have it. Okay, so now they have it, but I don't. Okay, so I'll get torticalis, that's fine. So don't mind that I'm not looking at you. It's the cursor. Now, okay, now they have it and I don't. Okay, you know what? I'll imagine I have it. Okay, yeah, so going back to front, here's the superior frontal gyrus, here's the middle frontal gyrus, and then you see here's pre-central, side to side, post-central. And you can see the pre-central's much thicker than the post-central. And this is that omega right there, that Greek omega. And so this is going to be hand motor. And unlike language, which is variable, that's going to be hand motor in everyone in the room. And so hand motor is gonna be right here. Hand sensory is gonna be right behind it. Shoulder's gonna be here. Leg's gonna be on the inside. And then further on the outside, we're gonna get more motor speech and oropharyngeal motor involvement. So if we go, let's see. So now when we look at the brain more laterally, this is the typical orientation of the Rolandic area motor sensory. So it comes down, hand here, post-central sensory here. Oftentimes down in here, there's a little bit of a gap area and then we get down into face motor, face sensory. And then at the bottom, most of the time it's a U like this. And then there's the artery that comes out of the sylveon fissure that runs right up in the middle of the central sulcus and supplies blood supply. And all that's very relevant for what we're doing surgically. And so here's another view here. So we're looking, so here's temporal lobe, frontal lobe. So frontal lobe, superior frontal gyrus, middle frontal gyrus, inferior frontal gyrus. Inferior frontal gyrus has three parts. The back part, which is the opercular part is right in front of the motor pre-central gyrus, face motor here, face sensory here coming up. And you can see on this brain, it's not a U, although it's almost always a U. Then in the temporal lobe, again, three gyri, superior temporal gyrus, middle temporal gyrus, inferior temporal gyrus. The front of the temporal lobe, we're worried about auditory naming. The back of the temporal lobe, we're worried about auditory and visual naming in terms of functions. The typical Wernicke's area for speech reception is right along here, super marginal gyrus and angular gyrus that we're mapping for. The typical traditional Broca's area, speech expression, back of inferior frontal gyrus. And then in the dominant hemisphere, usually the left, we're worried also about face motor. So these are the main areas that we're looking in epilepsy or tumors to map in terms of language functions, perisylvian. Sorry, let's see. In terms of language functions, perisylvian and then motor functions, motor sensory. Now, for those of you that follow this field, we get much more detailed into what we're mapping, but we're just gonna focus mostly on simple primary functions today, because honestly, we could spend all day, which would be great. So here's what it looks like when you compare an MRI. So when we have a patient MRI, so now we're looking, here's actually the three parts of the inferior frontal gyrus. This is the triangular part, the orbital part, the opercular part. Here's the bottom of pre-central gyrus, U-shape coming up into post-central gyrus. This now is inferior parietal lobe, super marginal gyrus, angular gyrus. So we're worried about language here. We're worried about verbal naming here. We get more worried about reading down in this area, particularly alexia without a writing problem. As we move towards the temporal pole, we're worried more about auditory naming. And then there's basal language sites involved in naming. So every spot in the brain, we're worried about testing for absolute specific functions based on the anatomy of what we're seeing. And then on the medial hemisphere of the brain, so here's the anterior frontal pole. So here's that same superior frontal gyrus. This is the cingulate gyrus right here that comes back. This is the pre-central area coming over the top. So this is leg motor here, sometimes some shoulder all the way to the top. Primary sensory here. And then as we come down below, cingulate gyrus. And this is how we tell on an MRI. We follow this sulcus above the cingulate gyrus, and it comes back and it ends up on top behind primary sensory. And then this is the inside of the parietal lobe right here, what's called the precuneus. This is the parietal occipital sulcus. This is visual cortex right here. So now we look at a real brain, corpus callosum. Cingulate gyrus right here. Cingulate sulcus, sometimes discontinuous. We follow it back. It goes behind primary sensory. Here's leg sensory. Here's the central sulcus over the top. Here's leg motor. Here's the precuneus, parietal occipital sulcus. Occipital pole here, so superior occipital cortex, inferior occipital cortex into the temporal lobe here. Here's that bottom temporal gyrus from the outside here. Then there's a collateral sulcus separating this. This is parahippocampal gyrus here, and the hippocampus is on the inside. So basically the brain anatomy, while there's lots of differences in sulci, it's very consistent from patient to patient in terms of what we're gonna see. So then we start looking at an MRI. Here's an MRI without a lesion. So corpus callosum, callosal sulcus, cingulate gyrus, cingulate sulcus. We follow it up behind. It gets a little bit confusing because it doesn't go all the way to the top, but this is actually the back of that cingulate sulcus. Primary sensory, primary motor, medial parietal, parietal occipital sulcus, occipital. So now we're trying to figure out where the lesion is here and what function we're worried about. So here's that cingulate sulcus. We follow it back, comes up right behind here. Here's the lesion right here. So that lesion tells you that's gonna be a lesion in primary sensory, predominantly leg and shoulder. So we're worried about sensory function to map leg and shoulder, and we're worried about hand right in front of that in terms of what we're primarily mapping on that lesion. So we look from the top again. So here's superior frontal gyrus, superior frontal gyrus. Always look at the normal side first to find your anatomy. So superior frontal gyrus. Here's precentral gyrus. Here's the hand omega right here. Here's hand motor. Postcentral gyrus, hand sensory right here. So now there's a lesion right here. So where's this lesion? So same thing, we follow it back. Here's superior frontal gyrus. Precentral gyrus, hand knob here. So that's that same lesion, medial shoulder and leg sensory with leg motor right in front of it. And so that's what we're worried about, and that's what we end up finding in the operating room. So here's another lesion. So where's this lesion? Normal side, superior frontal gyrus coming back. Precentral gyrus, thicker. Postcentral gyrus, thinner. Hand motor, hand sensory. Here's the other side with the lesion. So here's precentral. So this is in front of precentral. This is in what's called the supplementary motor area. So this is a supplementary motor area, low-grade glioma. So we know that we're interested in mapping supplementary motor function and staying in front of primary motor. So that's what we're doing preoperatively in every part of the brain. And then here on the basal surfaces of the brain, so this is looking from below. Where did my pointer go? There we go. So looking from below, this is the basal frontal lobe. So this is the olfactory gyrus. This is orbitofrontal cortex here. Orbitofrontal cortex, middle cerebral arteries right here. Here's temporal lobe from below. Here's temporal occipital junction from below. So let's talk about a few specific areas and risks of surgery in those areas, even with mapping. So here's a tumor right here that is on the medial temporal lobe. Here's a coronal view. So this is frontal lobe coming down here. Sylvian fissure, temporal lobe, the three gyri of the temporal lobe. Superior, middle, inferior. Collateral sulcus, fusiform gyrus. So this is actually anteriorly in the amygdala just in front of the hippocampus. And the difficulty with the amygdala is that right above it, it goes up into the basal ganglia. So the three areas that when I look at are most dangerous for us from a risk-benefit perspective are this medial temporal lobe around the amygdala, the insula right here buried beneath the frontal and temporal opercula, and the cingulate gyrus right here. So if we look at these individually, so here's the amygdala right here. This is a different case. Amygdala and hippocampal tumor and parahippocampal gyrus. Oops, let me back that up, sorry. So here's the amygdala and coronal view. Here's the amygdala and axial view. And so we can see right here, amygdala, head of hippocampus right here. This is posterior cerebral artery right here. This is the brainstem right here. And so if we look at the anatomy here, this is looking down from above. Here's the hippocampus here. Here's the amygdala right here. The brainstem's right here. It looks pretty simple until we throw in all the vasculature. So here's the hippocampal head. Here's the uncus and amygdala looking from above. This is the anterior choroidal artery, which comes along and feeds the choroid plexus and then continues on deeper into the brain and has to be preserved 100% of the time. And then if we look from below, this is the temporal pole. This is the back of the temporal lobe here. This is the bottom of the temporal lobe. This is the uncus. This is the amygdala right here. So when we're operating in that area, just on the medial border, we've got the optic tract right here. We've got the posterior communicating artery. We've got the carotid artery. We've got the posterior cerebral artery. We've got the anterior choroidal artery coming through and all these small little vessels going up to the optic tract and other deeper basal ganglia areas. And here's the other problem, the amygdala that I just showed you. The front of the amygdala is all within the temporal lobe, but when you get to the back of the amygdala, there's no boundary between the amygdala and the optic tract and the basal ganglia above. And so it's very easy to potentially go too far beyond where we want to be if you're not really, really careful and know where you are. And then also we have to understand that in this area of the temporal lobe and the amygdala and the basal frontal lobe, we've got all these different white matter pathways. We've got the uncinnate fasciculus here. We've got the, what's called IFOF, inferior frontal occipital fasciculus here. We've got the inferior longitudinal fasciculus here. Every one of these has a testable, mappable function. And this is where low-grade gliomas grow, so we have to understand the functions and be able to map the functions to figure out what's safe in the operating room. So here's just a brief video. This is a recurrent tumor case from recently. We're looking in. So here's anteriorly. Here's posteriorly. This is actually the hippocampus right here. This is part of the choroid plexus right here. So this is an amygdala tumor right here. And so what you'll see is that as we're very, very gently teasing this firm tumor off of the inside boundary here, you'll start to see if I hold here. So there's this tissue paper thin membrane, which is the arachnoid and the pia separating the temporal lobe from the internal carotid artery, the posterior cerebral artery, the posterior communicating artery, the third nerve, and everything else that lives in this little space. And because this patient's a reoperation and has had radiation before, this is a frail membrane. So we end up actually putting a hole in this membrane. We prefer not to, but in this case, you can see. So you come through that membrane, and here's the carotid artery. Here's the posterior communicating artery. The third nerve is right in there. If we keep going now back towards the tumor as it goes towards the choroid plexus, and I stop again, here's the choroid plexus. This is that anterior carotid artery coming along here, giving a branch to the choroid plexus. So if that gets disturbed, there's a carotid artery infarct here. We keep going a little further along, and so here's the choroid plexus in the ventricle. Here's the hippocampus. This is where the amygdala is. And as we keep going, here's the posterior cerebral artery right there. So we're working in that back of the amygdala up towards the basal ganglia, and it looks completely unchanged from anything else we've done, but as we go millimeter by millimeter, we're stimulating the brain. And right in this area, when we stimulate, we find the corticospinal tract, and we're getting contralateral motor involvement. So if we keep going on this last little bit, we're going to make this patient hemiparetic or hemiplegic if we're not actually mapping him in the operating room. Let's get this to advance. So this is a case, fortunately not one of mine, but unfortunately that we see, I see in my office three or four times a year, where somebody operating in this amygdala region gets too deep into the area and ends up giving a patient multiple perforator infarctions. And this is a patient who had seizures in a low-grade glioma who still has part of their tumor and is now densely hemiparetic and aphasic because of not completely mapping and understanding the anatomy in the region. So these are very tricky areas in terms of knowing where you are and making sure you stay safe. So the insula is the next area. So this is now a coronal view, frontal lobe, temporal lobe, insula right here, middle cerebral artery branches on top of the insula. So again, coronal here. So now moving on, here's a sagittal view. So the temporal operculum's been removed, the frontal and parietal operculum are removed, middle cerebral artery with all the branches running along the insular sulci. So in order to operate on the insula, you either have to open the sylveon fissure and dissect along the vessels to get into the insula, or you have to unroof the opercula if it's safe from a mapping perspective to get to the insula. And again, here's a sagittal view just looking at the insula. So here's the main middle cerebral trunk with all these middle cerebral artery M3 branches running between the five gyri of the insula, one, two, three, four, five. And so all of these arteries, and to the degree possible, their tiny little branches have to be preserved to operate in this area. So here's a blown up view. This is on a coronal view. Most of the vessels out of the insula come inferiorly into the deep, but about 3 to 5% are these long perforators at the top of the insula, which go up to the deep white matter and put you at risk of small but potentially very symptomatic strokes. So when we get into these back long gyri of the insula higher up, these little tiny vessels that are feeding tumors are continuing on to go to normal brain. And that's what gives you the major risk at the upper back of the insula. And that's why when Mitch Berger and Nader Sanai, when Nader was a resident, he's now a very successful surgeon at Barrow, they put together these insular zones of risk for low-grade glioma. And not surprisingly, the big zone of risk is the posterior superior zone because it's hardest to get to and it's where that vasculature is. So in order to get there, we either have to get the sylvian fissure all the way open or we have to map all of these areas that I was showing you earlier on the back of the sylvian fissure to make sure that they're safe from a language perspective to get a window into there. And sometimes you can remove some of the operculum to get there and sometimes you just can't. And so if you can't, you have to be ready to split the sylvian fissure to get there. So then you say, well, why not split the sylvian fissure in everybody? This is from Johannes Schramm, who's now retired, but he was one of the most experienced epilepsy and glioma surgeons on the planet. He was chairman in Bonn in Germany forever. This is his series, very large, 235 patients with tumors in this area. And you can see when one of the best people in the world went trans-sylvian, he had an 8% hemiparesis risk and a 6% aphasia risk, whereas when he was able to do a cortical window, he dropped those numbers down to zero. And so if you can get more room to work with, it's going to be safer for the patient, but you have to map the patient to get that room. And then finally, the cingulate gyrus is right here beneath the medial frontal lobe. And the most dangerous part of the cingulate gyrus for epilepsy or tumor surgery is right below primary motor sensory cortex. The second most dangerous area is this deep area here, deep to the posterior part of the brain. And I'll leave it at that so we can move forward. So when we talk about these types of surgeries, low-grade gliomas are very commonly located within eloquent brain areas. And so just these various critical regions that we have to be able to map oftentimes are involved by low-grade gliomas. And as I said, these tumors migrate along white matter pathways, so we have to be able to map those pathways for their specific functions to safely remove tumors. And then adding to the complexity, we've always known that gliomas cause seizures. Brain tumors cause seizures. But what's coming out in the last several years is that seizures themselves also probably promote progression of tumors. So it's critical in these tumor patients to not just remove the glioma, but to try to stop their seizures. And actually maximizing resection is the number one way to help stop their seizures. So the seizures are predominantly a gray matter brain problem. The low-grade gliomas are predominantly a white matter functional anatomy problem. And so to take care of these patients, we have to do both. We have to be able to map the gray matter surface of the brain and map the white matter propagation pathways to keep patients' functions intact. And so there's an overlap. There's some of these low-grade epilepsy-associated tumors, which predominantly cause seizures and do not progress in general to higher-grade gliomas. There's cavernous malformations that cause seizures and obviously don't grow or progress. They grow, but they're not tumors. They don't progress. But then we have all the low-grade gliomas that they do progress, and if you don't remove them, eventually they all become high-grade cancerous gliomas. So from a tumor perspective, we want to maximize resection of the tumor. From an epilepsy perspective, we want to make sure we're removing the brain areas that are actually causing the seizures. And I'll skip this slide just for time. So what do you need to do this? Well, you need a whole team of people. Typically we've talked about you need a surgeon who knows what they're doing, who's experienced and trained. You need really good anesthesiologists. This is Eric Heyer, who retired a few years ago, but we worked together for almost 20 years. You need anesthesiologists who are comfortable having patients wake up in the operating room. Sometimes they have airway issues, who don't panic when that happens, who are able to sometimes put in a laryngeal mask for anesthesia and then wake them up and then put one back if necessary. You need a great interoperative monitoring team to help with all of the stimulation aspects. This is Ed Gallo, who's been with us forever and is phenomenal, and I hope he never retires. And this is Marla Hamburger, one of our two neuropsychologists who are in the operating room testing patients with us every time we're there. And so again, developing tasks appropriate to the exact areas we're interested in beyond just basic language and sensory motor tasks. So this is George Ogerman, who I mentioned earlier. While their Penfield started all of this in Montreal, he was one of the people who really picked up upon it as an epilepsy surgeon in Seattle at the University of Washington, where I trained. Mitch Berger, who's one of the best known people in the world in the tumor area, was a junior attending in Seattle, learned from George, and I was privileged enough to learn from both of them. Hugh Dufault, who's in France and has really brought the field forward probably more than anybody, was a fellow with George when I was a resident. And here's the people who were my chief residents, who I was really fortunate to train with and under. And then this is a community of people who share cases and share experience. Lorenzo Bello in Milan probably knows more about some aspects or all aspects of motor mapping and other aspects. Rich Byrne, who's the chair at Rush in Chicago, Hugh and Mitch I mentioned, Jinsong Wu in China, Nader Sanai now at Barrow. We're sharing cases all the time. I sent three cases to these guys in the last month, and what was fascinating is I got multiple different opinions on what to do on the same case from some of the most experienced people in the world even now, because there's not always a right answer. And there's no set training for this. We don't know how many awake mapping cases make a surgeon safe and proficient. There's a specific set of surgical skills, and removing an insular glioma like this is totally different from a surface glioma or a cingulate glioma or even an amygdala glioma. And so it really is an aspect where we're getting more and more people interested in the field, but we haven't figured out what's actually necessary from a skill perspective to train. And you'll hear people say, oh, well, I've got fMRI. I've got great imaging at my institution. And what I would say about that is that imaging is really important. It can tell us cerebral dominance. It can tell us how the brain is organized with an fMRI and tractography around the tumor. For some tumors, you can have function within a tumor. We can figure out where are all the white matter pathways relative to the tumor. There's actually companies now doing different aspects of DTI network pathways, synaptic, omniscient, both here at the meeting, have really beautiful technology to help with this. But in my opinion still, this is a preoperative risk stratification. It can help you in the operating room, but ultimately there's nothing like having an awake patient who can carry out testing in the operating room. So preoperatively, we're also, we're most important. I mean, look at this is a crazy low grade glioma here that's going from the medial temporal lobe into the posterior fossa, compressing the brainstem, posterior cerebral artery and all of its branches running right through the tumor. So we have to know ahead of time, what's the vascularity? How are we going to get there? How are we going to save all the arteries and veins? What's the brain gyral and sulcal anatomy of our resection? And so really, we're finishing this surgery in our heads before we ever start the surgical procedure. And then awake testing, whatever function in the OR we need, as I said, modifying it to the patient's profession. If they're multilingual, you have to be able to test them in all of their main languages. And again, what tasks based on what functions and what parts of the brain, understanding how to white matter knowledge and how to stimulate for what we need. And so again, we're doing what traditionally was epilepsy surgery for brain tumors. And now as the brain tumor field moves mapping forward, we're flipping it around and taking the brain tumor advances into the epilepsy field. And again, critically preserving all of the vessels that are running along a tumor to the normal brain around it. So in the operating room, these are some of the tools we use. So traditionally, stimulation was done with an Ogerman stimulator that George developed, which was a bipolar stimulator where you have these two contacts here that can be anywhere five millimeters to a centimeter apart that you're stimulating the brain with. And I'll show you a minute, a monopolar stimulator can be used. But bipolar stimulation when done at low frequency has a greater risk of potentially causing seizures in the OR. So if we're worried about seizures, we prefer to use a monopolar stimulator now. This is somatosensory evoked potentials, which gives us a sensory response to monitor as well as a motor response in the cortex. Motor evoked potentials along the edges of things beyond the craniotomy. And then having patients awake so we know at the end of surgery what are reversible deficits if we're in the supplementary motor area. If the primary motor area stimulates at the end of surgery, we know that patient's gonna be okay. And then if we get a seizure in the operating room, this is something that Mitch figured out when he was a junior attending when we were all working with him as residents, that just cold saline in the operating room with an awake patient is all we need to stop it. So awake patient testing, like I said, there's nothing that substitutes for it. There's nothing better than it. So these are low versus high frequency stimulation, and we use combinations of these. So here's that bipolar stimulator that's used to stimulate along the surface of the brain. Here's a monopolar stimulator, which gives a greater area of spread. So this is gonna spread about five millimeters beyond the tips. This one spreads a millimeter per milliamp of current. So if we turn it up high enough, we can find fiber pathways up to two centimeters away. We can know how far away they are to protect those pathways as we get closer. So sounds simple, but you have to pick the right patients. You have to really know their imaging. You have to know what their pathology is, what your surgical goals are. You have to know what's important to the patient, what functions you have to preserve. You have to know your own limits as a surgeon and what you're able to do and not do. You have to know your team and know exactly how experienced you are for any sort of circumstance. And most importantly, we can always do more, and you have to know when to stop. So I'll show you a few simple cases, cuz we're just wrapping up. So this is a patient quite a long time ago. This is a left-handed patient who's right language dominant, who had multiple small intracerebral hemorrhages, and there's this small cavernous malformation here causing hand clumsiness, dysarthria, word substitutions. So now we're looking down on the brain. Medial is here, anterior is here, the ear's down here, the sylveon fissure's here, back of the head's here. So here's face motor here, dominant face motor in this patient right on top of the lesion. There's face sensory inside of the mouth, cheek, tongue, hand sensory, hand motor. We do a somatosensory evoked potential. We can find that motor's here, sensory's here confirming it. So if you go through this working cortex on top of this lesion, this patient's gonna end up with a deficit. So here, just simple mapping tells us we just have to open the sulcus right here in front of the precentral gyrus. So here's the somatosensory evoked potential. So you see there's a downward deflection here and an upward deflection here. That's the gap between motor and sensory right here. It tells us where it is. And so now we just have to work between this sulcus to preserve the gyrus, remove the malformation, and preserve her function. So here's a different case, complete opposite. So again, superior frontal gyrus, precentral gyrus, postcentral gyrus, premotor here. So here's a tumor invading the premotor, or sorry, the precentral primary motor cortex and primary sensory, mostly primary sensory. But what you see is you see this part of the tumor that's really dense white and this part that's kind of hazy. And what I can tell you from experience is that most of the time, when you have a really hazy tumor like this, that's gonna be a diffusely infiltrating glioma with functioning brain within it. And so this is not a case where we're gonna be able to remove all this brain, almost certainly. Once in a while, it's not 100%, a functional MRI can help predict that, imaging can help predict that. But it's very likely you have to tell this patient that we're just gonna be removing this part for diagnosis and enough pathology to get for studies and things, but we're probably not gonna be able to remove all of that diffusely infiltrating tumor. So how do we actually do this? So for a patient where we are trying to get to the top of the head here, hand motor all the way to midline, in general, we position the patient just like this. So supine position, straight up and down, midline's here, so we can get to there. If we're trying to be more lateral, down by the sylvian fissure, we're putting patients in a lateral position to get to the temporal lobe, the insula, the frontal operculum. And then we're worried about patient comfort, skull fixation, making sure their airway's okay. If their head's above the heart, making sure that we're minimizing the risk of air embolism, and really working with the anesthesiologist to completely control the environment. So this is that case I showed you right here. This is this tumor here, this MRI's always backwards. So here's this left primary sensory cortex. So here's, sorry, I lost this. Here's central sulcus, hand motor, hand sensory. So this is a hand sensory area tumor. So here's now the patient positioned in the OR, nose here obviously, midline here. Here's exactly where the central sulcus is and just behind it. So we don't need a big opening here. So this patient is sedated, but they're not intubated. We're just protecting their face so that they can be tested. The anesthesiologists have their right arm in hand so we can monitor it. So here's the monitoring of the right hand. We've got electrodes in to monitor both for median nerve somatosensory evoked potentials for motor stimulation. We do this before we wake up the patient so they don't feel the stimulation and then once they wake up we can monitor them awake. So here's a simple incision in that area. So here we are with the anesthesiologist on the other side of the drapes. They have access to the patient. They can see the patient, talk to the patient, follow their function together with our monitoring team. And so here we are. Here's the size of the opening. It's a couple centimeter opening. Here we're testing with an Ogerman bipolar stimulator. This is several years ago. Now we probably use a monopolar stimulator to minimize the risk of seizures here. And so here's the central sulcus right here. Here's hand motor. Here's what's remaining of hand sensory. We open along the central sulcus and just remove this lesion through about a one and a half, one centimeter opening, saving all the vessels along the way and his sensory function completely recovered. So here's a patient with an insular glioma. This is about the opposite. This is as complicated as it gets. So this is lateral position, which we have to expose all of the opercula over the sylveon fissure. So this is the left arm up here, right arm off the table, pad in place. This patient has a laryngeal mask because they were very concerned and anxious about being sedated. So they have a laryngeal mask, essentially for general anesthesia that the anesthesiologist will pull when we wake up and test the patient. And here you can see several opercular windows that we had to document were safe to get down into the insula to then remove the tumor down below. And every one of these little arteries is critical and has to be preserved while the patient's awake and testing for us. And eventually we had to stop at the back because we started to develop language problems at this last little bit right here in the white matter. And again, critically opening these windows and preserving every one of these vessels that are running along to normal brain because they're all critical. And so a simple way to start if you're building a program in this is actually with simple metastases in the motor sensory area. So again, we've looked at this superior frontal gyrus, pre-central, post-central, thicker pre-central, thinner post-central, hand omega. So here is a primary hand motor metastasis right here. So we have to map whether there's brain above it. In this case, there was a thin bit of cortex above it. It came close enough to the surface. This cortex was non-functional so we can make a small window in the pre-central gyrus. If we couldn't, we'd split the central sulcus here to find a safe area along the side. But you can see here, there's a fair bit of brain on the back of this. So the prediction is actually that's gonna be more risky and we're gonna wanna come from the top. And then we have to preserve all the arteries in the central sulcus. Even if they're feeding the tumor, the main arteries are going on to working brain. And even with a tiny little tumor like this, this is a tumor we would all gamma knife. Tiny little metastasis and we all agree, this was an older patient with health problems with metastatic lung cancer. But once in a while, even with a tiny little tumor, if there's already edema at the start, we end up with a situation that here's this patient three months later and his edema grew significantly after radiation and he ended up with a refractory seizure disorder and a weakness in his dominant hand from all of us making the decision that we thought was the right decision. So we often err on the side of being more aggressive in the primary motor sensory area with removal, particularly of metastases because of the fact that we find these patients are uniquely seizure prone if they develop radiation induced edemas. So getting back to one of these complicated frontotemporal insular gliomas. You know, I ran this experiment a bunch of years ago where I talked to people at a very, very busy academic medical center with a whole lot of accomplished tumor surgeons and I said, at your institution, how would this be handled? And what we came up with was a whole bunch of options. Some people would observe it, some people would biopsy and then observe, some would biopsy then treat, some would do a subtotal reception without mapping, some would do a subtotal resection with mapping, some would do brain mapping to maximize resection and some would even do what's called a supramaximal resection which has been popularized really by Hugh Dufault and now many others including Lorenzo Bello, Jinsong Wu, some of the people I talked about. At the same point in time, if you went to see Hugh in France and I made a restaurant analogy about what the menu would be, if you went to see Hugh in France, your only entree choices would be a maximum surgical resection with mapping or a supramaximal surgical resection because that gives the patient, if you can do it safely, the best chance of removing as much seizure as possible, of stopping their seizures, of minimizing malignant progression and of treating their tumor. And so we're still stuck in a situation where we have other places in the world where healthcare is super specialized often within national healthcare systems and we still have such a hodgepodge here in the US. And I would say we're getting better but it's somewhat at the expense of a learning curve. And so we still have a long, long way to go here and this is still a field where we need much more training, much more education and there's a lot of room for improvement. So I just want to acknowledge, as I said, George Ogerman, who I trained with, and Mitch Berger also, Hugh, who's been a great colleague and friend, Lorenzo Bello, my mapping psychologist. Over time, our neurophysiology epileptologist, our neurophysiology team, all of my neurosurgical colleagues and most importantly, in this session in particular, Jordana, my nurse, and Cielo, my assistant, because you guys all know that you guys are the people who keep our practices working, that you're the ones who take care of everything behind the scenes that allows all of this to happen. And so thank you guys for doing what you do. Have a great day. Thank you. So questions? Anybody? Yeah. I have a question. Is there a difference between ambidextrous and ambidextrous? It does, yeah. So ambidextrous patients are more likely to possibly have some aspect of right language dominance and so if somebody's ambidextrous, then you want to find out, a functional MRI will often tell you language dominance, but if somebody is right language dominant or mixed dominance when they're ambidextrous, then more often we're going to be worried about language and what typically would be the non-language hemisphere. What I ask all the patients is what's your handedness and what's your footedness? Because some people are right-handed because they got converted as a kid. So it used to be, not so much now, but it used to be, for instance, in the Catholic schools when I was growing up, all of my friends were forced to be right-handed. Even if you were a lefty, the nuns wanted you to be a righty. But if you ask somebody which foot you kick with, then they would kick with their left. That doesn't necessarily mean they were mixed dominant, it means they were probably converted, so you ask them. But if somebody is truly left-handed and left-footed, then you worry more about right dominance. It's about 30% right dominant for people who are left-handed, whereas it's 5% right dominant for people who are right-handed, or less. Other questions about any aspects of this? Yeah. Can you make some comment about the trans-Syrian approach and the trans-Syrian approach for a long time? What happened by this until the use of this approach? Yeah, so as I showed you, the trans-opercular approach does give you more room to get to the corners of the insula, but you have to be able to find a window. And so if you don't have a trans-opercular window, because it's not safe from a mapping perspective, you have to go trans-Sylvian on those. But also, you'll see, so say that it's an insular case with a smaller tumor in a patient who has epilepsy. A smaller tumor, the Sylvian fissure is not going to be pushed outwards by the tumor, by the mass effect, and so oftentimes, it's easier to potentially get an opercular window to get to the very back corners of that. If you have a big insular low-grade tumor, it's got mass effect, and so it's pushing the brain outwards, and it's opening the Sylvian fissure. So oftentimes, you'll look at the MRI, and the tumor's right at the surface, in which case it's easier in that case to go trans-Sylvian. So I don't think there's a right or wrong way. I know there are some surgeons who actually only do one. Like Hugh predominantly tries to go trans-opercular through whatever window he can find. Fred Lang down in Texas tries to go trans-Sylvian whenever he can. I prefer to change it up and combine it even based on the individual anatomy of an individual patient. Yeah? I have a question about competence of these cases. I'm sorry, about what? Sort of competence of these cases. Yeah. In the United States, are there any new ideas for mapping cases or white cases that are beautiful, and should we really be looking for a patient who's not necessarily that beautiful? So I think it depends on the case, right? I think that if somebody has done a fair bit of mapping and training, I think you should start with easy cases. It's like anything else, right? I mean, if you are a vascular neurosurgeon, even in the era of coiling, you're not gonna start with a middle cerebral artery aneurysm that requires a bypass in order for you to control a non-coilable aneurysm, right? That's a very specialized case. Similarly, I would say, for complicated, deep amygdala tumors that are going up into the basal ganglia, or for insular gliomas, I don't think that anybody should do one insular glioma a year. I don't think it's in the patient's best interest. But the reality of healthcare, depending on where you are, it sounded like maybe you're Australian, but the reality of healthcare is, in the United States, there's incredible pressure within healthcare systems for systems to hold onto their own patients. And so we see a lot of patients who somebody went in and took out whatever they could, where there's 70% of the tumors still left, and now that patient goes doctor shopping, and now they realize, well, they need a whole nother surgery. We have to figure out how we, within the confines of the healthcare system, try to minimize that behavior. And again, most importantly, is patient safety, right? I mean, when I say to somebody, a patient will come to me, and they'll say, well, why didn't this doctor take out more tumor? I said, because they did as much as they felt was safe, and they didn't hurt you. And that's the most important thing, because in these tumors, you can't give back a deficit. And if you give somebody a lifetime deficit on top of a brain tumor, you've failed that patient up front. Any other questions? Great, thank you so much. Okay, a little bit of housekeeping before we- The question is, who do you refer these patients to? And the easy answer, I would love for that to be, is me, of course, but there are dentists that can manage this, there are neurologists, there's a lot of ways to skin this cat. And then the last and most important criteria, finally, is relief. So this is actually called the suicide disease. And if you open up a textbook, the textbook description of trigeminal neuralgia is what we call typical. So that's typical face pain. Atypical, it doesn't mean common versus uncommon, typical versus atypical are two distinct definitions. So typical face pain is discrete, short, excruciating episodes. And it can be usually a stabbing, electric, lancinating pain, only on one side, and usually in a reproducible distribution of the sensation of the trigeminal nerve. And it's often triggered by sensory stimuli. So in the post-pandemic world, we actually saw more patients with attacks because they were wearing face masks, and that would actually trigger attacks. Putting on makeup, shaving, brushing your teeth, all things that can trigger attacks. And some quick stats on it. You can see this is pretty rare. There is a female predominance, and it's most common in patients between 50 and 70. And I'll explain why in just a little bit. The most typical distributions are V2 and V3. So that's the bottom portion of your jaw. As you get higher, you're in the V1 distribution. So what causes this? The general hypothesis, and this is still a hypothesis, it's not something that's been proven beyond all doubt, but it's vascular contact or compression of the trigeminal nerve. It's usually the superior cerebellar artery, and it can occasionally be a dolocoectatic or a big tortuous vessel that doesn't belong there. But it's usually a normal SCA vessel that causes it. And over the course of a lifetime, that blood vessel just pulsates on the nerve. And that's why we usually see this in older patients, because it's several decades of sustained pulsations on the nerve that actually create this problem and create a demyelination, which allows for a crosstalk between light touch sensation fibers and excruciating pain fibers. So that's why you typically won't see a 12-year-old or a 20-year-old with this problem. It actually takes several decades of contact before this happens and becomes a problem. Ah, there we go. All right, so this is a nice little cartoon that demonstrates the problem really well. Here we have a retractor on the cerebellum, and that's something, let me just try our pointer here. Perfect. So this is something we never use in surgery anymore. That retractor is something that can be a little traumatic. It can cause ataxia and imbalance after surgery. But for the purpose of the cartoon, it gives you a nice view. You can see this blood vessel here is just sitting on that nerve. And for reference, if anybody here likes angel hair pasta, this nerve is probably 10% the diameter of angel hair pasta. So we're really zoomed in here. But this mere contact is enough to cause this problem. What's unique about trigeminal neuralgia, 60% of the population, so 60% of the people in this room have this configuration of that blood vessel and that nerve. So the reason why 0.01% of the population develops trigeminal neuralgia when 60% actually has this anatomic configuration, we don't know. That's ongoing research. We really haven't figured that out yet. This is what it looks under the microscope in the OR. So again, this is a pretty small and seemingly innocuous vessel, but it has a point of contact or conflict with the nerve. In this case, it's not crushing the nerve. Sometimes it is. The bigger the vessel, the more mass effect on the nerve, the more excited we get that this is gonna be a good result. But mere contact alone is sufficient to cause this problem. And this is what it looks like on MRI. This is very subtle. You'll often see radiologists and even some neurosurgeons may look at an MRI and say this is negative MRI. But this is the brainstem, this is the pons right here. All of this bright stuff is CSF in a fluid cistern. And this tiny little circle, that little cross section, that's a cross section of a loop of the SCA vessel. And it is in contact, not obvious and not terrible with the trigeminal nerve. So if someone presents with the right typical symptoms, that's sufficient. Again, a couple more examples here. So very subtle, but it's in contact with the nerve. And here's a more blown up sequence on the left. You can see again, this is the trigeminal nerve coming off the brainstem. And in between the brainstem and the nerve at what we call the root entry zone, that little black dot is a cross section of a vessel that has contact. Now we're looking at a coronal view. So this last view was axial. So in the coronal view, this larger cross section is the trigeminal nerve and it's forming a U. That U is because it's indented by a vessel that's sitting right inside it. That also would be sufficient to cause this problem. There were some studies that were done that actually looked at asymptomatic people and they got these trigeminal neuralgia protocol MRIs. And again, these people are asymptomatic, but they have nerves and anatomic configurations that look just like this. Why they don't get trigeminal neuralgia, we don't know. Now it's also not always subtle because as you can see here, this is the trigeminal nerve and this is a pretty big circle there. So that's a larger vessel that is displacing it. And I always feel a little bit better when I see that because it's more obvious. The more obvious it is, the more confident we are that we can help someone. This is a massive blood vessel. So we call this a dolichoictatic vertebrobasilar artery. And this is a large blood vessel that can actually exert a lot of mass effect on the nerve. And the surgery involves slinging this off to the side to get it off the nerve. And that's a surgery that is a lot of fun, but can be somewhat high risk. And patients have a very difficult time reconciling. I have face pain. Should I be getting a complex skull base surgery that theoretically could kill me, give me a stroke? And it's very difficult for patients to agree to proceed with the surgery, no matter how bad and how debilitating their pain may be. There are other causes of trigeminal neuralgia. It's not always vascular compression. It can often be a tumor. So if it's a tumor that is wedged into that nerve, you can get the same exact symptoms. That's actually pretty rare. So as you see here, it's less than 1% of patients. The most common tumor that does this is a vestibular schwannoma. And you can even get pain on the other side when it's a tumor because of tension that's placed on the contralateral nerve. Tumors will more often cause what we call atypical face pain. So atypical is a pain that the episodes last longer. They're usually less severe, but it's more of a burning, gnawing pain as opposed to an absolute excruciating, stabbing pain. And if it's a tumor, a patient's more likely to have a neurological deficit, such as a sensory deficit on the face. These patients won't respond to Tegretol as well. And we're gonna talk about that in just a minute. So here's an example of a tumor. This is actually not a vestibular schwannoma. This is a meningioma. But this is a Petrus Ridge meningioma that's pushing on the pons. And you can't even, this is a normal trigeminal nerve, and you can't even see it in this case. So the management for this patient would be just take the tumor out. You decompress the nerve and they're gonna feel better. This is a tumor that is of a size, if the patient were asymptomatic, you wouldn't necessarily need to take it out. It's a benign tumor. You could observe it. You could deliver radiosurgery to it. But if they have severe trigeminal neuralgia symptoms, the tumor has to come out, even if it's small. That's the best way to treat the face pain. This is a tumor. This one is a vestibular schwannoma. This is much larger. So this is a big tumor that needs to come out anyway. And sometimes these patients will have significant symptoms with face pain. One of the other main causes of trigeminal neuralgia face pain is multiple sclerosis. And this is actually the same mechanism as patients that have vascular compression, because you have this demyelination event with crosstalk between pain and light touch fibers. So MS does the same thing that the vessel does, even though MS is more of a systemic autoimmune inflammatory problem. And it's very important that you diagnose MS because the management is different. A patient with MS and trigeminal neuralgia does not get a microvascular decompression because the blood vessel is not causing their problem. If you move that blood vessel, their pain will not get better. They need something ablative that damages the nerve and interrupts that pain signal. Whereas someone who has vascular-induced trigeminal neuralgia, the best solution is to move the nerve, then it's very likely they'll be cured of this problem. So as you can see here with multiple sclerosis, sometimes the nerve will actually light up, and that also helps to suggest that this is not a vascular problem, it may be something else. And of course with MS, we often lean on our neurology colleagues to facilitate a diagnosis, whether it's extensive plaques throughout the brain, or oligoclonal bands in the CSF, or most importantly, when you see these patients in the emergency department in the office, ask them, is this an isolated problem, your face pain, or are you having paresthesias, deficits, other symptoms throughout the body? If the answer is yes, maybe you suspect MS, especially if it's a middle-aged Caucasian female that fits the demographic, as opposed to just thinking this is isolated trigeminal neuralgia, because the last thing you want to do is a microvascular decompression in an MS patient, when we missed the MS diagnosis. So how do we treat this? If someone comes in with the right typical face pain, and they have a blood vessel on their MRI, as much as I love the microvascular decompression surgery, and that's what makes me get up in the morning, and as much as we have as a field refine that surgery so the patients are going home post-op day one, all of the risks are approaching 0%. The recovery is very brief. As streamlined as that may be, nothing's easier than taking two pills a day with no side effects. So we always start with medical therapy. I don't believe in jumping straight to surgery. So Tegretol is the gold standard. Trileptal is also very good, and that's used for patients that can't tolerate Tegretol, and you can see here 70% of patients have acceptable or even better relief. So if a patient can tolerate the medication, and they have excellent relief, just go with medical therapy. It may not last, it may fade, but that's what we start with. Not only because it's therapeutic and effective, but it's also diagnostic. Patients who transiently respond to Tegretol are better surgical candidates. Patients who never respond to Tegretol will actually do worse after surgery. So as a surgeon, it helps me to predict how are they going to do. Neurontin helps. It can act synergistically. What I prefer Neurontin for is as a salvage therapy. So someone who has failed all treatment, it can mute the pain. It will not give you fantastic results, but it does help to mute the pain. Not on this slide, but something that can be very helpful as well are antidepressants. Again, it's not a magic bullet, but it can help to suppress the pain when everything else has failed. So this is less important, but it's just to show you everywhere in neurosurgery and everywhere in medicine, we've tried to come up with charts and scoring systems so that we can communicate with our colleagues the severity of pain, the severity of a tumor, the risk factors. And this is the most commonly accepted sort of scoring system that comes from the Barrow Neurological Institute. And it basically reflects how severe is the pain. The higher numbers mean they're doing worse, and the lower numbers obviously mean they're doing better. And the variables that matter are the consistency of the pain, are we on medications, and how debilitated are we. So this is something you can use just to communicate to your colleagues what category a patient fits into. So surgical therapy. When do we start talking surgery? Number one is failure of medical therapy, and number two is when the risks and side effects of medical therapy exceed the risks of surgery. So even if that Tegretol is working beautifully, but a patient says, I feel very cloudy, my balance is off, that can happen pretty often with Tegretol. It was originally developed and designed with the mechanism of action of an antiepileptics, and those are side effects patients can have. And with the risk factors of surgery, those are side effects that we don't need to just tolerate with the medications. So let's start with radiosurgery. That's GammaKnife and CyberKnife specifically. I absolutely love GammaKnife. I love it for tumors more than I love it for trigeminal neuralgia, but it has a role for trigeminal neuralgia. If a patient has medical comorbidities to the point that they can't tolerate surgery, this is a good option. Now I will say the oldest patient I've ever done an MVD on was 95 years old, and obviously at that age you've got a lot of comorbidities. So this is a surgery, if someone can tolerate general anesthesia, they can tolerate an MVD. But some people can't tolerate that, and in that case radiosurgery is a very good option. If they are on blood thinners with fresh stents, and we absolutely can't take them off their blood thinners, they're antiplatelet agents, then GammaKnife is a good option as well. And if pain has been refractory to multiple procedures, then doing something, anything ablative can often help. It is the gold standard for multiple sclerosis face pain. So if a patient does have MS, then GammaKnife is a very good option for their face pain. The biggest risk is hypothesia. We are damaging the nerve by design. So if we're damaging the nerve, sensation is going to go down. And there is also a risk that that sharp episodic trigeminal neuralgia pain can convert into a more constant burning, gnawing trigeminal neuropathy pain. In some cases that's an improvement, but that still can be very uncomfortable and very disabling. So these are just a couple studies just to give you a sense for the efficacy of this. And this was a hundred patients and this study showed that 20% had some degree of hypothesia after their initial treatment, which then ballooned to 32% after the second. These are really high numbers, especially when you consider that MVD you're at about 2%. Now a lot of these patients would very gladly trade their face pain for numbness, but it's still something that we we seek to avoid. So this gamma knife paper, again about a hundred patients, it shows 71% transition to the Barrow scale 1 to 3, which 1 to 3 basically means acceptable, livable pain. And the median relief is 12 months, which 12 months isn't very good. But again, to be blunt, if you have an 82 year old patient with debilitating face pain and metastatic cancer, 12 months may be good enough. So maybe we're not considering surgery in that patient. And again, you see a pretty high number of patients with hypothesias. Also, as we move through this, please don't hesitate, raise your hand, call me out, ask questions. I would love to be interactive if you guys have any questions or comments as we go. So this is just yet another study. 88% of patients have pain relief at one month. That's a really good number. One thing to keep in mind, gamma knife, cyber knife, they don't give you immediate results. It can take one to two months for relief, whereas surgery and some of the percutaneous procedures give you instant relief. And that one month matters. There have been multiple recorded instances of patients committing suicide in that one month latency interval. It happens and the pain is that bad, so the latency matters. And these are some Kaplan-Meier survival curves that just show you the incidence of pain recurrence. And again, gamma knife can be very effective, but it doesn't last. It gives you anywhere, again, the median, depending on which study you look at, the median interval of relief is often somewhere around two to three years, so it's not that long. So now we're escalating to percutaneous surgery. It's less invasive than MVD, also a little bit less effective. To contrast this with gamma knife, though, it does give you immediate relief for a patient that might be in crisis. It's a very good palliative option if a patient has an unresectable tumor. So you can't take the tumor out to fix the pain, but you could do a percutaneous injection. If a patient has a limited life expectancy and we don't... yes? Absolutely. So there is no gold standard or widely accepted standard of care for exactly how to manage failing medications that still have some level of efficacy, whether it's gamma knife, percutaneous procedures, or microvascular decompressions. Everybody has their own system. So for me personally, if we're doing a gamma knife procedure, I will keep them on all of their medications until they have experienced definitive pain relief from the gamma knife, and at that time I'll start to wean them off. If I'm doing an MVD surgery, that's a little different because we are removing the cause of their pain, so I'll be more aggressive in getting them off their medications. But I also don't do it the same way every time. I try to customize it for each patient because depending on how bad their pain is and what their side effects are from the meds, that impacts how quickly I basically wean them off. So again, MS is... even though it's typically with gamma knife, you can still do a percutaneous procedure to treat MS, and it is good for patients with a limited life expectancy because again, it just doesn't last as long as MVD, but it does provide you with the immediate relief. So there's different types of percutaneous surgery. The general... the gist of it is it's a needle that is advanced into the cheek up to the skull base and through a foramen in the skull base to a cistern where part of the nerve is contained, and then you can do various things from a radiofrequency rhizotomy, a balloon compression rhizotomy, or an actual chemical lysis of the nerve. But the under... the common denominator for all of these treatments is that we're damaging the nerve, just as in gamma knife, so we refer to these as ablative procedures. For a radiofrequency rhizotomy, the patient needs to be awake because they're actually commenting on burning and symptoms. For a glycerol rhizotomy, that's a chemical injection that damages the nerve. They can be asleep for that. That has the lowest incidence of hypesthesia of any intervention besides MVD. And you see here, this is an incredible number, 97% with immediate pain relief because we're damaging the nerve. Yes. That's an excellent question. So if you go into the actual ganglion of the nerve, you can treat all three distributions, V1, 2, and 3. You can also do more peripheral blocks to target a specific nerve, but generally speaking, we will do a skull base injection more proximally because you can get all three distributions. But you can do peripheral blocks to target a specific distribution. So the 97% is great, but it's so high because we're damaging the nerve, so that pain signal is going to be interrupted. But unfortunately, the trigeminal nerve is a very robust and durable nerve. If I could redesign the cranial nerves for people, I'd make other cranial nerves that are far more fragile, I'd make them as durable as the fifth nerve. But because the trigeminal nerve is so durable, you can create this damage, and then it heals, and the pain comes back. And that's very reliable. And depending on which study you look at, you can see here we have 18 months. Some of the studies are 12 months, 24 months for the when you get very high levels of recurrence because this just doesn't last as long. We're not treating the underlying problem. And again, this is just another type of damage that we can deliver to the nerve. I don't actually do this procedure, many do, but it's an inflation of a balloon that directly compresses the nerve and can cause relief through that. And depending on which evidence you believe, this is a little bit less important, but we're just talking about percutaneous damage to the nerve. You can see the efficacy is fairly comparable, but the dysesthesia and numbness is a little bit higher for glycerol rhizotomy. All right, now for the fun part. We can talk about MVD. So if medication fails and the patient can tolerate it, this is the gold standard. So you see here, 80% of patients have 10 years of relief or more. And the reason our data can't extend well beyond 10 years, one, these are older patients in general that we're operating on, and two, when patients have a brain tumor, they usually will follow up for surveillance scans. When patients have pain that has been cured, their follow-up is less reliable. So that's why most of the data sort of trickles off at 10 to 15 years. But in general, we're expecting lifelong pain relief for most people who get this operation. And again, it's less effective with MS. So I showed you this cartoon before, that's the blood vessel. This is what we're doing. We dissect the blood vessel off of the nerve, and we put a microscopic pillow there. That's it. That's the surgery. And once you put that pillow in, those pulsations are no longer transduced to the nerve, and the expectation is the pain is cured, and you get lifelong relief. So this is an operative view under the microscope. This is the fifth cranial nerve, the trigeminal nerve right here. This is the pons, and this is that loop of the SCA, which is or was compressing the entry zone for that nerve. And this little cushion is what displaces that blood vessel off the nerve. And again, this is the entire operation right here. What makes it fun for the surgeon is that it's a very delicate operation under very high magnification, but this alone is what cures their pain. Unfortunately, not every patient is perfectly typical and cut-and-dried. I see a lot of patients who have failed other therapies. So patients who have had GammaKnife, had CyberKnife, they've failed it. They've had MVDs, they've failed those. So there are studies that show a salvaged microvascular decompression after other treatment is viable and effective, but patients just need to know it's less effective than an MVD up front. So patients are going to want to know, what's the percentage chance that my pain is gone after this operation? The more perfect their symptoms are, the more perfect their MRI is, the higher the number. And we basically deduct percentage points for everything that's a little bit more atypical or a little more concerning. Because depending on how disabling the pain is, we'll mutually agree there's only a 60% chance you get better, but it's still worth it to do the operation. But the patient needs to know how likely it is that they're actually going to get relief. And again, this is just another slide showing that there is efficacy with MVD after other things have failed, but we just need to acknowledge and the patients need to be informed that that efficacy has decreased. So this is the the bottom line and the next slide is the most important one. If you take anything from the talk, I want it to be the next slide. So when we're evaluating a patient for microvascular decompression, we need typical symptoms. And typical, as we said, it actually means a certain list of symptoms. And that's the sharp, episodic, debilitating, stabbing pain. We need the MRI to show a blood vessel, because if we don't see a blood vessel on an MRI, we're not actually doing anything with the operation. And it helps, it's not essential, but it helps for a patient to have a transient response to medications. And then with subsequent failure or intolerance of those medications. So this is the diagnostic slide for trigeminal neuralgia that I am thinking of in my head every time I see a patient. It's remarkably simple, but the more diagnostic certainty we have that the vascular compression is the problem, the more certain we are that MVD is the correct and only treatment for that patient. And again, just because the vessel is there, doesn't mean it's the cause of the problems. But the more certain we are, we have to do an MVD. As we trend towards either diagnostic uncertainty, because of more atypical symptoms, no blood vessel, or a diagnosis of MS, then we do ablative procedures. Because when we don't know what's going on, simply damaging the nerve is the most likely thing to help. When we know what's going on, MVD is the way to go. Just to, yes. Yes, two comments on that. One, we have to make sure we're looking at the right MRIs, because not every center does the right MRI. I have patients that come from a lot of different locations, and the quality in the MRI is pretty variable. So there's a specific sequence I like that really shows it. So it's ultra fine cut T2. Sometimes it's called a Fiesta, doesn't have to be. And that usually shows vessels really well in the axial and coronal plane. So sometimes the vessel's there, but the MRI just isn't equipped to show it. But specifically to your point, when you see a vein, there is good evidence that shows a vein is sufficient to cause trigeminal neuralgia, and displacement of that vein, or even coagulation of it, and resection of it, is sufficient to cause relief. But that evidence is not as good as arterial compression followed by decompression. So that's a little bit more controversial. There are some people who will say, you do not take those patients to the OR, you're not going to help them. Other people say you absolutely can. So that's controversial. But there are pretty good case reports, and there is some data out there that show you can help these patients, but it's not as robust as arterial. Just to give you a sense for what we're doing, what it looks like in the OR for these patients. So this is a surgery that's always done under microscope, because you cannot visualize this nerve and this artery without a high magnification microscope. So this is my philosophy when we're doing these cases, or really any case under microscope, is comfort. You need to be comfortable, you need to be relaxed, and you can see here, this is, you want this to be like sitting in a Lazy Boy in your living room. These are fairly quick surgeries, usually 60 to 90 minutes, but still, if you're not comfortable, then you're exposing yourself and your patient to complications and misadventure. This is what the incision looks like. So here we use skull landmarks. This should be the transverse sinus, right here. The sigmoid sinus is going to follow a contour like this, and we want to stay away from that. They're highly vascular structures. If you damage them, that can be pretty morbid to the patient with a lot of blood loss. So we designed the incision and the exposure to avoid those sinuses. It's a very small incision, usually four to five centimeters. The smaller the incision, the less post-operative pain the patient has, the sooner they go home. But you can't get too cute with the incision because you need to visualize the job that you have to get done. So depending on the surgeon's experience, you may need to get bigger with the incision. But this is how we mark the patient. Right around here is where we'll create our cranial access. And this is that same patient after surgery where we put a little strip over that. What you may notice here is a little tube that's basically a headphone, a little earphone going into the ear. Because the primary risks that we talk to patients about for this operation, one is hearing loss. That risk should be well under 1%, but it is a risk. So we actually monitor hearing during the operation. And the hearing can start to fade. And that actually gives us a heads up before they have unilateral deafness where we can stop. We can let that nerve basically give it five minutes and it will actually improve. But that's a warning sign we get that hearing is about to go out. Yes? We don't do it before surgery unless the patient says they're already having hearing loss. Because if they are already having it, then it's, for lack of a better term, it's just for protection for us to say it was like that before we got there. But the expectation is that they will not lose hearing. And we can get baselines in the OR when they're asleep in any way. So we'll know if there's a deterioration. Yes? Some people use navigation. I do not. The goal of navigation, if somebody were to use it, would be to plan the craniotomy. Because you can use that to avoid the sinuses. So you can use it, but I usually will not. Yes? If the fifth wave of the VAEP is gone when you do this surgery, how does the patient fare after the operation? Is the hearing improved or is it gone? So if you lose that, then the overwhelming majority of time is the patient will wake up without hearing. Then when they wake up without hearing, it can come back. Sometimes you can put them on steroids. It's sort of like holy water. There's really no evidence that it helps. And some people will believe that that makes it more likely that the cranial nerve will heal. So it can come back. When it does, it usually comes back in some way deteriorated. If someone wakes up without hearing after the surgery, usually it's not coming back, though. So that's an excellent question. I'm going to show you, I'll answer that for you when we get to one of our anatomy slides in just a minute. But it's basically from tension on the nerve. So I'll show you in just a minute. So this is the underside of the brain. And this is the trigeminal nerve here. So what we do with our approach is we slide under the brain in this direction to access the entry zone of the trigeminal nerve. And when we get to a couple more anatomic slides, it'll be easier for me to show you why you can damage cranial nerve 7 and 8 in the approach to 5. So again, this is the same picture here. We slide in like this. And this is that SCA loop that can be sitting on the entry zone of 5. This is our approach. So it's called a retromastoid craniotomy or craniectomy. And 5 is all the way down here. To fully visualize 5, we have to put some tension on the cerebellum. Tension on the cerebellum puts tension on all of these cranial nerves. And the surgery is a balance between dissecting around these cranial nerves, because there's arachnoid bands that are stuck to them. If you dissect all of those arachnoid bands, when you put tension on the cerebellum, there's less tension on the nerves. It's also inefficient to be dissecting around all of these cranial nerves when the surgery is here. So it's a balance. But we have to go, this is cranial nerve 8. That's hearing right there. We're going in this trajectory towards 5. So if we were to bang into that nerve, if we put too much tension on it, that's how you lose hearing even though we're working on 5. Just underneath 8, which you can't really see here, is 7. So technically you could have somebody with facial weakness after this operation as well. That should almost never happen, but it's something we still counsel patients on that could happen. So for the risks of this surgery, damage to the cranial nerves here. And these are all blood vessels. We're specifically cutting and moving a blood vessel off of 5 so you can have a stroke as well from this operation. We're zoomed in a little bit more here. So this is a posterior and side view of the brain stem. These are cranial nerves coming off the brain stem. This is the 7-8 complex. They run together. And this is the 5th cranial nerve all the way in the distance. And this is a loop of that SCA that is sitting on the brain stem right there. So another view. 5th cranial nerve. We're zoomed in. And there's all kinds of compression here. I love it when I see something like this because this is going to be more fun in the OR. We've got an SCA loop here. We have the anterior inferior cerebellar artery here. And we have a vein here. So if we want to reliably give this patient pain relief, all of these blood vessels need to move. And we need to make some sort of sleeve cushion around this nerve to protect it. This is a patient, just to sort of condense all of this information, this particular patient I saw they actually didn't have trigeminal neuralgia. They had glossopharyngeal neuralgia. So you can have vascular compression and neuralgia of any of the cranial nerves that have a sensory component. And it's the same symptoms, but it's in the throat. And this is exceedingly rare. This patient lost about 30 pounds, wasn't eating, wasn't drinking. They had all kinds of electrolyte abnormalities. Nobody could figure out what it was. And as much as I would love to take credit for it, I got a consult in the electronic medical record that just went straight to my phone and said glossopharyngeal neuralgia. And it was from a hospitalist. And I figured, yeah, right. They don't even know what glossopharyngeal neuralgia is. And I saw the patient and it was, they nailed the diagnosis after a couple neurosurgeons and multiple neurologists couldn't figure out what was wrong with this patient. So it was amazing that they nailed that diagnosis. But what you can see here, this is a blood vessel. In this case, it's pica, the posterior inferior cerebellar artery. And it's completely encasing and covering the ninth cranial nerve. And what we have here is now you can see as we're slowly displacing this blood vessel away, and these are adhesions that need to be sharply cut, this is the ninth nerve coming into view. So let's hope our video works. So this is that pillow going in. And we're trying to dissect this blood vessel. And we're pushing it away from the nerve. You can see the space is getting bigger and bigger as I push that vessel down. So proximally we have space. And now distally we're working to create space. So when this patient woke up, their pain was completely gone. And they had durable, long-lasting relief. This is what the incision looks like after about two weeks. So ideally, you really won't even be able to see it. And this is another patient with the same incision. So the hair should really grow right over that, and you'll never see it. Just to condense all this information, again, the reason these patients are special to me, in neurosurgery we deal with a lot of pain. Nobody really enjoys managing pain. And the vast majority of pain in neurosurgery is sort of that 5 out of 10 annoying, gnawing pain, which can be disabling. And a win is reducing that maybe to a 2 out of 10, where it's a war of attrition. We can't eliminate the pain. We just try to better manage it for the balance of their life. Trigeminal neuralgia is a pain that blows that out of the water. I had one patient who we did an MVD, who did really well, got in a car accident and was ejected through the windshield. And she basically skinned herself alive and had crepitus and subcutaneous air throughout her body. I was actually consulted to see her for neurotrauma. She also had a fracture in her back. And she said to me, Doc, this pain is nothing compared to any of my episodes of trigeminal neuralgia. And that really made it real for me. So trigeminal neuralgia is a type of pain that is horrible. It's why it's called the suicide disease. But when properly treated in the proper patients, we can convert that into a 0 out of 10 pain for life. So that's why I really love this. It's not like we're fighting this losing war of attrition. We can actually beat this. It gets a little trickier when it's atypical pain. But these are patients that have a hard time finding someone to sympathize with them. Because when you say, oh, I have face pain, but nothing's wrong with me, nobody really understands it. And there's a lot of resistance to getting surgery for something that's a complex brain surgery for pain. So that's everything I have for this. I think I'll be talking to all of you tomorrow as well for some things you might see in the emergency department. But are there any other questions? Yes? Thank you very much for this nice lecture. I have a question about elderly patients with comorbidities and vascular compression. And would you consider them as a good candidate for SRS? Consider them what? I'm sorry? Would you consider them as a good candidate for a radiotherapy? Yes. So elderly patients, it really depends. It's a case-by-case basis. I said earlier in the talk, the oldest patient I've ever done an MVD on was 95. So if we can do the surgery in an hour with about 5 cc's of blood loss, even an elderly patient with vascular compression, an MVD may still be the right thing for them. But if it's just too much, if they're too frail, radiosurgery is an excellent option. It really is. And there's also, I don't like to get into the habit of doing radiosurgery because it's non-invasive, and then surgery if they fail, because surgery really is the better option that treats the underlying cause. But it's also possible in someone over 90, if they are just very resistant to surgery, you can start with radiosurgery and then transition to the microvascular decompression if it just definitively fails. Yes. My question is, do you consider this kind of surgery as a completion? Do you have the patients go home in the day, overnight stay, and then how long do you keep all of them post-operative? So, another great question. One area of innovation in the community of people who do this surgery a lot, there has been discussion about sending them home same day. I will never do that because if they have a bleed at the surgical site, in the posterior fossa, that can be deadly. If that happens in the hospital, we would take them back to the OR and they would be fine. If that happens at home, they could die. So, in my opinion, it's worth one night of observation in the hospital. I, knock on wood, haven't had that complication before, but I will always keep someone in the hospital overnight. And, again, there's, on post-op day one, they may have some vertigo, they may not be good on their feet. I just feel that I can control things better with one night in the hospital. Almost all patients go home the next day, but I'm not quite ready to call this an outpatient procedure. As far as follow-up, the first thing that matters is what we're going to do with their meds. So, if there's someone who couldn't tolerate the meds, I'll turn them off instantly. If there's someone who was tolerating the meds, but they were just starting to fail, I'll turn them off over the course of a two-week wean, because I don't want to pull the rug out from under them, because sometimes, even after a good surgery, you can get an attack just from manipulation of the nerve. So, I like those two weeks of protection on the meds. I'll see them at two weeks to check their incision. If they wake up well from surgery, I actually don't get any imaging. And, if they have no pain at two weeks, at that point, I tell them follow-up is optional. But, just for research purposes, I always try to check in at different intervals, so we can follow up on our outcomes. Well, thank you again for having me, and I will see you all tomorrow. Okay. So, here comes the interactive session. So, everybody get your voices ready, and opinions, and all the other things. So, those that wrote down on the note cards, we have a compilation of those, and we can discuss that if you have a comment that you would like to make, or you have additional questions about it. It's pretty much the gamut. And, I'm going to start with the question one, which was, what would you have wanted to know before you went into neurosurgery? The first answer that I pulled was quite humorous, that, and I'm not going to put this in my words, quote, unquote, surgeons are needy. For all the APPs, you know what that means. So, I feel like, from my standpoint, I've been doing this before EMR was EMR, where I worked. I was actually on paper. And, being on paper, I remember the charts being slung to me in medical records, and, you know, I would have to help my doc sign, and date, and stamp every little last thing. I think along with this comes licensing on each state, and do you require a co-signature, and does your facility require a co-signature, and does your doctor require a co-signature? I get those questions a lot, so let's talk about that for a little bit. If your state does not require a co-signature, right, do you require a co-signature? Well, then it's up to your facility. If at any point is a yes, then everything has to be signed off. If you're signing off in an EMR, and then it's going for co-signature, and then your doc holds up the co-signature, the bills are held up, and then you're probably getting the administrator after you that your bills are getting held up. So, I would understand, at your level, who requires it and why. Does anyone in the room? Let's do hands first. Who requires a co-signature on what they do? Just raise your hands. Wow. Okay. Of you, who's requiring a co-signature because of state law? Fewer. So, the ones that are requiring a co-signature that aren't state law, why is that? Does anybody want to comment? Facilities requiring it? Okay. Is it annoying to you? No. Because it's not going into your bucket. It's going to them after a while. Okay. That's good. Other part. Orders and everything else, imaging. Are you putting it in? Raise your hand if you're putting in all the orders for the doc and everything else into the sign. Yeah. And you're getting all the results, aren't you? Isn't that amazing? The work goes through you and now the work comes back to you. So, with that, I think all of this has changed what we do. Obviously, back in the day, I could say, oh, I lost your chart. I can't find it. They didn't fax your report. We don't know. There was a lot of no's. Now, it's all there for everyone to comment on. Where I work, Consul's in the back. She's PA that works with me. So, if you want to hear the dirty part of it. But I am administrator and PA in clinic. So, I see both sides and it is a hard world. I would preface anything that you do to talk to the administrator that you work with and hopefully they understand where you're coming from. The other part of surgeons being needy, I'm sure that kind of goes across the board on everything, right? We answer the questions. So, the next comment I have is that, I love this, that, you know, everybody wants an answer and that goes into the misconceptions later and are we answering all the questions for all the people and we're like the answer hub. Some people said that it was challenging more than they thought it was. Others thought that it was better than they expected being a neurosurgeon. They loved it more, which is great. Someone mentioned online startup class. There is an onboarding, little plug for this, for the SNAP course on AANS. There is an onboarding course. So, if there's anybody new to your group or you feel like you're behind maybe or subspecialties, there are online courses through AANS that hopefully you can get your employer to pay for so that they will, you kind of have a hub of all the general information. Danielle and a group are working on SNAP 2.0, which is like the more advanced. So, if you've already SNAP 1.0, then be looking for the 2.0 and it might be able to give you some more advanced content. And then, other comments were that neurosurgery is not as scary as it seems to be. I have to say for one of the ones that employs PAs or, you know, does all the interviewing and goes out and gets the whole process. I never wanted to go to neurosurgery. I've been in it 16 years, but I thought it was scary as all get out. And when I was approached for the job, I was like, yeah, right. I'm going to go over here and go into cardiovascular. That seems way more straightforward than all of this. And then I got sucked in, started the job and never left. So, I will say that it is hard. And I think during your career, you kind of have to do the work-life balance and it's really, really hard. There are some jobs that do like an eight to five. There are some shift work, but we'll be discussing that later today as well as tomorrow. Okay. So then, any comments? Yeah. I completely agree. It really bodes well if they do have that much confidence on you and lean on you. They're not going to lean on somebody they don't trust because in the end it comes back to them. Right. And I do think that early on in my career, I'm sure you felt the same. It wasn't really easy to delineate your lane because with paper charts, it was kind of everywhere and we really didn't have a good way of communicating. This is, yes, I order the test. The test comes back to me. I review the test. I determine what the next step is, if I think it is, and then check it off with the doc if I need to. So, I do think that the age of electronic medical records and what we do now does give us lanes better, but I would wholeheartedly agree that I think neurosurgical APPs are, in large part, you know, the gasoline that makes the whole thing go and the neurosurgeons know that when you're walking around you're probably gonna find a neurosurgeon Oh, you're an APP. I need one of you. I get that at all the annual meetings I need one of you, right? Do you have another one? In fact, I need some more. So if anybody would like to come work with me, that'd be great So everybody needs one and I think that's also a great thing You know to be needed as a good thing, okay any other comments Okay Danielle's up and if you come up with anything or have any other comment or anything that you want to hear back on from The audience or anything just let us know All right Question number two was what what do you wish you knew before you took your current job? Some similar sentiments as to just neurosurgery in general in general Very insight insightful comments, you're not gonna know everything Nobody knows everything you're gonna learn something new every day. I've been in this over 10 years I'm still learning new things, you know Just when you master the ICU you move to consult service when you're mastering your consults You move to outpatient when you're done with outpatient. You're in the OR and there's so many Different things in neurosurgery. I still feel like I'm learning every day. So if you're new to this don't get frustrated, you know That's why we are trying to help educate APP is because I know when I came out of school There weren't a lot of options as far as content for me to learn. I think neurosurgery in PA school for me Was maybe like one lecture like when to call for help But I didn't learn anything else about neurosurgery. So it's a lot of on-the-job training and we know that's difficult and so Look for resources events like this where you can network and get ideas from people is really helpful Very insightful though. You're not gonna know everything. Don't expect to know everything Don't be afraid to you know, call up your physician ask ask them a question if you don't know the answer Again came up neurosurgeons are needy. We know that But I agree they're very confident in your work And so they wouldn't place these responsibilities on you if they weren't confident in what you do We have termed it in some of my workspaces learned helplessness It's they know that you're gonna take care of things and so they become less and less involved But it doesn't change the fact that they are very confident in you and your abilities And so that is a compliment to us as a PPS There are a couple responses regarding clarification of responsibilities To sort of fully understand what you're getting into before you sign on to a position I too have had difficulties with this it sort of depends on the job How used to a PPS they are or you know a hospital system if you're onboarding their Credentialing they'll have an outline of all of the things, you know, you're checking 300 boxes to get your credentials, but I do find that that doesn't always Correlate with what you're actually doing on the job, you know, someone in HR is typing up responsibilities retracting skin closing wounds But maybe doesn't necessarily Capture the things that you're gonna be responsible for So how many people? Have a list of competencies Aside from you know hospital based where they just sort of list out things that a PPS can do Did anyone when they started their job to have an onboarding? Packet with tasks that you need to be signed off on before you are considered off training Oh Okay, only a couple people so if you are in management or you're onboarding or hiring people there's something That that I used to do When I was in my leadership position is a list of competencies for people who are entering the job You make it clear. These are things that you need to be able to do You need to be supervised in doing these so you're safely performing them on your own when you're signed off But that too helps clarify sort of exactly what the expectations are for your position And then when those are complete, you know Everyone's satisfied that you're properly trained and you know what you're getting into Some final comments some people mentioned Just sort of knowing how much work is involved Especially now with electronic medical records and that dreaded inbox that just fills up with results in patient questions and You know You're in a full day of clinic and then you click on your inbox and there's 47 unread messages that you have to sort of triage through so Agree, that's with EMR things are much more challenging patients can message you directly They're so kind and radiology when they read things They just push the report right through to the patients And so they read the report and then you know are concerned Because they haven't heard from you or you may not even know it's done yet And they're calling, you know five times to try and figure out what the results are. So In general, you know understanding what responsibilities you will have Whatever the setup is with you and your physician if you're ordering the study, are you interpreting the results? Are you responsible for calling the patient back? Do you have time built into your schedule to do these things? Do you have an administrative? Afternoon or an administrative day where you can catch up on your charting catch up on all of your inbox items important things to think about when you're looking for jobs That's really it anyone have any comments or anything to add Okay Okay, so her question is do you have someone else in your practice that helps you triage these items Whether it be an MA or a nurse or someone who's calling patients back So if you do, can you raise your hand? All right, good number Okay, we're on to question number three misconceptions a lot to do with questions One is a surgeon is needed to answer your questions. Don't we get all of that, right? I think that Comes With the territory and it does kind of wax and wane depending on the delivery, but it also is dependent I feel like on the relationship you have with your physicians and how much your physicians speak about you There are ways to do clinic I find it a stark difference between when I do clinic with physicians because where we are people get third fourth opinions So we actually see the Patients with the physician and do the majority of the work and then we bill it under us But if I go over that patient with a physician and I give them all the information and they walk in and say hey I spoke with Alice and she said you have X Y & Z and you've already done this and I've been looking at your MRI This is what I think. Is that all accurate? That's a different approach to that and gives me more I think it lays the foundation for respect to that APP different than if they walk in. They're like, hey, what you doing here? How'd you get here? What's going on? And it's like what did I do all that work? Didn't you listen to me didn't you know? So and then they've and then the patient feels like they're doing double work and saying it all over again And why were you even here and you weren't even needed? So I think that is one simple way of getting across that you can have those questions and you can have those answers Same difference at the end of the visit or in other instances. So then there were other comments on That we answer all questions for everything how many feel like that they are a primary care provider at times Like I have a stomach bug what can I do for it my foot hurts what's this, you know? Oh my it it's everything and like not me not me not me. That's why I went to neurosurgery I remember the last day in my general rotations for PA school and the person brought like a Plastic bag on the counter for all their medications and I looked at that bag and I was like subspecialty subspecialty subspecialty Because they were asking about every medication there was another primary doctor that I did a rotation for that literally at the front It said you're allowed to have two Complaints today if you have more than two complaints today in different areas you have to come back tomorrow And I was like, oh wow, that's but yes, I mean it just balloons up so we can't have answers to everything and I think the way that you frame that with a patient or even the Way you answer some things in the very beginning can maybe lay the foundation for that Okay, you tell me if you feel like jumping in Daniel, okay One of these other comments was great two of these are more of administrative and liking Independence versus extension of the neurosurgeon and what's better. So let's raise our hands if we feel like we're an extender Nobody do we know what extension of the physician nobody everyone is independence Okay, raise your hand if you're independence Compared to the physician We got a lot of people in between apparently Or completely reliant. I don't know Okay, so From a PA perspective we've gone on from I don't know if you've heard the big terminology change with a PA and some other things but it's not no longer going to be physician assistant, but physician associate and One part of that is what does that mean? And I think that's part of a patient world as well, right? How do they deem us? Are we in lieu of or are we in extension? Are we independent? Let's raise our hands if we have our own clinic Okay in your own clinic are you seeing spine Yes, are you seeing brain and no spine Excellent any okay, how about functional like purely functional and not You know, okay So there is those different worlds of The independence and I think that's probably dependent upon your physician and right your administrator which gets the next comment Some administrators don't understand scope or capabilities Let's raise our hands if we feel like we are our administrators understand our scope and our capabilities Do do understand? Or barely half maybe So something that you can You know ask for in your institution is a person above you, you know, usually in the world of Union or Academic medicine you have to have someone that's clinical above a clinical person In other institutions or other facilities, you can have somebody above you That's actually not clinical and then that can bode a little poorly on if they understand your role But we can discuss that again tomorrow at our luncheon anything Anyone wants to ask or have any comments on Yeah I And so knowing what my role is my scope in New York specifically We've been able to really get me stuck Where there are patients? I have no idea And I think that you've been my best advocate for You know my administration So if you can do that for yourself I Completely agree and for the first one where you're like the PCP because they don't come back right there Just come they're only coming to you because they had some massive something happen And otherwise, they're gonna be non-compliant on the other things because they don't have a mode in some institutions There are some liaisons that will help and get those patients back But it is very very difficult and a lot of those stroke patients are in that They wouldn't have been to the doctor had that not happened And I've seen many patients from other countries saying I saw another day that said listen We don't go to the doctor in my country unless something is horribly wrong And so she hadn't had any preventative care in decades, and she hadn't had it You know so it's just not the norm as to where we are so yeah They get to you And you have a lot of and thank you for doing what you do right because if you weren't the advocate for them nobody Potentially could be Yes physicians are your best advocate and your relationship with your physician is your best source to come to solutions about Everything and I think that probably I would say if you're here in this room You're most likely paid for by your employer right in some capacity or another meaning that they support you and they understand that so that Just bodes well for the people in the room as it is You're already supported in this the people that aren't able to come because of CME money That's been pulled away, or they'll say we don't have anything for you. You'd have to pay I think that's that's where they don't see your value, but the people in this room I feel like you know the majority of you. I would say they understand your value, and there's no questions about that Oh I'm sorry just because I'm a PA. I usually have an NP with me that says NP and all of the other things Yeah, it's equally distributed, and we'll do the hands you know from an administrator perspective Neurocritical care units in stroke is a lot of the majority is nurse practitioners in the OR the majority is usually the PAs And there's a mix everywhere else So that's usually kind of the neurosurgical yes, but we'll raise hands nurse practitioners PAs oh We're about 50-50. Yeah, that's excellent. Which is practically the world of what we live in I think a lot of other Worlds are more PA or NP dominated and the lovely part of neurosurgery is we get a mix of everything right we get babies and Adults and benign and malignant and nurse practitioners and PAs working together Okay the last subset of just sort of general questions, and we had a few questions regarding APP specific conferences or content Yeah hard to find I think in general, but the AANS has really invested a lot of time And funds into building what we think is a subset. That's sort of Overlooked sometimes and so just so you guys are aware. There is an APP We have termed it from cranial to spine APP only conference AANS does this once a year. It's looking to be late September, and it will be virtual this year So that's coming up That's a great mixture of topics. We tried to hit on you know a lot of the big stuff trauma spine tumor so that's coming up and then the AANS also has a large online offering SNAP modules, there's a lot of onboarding if you're new to neurosurgery We're currently working on a SNAP 2.0 which is going to be more advanced surgical technique surgical videos surgical Explanations so even if you know if you're in the OR great and that will be helpful to you But if you're in the office or not in the OR you're still taking care of these patients and understanding There'll be sort of condensed videos that show you the highlights of surgery the risks of surgery the benefits So things that you can go through with your patients wherever you are in the hospital in the office whether or not you're in the operating Room, so that's ongoing and hopefully will be launched Maybe later this year a lot of people had questions on how you can become more involved as a member We can obviously speak to the double ANS We're always looking for APPs We have many different Aspects throughout the double ANS that have APPs involved We have educational committees And subcommittees we have committees that are building out these educational offerings We have conferences if you want to if you're interested in speaking Obviously this subset at the double ANS for the physicians And then also the APP only conference is coming up in September So if you have any interest, please stop by talk to us. We're here today We'll be at the luncheon tomorrow, and we'll be here all day tomorrow As well, so we'd love to have you guys if you're interested And there's a lot of other things that aren't as visible as just a conference that we love to have APP input for We always try to like get with the content figuring out Who's attending the annual meeting versus our other content so can you raise your hand if you're in your first one year? Awesome okay first five years Okay and beyond five years and Then beyond I'm sorry hold on up to like ten years Okay, and then beyond ten years Okay interesting a mix we used to always have like the ones that were like Five years plus ten years plus at this meeting and not the ones that were less So we just need to make sure that we're providing enough content that kind of spans all of that we have Probably about five minutes before the next lecture Maybe actually four according to our little scheme But if you want to take a quick break run to the restroom whatever you need to do And then we will have lunch break after our next lecture. Thank you I Know Yeah, it's electronic records like you can't escape it's like every time I walk away You Great, well, I'm just here, I'm just after Jefferson, so. Yeah. Hello. How are you? Good, how are you? How are you? Thanks, thanks. I'm moving, so we're only, I can't show it to you. I work at Jefferson. I'm, there's staffing company, but yeah. He's probably here by chance. I'm sure he'll track me down. Good to see you. Good to see you. All right, are we ready to get started? All right, we're gonna move forward with our next speaker. We have Dr. Laxton here. He is an associate professor at Wake Forest University. He is the director of functional neurosurgery and specializes in cranial neurosurgery, including neuro-oncology, epilepsy, trigeminal neuralgia, and deep brain stimulation. We also have one of his PAs here, Caitlin. Hello, everybody. So, it's great to be here. Thanks for the invitation. Caitlin and I have worked closely together for five years now, and I think it's a key part of our practice that our team is doing well, if our patients are gonna do well. And so, what I'm gonna talk to you today about how do you, what do we do, how do we do that. Hopefully, that'll have some relevance for you in the context of functional neurosurgery, which is my subspecialty. And so, we're gonna talk about functional teams, meaning we are functional and we work well together, and the topic, of course, is functional neurosurgery. And so, we don't just work together, we thrive together. So, I hope at the end of this presentation, you'll have a better understanding of functional neurosurgery and a better understanding of how, through collaboration and cooperation, the complementary roles of the neurosurgeon and the APP can optimize our patients' outcomes in functional neurosurgery. So, what is functional neurosurgery? So, it's that subspecialty which is concerned with stereotactic and physiological techniques, including framing, or framed and frameless stereotactic systems, stereotactic radiosurgery, electrical recording, and electrical stimulation for localization and treatment of target structures in the central and peripheral nervous system, and the surgical alteration of the nervous system to treat neurological disease. So, big mouthful, but I think some people don't actually fully understand what it is. That is a detailed but very accurate description of what we would call stereotactic and functional neurosurgery, which brings up, what's stereotactic? So, here is another wordy definition, but again, very accurate, involving, being, utilizing, or used in a surgical technique for precisely directing the tip of a delicate instrument or beam of radiation or other energy in three planes using coordinates provided by imaging in order to reach a specific area in the body, okay? And of course, we use stereotactic techniques in spine surgery now. We use stereotactic techniques in oncology, right? In tumor surgery, it's a core part of neurosurgery, but certainly, the functional neurosurgeon, that's what we've spent a long time trying to perfect. So, we can't just be close. We need to be incredibly accurate with where we're trying to use our techniques, and we'll talk about DBS in a little while. So, precise targeted surgical techniques modifying neurophysiological function to treat neurological disorders. For Caitlin and I, our practice involves movement disorders, epilepsy, trigeminal neuralgia, and neuro-oncology. Other functional practices, and I know we're a big general group here, but for those of you who maybe are in a functional practice or maybe gonna be joining one, they're all different, just as even every spine practice is different. But other functional practices can include pain, pediatrics, trauma, neurovascular stroke, and spine. And so, our functional practice involves a lot of DBS, a lot of laser surgery, right? So, MRI-guided laser interstitial thermal therapy, stereo EEG, right? And I think Dr. McConn talked a little bit about that. Stereotactic radiosurgery is actually the thing I probably do the most, and craniotomy is the thing I do second most. So, that's our practice, but other functional practices are gonna be very different. Although I was trained in spinal cord stimulation, I don't do that anymore. So, but other practices have a huge role in spinal cord stimulation, and APPs may have a huge role in managing those patients. Intrathecal pain pumps, baclofen pumps, high-intensity focused ultrasound, spinal surgery, and other forms of stereotactic radiosurgery, right? So, some places have CyberKnife, some places have ZAPx, maybe others, right? Other types of LINAC systems. So, the key principles of our collaboration, and really these are the key things, I guess, of any successful collaboration, is mutual trust and respect, open communication, right? Empathic, patient-centered care. And I should just say, everything I'm talking about, they're interrelated, they depend on one another. It's hard to have one without the other, but really they're the fundamental essentials of a good collaborative team of APPs and neurosurgeons. So, clinical excellence, right? So, we can't do any of this other stuff if we're not having and desire to have fantastic outcomes for patients and continually working to improve those. And that also means knowledge, right? So, do we have the knowledge, do we have the technology, do we have the skill sets to provide optimal outcomes for patients clinically? Professional standards and ethics, and all sorts of domains, and all domains. But, you know, there's a lot of pressures in medicine and in surgery. The only thing we should be thinking when we're seeing a patient is, do we have treatments, do we have management options that will help this patient, right? So, we're not trying to fill our days, we're not trying to put our numbers up. The only thing that's in our mind is, what's happening with this patient, what could help them? Are we able to provide that? And that's the key part in my mind for professional standards and ethics. And then continuing medical education, how can we do any of this other stuff if we don't continually strive to do better and to improve? And so, you guys are all great examples of that right today. And then, of course, a team-based approach. So, we all are gonna have roles, we don't wanna double up, we don't wanna, you know, do everybody doing the same thing. No, we wanna maximize what we're accomplishing. And again, going back to dialogue and communication, are we doing that, is your skill set being used, is my skill set being used? Are we unnecessarily duplicating things? And how are we integrated with others? Medicine's incredibly complex, it's multi, multi teams of multiple, multiple people, and it's the integration of those teams that optimizes our patients' outcomes, again. So, how do we optimize that? So, in terms of little more nuts and bolts of what we do as a team, we have review and triage of referrals, clinic evaluation and management plan, we have the management or the procedure, we have post-operative care, early and in-house and outpatient, and then the ongoing follow-up. So, for review and triage, can we help this patient, right? We were just talking, you know, somebody comes with their big bag and talks about their toe pain and everything else. Yes, our patients are complex, they have lots of issues, but we're a highly sub-specialized practice, right? And so, you have to acknowledge that, and for those appropriate patients, we're gonna have excellent therapies for them. So, we look at that, and then if we think, yeah, this is a problem we can help them with, do we have the information we need? Do we have the labs, the imaging? And if we don't, how are we gonna get that? And again, that's coordination amongst ourselves, it's coordination amongst our nurse navigators, our schedulers, our other team members, to make sure that happens, because if a patient shows up in clinic and none of this stuff is there, that's a waste of everybody's time. And then, how quickly should this patient be seen? Maybe they need to be seen today or tomorrow, maybe they can be seen in a couple of weeks or even, you know, several weeks. So, we have to make those decisions. So, in clinic, the way we divide up things is Caitlin generally goes in and initially meets the patient and gets a good sense of what's going on, what's their level of functioning, what are their problems, and then I'll be reviewing imaging, I'll get the story from Caitlin, and I'll sort of formulate an assessment and a plan. And then, how is that all documented? How are the insurance issues sorted out and kept clearly in mind? It's not just annoying when insurance issues arise, right? It's negatively impacting patient's health. So, we need to be really proactive and be on top of that ahead of time. How can we minimize denials? How can we make it smooth and streamlined, the process for a patient who desperately needs our help to get that help, right? And so, we have to be very explicit in addressing those things. And then, once we've got this plan in place, that patient's gonna need, and their family, likely is gonna need prep and support for the treatment and for the next steps involved. So, for the management, maybe that's just observation. Maybe they don't need surgery right now. Maybe they need radiosurgery. Maybe they need some type of surgery, open resections, other types of minimally invasive procedures. Maybe they've had imaging and they need their shunt reprogrammed. Maybe they've had their DBS already and they might need DBS programming. In some practices that you work in, you might be quite responsible for that. In our particular practice, the PAs in neurology take care of a lot of that in association with their neurologist. But at a minimum, you need to know how to program it and what's involved, if only to interrogate what's their setting right now, right? So, there are at least three commonly used systems. And so, if you're in a practice or in a referral zone that uses all three of them, you should have some familiarity with that. And where is the equipment? Who has it? Do we know how to use it? These are crucial, crucial issues because everybody will call you, right? So, cardiac surgeons doing a procedure, they notice this bump in the patient's chest and they have questions and they wanna know about how to turn it off and can they use cautery and all this. So, you need to be really aware of what's going on with your patients. In our particular practice, we don't use a lot of medication management. Our practice is focused on surgery. Other practices might have a big medication component. But even in ours, it essentially doesn't involve medication. You're gonna need to know about our core neurosurgical meds, right? Decadron, epilepsy medicine, pain medicine. What if they have an infection? What are we doing for antibiotics? And then there might be procedures that are actually happening in clinic, right? So, sutures, dealing with wound issues, aspirating pseudomeningoceles possibly, LPs. And so, that's all part of our practice. The early post-operative care, that's Caitlin and I walking around the hospital and seeing these patients. So, exams, wound checks, looking at any imaging as relevant to this patient. Are they gonna need PT, OT, speech? Do they need referrals to other people? What's the timing on that? Do they need to see them in-house or can that be outpatient? And then, dispo planning, right? So, is this somebody who's gonna go home today? Are they gonna go home at some point? Are they gonna need to go to a rehab center? Are they gonna need to go to a skilled nursing facility? How do we facilitate all that stuff to make it as efficient as possible for patients? And then all that involves orders and documentation. How is that getting organized? Who's doing it? How is this integrated with, in my case, residents and fellows who are in my teaching hospital? And that's another important relationship and dynamic that we all have to navigate. And so, as an outpatient, we may be checking on them or our nurse navigators may be checking on them. How are you doing in the first couple of weeks? They'll be coming back for wound checks and suture staple removals. There may be imaging to review in that sort of four to six week period. Did all the appropriate referrals happen? Was this a tumor patient? They need to see HEMOC. They need to see RADOC. Who else do they need to see? Do they need more follow-up with the epilepsy team or the neurology team for their seizures or for other things? Do they have other comorbidities? And they have their other chronic pain management that needs to be ongoing. Patients often will need and ask about back to work. Can I go back to work? What are my restrictions? Do I need documentation for that? Who's gonna do that? Is that gonna be me? Is that gonna be an APP? Is that gonna be our nurse navigator? All of these things are important. And then what's the next follow-up for that person? So at that time, say we're at six months down the road, we're probably obviously getting a clinical update. We're possibly looking at imaging, depending on what the issues are. And maybe we're always redeveloping and reassessing the plan and then arranging more follow-up. So in terms of our team, our schedule is integrated and separate. And so on Mondays, I'm in the OR. Caitlin's in an independent clinic, right? She's seeing a lot of my follow-ups, but she's also seeing other neurosurgeon's patients. And that's something we continue to work on. How can she see and her practice be sort of exclusively in our domain and less so in other domains? Other people's preference may be to remain completely general in their independent practice and only sort of focused on that team again when you're working with the neurosurgeon. Tuesdays, she and I do Gamma Knife. And later in the day, we have admin and meetings that we attend. Sometimes those are different, sometimes those are the same. As a team, my Tuesday is meeting with the epilepsy team, meeting with the DBS team, meeting with the oncology team for Brain Tumor Board. Does it make sense for you to go with your neurosurgeon to these? Is that a good use of your time or is that a waste of time? Is that informative, educational for you, or is that just delaying you getting important paperwork or other stuff done? And so that's a good point of discussion, right? Should you be attending, should you not? And if not, what else are you doing? Wednesdays, we have our big combined clinic day where we're working together in clinic. Thursdays, again, I'm back in the OR and Caitlin has her independent clinic. And then Fridays, I do Gamma Knife. Sometimes she may be involved in that. We also have a morning clinic, so she'll get that started and then I'll come up and do the clinic. And then we have admin and meetings on that day. So put that schedule out there just for you to think about, is my schedule optimized? Do I like my schedule? Do I like my week? Do I think of, oh God, Monday. What can we do to make it not an, oh God, Monday? It's like, oh great, here we go, let's do it. I feel valued, I feel like I'm doing good work. My patients are getting great outcomes. I like my coworkers. That's, I think, a big part of it. Obviously, first and foremost, an effective functioning team's about patient outcomes, but it's also about our own job satisfaction, our own life satisfaction. So let's get into a little bit of the specific topic of functional. And so again, going back to clinical excellence, we can only provide excellent care if we understand what clinical domain we're working on. And so the most common movement disorder conditions we treat in functional, and certainly in my practice, are Parkinson's disease and essential tremor, and to some extent dystonia, although much less frequently than I treat the other two conditions. And so the Parkinson's is characterized by tremor at rest, right, that's at low frequency, sometimes described as pill rolling. You can have a mixed component, that is, when they try to do something, they might have a tremor, but in general, their tremor might actually stop when they try to do something, and it's only present at rest. And it can be unilateral, especially in the beginning. Rigidity, slow movements, bradykinesia, postural instability, shuffling or festinating gait, and difficulty with transitioning movements, all very classic. Decreased emotional expression, classically described as masked faces. A quiet voice or hypophonia. Parkinson's patients often have pain, okay, so that's a very key feature, not always discussed, but they often have pain. And in addition to their medication, levodopa, our DBS can actually improve that, too. And we may wanna look at other types of conformations, so what are called DAT scans, which is a nuclear medicine scan looking at stridal uptake of dopamine. So again, our patient's medication is managed, and the majority of their care is managed by their neurologist, but we have to have some understanding of their medications that they're on, right? So they're on levodopa and a mix of medications to decrease the rapidity at which that levodopa is metabolized and useless, right? So that's what Sinemet is about. That's what some of these other drugs are for, as well as drugs that are just supposed to increase dopaminergic activity. And so that's what they're on. And so in terms of essential tremor, this is not the same tremor as Parkinson's disease, so this is an action tremor. When they're trying to do something, that's when you see it, and it's very debilitating because whatever they're trying to do, it's derailed by this tremor. Now, everybody has a little bit of tremor, and so what happens with these patients is they sort of bear with it for many, many years until it's just so debilitating, and that's when they see us. The other sort of sad part about that is it's really, I think, poorly understood that we have surgical treatments that can eliminate tremor, like just eliminate it, and I think, unfortunately, there's a lot of patients that suffer needlessly with this condition, and this is one of the most satisfying areas of a functional neurosurgery practice, certainly one of my most satisfying. I agree with the earlier speaker. Doing MVD surgery and curing somebody's facial pain is incredibly rewarding. Equally, though, is eliminating somebody's tremor because tremor is incredibly debilitating, and that's what essential tremor is. It can affect the trunk, it can affect the head, it can affect the voice. It can be made worse with caffeine and stress, and it can be improved with alcohol. You'll have some of these patients who actually become alcoholic, so you have to, that becomes part of the management issue, and it can run in families, and it can, as I say, get worse over time. These patients are often older. So there is medical management, and part of that is just reducing their triggers. Propranolol and primidone are two of the medications, but they're really not very effective in general, not even in the ballpark of the medication management for Parkinson's disease. So they still just suffer in general, and they might take this medicine, and the medicine can have side effects. Eventually, though, if the tremor becomes debilitating enough, they come and see us. The issue for Parkinson's patients, when their medication is actually effective, is that they have other issues. So what they're getting is this effectiveness is becoming less effective and for shorter periods of time. So these are on-off motor fluctuations. As they require higher and higher doses, they can get levodopa-induced dyskinesias and abnormal movements that are disabling. And then they can also have disinhibition and hallucinations as side effects of the medication, and so they need alternatives. And so these include ablative techniques, radiofrequency ablation, stereotactic radiosurgery, focused ultrasound, and deep brain stimulation. And so with deep brain stimulation, some of you are probably involved in this, and others may not be, but a DBS lead is placed in a specific target in the brain, or a circuit, we think of this as a circuit therapy, to intervene in a particular function. Obviously, in movement disorders, that's motor function. And so we can see here the globus pallidus, or the subthalamic nucleus, are the common targets for DBS in Parkinson's disease. And so what do we treat typically today? So the two most common things are Parkinson's and tremor, and dystonia to a lesser extent, epilepsy becoming a bigger and bigger part of my practice now. It's, in the last few years, that's been FDA approved, and this can be an excellent option for epilepsy, certain epilepsy patients. So who are the best candidates for this? They're actually medication responsive, and so again, going back to that clinical excellence stuff, that's kind of counterintuitive to say, right? So I'm getting surgery because my medication's effective? That doesn't make sense. Well, it's effective, at least initially, but in the ways that we just described, it's becoming less effective, okay? So the things that medication doesn't help, and never has helped in a Parkinson's patient, let's say, those are the things you have to counsel the patient on, that DBS is not very likely to help them either, okay? And so understanding that is important into accurately counseling patients. DBS is excellent for tremor. It just eliminates tremor. And so those are good candidates. Patients who have these levodopa-induced dyskinesia is a great candidate, and essentially, particularly in the tremor patients, essential tremor patients, anybody whose quality of life is impaired because of their movement disorder are a potential candidate. So patients in the Parkinson's group who have this Parkinson's Plus, they don't have idiopathic Parkinson's disease, they're not good candidates. Patients who've never had any response to medication, with the one important exception, and that is even if a PD patient's tremor doesn't improve with their Sinemet, it might improve with DBS. So that's a really, really important thing. And so if they have moderate to severe dementia, there may not be a good candidate. Severe psychiatric comorbidities and poor family and social support. Those are all probably not good signs. DBS is not a come in, we do your thing, and see you later, right? It's huge workup, lots of visits. It's a two-stage surgery. It's lots of follow-up visits, optimizing stimulation programming, et cetera, et cetera. So if you don't have the support to get through that really, really big process, you're probably gonna struggle. And maybe there are alternatives that might be more feasible for you. So timing of DBS surgery. When I first started, the family would wheel the poor patient in, slumped over in a wheelchair, and like, can you do something? Well, you know, that's the end stage, severe, severe Parkinson's disease. We've really lost our window to help them. Now we think, you know, much, much earlier, there's even studies that show within the first two years of diagnosis, depending on that person's particular clinical course, they may benefit from DBS. So we like to apply it much earlier than we once thought. And we're able to help all of these things very well, the dyskinesias, the tremor, the rigidity, slowness of movements, and gait, but this is in a decreasing level in that list. And so gait is the thing that seems least responsive to DBS. And knowing and having a flavor of that is very important when you see these patients in clinic. Because if they're saying, oh, the only thing is my gait, it's never been helped by medication, and it's terrible, and I'm having falls, you need to talk to them about expectations, and this may not help them in the way that they hope. And so what are the targets and movement disorders? Subthalamic nucleus, globus pallidus, and thalamus. STN-DBS improves the cardinal features of Parkinson's, and it is able to achieve the greatest reductions in med doses. And that can be very important for people if they're having side effects to their medication. It might influence our target choice. GPI-DBS is the other important target. And so also good at treating the cardinal features, and it's particularly effective at reducing dyskinesias. It's the target, in fact, for dystonia, and it has a very direct anti-dyskinetic effect. The effect STN-DBS has is you can reduce the dyskinesias by reducing the medication dosage, but GPI can have a direct anti-dyskinetic effect, which might be relevant for a particular patient. So STN versus GPI, how do you choose? Who gets what? So the best evidence we have, in fact, shows them to be pretty equal in their effectiveness for Parkinson's disease. However, as our practices have evolved, really, we tend to favor STN. And it's just, we see the clearest and earliest, especially improvements in tremor, after STN-DBS. And we may favor GPI when dyskinesias or dysktonia are a prominent feature for the patient, or when the patient has psychiatric comorbidities. We call it a sort of a cleaner target than STN. So with thalamic DBS, we're treating tremor. And so this is the target for essential tremor, but also perhaps somebody has a Parkinsonian tremor, and you may choose a thalamic target for one reason or another. Perhaps if you're using an ablative technique for whatever reason, whether that's focused ultrasound or radio surgery, or for MS tremor. And so, as I mentioned, for dystonia, we would favor the GPI. So what happens during the surgery? So I have to plan the case. So in our particular practice, that's me. I don't know if any of you are involved in that sort of thing, if you have that as part of your practice. Certainly there is variability as to who's involved in treatment planning. In some teams, it's the neurology team that's doing it. But I'd say mostly it's the neurosurgeon, plus minus an APP. And so that happens. And then of course, we have to do the frame placement and have the intraoperative. So that may be something that an APP is assisting with. That may be something that an APP and a resident does together. In my practice, that's something I do with residents. So understanding and knowing frames and understanding the issues around frame placement, though, I'd say is crucial knowledge for an APP in a functional practice, for sure. And then we have the prepping for surgery. Again, here's a resident doing that. That might be an APP. That could be you. Or it could be you working with a resident. And as you've sort of been seeing here, I use a CRW frame. Other practices, and maybe your practice uses other techniques. So there's a huge host of ways to get DBS leads where they need to be, or other stereotactic procedures done appropriately. And I would say, even if you're not in the OR, if you're part of a functional team, or whatever team you're part of, you should know the techniques and the technology that is being used, okay? Because there are specific issues that relate to them, and the patients may have questions about them. And so you're a more valuable resource to your patients if you understand all these nuances of your practice. So here's a patient, and here's a full view of ROR, right? And so you see all sorts of people, nurses, residents, anesthesiologists, nurse anesthetists, physiologists, neurologists, other types of residents, and obviously neurosurgeons. Maybe you, maybe you're helping the neurologists, maybe you're helping with the actual procedure. And so in our particular practice, we do awake DBS surgery, although I do asleep DBS surgery as well. The patient, not me. And so with awake surgery, I'm recording neurons, right? I'm doing microelectrode recording. And so here's an example of that's how we start things off. In my OR, I work collaboratively with my neurologist too. Some ORs, that doesn't happen. It would be me or some other physiologist doing that work. So we work very closely together, and we're measuring neuronal activity right here. And so in my OR, my OR is my lab. So I'm also doing cognitive neuroscience in my OR. So here's one of my research collaborators, and here's a patient who's actually doing a task while we're recording their neurons. And we're actually recording fluctuating neurotransmitter levels in their striatum during this. And so now you might not even be involved in consenting them for this procedure, this part of the procedure, but if they're doing it, they're definitely gonna have questions about it. So you may be very involved or you may not be involved at all. But if you're working in a practice that has this kind of a thing, we're doing research in the OR, we're doing research in the epilepsy monitoring unit, you should at least have a very working knowledge of what's going on because your patients are gonna ask you. Okay, after that first DBS implantation, we then move to the second stage, which is the implantation of the internal pulse generator. And so that's a much shorter operation, happened three weeks after, when they've healed from the first surgery. And that's when we're connecting that DBS lead to the programmable power source. So they heal up from that, and then they get back in our practice to their neurology team, PA and a neurologist, to begin initial programming of their DBS. And so again, you may be more or less involved in that as an APP, but a working knowledge of DBS programming is important. And then with every condition, we like to talk about our great outcomes and why we're doing this, but we also have to be aware of our complications. And so this is something that the APPs often manage and something we need to be aware of. And it's also something we need to counsel our patients about, right? So in DBS, we have hemorrhages, seizures, infection, wound healing issues, potentially neurocognitive issues, pain, we have hardware technical issues, and we can have treatment failure. So why is that? Is the lead in the right place? Is it not in the right place? Is it just disease progression? And so we need to work with our patients on all of these things potentially. So I'll quickly talk about epilepsy, another big part of our functional practice. And it's a common condition with a third of patients not being helped by their medication, and those people are surgical treatment options. And we talked about stimulation for movement disorders. There's a lot of good stimulation options for epilepsy as well, including anterior nucleus thalamus, DBS. There's something called responsive neurostimulation, or RNS, or Neuropace, and which is a closed-loop system where we're putting electrodes in the brain that record activity and then provide stimulation based on those recordings. And then, of course, the much older vagus nerve stimulation. There's increasing evidence for the effectiveness of all of these therapies. We looked at what DBS looks like. This is what RNS looks like. This time, the internal pulse generator that's in the chest in DBS is in the skull in RNS. And so managing these patients, you need to be aware of these differences. The surgery's different. And so with VNS, IPG's back in the chest, but now we've got incisions in the neck, and that's a coil electrode around the left vagus nerve. So one of the more common conditions we treat is medial temporal lobe epilepsy. And we've established with outstanding studies that there are great treatments for that, specifically temporal lobectomy. And we achieve far superior outcomes in terms of seizure freedom with surgery versus ongoing medication. And so around 60% of patients who get a temporal lobectomy are gonna get seizure freedom. And so, and that greatly enhances their quality of life as well. And so unfortunately, that is very heavily underutilized and has been forever. And so why aren't patients getting the treatment? It's because they're afraid of it, right? Everybody's afraid of brain surgery, and these patients are suffering instead of getting surgery. So over the last 10 years, a much less invasive way to do this surgery has developed, which is MRI-guided laser interstitial thermotherapy. And so instead of a larger incision, we're talking, I don't even shave patients for lit anymore. They have a quarter-inch incision, and you can't even see it from day one. And so the important thing, though, of course, we're not doing it just for, so they don't have to have their head shaved, is that it works. And again, accumulating evidence that around 60% of these patients are achieving seizure freedom. It's in the realm, 50 to 60, and that's in the realm of an open resection. And upwards of 80% of patients are getting outstanding outcomes where they either have no seizures or have a rare seizure. And so again, we need to be aware of potential adverse effects of that. But they're much, much less than open surgery, and patients love it. So that everybody I see with this condition, I present both options. And I have to say, it's actually been several years since I did a temporal lobectomy because everybody opts for this. And so there are many other applications of lit in epilepsy as well. And so this sort of emerging effectiveness has been acknowledged and reported by the American Society for Stereotactic and Functional Neurosurgery in a position statement a couple years ago. And so there's two companies. We talked about the three companies in DBS, two companies in lit, which is Monteros NeuroBlade and Monteros Visualize. Your center may use both, may use one or the other. I think having a working knowledge of them is very important. This is an example of a lit case for a medial temporal lobe epilepsy. And you can see with this straight laser probe, we're able to achieve a very good ablation of the medial temporal lobe amygdala hippocampus. And this is an example of somebody who's seizure-free. Now I think we're at seven years. I won't talk too much about trigeminal neuralgia. Very common condition. This is a core part of our practice. You heard about the features, severe disabling pain, the suicide disease. And so although there are medication options, important to know that opioids are not one of them, right? So we talked about these anti-epileptic drugs. So that's one good thing is if you're on a functional APP neurosurgeon team and you see somebody coming in with opioids, if it's for their facial pain, that's probably a bad thing and we need to help them get out of that trap. And so for the many people who fail those treatments, there are the surgical options. And you heard about those earlier. In addition to MVDs, I do a lot of gamma knife for trigeminal neuralgia. And so this is an area where Kaitlyn and I work together. And so one of the issues you do is frame application, right? And so here she and I are recently in the gamma knife unit putting a frame on. This is one of our very kind colleagues who would sit there and we weren't actually doing it to her, don't worry. But yeah, so that's what it looks like though nonetheless. So that's our Tuesday mornings. We're putting, we probably have five or so patients that we're putting through this treatment for various things, trigeminal neuralgia being one of them. And so once the frame's on, they get their imaging, we do the treatment planning, they go in for treatment and another part of the team, a physicist, right? So Kaitlyn needs to know them. We all need to know each other and work closely together. As we talked about, you don't get immediate pain relief. You get pretty good outcomes initially but there is a high risk of recurrence. And so in our practice, Kaitlyn is the one who follows up with them. I don't even arrange to see them for four months because it's a delay to effectiveness. So she'll see them. If at four months they don't have pain or if they still have a bit of pain or they're still on the medication, we may let them wait a little bit longer. And when it gets to six months, if they haven't really seen pain relief or sufficient pain relief, that's when we start to reevaluate. Have we got the right diagnosis? Are there other options for them? What else do we need to do? What other treatments do we need? Should we just go with an MVD? Should they get Gamma Knife again? These are the questions. So basically the collaboration essentials are understanding the condition, understanding the management, the roles pre, intra, and post-operatively, and how that is all coordinated. So one big thing I think within an APP neurosurgeon, team in neurosurgery, is all of us have to have flexibility. So I'm the Director of Stereotactic and Functional Neurosurgery. I have a functional practice. Caitlin and I are on this functional team. The number one thing we treat is brain tumors. So you may be on a team where the number one thing they treat is degenerative spine disease. So we have to be flexible. There's on-call issues, brain trauma, hemorrhage, subdural hematomas, hydrocephalus, abscess. Caitlin often has clinics where she's treating other neurosurgeons, not only my patients. So this might be a spine surgeon. This might be a pediatric neurosurgeon. So although we are focused and we are a functional team, there is some need to be able to understand and manage these other conditions within neurosurgery. There may be imaging follow-up. In general, Caitlin will look at imaging, but in our team practice, I will always sort of give the last word in terms of what I think the imaging is showing and what that means for our management plan. And so that's where we communicate and discuss. If the patient's had imaging for, and they've got a previous shunt, Caitlin might need to reprogram the shunt and put it back to its proper settings. And there may be wound care issues in all kinds of ways. So for the team to work effectively, there needs to be continuous reevaluation and optimization. So are the patient's needs being met? Are our roles effective? Are there new practice patterns that are either being inflicted upon us or that we are recognizing as this would be an improvement? And are there new therapeutic options we need to be aware of and maybe to integrate? I think to remain engaged and excited about our professions, we need ongoing professional development. And the better we feel as individuals, the better we work as teams. So that's mentoring trainees, attending courses, teaching courses, doing research, knowing the literature and adding to the literature, remaining open about new ways of doing things, technologies, therapies, and also possibly taking on new roles and responsibilities and being open to innovation. So innovate, let's make things better. Let's acknowledge what we're doing well, but let's try to identify where could we improve. And so for optimizing of team dynamics, first and foremost, are we optimizing patient care? Is our team effective? Are we actually accomplishing the whole purpose of what we're doing? And we need to talk about that. Are we enhancing, optimizing each other's career and life goals? I don't know if that sounds like above and beyond, not my opinion. If we're not helping each other achieve what we wanna achieve as individuals and as a group, then that's a problem. So let's work together and try to make sure that happens. There's been times when Caitlin's practice has veered into areas where she was not wanting it to go into. We're supposed to be a functional team. Why am I seeing only PEDS patients right now? Because she's really good and people can kind of try to capitalize on that. So we've had to identify what are the patterns that are making things go in a direction neither of us want. A nuts and bolts issue was that for whatever reason, some of the schedulers were booking all my followups with me and everybody else's followups with her. So we just had to say, no, no, that's not gonna happen anymore. So she sees my followups, right? And so these kinds of things, it's not just sitting there suffering. It's having a good discussion, good open communication to first identify and then figure out ways we might be able to fix it. And so yeah, so that goes with are we happy? Let's talk about it, open dialogues. And again, respectful communication keys. And when it all clicks, these are some patient comments we've had over the past six months. So Dr. Laxton has an amazing team. They are wonderful, right? Thank you. Dr. Laxton and the team were absolutely the best, right? I will be forever grateful. Caitlin is wonderful. We feel confident in her ability and expertise. Love her, right? That's what we all want. We wanna do our best for our patients and we love it if they feel we have done our best for them. And so functional is an incredibly fascinating clinical area and you can have a hugely positive therapeutic impact for patients. And I think that optimal APP neurosurgeon collaboration is essential for achieving that optimal patient care. And here's our big functional team at Wake Forest and thank you for your time. And happy to answer any questions. Yes. Dr. Rourke, he is an assistant professor at the University of Colorado. He serves as the director of inpatient neurosurgery also at the University of Colorado and the associate director of the department's residency training program. He has extensive training in all treatment modalities for the full spectrum of cerebrovascular disease. This includes ischemic stroke, intra and extracranial stenosis, cerebral aneurysms and vascular malformations. He's gonna talk to us this afternoon about vascular vignette with imaging. Thank you. That's a large crowd I hear. That's good. I'd rather be the first one after lunch than the last one before lunch. So we're totally fine. Let's see here. How do I advance? No. Sure. There we go. Awesome. All right, disclosures. I used to say sadly I have none but I'm the PI for the embolized trial which is just middle meningeal artery embolization. No direct funds from that. The way I'm gonna break it up today is I'm really just gonna do three kind of case examples from vascular neurosurgery and then go through some of the imaging, talk about some of the pertinent literature. At the end of the day, these are, any of these could be multi-hour presentations so this will be more of the high-level overview. If you have questions, feel free to interrupt. So we'll jump right into it. Case one, 53-year-old male presents with an NIH of 10 and the symptoms are consistent with right hemisphere dysfunction. So his left face and arm, base arm and leg are weak. He's got stuttering symptoms. The leg weakness has been maybe clumsy for a few days, not quite sure. Technically, what the stroke gave him was a wake-up stroke so his last known normal was the night before and they did a CTA and a CT perfusion and it showed occlusion of the right ICA and the right MCA. There was a small core infarct with a big penumbra and so at that point, we think as vascular neurosurgeons, there's a lot of brain potentially to save. The problem is those words that I said where I mentioned occlusion of two different vessels and this is not the picture we want to see when we start a thrombectomy case. Like this is miserable. And then just a preview, once you can get by that lovely occlusion and then get a picture that looks like this where this is the carotid coming up and that's where the middle cerebral artery should be and it's just a nice big blank space. Same thing there. There should be a whole bunch of blood vessels right there. So what I'm really talking about is the concept of a tandem lesion and so what is a tandem lesion? It's defined as a severe stenosis or occlusion of the cervical internal carotid artery and then an intracranial large vessel occlusion, usually the middle cerebral artery. In the ESCAPE trial, there were about 16% of the patients presented with a tandem occlusion and in other series, there's 10 to 15%. So this is not an uncommon presentation and again, like the worst words the stroke neurologist can tell us on the phone is, oh, the carotid's out too and then you start to think because when they say the carotid's out too, there's a lot of things that go through your mind. Okay, is it a dissection? Is it atherosclerosis? Do I need to stent? Do I stent now, stent later? Should I use a balloon? Stent first? Should I stent second? Should I refasterize the brain first? I don't know, time's brain. Can I get there? Embolic protection, balloon guide, shuttle. Are they on hospice? Can I just not do this? Which carotid stent should I use? Other stents. There's that Zilver thing that goes in the biliary system. I can use that, whatever. Can I drag a stent through a new stent? That seems dumb. Okay, how about an aspiration catheter? What if the wire doesn't cross? I'll use that wire, that wire, that wire, that wire. And then can I use a stent to deliver a carotid stent? I don't even know. And then why didn't I go into banking? Because they don't do these things ever, and no one dies. Thankfully, we have the guidance of our predecessors who write articles with titles like this, lack of consensus among stroke experts, which is good and bad, because at the end of the day, you can kind of do a whole lot of things, because we don't really know what the best management of these are, okay? We try at our institution to be flexible and deal with what we get. The big divide in tandem lesions is, they talk about, do you open the carotid first or the head first? And again, we tend to think, if I can get through the carotid lesion and get the blood, the clot out of the MCA and allow the brain to maybe give collaterals to itself while I work on the carotid, that's great. In practice, if you have someone with one of these, that has rarely been the case for me, that I can get anything large enough to work in the head without first fixing the carotid. And the whole thing with carotid occlusions, it's kind of, if you're gonna boil it down to like, what is the thing here? And the thing is, do you stent now or stent later? And the reason for that is because if you stent, you then need to put them on a bunch of antiplatelet medications. And so then, a lot of these patients have had TPA. So now you're talking about TPA, where if you look in the TPA guidelines, if you give them TPA, you got about 24 hours where you're not supposed to give them any antiplatelets, any anticoagulants. And now you're talking about dropping the stent, loading them with aspirin, Berlinta, Plavix. So that's the thing. And so what I did in a talk I gave about this a few years ago is I just went through literature and looked for what are the hemorrhagic complications. And so there's several studies out there, and I'm gonna try not to bore you, but there's just, I made the point in points in red. But so there was a 2018 study that had about 400 patients. And in that study, about 2 1⁄3 of them had IV lytics, 2 1⁄3 of them were stented, 2 1⁄3 of them had antiplatelet therapy, and they're symptomatic, that SICH, it's all over our literature in vascular, is symptomatic intracranial hemorrhage, 5.3%, which is very in line with people who don't get stented. There was a study by Nolan. Now theirs, they had a little higher rate, but that tended to be the outlier of the studies that I had found. A nice set of studies from this group in 2018, they had between the two groups, over 300 patients with stents in the acute setting, and they had between a five and a 9% symptomatic intracranial hemorrhage rate. So it's not as if you're taking these people by any evidence base up to like, oh, there's a flip of a coin chance that they're gonna bleed, it's not that high. This was one more study where they just, they had 45 patients that they stented, they looked at their rate, it was 4 1⁄2%. This is the last study I will hit you with. The interesting thing I thought about this study was they looked at their 600 patients in a registry overall, and then they had a subset of when a stent was used. At the end of the day, the outcomes were basically the same. There was a trend towards an improved outcome with carotid artery stent that wasn't significant. There were actually a little few, just a tiny bit less of the intracranial hemorrhage rate. The favorable outcome rate was about the same, 50 versus 53%, and the mortality was about the same. There's not data out there that says, oh, this is the worst thing you could do for a human being. It's really fairly equivalent if you just look on a population level. This is just the regression analysis where they looked at the predictors of successful reperfusion and a good outcome. I think some of these are truisms, like, hey, if you're younger, you'll have a better outcome. If your stroke is smaller, you'll have a better outcome. Things like this, I don't, it's good to know, but at the end of the day, they tell us things I think that we already know. Just because I don't wanna only bore you with slides, we'll show you, you know, odd pictures of angiograms. This is kind of a typical flame shape where the carotid is out. Here's the common carotid. There's the normal external branching pattern, and then the internal just flames out. You actually don't see any intracranial perfusion. This is after I had gotten through that, and so I've kind of burrowed my way through that at this point. I haven't put a stent in yet, and I'm just doing pictures to see what's going on in the head, and you can see that there's branches that are out and there's branches that are missing, okay? So on this patient, I couldn't get anything large enough by to fix without getting a stent in, so we placed a stent, and then at this point, I did a Dyna-CT to make sure there wasn't any bleeding, and then we revascularized the head, so, and that, again, for this one, I had to stent the neck first. If I could have gotten all the way there without the stent, I would have done it. I'm gonna stop, because this is the end of case one. Are there any thoughts, questions, concerns about tandem lesions? Cool. Case two. So, 75-year-old female. She has two weeks of right eye pain, progressed to double vision. Felt like a sinus infection. Pain progressed to her right temple, and so she went to the doctor. They sent her to the ED, and at that time, the eye's moving normally. She's been a smoker for about 25 years, no family history of aneurysms. A long time ago, she had been told, you have hypertension, you need to take medicine, but she didn't enjoy the way she felt on it, so she's untreated hypertensive. No weakness, numbness, or complaints, aside from this double vision. And her eye didn't really hurt by the time she was seen. But it's really difficult to keep it open, so she has an eye that is not terribly open, and it's not moving well. She had a bunch of imaging. The first one I'll show you, this may be a subtle finding. It's one of those where you look, and it's like, oh, things kind of generally look okay, and then once you see it, you kind of can't unsee it, where she's like, hey, that thing on the right is not the same as what's going on on the left. So what does that lead to? People like me, taking catheters and doing more pictures. So what we have is a partially thrombosed, cavernous carotid aneurysm. And so this is the filling part of the aneurysm. The aneurysm that you saw in the MR is actually more like this. She actually has this incidental little anterior caroidal artery aneurysm at the time. It's up in the communicating segment. And so we tried to figure out what to do with this, and we're kind of looking at the pictures. These are the 3D reconstructions. So you can see this. There's the partially thrombosed. That's the filling portion of the cavernous aneurysm. She's got this thing up here. And one of the things, as a neurosurgeon, that we know is that those aneurysms in the supraclinoid area, they can touch the third nerve. And so the question is, in general, if you see somebody with a large aneurysm and a small aneurysm, it's the large aneurysm that caused the problem, right? If someone shows up with diffused subarachnoid hemorrhage, a 13 millimeter ACOM aneurysm, and a three millimeter MCA, it's the ACOM that ruptured most likely, okay? But this one, we were a little suspicious. So we decided to do an MRI with one of those little KISS sequences that the other guys used to look at cranial nerves. And lo and behold, this is the third nerve, and this is the aneurysm denting it right there. And there it is. So this is the bottom of the aneurysm. I'm not smart enough to make videos on, I wish, I'm sorry, I could have made you a video. But trust me, that dot, that is the tip of that aneurysm denting right into the third nerve. So what we decided to do with her was, the fix for the big aneurysm is a flow diverting stent. So then we get to talk about all the antiplatelet stuff I was just talking about, and what can you not do on dual antiplatelets, clip an aneurysm. So our thought was, hey, this is physically touching the nerve that isn't working, let's go clip this. If her third nerve gets better, cool, we'll come back and address the other thing later. If her third nerve does not get better, within a week or two, make sure she does well from surgery, and then we'll fix the larger aneurysm. So her third nerve got better. So this was a good one, because we actually thought about what we were doing, it didn't just fix the giant aneurysm. It was denting the third nerve, absolutely as expected. And she had relatively immediate improvement, not resolution, but relatively immediate improvement of her third nerve palsy, which was really fun. And then I think I'm seeing her in a week to treat the cavernous thing, as long as she's doing well. That leads me into just a very brief, again, high level overview about third nerve palsies. So when we think about the symptoms of a third nerve palsy, we're talking about ptosis, diplopia, pupillary dysfunction, and ophthalmoplegia. When we think about the differential for these, it's kind of two broad buckets. There's the non-pupil sparing and pupil sparing, right? So the non-pupil sparing is your pupil is large, it does not work. We think about things that cause pressure on the third nerve. So we're talking tumors like Clival meningiomas. Then we think about vascular things like PCOM aneurysms, Basler tip aneurysms, uncle herniation, everybody knows that one. Somebody has a blown pupil, that's because the third nerve's getting smashed by the uncus. And then you think about cavernous sinus lesions. A lot of cavernous sinus lesions, if they're causing the third nerve palsy, they could be causing a lot of other cranial neuropathies as well. So you start to think about not an isolated third nerve, but you see the fourth, V1, V2, things like that. There's the pupil sparing, which that's not necessarily the neurosurgical world. It ends up being the neurovascular world sometimes when you're dealing with athero or giant cell arteritis. But those are things like diabetic neuropathy and myasthenia, okay? Specifically to dial in on aneurysms and third nerve palsies, the most common is the posterior communicating artery. So to be fair, the first time I looked at this when I was doing the aneurysm, I'm like, oh, it's a PCOM. And as you look closer and closer, it's like, oh, no, the vessels coming out of it are clearly going where the choroidal goes. But so about 25% of brain aneurysms are PCOMs. They're a very common location to rupture. And it's also the most common location to cause a third nerve palsy. There are some studies out there that cranial nerve three palsies can be seen in up to 20% of patients with PCOM aneurysms. Next, since that was this case, is the anterior choroidal artery. It's actually, anterior choroidal artery aneurysms are only about two to 5%. They're a very small slice of intracranial aneurysms. And the best I could find in the literature is about 3% of cranial nerve three palsies are caused by anterior choroidal aneurysms. Cavernous aneurysms, that's a very small, less than 1.5% of all intracranial aneurysms and an extremely small slice of pure third nerve palsies. The controversy, because who doesn't want to talk about controversy in this is do we clip them or do we coil them? That's a fun rabbit hole to go down if you have no life like me, but there's a shocking preponderance. I know this will shock all of you, but when you look at most neurosurgical journals, the papers published would strongly imply that clipping is a lot better than coiling. And then when you look in the radiology journals, there's a whole lot of papers that say that coiling is just as good, if not better than clipping. I mean, there was one paper where they literally quoted with coiling a zero to 100% rate of improvement in the literature. I don't even know what to do with that number. What you tend to see is I do think there is good arguments for clipping these when you could go either way because the idea is people think it's part mass effect, part pulsations, and clipping really takes care of both of those. If you pack an aneurysm with coils, you are doing nothing to improve the mass effect of that. Full disclosure, I coil PCOM aneurysms and I've coiled PCOM aneurysms with third nerve palsies and a good amount of them get better. So I don't think we really understand exactly what's going on with all of these. I'll say the PCOM, it's a nice place to coil. It also has a fairly high recurrence rate. Like when I think about the aneurysms that I've coiled that I have to retreat, PCOMs and basilar tips, they're right up there. I do still think it's better that basilar tips are coiled because of all of the thalamoperforators and everything going on and the lack of surgical experience. But just when you coil a basilar tip, you're telling the patient like, there's a good chance this is gonna recur and we're gonna have to put more coils in. And it's kind of become the same with a PCOM. You can get nice results and flow diverters are helping with the PCOM. And flow diverters may also change the way we can treat aneurysms that cause third nerve palsies in the sense that if you can, there are people out there who are putting a flow diverter over the PCOM origin and then loosely packing it with coils so that ideally you're not putting a bunch of mass effect on the nerve, you're getting rid of the pulsation artifact. So we'll have to see with time what happens there. But the general agreement I would say, whether you like to clip, like to coil, whatever, is that the time from onset of symptoms is inversely correlated with a good recovery. If somebody shows up either in the office or in the ED and they've had a third nerve palsy for several weeks, it's gonna take a long time and it may not get better. So those are the people where we're saying, the damage may already be done, but we should still fix this because it may have grown acutely and that's why you have this. And also the people who present with a complete palsy don't tend to get the recovery that those with an incomplete palsy. So that's really that. Any thoughts about third nerves? Yes. In terms of the use of it and the role of the mass effect, do you change the orthographic epidermic with extending for an L? Not with her. No, we did, you know, she got our institutional policy, not institutional, typically with anesthesia, they get tenodecadron with induction of anesthesia and we do kind of four Q6 after for a few days in a rapid taper. We don't, we didn't extend it for her. Also because she showed pretty quick improvement. It's like, okay, I think we got the problem fixed, so. Thank you. Yes. When you've got a patient who's anterior. I just did it in this case because I didn't I was concerned that there was kind of a red herring. I think the giant cavernous aneurysm for her was the red herring and it almost was more because we're academics like well we should probably investigate this. I if I'm being honest I was gonna go explore that aneurysm anyway but I kind of wanted to know I mean if it had shown that it was clearly pointing the other way okay maybe. The problem is just when I knew if you know you're gonna put a flow diverter in I mean and I I know that the the new pipeline you can stop the second antiplatelet agent after three days but in our institution we're still really not doing that yet so if I put a flow diverter in somebody that's six months of dual antiplatelet therapy and so I'm kind of committing them to really no intracranial procedures and so with this one I had kind of a low threshold I was ready to explore it anyway and we kind of just wanted to see we wanted to see if we were right and see if that's what we were going to be looking for if that makes sense. Yes sir. I'd say 15-20 percent I mean it's it's not I mean if you think but not of all my aneurysms so if you think you know if PCOM is about 25% of the aneurysms and then about 15 or 20 percent of those I mean this is not an everyday thing where we're dealing with someone with a third nerve palsy we end up seeing it you know every couple of months something like that. Yeah. Cavernous carotid aneurysms basically have to be coiled and I there was a time my chairman was Dr. Haynes who he's kind of the doubt he's the doubting Thomas of neurosurgery he's mystery evidence he wrote the evidence-based medicine in neurosurgery textbook it's that thick which I gave him a hard time about but I drank his Kool-Aid I got a master's in clinical research at his urging and I love the man but we he talks about the days when a lot of cavernous sinus surgery was done and it was very bloody it was very unsatisfying for the people who did it. This is an aneurysm that has truly been revolutionized by flow diverters I mean the pipeline stent for cavernous carotid aneurysms I mean it works over 90% of the time it is a 20-minute case and within 6 to 18 months with these aneurysms you have a normal angiogram I mean it's really that it's that's actually what it was like the FDA indication is for aneurysms in this low in that location so that this is perfect for a flow diverting stent because there's no great surgical option for this you know cool questions you guys are actually listening nice I said glad I didn't catch it before lunch all right last case I talk fast so I'm probably gonna be done early so I'm sorry last case 69 year old female brought to the ED by an ambulance one hour status post onset of upper extremity weakness in the left apraxia her NIH is 3 okay past medical history is hypertension she's had basal cell carcinoma and she used to smoke non contrast head CT was negative for any acute process so in your minds what are you thinking is coming next there's probably TPA things like that these are her pertinent labs and vitals I put the blood pressure in red because if you're starting to think that someone needs TPA that number can't be you have to drop that a little bit I'm not gonna give you a slide about the TPA inclusion criteria because they're very strict they're very rigorous I just finished call this morning after a week on call and I think two days ago we got TPA in somebody because five minutes before their window ended they confirmed the last known well and like had it been six minutes later that patient would not have gotten TPA there's they're very strict with the inclusion criteria patient got an MRI showed that little thing right side no thing and then there's her crowded the patient's crowded Doppler so it's stenosed a lot of Dopplers get done I like CTAs because since I do stroke most of the patients I end up treating have CTAs just gives me more information about where the lesion is relative the jaw things like that so what what you see here is that is calcific plaque this is the common carotid there's the bifurcation there's a post stenotic dilatation right there so this is what we would call symptomatic carotid artery stenosis when we think about that we start to think okay what to do plaque morphology so what are the characteristics that can increase your risk of symptoms if you see these ulceration intraplaque hemorrhage obviously an intracranial embolus okay so we're gonna talk a lot about an asset which was kind of a landmark trial done for this way back in the day I do want to go a little bit beyond that and tell you some of the stuff we've learned since NASA about some of the subgroups but in NASA the medical group if they had a high-grade stenosis with no ulceration they had a 17% to your stroke risk if they had that if they had an ulceration there was a 30% risk when we think also about stroke we think about who are the high-risk groups for having repeat events so we think about older age men people who present with a stroke are more likely to have another stroke than those who simply present with a TIA and people who only present with ocular symptoms are actually less likely to have a stroke than either of those two okay we think about the time since the last event and then irregular plaque morphology and this is another one where the trials we have have shown a reasonably good correlation between the percent of stenosis and the risk of stroke this is a heat map for men and I'll do it there the next slide is for women and I just think it's nice because well it breaks it into age groups so this is young so less than 65 65 74 75 plus and then we have the different types of presenting symptoms so ocular TIA and stroke and that's for each one and what you tend to see is as you get older with more aggressive symptom presentation this is your percent risk of stroke in a couple years and the reason I like the heat map is because I specifically like to compare the male to the female one and so we see a lot more green a lot lower percent risk of stroke in the female side than in the male side still obviously if you present with a stroke with an ulcerated irregular plaque that is highly stenotic you're at a high risk of having a stroke okay so just the quick recap of NASA it was done in the mid 80s randomized prospective multi-center trials published in 91 they did endarterectomy versus medical management in patients with symptomatic carotid disease okay there have been a lot if you if you want to think about a condition neurosurgeons treat that has been studied well by good quality evidence and good quality trials look no further than carotid stenosis because there's a lot of randomized trials a lot of large cooperative studies have been done to look at symptomatic and asymptomatic stenosis and our direct me and stenting in this one patients who had had a hemispheric retinal TIA or a non-disabling stroke within the last 120 days if they had carotid stenosis from 30 to 99 percent they were randomizing the medical arms and surgical arm which was everybody got medical therapy and then surgical arm got an endarterectomy they found first patients with severe stenosis which they determined they said was 70 to 99 percent that trial was actually stopped early because of the significant benefit so at two year the risk of an ipsilateral stroke was 9 percent in the surgical group it was 26 percent in the medical group so that's a number needed to treat of six to prevent a disabling stroke okay actually there was a more benefit seen for endarterectomy in patients over 75 years of age that has borne out also when you compare endarterectomy to stenting and I'll get to that in just a bit moderate stenosis is where things I don't want to say they get more murky but I mean for the most part if you have a patient with symptomatic high-grade stenosis you're not thinking about if you're going to treat them unless they're near the end of their life or have other things you're largely about how you're going to treat them when you get into moderate stenosis this is where there's a little more nuance because the benefits are they're not quite as robust as they are with severe stenosis so NASA had about 850 patients who had moderate stenosis that's 50 to 69 percent I'm not gonna waste a slide on it if you have less than 50% stenosis none of these trials said that you should get a surgical intervention so the five-year risk of ipsilateral stroke for moderate stenosis was 22 in the medical group and 15 or almost 16 in the surgical group so now we're getting into a number need to treat of 15 to prevent one one you know major stroke it's hard to because if you look at this is over five years now and you're talking about roughly 6% reduction over five years you're about a percent per year if you have patients who are getting older or more frail they start to think about these numbers and they're like I don't know if I want to go through that for a 1% less risk per year and that that becomes kind of just a discussion between you and your patient I will say that men did better than women within our direct me there's actually a lot of medical studies across specialties that men tend to get a lot of better outcomes with different types of interventions and there's not a lot of good theories as to why but for this one it was this was striking that for moderate stenosis the number needed to treat in men to prove it was 12 it was 67 in women now women had a lower risk of five-year stroke in the medical arm it was 15% for them and 25% for men and again more benefit in the elderly sorry I just had a thought that then left me so apologize we'll switch to stenting there have been a bunch of trials with stenting and I'm not gonna bore you to death with all of them crest is the one I'll talk about what time what time am I done okay for a minute I thought I had to sorry so the crest trial was randomized and this is this is stenting versus endarterectomy and so they had symptomatic stenosis and they also had some asymptomatic but the primary endpoint was peri procedural stroke am I or death okay if you read the abstract of crest it says there's no difference between the two they're equivalent in their primary endpoints so when you dig into the data which is fine that's what we're supposed to do you'll see that the peri procedural stroke protection was better in the endarterectomy group there were more peri procedural myocardial infarctions in the endarterectomy group but there were more strokes in the stenting group and so we have this balance where overall the risks kind of evened out some of the critiques of the trial were that they included as a myocardial infarction people who had asymptomatic troponin leaks and so be like well you're kind of you're holding us to a different standard if you if you look at some of the things published afterwards even patients who had that asymptomatic leak they had a higher mortality in two years so there is reason to include it but the quality of life was actually affected by a peri procedural stroke overall in the study whereas the peri procedural mi was not what this has really led to is that I think in the vast majority of practices where you have both the technical ability to stent or to do endarterectomies like a lot of academic centers like it's really an endarterectomy first it's like an opt-in to endarterectomy because it's got better stroke protection and some people like I was trained I did my fellowship at University of Michigan and Dr. Thompson he does all of his endarterectomies awake because like he says he's Irish he has the gift of gab and he chats with him the whole time but he also they it kind of takes away that increased mi risk from general anesthesia I have yet to do on awake since fellowship because I always tell people I can do this awake or asleep and I have yet to have someone choose awake he just tells them I do this awake so but also stenting the complication rate for stenting goes way up as you age there's pretty good data that really if they're over 75 they actually do much better with endarterectomy so again if you have that equipoise where you think you could stent or do the endart the endart is typically preferred the other thing I wanted to note and I don't have it on a slide but I thought this was very interesting the big problem with the trials now it's just how old they are medical management is completely it is improved quite a bit since those trials were done and so somebody way back in the several years ago they did a study where they looked at the event rate of the medical arm in these trials before and after the year 2000 and so the stroke rate before 2000 was about 2.3 per hundred patient year of life and after 2000 it was one and that's just in the medical arm so what we know is that medical therapy has gotten a lot better and I think that is I'm not going to dive into asymptomatics but that has really cut into the indications for asymptomatic carotid endarterectomy or carotid repair I should say but I just do think that the big issue the big the biggest thing I tell my patients when I'm talking about these surgeries is these are the best level of evidence they're fantastically done trials they were finished when I was in high school like they are these trials are old because I'm getting old and that's the problem and that's what we don't know there's new trials where they're trying to do it and like crest to there's taking a long time to enroll so discussion for this one again she had an acute ischemic stroke to be TPA eligible let's get that blood pressure on 185 MRI she had small right hemispheric infarcts that then the timing of intervention is always missing because there's there's this kind of general thing of like well you got to get it done within 14 days that really only applies to endarterectomy but it does apply so if you look about a little over 10% of people who have their kind of first stroke their index event if you will about over 10% are gonna have another stroke within two weeks and so what it really comes down to is that your your risk reduction is much better if you get that CEA done within two weeks so it's about 30% in two weeks if you go two to four weeks to 17% one to three months it's 11% then this is counterbalanced by the fact that there's good evidence that your rate of periprocedural stroke which like I said diminishes quality of life is actually much higher if you stent early so if you stent within a week they tend to think you could have a three time a threefold increase in your risk of periprocedural stroke if you stent within two weeks it could be two so a lot of people would argue that if you need to do an acute intervention on somebody and they can get an endarterectomy that's what they should get because the actual risks are just higher when you stent somebody early the other thing to consider though that you have to consider excuse me when you're talking about decision-making is is the endarterectomy technically feasible so we think about a high lesion that gets behind the jawline we can't get up there very well if they have prior radiation to the neck they've had prior surgery on that carotid even if somebody has had an ACDF you know you're I think in my practice I actually send those patients to ENT to get scoped to make sure they don't have an asymptomatic unilateral local cord paralysis so if someone has had surgery already then that makes the their scar tissue it makes the dissection more difficult radiation because I deal with those also when they have carotid blowouts a radiated vessel can fall apart in front of you that's unpleasant you have to think of the technique and this is very institution specific of how you assess perfusion dr. Thompson's way is leave him awake put a rubber ducky in their other hand and every five minutes they squeeze the ducky in here and you know they're following commands and can move and when they stop squeezing the ducky they get their shunt other people do SSEP EEG a lot of vascular surgeons really like stump pressures and then you think about antiplatelets heparin different things that you use in the operating room none of those are really none of those usually are germane to your decision about what to do and that's it so and that was the third case so any questions concerns comments thank you it's okay it's okay I have a question so wait we're doing it by table or by individuals at the table individuals at the table okay so we'll definitely need some help spotting people as those hands go up and yes I was tasked to put this this talk together about spine jeopardy and it was a little more complicated than I first planned just to get a get a sense of the room at University of Miami we work with a lot of a PPS both nurse practitioners NPAs could I just get a sense of kind of where everybody's coming from could NPS raise their hands okay okay and PA is raise your hands okay so it is pretty even evenly matched that's a good thing for today and then the next question is does anybody spend time in the OR raise your hands oh a lot of people that's great okay and then are most people hospital-based raise your hands okay and what about just clinic based okay great so there's definitely gonna be some things from all of those places in in this spine jeopardy today so and some of the things you may have to dig back or use chat GBT to quickly figure out so I see some phones you know in front of everybody there so don't think we didn't see that that's that's okay though there's there's no rules here okay anybody want to start us off don't be shy yes okay let's go some of these are pretty easy and then some of them we'll see how it goes let's go degenerative conditions with a question mark because most of them are degenerative conditions but there are some some things that may take you by surprise here so let's go DGN conditions for 100 okay I'm seeing something different here you Okay. Perfect. So I guess I'll work it maybe backwards here. Okay. That's fine. Okay. So first question. Degenerative conditions for 100. I see a hand up in the back. Yep. Let's see. Who's up next? Okay. I saw that gentleman's hand go right up. S1. Yeah. The only choice, okay. All right. We got 100 points on the board. Okay. You want to decide on which one goes next? Trauma for 500. Oh, wow. Okay. Here we go. So this one has a little bit of words in here, and it is multiple choice on the left. So I'm going to read it, okay? And this is trauma, but all of them have a question mark next to those things because it may be something different. So a 65-year-old male comes to the hospital after a motor vehicle accident complaining of neck and back pain. Further questioning reveals that the patient has a history of chronic neck ache in the morning with back stiffness. He also admits to having mild dysphagia with the sensation of a lump in the throat. Initial x-rays show significant vertebral osteophyte formation but are otherwise negative. Hip x-rays show normal hip and pelvis joints with no fractures. What is the patient's most likely diagnosis? In the back. Next person. You're going to have to help me out here. I think it was right up front here. Right up front. Dish. Yes. Absolutely. So Dish, they admit to morning stiffness, chronic axial neck pain, the sensation of a lump in the throat with dysphagia, and this is Dish gives you the formation of osteophytes and spares the SI joints. So all those things help point to Dish. And just as a point, these bridging osteophytes with Dish do not provide added stability. Okay. Go ahead and pick the next one. Trauma, 400. I'm seeing a theme here. Okay. A C6, spinal cord injury patient experiences hypotension bradycardia. Name and explain the mechanism of the syndrome. You back there. Okay. I'll take that one. Do you know the mechanism? For an extra ‑‑ sorry. Some of these questions have second order questions on them. If you get the second part, we'll give you extra points. An extra 100 points. Impairs the sympathetics? I like it. Good. So that was 400 plus an extra 100. So 500 points. So here we called it neurogenic shock, but autonomic dysreflexia, it's kind of a subset of that. Okay. Go ahead and pick the next one. Trauma for 300. Okay. So which of the following statements about high dose methyl prednisolone protocol for use in spinal cord injury is false? False. Which one is false? No hands yet. Oh, okay. Got it. Okay. So A ‑‑ remember, there is swag on the line, so feel free to come up closer. A, administration should not be undertaken greater than eight hours after the injury. B, some of the apparent benefit of methyl prednisolone may have been the result of patients recovering from steroid‑induced myopathy. C, an almost equal number of studies have shown a benefit from employing the protocol as have shown a lack of benefit. Or D, risk of high dose methyl prednisolone involves sepsis, pneumonia, GI bleeding and deleterious effects of elevated blood glucose. Again, this is for false. Which one is false? Sorry, which one was first? Yep. Correct. Next person. Yep. Right there. C. Correct. Okay. So everything else was true, but the benefit initially demonstrated could ‑‑ that's supposed to be could, not count, but could not be replicated in any other study encountered in a meta‑analysis of the literature. Okay. So go ahead and pick the next one. Tumors for 500. 500, you said? Wow. Very impressed with everybody. Okay. Okay. A 65‑year‑old Japanese male comes to your office complaining of not being able to keep objects in his hands and dropping things. Your exam is positive for bilateral Hoffman's, hyperreflexia, weakness in his hand muscles, cervical MRI with central canal stenosis and cervical dynamic X‑rays are normal. Careful analysis of MRI indicates a hypo‑intense signal on T1 and T2 lining the posterior side of the vertebral body at C3‑5 with sparing of the disk space. What is the most likely diagnosis? Those are the letters on the left there. The gentleman. Which one was that? D. You are correct. Okay. So segmental OPLL or just OPLL, and it's calcified lesions are hypo‑intense on T1 and T2. Obviously most of the time we're getting a CT to get a better sense of what the bones look like. There's obviously a higher incidence in the Japanese population. Because the area behind the disk was spared, this type of OPLL is classified as segmental. There's a couple of different types of categories of OPLL as we can see here. One is flowing and continuous here, segmental as it was in this question, mixed where you can see a little bit of both, and then this other type. Okay. Would you like to pick the next one, sir? Any category 500. Okay. Imaging is very close to my mouse, so I'm going to take it. What is this? What are the treatment options? I'll take it. Treatment options for extra points. Okay. And another set of additional points, if you can name another one. No, as far as treatment options. You got the diagnosis, right‑sided synovial cyst. Okay. Okay. Well, we're here with a bunch of neurosurgeons, so we're going to decompress first, usually in our line of thinking. But no, you're absolutely right, that is one option. And then one of the last options that I'll bring up is just a cyst ablation. So sometimes if you have a very good interventionalist, people can go in and try and aspirate or try and ablate the cyst itself, and it's usually not a permanent solution. So decompressing that cyst is usually our first line of attack. If it recurs or the patient, you know, generates some instability at that level, then absolutely we do fuse. Okay. So definitely give you 600 points for that one. Okay. And go ahead and pick the next one. Anatomy for 500. Everything else is going to be easy for you guys after this. Okay. Compression of the nerve root in the neural frame and most often results from hypertrophy of which articulating process? I'm sorry, which one? Yes. Yes. Which one? Okay. We'll go to the next person. »» Superior. »» Yes. Superior articulating process. Okay. All right. I'm going to pick the next category. »» Anatomy 400. »» Anatomy 400. Okay. How can one differentiate an L5 radiculopathy versus common perineal nerve injury on exam? »» On exam, they're able to invert. »» Okay. What would you see with which one? »» If L5 is intact, they're able to invert. If it's not, they're unable to invert. »» So if L5 is intact, they are able to invert. »» Yes. »» Correct. So if you have an L5 radiculopathy, you'll have difficulty with foot inversion. And if you have a common perineal nerve injury, you will have difficulty with eversion. Okay. Go ahead and pick the next category. Imaging for 400. Okay. Sagittal T1 weighted with gadolinium contrast. What is this? What lab value is best to follow? What is the most common etiology? So you can get extra points for this one. Yep, right here up front. Yes. Okay. Do you know which one is more sensitive? But you already named one of them. Yep. And do you know what the most common etiology for the third bonus points? Or second bonus points on top of the original? Oh, as far as what bug? Okay. There we go. Staph or strep. So yes, what we were looking at was C6-7 dischitis vertebral osteomyelitis. There was ventral epidural abscess with spinal cord compression there. We usually follow C-reactive protein to see if our antibiotics are effectively working. And, again, the most common etiologies are grant-positive organisms, such as staph, aureus, and strep. So that was you did 400 for imaging. So that was four. So you got 500. Perfect. Okay. Next up. Oh, really? Okay. Look alive. There's a lot of the board open. So just raise your hand if you have a choice in there. You can't go wrong. Okay, go ahead. Clinical for five. Describe the typical findings of an intradural dorsal fistula on MRI, and what is the gold standard treatment for the bonus points? Can everybody see what's going on there? Sure. Next person. Well, describe the image first, as far as what we see there. And then the gold standard treatment will be for the bonus points. So, yeah, you got the gold standard treatment, so it's almost, almost. So with the intradural dorsal fistula, you just want to clip or ligate the posterior draining vein, okay? And typically we'll describe what we saw here are dorsal flow voids, that's what all that serpiginous kind of dark material was posterior or behind the spinal cord. And then you can see extensive signal change and variable and patchy enhancement, basically due to swelling of the spinal cord and congestion, as there is just a backup of flow of blood. So too much blood is going in, and decreased blood flow is going out on the backside. So for the treatment for this, when it is on the backside, you go in and you ligate that draining vein. So you put a clip across it, or you can just coagulate it and cut it. So you did get part of that, so 100 points to you. Okay, you want to pick the next category? Only 500, okay. Okay, spinal deformity and sagittal balance. Above what value is the sagittal vertical axis considered abnormal? For extra points, what is the ideal relationship between lumbar lordosis and pelvic incidence? In the back. Yep, that was you. Okay. I agree with the second part, but the first part, could you just say that part again? You're very close. Yeah. So, above what value is the SVA considered abnormal? Yeah. Okay. Perfect. So, the line we're talking about here is this line that's kind of hard to see, but it's a plumb line. It says SVA pointing to this thing here. Plumb line that we dropped down from the level of C7, and the SVA is measured from the post here, superior part of the S1 vertebral body, right here where the mouse is. And generally, you want this number to be less than five, and that's more of a normal type of number. And then, the ideal relationship between lumbar lordosis and pelvic incidence, let me click on this here. Okay. So, lumbar lordosis is a measurement between the superior end plates of L1 and S1, and that is a variable that we change in surgery, that changes throughout our life. Pelvic incidence is this angle here that we measure on standing x-ray films from the middle of the femur up to the middle of the S1 end plate, and then we draw a straight line here. And that angle is the pelvic incidence, and that is a static measurement in our life. And so, ideally, we want the mismatch between lumbar lordosis and pelvic incidence to be less than 10 degrees. So, many people will come in with significantly reduced lumbar lordosis, and that's why we do deformity surgery to give them more lordosis to try and get those two numbers to be less than 10 degrees or less than 10 as far as a mismatch. Okay. How much was that one? That was 500, and you got the second part as well, so 600 points. You go ahead and pick the next one. 300. Okay. And how are we doing on time? Pretty good. Okay. A 35-year-old male who has previously undergone a lumbar microdiscectomy for an L45 herniated disc presents to you with an acute onset of recurrent lower extremity radiculopathy eight months after his previous surgery. Recurrent disc herniation versus epidural fibrosis, what MRI sequence? Yep. Right up front. T1 with contrast. That is correct. And then for the second order question, can you describe which one would show you what as far as which one will show you fibrosis, which one, what will enhance, either the recurrent disc or the fibrosis? Fibrosis. You got it. Okay. All right. And that was 300 plus an extra 100, so 400 points. Go ahead. Clinical surgery for? Four? Okay. What imaging modality is gold standard and mandatory for all spinal arteriovenous lesions? You got it. You already said it back there. Your colleague next to you, earlier. The gentleman right next to you, earlier. Yeah. Okay. Good. So that was, I think that was for 400 clinical. So you have the floor. Trauma, 200. Okay. A 70-year-old female presents with significant neck pain after a fall. Imaging demonstrates a type 2 odontoid fracture with 5 millimeters of displacement. What treatment would lead to the lowest mortality and highest health-related quality of life? Sorry. Right up front here? Yeah, you were first. Hey. Next. I think it was, oh. Yeah. That's correct. Okay. So for type 2 odontoid fractures, generally surgical. If there's greater than 5 millimeters of displacement or angulation greater than 10 degrees, and usually people do better with surgical treatment greater than 50 years old. With a geriatric odontoid fracture, as it was in this case, if they're healthy enough for general anesthesia, C1-2 fusion should be done if possible. Do not treat in a halo. There's an increase of dysphagia and death. Okay. So that was for 200, and you still have the floor. Tumors, 400. Okay. Which is the most important predictor of survival in patients who have a spine tumor? A, presence of mets in the liver. B, histopathology of the lesion. C, number of spinal levels involved. Or D, local invasion into paraspinal tissues. Who was up first? Who? I'm sorry. The gentleman in the blue shirt. Yes. I'm sorry. D? Who's up? Right here. Yes, correct. Okay. Histopathology of the lesion. Okay. So that was tumors for... I'm not sure. I forget. Is that 400? Okay. All right. Causes of spondylolisthesis include all the following except... Except which one? Correct. Neoplastic. So, clearly degenerative conditions and the other ones listed there can cause spondylolisthesis. And I'm sure you all are very well aware of the multiple classifications of spondylolisthesis. Normal, having no slip. Grade 1, 25%. Grade 2, 25 to 50%. Grade 3, 50 to 75%. Grade 4 is up to 100%. And then spondyloptosis is all the way off, essentially. Okay. Great. So that was degenerative conditions, I believe, for 400. Anatomy for 300. Injury to this tract results in pain and changes in temperature. Right there. The gentleman in the blue shirt. Spinal... What was it? I'm sorry. Spinal thalamic. Correct. Okay. That's 300 to you. 300, clinical surgery. A patient wakes up after ACDF surgery with this exam. What was injured? And for more points, where is the structure located? I think that gentleman there. I'm sorry. Yes, correct. Go ahead, sir, in the jacket. No. What's that? No. Yep. Go ahead in the back there. Okay. Do you remember the name of the Horner syndrome? Absolutely correct. And do you know where that's located? Okay. It's... Here, I'll show you. Here. So sympathetic chain overlonging... Sorry, overlying the longest coli. So you named it correct, and you got the sympathetic chain part as well. So we'll give you 300, so 400 points. And this overlies the longest coli. We're looking at an axial image here of the neck at the cross-section of the C5 level. Here's the longest coli on one side. Here's the longest coli on the other. This is where we attack the disc here. And here's the sympathetic chain on each side. And then just... We'll leave it at that for now. Okay. So what would you like next? Degenerative 300. Okay. 60-year-old male has painless diffuse weakness of the upper extremity with reduced reflexes and has hyperreflexia in the lower extremities with bilateral up-going toes. What pathology is most likely the cause? Yes. Cervical myelopathy? No. Oh, sorry. It was in the back. I apologize. Oh, yep. Yeah. No. The front? No. Uh-huh. Key word, painless weakness. Painless weakness. Yes. No. No. We're getting a little warmer. Yes, I'm so sorry. I didn't see you. No. No. I promise there is an answer. Yeah. Yes. No. Painless weakness. Yes. Correct. I should have put that one for 500. Oh, okay. Okay. So, anyways, motor neuron disease or ALS amyotrophic lateral sclerosis will present without dermatome involvement. So, painless weakness, upper and lower motor nerve involvement. So, that's a big one for our boards as well. If you operate on somebody with painless weakness, usually they're going to end up getting worse and worse, and you never help them. Okay. So, we'll continue. Where do we want to go next? 300, tumors. Okay. Which is the least common histology of metastatic tumor arising in the spine? Okay. Is it breast, prostate, non-small cell lung adenocarcinoma or transitional cell carcinoma of the bladder? Yes, sir. Oh, wait, I'm sorry? All the way in the back. D, final answer? You are correct. 300. Okay. So, we know metastatic spine tumors are more prevalent than primary spine tumors. Of the 1.5 million cancer cases diagnosed annually, 10% result in symptomatic METs, and then bony spine METs are the third most common site of METs, and it's commonly in the thoracic spine. And the most likely METs, like we saw previously in the question, are the breast, lung, and prostate. And then we usually use the NOMS criteria to guide our care. NOMS is the acronym for Neurologic, Oncologic, Mechanical, and Systemic Burden of the Disease to basically help guide our care, I'm sure, as you all know well. Okay. Where would you like to go next? James? Oh, I'm sorry. You've got trauma, tumors, degenerative conditions, anatomy. Tumors? 200. Tumors for two. Got it. Okay. True or false? Adjuvant radiation therapy for incompletely resected ependymomas has no effect on progression-free survival. I'm not sure whose hand was up first. Yep, you in the middle, sir. I have to read it now. So, next one? Sorry, who? False. False. Adjuvant radiation therapy. See? I mean, it was a 50-50 shot. That's good. Way to get your hand up in there. You get in the game. False. Adjuvant radiation therapy improves progression-free survival. The dose is 50 gray and 1.8 gray daily fractions. So, basically, if there's a residual tumor, a lot of times people watch to see if there's any growth. As soon as it grows, we go ahead and radiate it. Okay. Clinical surgery, 200. A patient comes to clinic with complaints of retrograde ejaculation. What procedure did he have it done? And for more points, what was injured? Yep. What's that? No. In the back? Yes, correct. And for more points, what was injured? Okay. All right, so ALIF, injury to the superior hypogastric sympathetic plexus can result in retrograde ejaculation, that's supposed to be ejaculation in males, with rates ranging from 0.42 to 5.9 percent. So typically there's a lot of people that will avoid doing this procedure on younger males. If they do, we always recommend people to go ahead and bank their sperm because it can happen. Okay. Okay. What category would you like next? There is. There is one last tumor. Okay. That's the one. Okay. A previously ambulatory patient having no comorbidities beyond breast cancer diagnosed five years ago presents with a single metastasis at T6 causing radiographic spinal cord compression, mechanical back pain, and three days of leg weakness requiring a walker for ambulation. Which treatment is recommended? Is it A, surgical decompression and stabilization, B, surgical decompression and stabilization followed by radiation therapy, C, external beam radiation therapy alone, so EBRT alone, or D, SBRT alone, which is stereotactic radiobeam therapy alone? B? That's correct. A hundred. And this was mostly proved to us years ago in 2005 by Dr. Patchell. You've probably heard of the Patchell studies that just showed that maximal decompression and separation surgery followed by radiation will best preserve ambulation and their functional status in patients. Okay. What next? Anatomy 200. This artery, radicular artery, usually enters at the spinal canal on the left at T9 through 12 to supply T8 to the conus. Yes. That's correct. And for another hundred points, just kidding, how else is it pronounced? Because everybody in this room, I'm sure, is going to pronounce it differently. Anybody? Adunkovich. No, I'm sorry. Everybody pronounces it differently. Yeah. Nobody really knows how it's actually pronounced. That is correct. Two hundred. Okay. Anatomy for a hundred. Okay. After posterior cervical decompression, this is the most common radiculopathy palsy, difficulty with shoulder abduction. Same person. Okay. C5 palsy. Correct. That's a hundred points. You got pretty far with it, so I think we're gonna give it to you. So we'll give you 300 points. So yes, the rule of Spence, greater than seven millimeters. Looking back at that image, you're looking at the lateral masses. It's injury to the transverse atlantal ligament. It's going horizontal, okay? And a C1 lateral mass fracture. You're gonna see the lateral masses start to slip off. There's a lot of these measurements and things that we've briefly seen and studied, but immediately pushed out of our brains because we assess all of these things with MRI now. So really that's the gold standard to assess the integrity of that ligament. Okay, we're next. Clinical for 100. A patient has numbness rating to digit number three. What dermatome is this? And for more points, what motor weakness may they demonstrate in their wrist? Right up front. Yes, okay. And for more points, what are they gonna have a problem with in their wrist as far as motor weakness? Final answer? Difficulty with flexion. Yeah, it's okay. You got the 100. And the way to remember that is your, when you bring your wrist in, that forms a seven. Oh, okay, that forms a seven. So hopefully you won't forget that, okay? Where to next? Imaging for 100. What number results in a PARS fracture as it slowly downloads? So I can keep my head in the correct direction. You, sir, in the blue shirt. Next person. In the back, right? Yep. Four? That's correct. Okay. All right. So anyways, looking at oblique angle of part of the lumbar spine. And there we go. Number five is the antevertebral body. Number two, sorry, that's the teepee, I apologize. Number two is the, that should probably be part of the pedicle there. This is the SAP on the left. This is the SAP on the right. And then the IAP of the left is number six. IAP on the right is number seven. And again, the PARS, which is the space in between the two joints here, between the SAP and the IAP. Here's the PARS. And a fracture there would give us a PARS fracture. Okay. It's true, the temperature is dropping outside and there's only one jacket here, so the stakes are high. Let's make it happen. Okay, go ahead. You're picking the next category. 200, okay. An L4-5 far lateral herniated disc will compress which nerve root? Shrine. Shrine. Yes. So, most herniated discs, as you know, L4-5, more central or at least within the canal, are going to compress the traversing nerve root. So at the L4-5 level, that would be L5. A far lateral disc goes out the foramen and is usually compressing the exiting nerve root above it. Okay. Ah, the last one. List these incomplete spinal cord injuries in the order of best to worst prognosis. Best to worst. You have brown saccade, anterior cord, and central cord injury from best to worst. Blue shirt? D. You're saying D? From best to worst as far as their prognosis? B. B as in boy? Is that correct? Yeah. Okay. So, central cord, no. Next. D as in dog. D as in dog. From best prognosis, anterior cord, central cord. From best prognosis to worst? No. Yep. Brown saccade, anterior cord, and central cord? No. Blue shirt? Yes. C. Brown saccade, central cord, and anterior cord. That is correct. Best prognosis to worst prognosis. And the reason for that being, these are incomplete spinal cord injuries. Brown saccade is a hemi-infarct or hemi-injury to half of the spinal cord, so you're only going to lose half of your motor function on one side of the body, and then also end up with sensory abnormalities on the other side of the body. So these patients actually do, within the realm of the injuries that we're looking at, they do the best as far as longer-term prognosis. Secondary would be a central cord syndrome, and that, as you know, usually ends up with people. The darker color is a motor injury, so they'll be weaker in their upper extremities, and their lower extremities will have strength but sensory changes, and it affects more of the proximal versus the distal motor function. And then lastly, worst out of all of these would be the anterior cord syndrome, which would give you essentially hemiplegia and sensory abnormalities below the level of the lesion because it knocks out both descending and ascending fibers. Okay. That's it. Somewhere in there was supposed to be a daily double, but I'm not sure how that didn't work. Okay. So who's the... With us now is Dr. Fagan. He is the Helen and Morris Marburger Chair and the Head of the Division of Neurosurgery at the University of Cape Town. His clinical and research interests span pediatric and functional neurosurgery and global surgery. He has served organized neurosurgery as the president of the Continental Association of African Neurosurgical Societies, the International Society for Pediatric Neurosurgery, the Society of Neurosurgeons of South Africa, and is president of the 18th World Congress of Neurosurgery that is scheduled to be held in Cape Town in 2023. He's going to speak with us today about world neurosurgery. Great. Thank you, Danielle. And hi. Good afternoon to all of you. I'm really sorry. I was kind of double-booked, so I just had another talk that finished. So it's kind of a very modest title to talk about world neurosurgery. So I'm afraid what I've done is I've taken that and I've kind of interpreted it from the point of view of where I work, which is in South Africa, just to talk a little bit about kind of the kinds of issues that we deal with as neurosurgeons in South Africa, more broadly in Africa, and hopefully giving you a bit of a perspective. But, I mean, this is kind of one point of view, and I'm not going to try and cover sort of neurosurgery across every single country in the world. I do come at it from a couple of different points of view. I am a pediatric neurosurgeon. That's kind of my core identity. How many of you here work in pediatric environments? Great. Okay. So if I get into trouble, please rescue me. Okay. So I'm primarily a pediatric neurosurgeon. I am currently the chair of our overall Division of Neurosurgery and the Department of Surgery, which has been a really cool opportunity to develop global surgery as a discipline that spans all the different surgical disciplines in our university. And we're hosting the World Congress of Neurosurgery in Cape Town in December. And I want to actually pose a question, which maybe we can discuss either kind of at the end of my talk or maybe at the global reception over a drink or something, and that is the notion of how we kind of increase neurosurgical kind of, I don't want to use the word manpower, personpower, kind of neurosurgical kind of capacity on the ground. And, I mean, this group really is, I mean, I'm really thrilled to have a chance to engage with you because in our country we don't have nurse practitioners. We don't have physician assistants. There's this very stark dichotomy between doctors and specialists, neurosurgeons and nurses. And it feels to me there's a huge gap there, and particularly as one looks across different African countries and countries that have very limited resources in terms of trained neurosurgeons, there must be ways in which one can kind of increase the capacity to treat patients by learning from the way your careers have evolved and the kinds of work that you do. So I'm really hoping to learn something. And maybe if any of you are keen to come to Cape Town, we can put together some sessions in Cape Town in the program to actually look at this and maybe try and look at it from a global point of view. So no particular conflicts of interest. Just to be clear, I speak from Africa, but I do not profess to speak for Africa. Okay, so I'll tell you a little bit about where I come from. I'll tell you a little bit about neurosurgery in my country and on my continent. I'll tell you a little bit about what I think is interesting and exciting about pediatric neurosurgery and global neurosurgery. So we all know, and I just want to start with a couple of slides that I usually use at the start of talks like this, the definition of neurosurgery, and it's incredible. I mean, I've just finished a term as I mentioned chair of the Department of Surgery and really gave me a chance to understand in much greater detail what all the different surgical disciplines do. And there's nothing that has the breadth and complexity and excitement of neurosurgery. It's such a rapidly growing discipline. And with 10 different completely separate subspecialties, each of which people can spend their entire career in. And what's exciting is not just that we have those subspecialties, but we don't even know what's kind of in the future. I qualified as a neurosurgeon maybe 25 years ago, and neurosurgery today is fundamentally different to what it was when I finished my neurosurgical training. And it will be completely different in 25 years' time. And I think neuromodulation and kind of stem cells and all these other kind of interventions are clearly things that are going to completely change the face of what we do. But whatever the future holds, the current reality is that the world is short of neurosurgeons. I was part of the study done by Michael Dewan, who's now at Vanderbilt, looking at neurosurgical capacity around the world. And we counted close to 50,000 neurosurgeons in the world. But there's a massive shortfall, and we need kind of 50% more than that just to meet the current needs of neurosurgical patients all over the world. It's even kind of starker when you look at pediatric neurosurgery. Pediatric neurosurgeons comprise only 4% of all the neurosurgeons in the world. The truth of the matter is that the vast majority of kids around the world are not operated on by pediatric neurosurgeons. They're operated on either by neurosurgeons, very good general neurosurgeons who operate on kids, or general surgeons, or pediatric surgeons, or medical officers, or clinical officers in some African countries who don't have a medical degree but are well-trained and have kind of surgical skills and surgical capacity. And there's a very interesting kind of interface between that and the sort of notion of how one's going to actually try and extend the capacity to treat the patients who need treatment. It's one thing providing emergency care, but obviously kind of elective surgical treatment, and particularly when you start to look at functional conditions like epilepsy surgery, the gap is just massive, and there's absolutely a huge, huge need here that has to be filled. Does it matter? Well, certainly if you talk to neurosurgeons in low-income countries, for sure it matters. They feel very, very strongly that we need to find ways to address this incredible shortage. So perspective does matter, and as I said, I'm going to just give you a little bit of a perspective from the southern tip of Africa. There's no particular reason that the world is always drawn the way it should be. We're a planet just like somewhere in the universe, but somehow the way the world has always been represented is the northern hemispheres on top. But maybe that's going to change in the next few decades. So there's no reason for that. So I work at the University of Cape Town, southern tip of Africa. South Africa, as I'm sure you all know, is a country with a very complex political history, and that continues to play itself out. And many of the issues which are relevant to global surgery are issues that we've had to grapple with as a country, and I'm going to come back to this a bit later. We have two hospitals. So Critter's Care Hospital is an adult hospital which became world famous in 1967 when Chris Barnard, on the 3rd of December 1967, transplanted a human heart for the first time. And if any of you ever come to Cape Town, there's a very cool museum with an operating theater where that happened, kind of reenacting that first heart transplant. And we have a children's hospital as well. Just to mention Barnard, so I'm sure you've come across this idea of clinician scientists, that you have doctors who are kind of finding a way to bridge doing basic research and also being clinicians. It's very hard to think of anybody who did that better than Chris Barnard. The heart transplant was almost like just an extra thing that he did. He did so many different things in his career. He was head of surgical research at our university and discovered the cause of intestinal atresia, did his doctoral work on tuberculous meningitis, did a lot of other really profound kind of basic laboratory research, did a heart transplant. And then probably his biggest scientific contribution was really pioneering the concept of brain death, which is obviously something that's very relevant to all of us in neurosurgery. Just the other person who did work that's very relevant to neurosurgery, Alan Cormack, who's a physicist, and it's a story I love telling people. Cormack was a physicist who had no intention of ever going to a hospital. He wanted to be in the lab doing basic physics research. And South African law, and in fact it's true all over the world, if you're going to give radiotherapy, you've got to have a physicist to check the doses. There's nothing more dangerous that we do in all of medicine than give radiation treatment. So you've got to have somebody who knows what they're doing to check the doses. Cormack got sent down to hospital. He absolutely hated it. He did not want to be there. But thrown into a completely unfamiliar environment, he had an original idea, and that was looking at these x-rays. As a physicist, he was looking at them kind of from a mathematical point of view and kind of realized, and this was in the 1950s, he realized that x-rays really are about attenuation of x-ray beams and you can describe that physical phenomenon mathematically. And if you took x-rays from different directions, you could work out the density of the intervening tissue, which was the basic concept of tomography. And he wrote a couple of papers in the 1950s, which got published in journals that nobody ever looked at. And there were no computers in those days, so it was all completely hypothetical. And 20 years later, a British engineer called Hansfield came up with a technical solution of how to build a computer tomographic scanner. And Cormack's algorithms were long forgotten, were dusted off, and became the basis of the software. And they both got the Nobel Prize in 1979, so it's a cool story. We've had a neurosurgery department in Cape Town for nearly 70 years. And we have a range of different specialties, particularly very strong in endovascular. About 90% of aneurysms in our place are treated endovascularly. Certainly, it's a very, very strong component of our program. For those in a pediatric environment who are familiar with selective dorsal rhizotomy, Warwick Peacock, who's a neurosurgeon who introduced selective dorsal rhizotomy, did it in Cape Town. So we've been able to follow up those kids who operated in the 70s and 80s, who are now kind of 40-, 50-year-old adults. And just to make the point that what we do in neurosurgery really has an impact on people for the rest of their lives. And it's really important that what we do has an evidence base and that we really know kind of that what we're doing is going to be durable and really make a difference in the long run. So just to give you a couple of numbers. So in the United States and Canada, you have incredibly well-resourced hospitals, large numbers of health professionals. That's sadly not the case in many other countries around the world. If you look at South Africa, so the OECD is the sort of collection of largely upper-middle-income countries. On average in these countries, there are around about 250 specialists per 100,000 population. In our country, there's a huge mismatch between the public sector and the private sector. And this is something you will find in many, many other countries around the world, that you have a public sector that is funded by government that cares for the majority of the population, and a private sector that's obviously funded largely through insurance and private payments that cares for a much smaller proportion of the population but has much more resources. And the point here is just to show that there are enormous disparities around the world in terms of the number of specialists. And this graph, I'm not going to go into details, but it really just shows the ratios of a whole bunch of different specialties in private practice, which is the red bar compared to green bars. So just to make the point, when you're looking at provision of neurosurgical care in the rest of the world, there's often tremendous inequality in access to care. One of the other really interesting demographic changes that's happening is the rapid rise in the number of women who are neurosurgeons, which clearly has happened, I think, very strongly in the United States and in other countries is starting to happen. And if you look at the ages of specialists in our country, there's no doubt that there's this rapid rise in the number of women. In fact, at our medical schools, more than half the medical students now are female. And there's no question that the way in which we function is clearly going to change to reflect the fact that we have a much more normal kind of workforce and a much more normal, I think, in many ways, sort of balanced approach to how we run our healthcare system. So this kind of gets factored into policy, and it really is about training and how you're going to start matching the number of specialists to your population. I'm not going to go through the details, but just to give you the notion that countries around the world are really having to find ways, not just to train enough specialists for their own countries, but to train for the huge exodus that happens. And for many, many countries, and South Africa is definitely no exception, and probably many of you have had the experience of meeting a South African nurse or a South African doctor who's working somewhere in the U.S., there's a huge kind of net exodus. So we spend a lot of time kind of workshopping and planning and trying to think of ways in which we can try to retain people in the country and not have them leave. So I just want to touch briefly on pediatric neurosurgery. And as you'll see, I think pediatric neurosurgery has enormous relevance when you're talking about provision of neurosurgical services around the world. So I'm very proud of this organization, the ISPN, the International Society for Pediatric Neurosurgery. One of the things we've done in the ISPN is made sure that nurses in particular and nurse practitioners are able to join the ISPN, complete the equivalent level to any of the neurosurgeons in the ISPN. And the idea is that we're talking about health care for children, and it really is about multidisciplinary team and completely abolishing hierarchy in terms of how you're going to provide clinical services. And as all of you know in your day-to-day practice, that hierarchy actually really gets in the way of delivering care, and particularly in a pediatric environment. There are a couple of things that I think are kind of special about pediatric neurosurgery. In many respects, it is the last refuge of the general neurosurgeon in that pediatric neurosurgery spans an enormous range of different disciplines. But within that, there are a whole bunch of really sophisticated subspecialties like pediatric functional neurosurgery that are starting to emerge. Teamwork is absolutely essential, and I think it's one of the really nice things about working in a pediatric environment. It's a deep sense in which that is appreciated and celebrated by people who choose to work in those environments. Many people kind of disparagingly dismiss pediatric neurosurgery as putting in a shunt or closing a myelomeningocele. But in fact, there's some really interesting and I think quite challenging technical challenges in pediatric neurosurgery. I'll talk a little bit about that. But the question is, what differentiates a pediatric neurosurgeon from just a well-trained general neurosurgeon who's treating children? There are a few things that I think are important, and those of you who work in children's hospitals I think would probably agree with this. The first is that the clinical assessment is clearly different in children. It's easy to kind of have a cursory look at a kid and say they're normal when they actually do have a deficit. if you don't pay attention to that and you then operate and it's clear the child has a deficit post-op, well, you need to kind of take responsibility for that. So the clinical assessment can be quite challenging. And imaging, which is often much easier to default to in adults, much harder in kids. CT scanning, obviously, is radiation, and MRI scanning requires an anesthetic, and that's problematic and often limits the access. And then you've got to think about development. It's not just about neurodevelopment, it's also about musculoskeletal development and to think long-term. And I mentioned these little guys who had rhizotomies 30, 40, 50 years ago who are now adults. And if you're going to do an operation that's going to work really well for 10 years, but by the time the patient's an adult, they're going to have terrible complications, then you're really not doing them a great service. I think a goal is a treatment, and I think that's a really important aspect of neurosurgery that oftentimes, actually, that's the wrong word, not oftentimes, but sometimes, we see patients that we just can't treat. Patients with really horrendous glaublastomas, children born with absolutely devastating congenital malformations, patients who've had catastrophic subarachnoid hemorrhages, patients who've had terrible traumatic brain injuries, and even though you can't do anything to necessarily change their underlying pathology and offer them a cure or even any meaningful improvement in their condition, there's often a lot that you can do that will not only improve their quality of life, but improve the quality of life of their family. And I think that's a very special aspect, I think, of the work that we do. But when you look at pediatric neurosurgery in children around the world, when you do the numbers, it's clear that more than 80 percent of kids around the world are not being operated on by pediatric neurosurgeons, and I think there's a strong responsibility for pediatric neurosurgeons to pay attention to that and to see how we can change that. So I'm not going to go through all of these, but these are just kind of a few things that I've reflected on over the years that have really changed our practice. I'm going to just touch on the ones that are in blue there. Those of you who manage patients who've sustained traumatic brain injury, one of the coolest things that I've seen in my career is multimodality monitoring. So we're monitoring patients not just with ICP monitoring, but brain tissue oxygen monitoring, EEG monitoring, often using transoral ultrasound and other modalities to really get a kind of a multidimensional view of what's happening in the patient. My colleague Tony Fugagi, who's a pediatric neurosurgeon who's really kind of led the development of this in many respects worldwide, has demonstrated that it's dramatically improved not just survival, but patient outcomes. So that really makes a difference. But the truth of the matter is that the vast majority of patients who sustain a traumatic brain injury do not do that in a context where they have access to this kind of expensive, sophisticated monitoring and high-end treatment. And that's a big issue we need to deal with as a profession. Spina bifida is a really, really key condition and probably is the emblematic condition for pediatric neurosurgeons. The single most important thing that anybody needs to know about spina bifida is it is preventable by women having folic acid on board at the time of getting pregnant. That has clear public health implications. And folic acid fortification, the United States and my own country, South Africa, have both been very progressive in having legislation that compels food to be fortified with folic acid, which reduces incidents. But this is a really interesting condition to treat. And one of the most interesting aspects is the way in which society's approach to kids to spina bifida has changed over the years, from quite a nihilistic approach in the 60s and 70s, the most extreme example of which was in Holland, where they had the so-called Groningen Protocol, which, in fact, allowed these babies to be euthanized after birth, which was really quite catastrophic, to the modern era with fetal surgery. And how many of you have fetal surgical programs in your hospitals? I mean, it is something that I think is getting increasing recognition in the U.S. Obviously, in low-resource countries, fetal surgery isn't an option. But I think what's interesting about fetal surgery is that it has kind of driven a kind of a resurgence of interest in how we manage these children. One of the few totally and truly and absolutely incontrovertible facts in all of medicine is that having folic acid on board at the time of getting pregnant reduces the chance of having a baby with neural tube defect. So this has been proven all over the world, that folic acid periconception reduces the chance of neural tube defects. And that's created a very powerful opportunity for advocacy. And we just had a really great presentation in the Global Session by Kimmel Gottmay from Columbia, who's really led a kind of a worldwide campaign to get the World Health Organization to take this on board. And there will be a resolution, hopefully, at the World Health Assembly this year, ensuring that this happens all over the world. So that's kind of what we're pushing for in neurosurgery is to try and prevent these conditions. I mentioned fetal surgery, and just to say that for certainly in our country, it's a completely unattainable treatment option. Close to seraphism, just to kind of touch very briefly on the fact that there's some interesting technical challenges in pediatric neurosurgery. So here's a kid with a lumbosacral lipoma. When I was a junior trainee, I was incredibly disillusioned with the outcome of our surgery. And then Dachling Pang, who actually worked in California, just up the road in the Bay Area in Oakland, published work where he described this radical resection of lumbosacral lipomas. And in fact, when I went to go and visit Dachling at his hospital in Oakland, the person who's doing most of the surgery was his physician assistant, who he had been working with for 20 years. And it was the first time I'd really actually encountered physician assistants in the operating theater, and it just blew me away. And I think it is such an amazing example of how one can really sort of extend capacity to kind of deliver really top-end, high-quality neurosurgical care through professions such as you all have in your day-to-day work. So this has been published. It's clear that this particular operation makes a massive difference, and it's a very cool operation. And it's one of those operations that you do, and you know for sure at the end of the operation that you've really, it's just kind of obvious, which is not always the case in neurosurgery, that you've done the job. And just to show you what that means, here's a kid with a lipoma attached to the spinal cord. You can see the fatty mass over here. And then when you've done the operation, you've completely detached the fat over here. You can see the spinal cord lying free here in the dual sac. And there's no question, if you do this operation correctly, you have a really good chance of a meaningful long-term outcome. And once again, just the same sort of story, patients had the lipoma resected. And you can see the spinal cord sitting here. Oops, you can't see the arrow, but anyway, you can see the spinal cord sitting there nicely free and detached. So just a couple of things from a global perspective point of view. So we know where the children are. And the vast majority of children in the world now are in Asia and in Africa. But the vast majority of children's hospitals are not where the children are. Now that's fantastic for children who have access to children's hospitals, but I can tell you between our hospital in Cape Town and Mbali in eastern Uganda and Egypt, there are no other full-time dedicated children's hospitals in the rest of Africa. The children who go to hospital are treated in general hospitals. And that's probably okay because actually there are much bigger challenges in terms of developing healthcare services, but in the long run, that's going to have to change. And one of the most important demographic things that's going to happen over the next 70, 80 years is by 2100, half the children in the world are going to be African. And you can see that from the rapidly growing population of Africa, with the median age in most African countries of less than 20. So that's important, and organizations that care for children like the ISPN need to pay attention to that. By 2100, five of the top ten cities by population in the world are going to be in Africa. And if none of those cities have children's hospitals, we're going to have a big problem. So this is an issue for all of us all over the world, to make sure that there are correct resources to take care of these people. So one of the most gratifying aspects of my career has been training a whole bunch of really outstanding neurosurgeons who've come to us from other African countries, been through our training program, have got exactly the same qualifications as any other South African neurosurgeon and have gone back to their countries, particularly in Uganda. We've had a really, really powerful alliance with a children's hospital in Bali in Uganda. So that's about education, and as Nelson Mandela said, education is the most powerful weapon that we have in order to change the world. It's really difficult, and it kind of doesn't feel quite right to contradict Nelson Mandela, but I think education may be the most powerful weapon, but it's not the only weapon. And one of the other weapons we have is leadership, and I'm sure you've heard again and again about global surgery, and I think for me, one of the really fantastic things about global surgery is the extent to which it's been a multidisciplinary, multi-professional kind of movement that has taken healthcare practitioners across the spectrum together to advocate for kind of increased access to patients who require surgical care. I'm sure you've all come across one way or another this Lancet Global Health Commission that was published in 2015, and the bottom line of this was that 5 billion of the world's population do not have access to adequate surgical care. That's a massive number. And the other very amazing number that has come out of this work is that if you add up the number of people who die from tuberculosis and HIV and malaria, each of which are massive worldwide infectious disease epidemics, if you add up the total number, and that adds up to nearly 4 million people, more people die from traumatic brain injury and car accidents and trauma than that whole number put together. And the truth of the matter is that that's really not been focused on much by governments and health systems. So the question is, why did it take so long? And I think it took such a long time, because for all of us, we'd much rather be in the operating room, at the operating table, rather than at the policy table, where the politicians are, where they make these boring decisions and where all these boring committees function. But what's changing that is global surgery. So when I was heading up surgery at UCT, I was incredibly lucky to be able to recruit Salome Maswimi, who is an obstetrician who came into the department of surgery to head up global surgery, and right from the outset, Salome recognized that what was really going to make a difference here was leadership, and that's really been the key ingredient of the way in which we've gone about developing global surgery. So it is about education, it is about doing research, it is about advocacy, but most importantly, it's about implementation, and you can't have implementation without leadership. So this is something we've really paid a lot of attention to as we've developed surgical services in Africa. So you can see there are many different African countries now where we've really tried to make a difference, and it's really about kind of growing leadership. And this leadership, just to state the obvious, that leadership is not just about the surgeons who are kind of taking leadership. It's about the anesthetists, it's about the operating room nurses, it's about the primary care doctors, it's about the people working in pre-hospital care, it's about hospital administrators, it's about everybody in that ecosystem stepping up and making a difference. One of the other things just to touch on is the fact that when you talk about global health and global surgery, it's also really important that it's about empowering people and making sure that people in low-income countries actually really are in charge of their own destiny and are not just the recipients of kind of policies that come from abroad. And this has kind of coalesced around the idea of decolonizing global surgery and actually saying you've got to step back and really let people in particular countries sort of really be in charge of their own destiny and not recapitulate the kind of colonial era when kind of people from other countries came and kind of figured out or thought they could figure out what was needed in other people's countries. So an important part of that is the notion of equity and actually making sure that what we do in helping people doesn't actually remove their capacity to kind of determine their own destiny. So that's kind of South African neurosurgery in 1970, it's a pretty pathological bunch of old white men. As you can see, African neurosurgery has really changed. This is a meeting we had a couple of years ago in Cape Town and it's unbelievably energizing to see the massive growth of neurosurgery across Africa. I mean in the course of my career it's just changed in absolutely untold ways. A couple of months ago we had the fourth Continental Congress in Nairobi in Kenya and it was just so cool to have neurosurgeons from across Africa coming to a really good meeting on African soil, presenting to colleagues and actually having this really rich discourse which kind of really showed that neurosurgery certainly in Africa is equal to any in the rest of the world now. And the last thing I just want to touch on is research and I think one of the magnificent opportunities we have as clinicians working in neurosurgery is that we kind of engage with the brain every day. Russ Lanzo, who many of you will know, works here in the US at Ohio State, has documented the enormous rise of research in neurosurgery over the last couple of decades. So that's where we are in Africa. We had this old building that I managed to kind of get permission and raise some money to fix up as a neuroscience institute. We opened it literally just as COVID arrived, got some labs in the building, but the most important thing is it's about a vision for developing world-class neurosurgical research and neuroscience research in Africa and kind of at first glance that may seem impossible and why are you going to try and do this in Africa because Africa's got such big problems. The fact of the matter is that there are some unique advantages and, you know, if we look 20, 30, 40 years into the future, this is a publication that's starting to document research coming out of Africa. You can see most African countries have some kind of neuroscience research and we did some work with the Wellcome Trust, which is a big research funding organization, looking at areas where African scientists can start to make really world-class contributions in neuroscience that cannot happen in the rest of the world. And I think, you know, this is for me probably been the most exciting part of my career in the last few years is to see not just the growth of neurosurgery, but now on the back of that a very rapid rise in neuroscience research. But just to kind of make the point that Africa has to be represented, this is looking at data in kind of genomic research and African populations are represented here in purple and you can't even see any purple here. There's just absolutely virtually zero representation of people of African descent in current genomic databases and that's, you know, it's bad for everybody and it's not least of all bad for science in that the greatest genomic diversity in the world is in African populations because of historically that's kind of where we started. We're all Africans originally and African ancestry has to be represented in genomic databases so Africa has a lot to offer the world. So in summary, neurosurgery has got a fabulous future. The world needs a lot more of all of us in the room to manage patients in neurosurgical conditions. I just want to put in a little plug for pediatric neurosurgery as a special part of that tapestry of neurosurgery. I hope I've made the point that global surgery is a very powerful kind of lever to really increase the impact of neurosurgery primarily through leadership which all of us in this room have the capacity to step into the role of leadership and in doing our work not just to make patients better but also to contribute to neuroscience. So I always love ending off with, I quoted Nels Mandela earlier and other beloved lately departed South African Archbishop Desmond Tutu used to talk about Ubuntu which is a deeply embedded African concept that all of us are human beings through our relationship with other people. The none of us is an individual on our own and who we are and what we are in the world is determined by how we relate to other people. It's a very, very powerful concept and I like to think it's probably the kind of lifeblood of global surgery. So none of us would be here unless there were people at home actually doing the work so just acknowledge all of my colleagues back home and then I'd really love it if some of you were keen to come to Cape Town and we could think about how we could have a session like this and actually really start a broader discourse around the world at how we increase access to neurosurgical care through creating more career pathways such as the ones that you've had in years in Canada. So on that note, thank you very much. It's really been a privilege to be part of this meeting. They're probably stunned. Thank you so much. You're very welcome. This was very nice. Thank you. Is Dr. Batterson in? I thought so. We're back here. Hi, so we have Dr. Joshua Betterson from Mount Sinai with us today. He is a faculty and chair at Mount Sinai and director of the clinical program of cerebrovascular disorders. Back in 1992, vice chair up until 08, director of residency program until 2009, and he has been the chair since 2008. He received his medical degree and completed his residency at University of California in San Francisco, so west to east, and while a resident, he did advanced study programs in neuropathology. He's done a ton of research as well as clinical work, and we are very fortunate to have you with us today. Thank you. Thanks, Alice. Thanks, everyone. Great to be here. I think this is the most recent one. Yeah, I think that's it. The title is about advanced digital technology in neurosurgery, but I really hope to focus on the role of PAs and advanced practitioners in a practice that uses this type of technology. Here are some of my disclosures, and I want to point out this last one, that my work and my whole practice are strongly influenced by my physician assistant, work partner and friend, Leslie Schlechter. If you're in neurosurgery, you probably know that it's easy. It's like riding a bike, except the bike's on fire, you're on fire, and everything's on fire. It's a lot easier when you've got a partnership like I do with Leslie. Do any of you know Leslie from her social media and that sort of thing? Good. I'm glad. You know, she's a force of nature, a former professional basketball player, 6'4 or so, and seems to be everywhere, all over the place in the hospital, and really has created a leadership role for herself in my practice in the department, and I believe also in national neurosurgery. I work at Mount Sinai Hospital, which was founded in the 1850s. It has continued to grow over the years, even recently continuing to grow, and it's really a big place now, with 43,000 employees. It's Manhattan's largest private employer, and to give you a sense of scale, Delta Airlines has about 80,000 employees, so it's really a socioeconomic force in New York. The health system sees about 1,500 new patients every day of the year, and it's really a big research organization as well. The neurosurgery department was founded in 1914. I'm the eighth chair. We currently have about 50 faculty, and we have 117 APPs, most of which are physician's assistants. This is a large group of people, and it didn't start that way. When I was chair, we probably had around 10, but the department has grown substantially, and there's no way to take care of the 5,000, 6,000 operations we do every year with the 50 attendings and 14 residents. It's just not possible. I organize the department kind of like a company, if you will, with administrative areas, but really we're organized by our service lines, each of which define our areas of research and clinical areas of expertise. It's a big service doing, as I said, about 5,500 cases each year, and it's a health system that is spread across eight hospitals in the New York area here, which has many other health systems such as Columbia, Cornell, and so on, so it's a very target-rich environment for neurosurgery. But having a big department has allowed us to recruit excellent neurosurgeons, each of whom partners with their PAs and nurse practitioners. We have organized ourselves in a way that started out providing neurosurgery services wherever patients arrived, and here you see the seven or eight hospitals. From this system, we went to one that focuses each diagnosis in a center of excellence in one or two of the locations, and what this has allowed is to concentrate diseases. So whereas before, if we had 150 or 450 intracerebral hemorrhages in a year spread across eight hospitals, 12 here, 100 there, 50 in another place, now all 450 are brought to one location, and so the team, the APP team and the neurosurgical team, the researchers, now have all of those patients to concentrate their learning on as well as the research. Here's how we've organized our APPs across the different hospitals. We've got almost more than 50 at Mount Sinai Hospital, and as you can see, there's a ratio of about one or two to 10 full-time and per diem, and the reason is that we're constantly growing, and so we sometimes grow faster than we can hire, and we're bringing in per diems who we hope like it and stay, but it's not just about hiring and staying. Being an APP, and I hope you don't mind if I use that term because it's both nurse practitioners and physician's assistants, in a big health system like this really requires a program, and this is one that Leslie created about five or six years ago called APOP, the Advanced Practice Provider Optimization Plan, and it starts with recruitment. She and we are connected with the PA schools all around the tri-state area and nationally. We have a social media presence. We're trying to present at meetings. We're trying to get the word out there about our program to get the attraction and the interest of PAs who might want to move to New York or work in New York. There is a significant recruitment and onboarding process that includes didactic education, hands-on education, seminars, quite a bit of hands-on training, at least six months of probation in which you are getting used to us and we are getting used to you. There's a chance for feedback, and almost everyone who comes stays. We then try to optimize your experience with ongoing education, making sure that we check in, that your experience is what we think you want it to be, adjusting it as needed, and then trying to develop leadership and higher roles for you as you rise in the system because there is room, as the previous speaker mentioned, for leadership. We've got seven, eight, seven, 11, 12 across the different services, as you can see here at our different hospitals. There are many different roles that the PA has. The one that I think is the most important is the one that spans the full gamut of neurosurgical care for the patient. You serve, I believe, as the connection to the patient through their neurosurgery journey from the onset of symptoms to the introduction to the physician and the team that's going to take care of you, through the experience in the hospital, discharge, communication with family, and then follow-up and that. This requires a full spectrum of knowledge, I believe, including in the operating room. Here you can see just random pictures of Leslie in her various roles. I love it when she scrubs, although we have to raise the table a little too high for my own comfort. I like to operate with her, but I think it's mostly so that she fully understands what goes on in the operating room. She can walk in, in the middle of a five-hour case, look at the screen and know exactly how it's going, where I am, when she can expect me in the office, when she can call to drag me out if needed, so on and so forth. As well, she supervises the acquisition of scans and the setting up of advanced technologies so that it all works well. But mostly she's there so she can guide, in the operating room, so she can guide the patient into and out of the operating room and develop that strong relationship with them and the family. Here you see her in her various roles, definitely with the technology, supervising, going to courses, sometimes lecturing at courses. She's a huge team builder and leader within the institution and outside. She does lecture, of course, and she travels. She sort of advises some of our other attendings in how best to implement some of their technology. She's a huge advocate for PAs, and I strongly support this. So I wanted to then turn to how we apply advanced technology in the operating room as part of our research program here, and I actually consider this part here, brain access that neurosurgery has, as one of our service lines, almost the same as brain tumors, because it's something quite unique for neurosurgery. Our department is number one in NIH funding in New York State, and we have focused a lot of our research on innovations in advanced digital technologies. This was an article that I wrote for Science Magazine a couple of years ago, and here's the picture that described the use of ARVR in the operating room, and I hope to bring you through to the point in this lecture, just in a few slides, so that we can fully understand what these pictures mean here. Here's the simple problem we face in neurosurgery. There's a tumor. We know that underneath that tumor you're going to find the optic nerve, carotid artery, and the third nerve, but the problem is when you start the operation, you can't see any of those things, and many of the tools that we use to remove the tumor are very dangerous to an optic nerve or carotid artery. So if we could see ahead and use advanced technologies to guide us, we might do it safer. I view this kind of like I do a sculpture in which the sculptor envisions the beautiful anatomy that is embedded maybe by stone or tumor, and then chips away at everything that doesn't need to be there, revealing the beautiful anatomy underneath. We apply virtual and augmented reality to do exactly this, and I'm sure you know from previous experience that virtual reality involves interacting only with the virtual reality and not with the physical world, whereas augmented reality overlays a virtual scenario onto the real world. Some terms that we use here, navigation, otherwise known as stealth, brain lab, synaptic, and others, navigation gets you where you want to go. Simulation, planning, surgical theater, brain lab, et cetera, is planning and thinking about it before you do it and while you're doing it. Augmented reality, I believe, helps you do it better. There are three major steps in the workflow. The first is to create the simulation. Think of the movie Avatar. What we do is combine CT scans, MRIs, NGOs, blend them all together and create the virtual reality scenario. We then link that virtual reality scenario to the patient's actual anatomy, and this is similar to GPS for your car. We then take a certain amount of that information and project it into the eyepieces of the microscope to facilitate the surgery. Another way of thinking about this is preparation, planning, and practice. The preparation part involves getting your scans just the right way, and I'll go over that, defining where you want to look to select critical structures, define your surgical approach, and then link it all together. There are 20 uses of mixed reality, and I'm not going to go over all of them, but I wanted to focus a little bit on what is the PAAPP workflow in this whole scenario here. The first is in consultation, and frequently we do consultations only with an X-ray and a history. Recently what we've done is we've created either a patient-specific or a pathology-specific consultation, which means we take their scans, we create a simulation, and then we present them with that 3D virtual reality scenario in the office so they can fully understand their own anatomy and understand why we're choosing certain approaches. Here's an example of a 39-year-old sailor presenting with hearing loss and decreased balance. We printed a 3D print of his tumor, and then I spent 45 minutes in the office explaining it to them, turned it over to Leslie, and here's what she had to say. the brainstem and all these little itty bitty foramen is where they come out and go to where they're supposed to go, all right? So ones that go through to the eyes come through here. The ones that go to the tongue come right through here. That's why we were checking how do you do all those things because all of the cranial nerves have their own little home that they kind of scuttle into. I call this look the aha moment. Even after I spent an hour with the patient describing it brilliantly, in my view, it takes just 10 minutes with Leslie and they finally understand it. Leslie and the simulation, this was a patient-specific simulation-based consultation. And you can see that the challenge of simulating this sort of thing is really significant. Here you see the tumor. Here's an area that has the seventh and eighth and vestibular nerves. And you can see this is a two millimeter marker. And just to give you a sense of scale, the dime is about 15 millimeters. Here's a one millimeter marker. And the seventh nerve is just a fraction of that. So it's really important to save it, obviously, and very useful if we have any help in doing that. To a colleague, and that's when it all hit home, actually writing down that I need a brain surgery to actually see your face and see the route that they're gonna take and the openness of the whole team. I mean, to be able to sit with them, see what the process is, actually meet the folks that are doing the 3D, that was incredible to me. And actually seeing, okay, they have sort of a very clear roadmap of what they're gonna do. It brings up the confidence level on the entire team quite a bit, and sort of that shock factor down a little bit. You're still scared, right? I'm still scared, but I feel much more confident. So, and there was a human touch to it as well. So it wasn't only the topology of it, but you could feel the passion of the team. That means quite a bit. That's the PA right there. I mean, that's the APP. You know, as human a touch as we like to have on the neurosurgery side, I think there's sometimes something more that can be added to it. You know, this is a lot of detail, I'm not gonna read it, but one of the things that the APPs do learn, and even the front staff, the front office staff learn, is exactly how the scans need to be acquired. So when you make the appointment for the consultation, if you haven't had your scan yet, we will order it like this, or give you instructions so you can order it, and this then allows us to create a good simulation. You can't create a simulation with every scan that comes off the street. Has to be done with certain parameters, and that's pretty important. Again, each diagnosis, here we're looking for acoustic, so, or pituitary, or posterior fossa, each one has its own protocol. One of the things that we focus on in the difference between non-simulation scans and simulation scans is getting them with a small field of view. A large field of view is necessary because it incorporates the whole head and the face, and we use the facial features during the surgery to register the patient. The small field of view blows up the area of interest, and we overlap those and link them together so that we can first register, and then we can navigate during the crux of the operation. So I'll go, I'm not gonna be too long. I wanna get ahead of the schedule here, but I'll go over a couple of surgeries and how we actually apply this. So here's the room set up with the simulation computers and so on all along the side for us to look at. And here's what it looks like in surgery. You have the operating microscope connected to the computers, and you have both navigation and simulation. One of the key components here is that we link the movement of the microscope to navigation. And what you see here is as I move the microscope, you're gonna see the navigation. You see, there's the operating. Now you move the microscope, and you saw the navigation and the simulation update. So linking the movement of the microscope now takes the place of the handheld wand that we used to have, where you put that into the field and navigate a handheld wand. This is pretty important, because what it allows you to do is inject some of that mapped out information into the eyepieces of the microscope. So during the prep here, I'm standing above my patient's head. You can see the left side's exposed. And as you come up to the eyepieces, and this is seen in both eyepieces, you'll see his tumor, the optic nerves, and other things overlaid right onto the surgical field. That's really a very different protocol, because in the past, you would have to stop the operation, look away at the screen to see the navigated information, and then restart the operation. Here, it's in the eyepiece, so you can keep doing what you're doing. Here, we're using it to position a patient. It's not only used in consultations and during the surgery, but even to position the patient. So here you see a fellow with two large hemangioblastomas. See them here. It's the front one that's actually causing problems now, so we're gonna be operating on this one. We don't need to go after the back one on this operation. When we first get into the operating room, and I come to the microscope after he's been positioned, we see that the tumors are projected through the eyepieces way up high on his head. That means if I were to operate like this, I'd have to lean all the way over and look back. Instead, all we do is drop the head a little bit before we start, and you can see now these two tumors, looking through the eyepieces, are lined right up with my trajectory over the eyebrows. So here, the heads-up display has helped with the patient positioning. Here's another way that it can help. This is a 47-year-old woman presenting with cerebellar findings. She's bumping into walls. As she said, she had just given birth to her fifth child, and she thought it was just expected after having so many kids, but she really was losing cerebellar function, and at surgery, here's what the heads-up display initially showed. This is really too much information. All of these squiggly lines are just getting in the way of doing the operation, and so what I then do is subtract out the things I don't need, and what I really do need to begin with is where is the tumor in relation to my opening? And here you see this. Here's what I'm gonna have to take out towards the end. As we progress through the operation, now the dura's open, we see, okay, well, I'm beginning to approach the back end of that tumor here. You see the line of the tumor, and I'm almost there in my surgical field. Another really important structure is her seventh nerve. We do not want her to have a weak face at the end of this, so here we've been able to visualize the seventh nerve, painted it before surgery, and now I can navigate either to it so I can identify it or stay away from it, and here I've identified it. I'm confirming it with a nerve stimulator, and I'm able to spare it, taking the rest of the tumor out, and you could see the tumor's out and the happy smile on the patient, but also me because this was Jeanne Gaffigan, Jim Gaffigan's wife, and I really did not want her to have a weak face. So let's put it all together. So here's a patient with a huge tumor, as you can see. First thing we're gonna do is select out the critical structures, and this is called the smart brush. This is what the PA will do, and actually now the PA has trained people who are in the office and quite advanced in what they do, but they're not with specific medical training, so with time this knowledge passes through the whole health system team, the neurosurgery team. So first we select the critical structures, tumor, blood vessels, bone, brain, and here you see Holly painting it out, and now we've selected tumor, blood vessels, bone, brain, and I'm just gonna stop this here. We know that we're gonna have to take this tumor out, and one of the critical features here is gonna be to identify the internal carotid and middle cerebral arteries, as well as this combined posterior commuting, cating, and anterior carotid artery, because even though these arteries are small, if you hurt them, they can paralyze the patient. So we just continue with, we start with the operation, as you see. Now, before we make the skin incision, we can see through the tissues where the optic nerves, the blood vessels are gonna be, the brain stem, and so on. After the soft tissue's been opened, before the bone opening, we can help define the bone opening, we can see where the tumor's gonna be after we open the bone, and then after we've opened the bone, as we're approaching, we know exactly where the optic nerves are gonna be, and before we get there, where the internal carotid artery is gonna be. So now, as we're operating, we see the optic nerves in virtual reality, augmented reality, the internal and middle cerebral arteries, and the tumor, and that's what these structures represent. One of the most critical parts of this operation is gonna be to define that posterior communicating artery, and I'm stopping the video here because the virtual reality shows it about the internal carotid artery, about a millimeter before I find it, and about a second before I see it. And there, boom, now you see it. So the machine showed it to us just a few seconds before. Sometimes that's all it takes, a millimeter or half a second. If you're a millimeter or half a second in advance of a critical structure, you're gonna save it. If you're one second too late, you can damage it, and damaging that fine artery can result in a very bad outcome. So for me, the whole point of the virtual reality, augmented reality, is to give me that half second just before I find that critical structure. So once we've identified it, for me, the operation was almost over at that point, even though it wasn't over, because I knew I had found one of the critical parts to safety, and then we were able to sort of remove almost all the rest, leaving a little bit behind, but having a good clinical and radiological outcome. So that's how we use it. And that's how the whole system is integrated to make it safer for the patient. We use it also in transnasal surgery. I'll just show one last case. This is a transnasal endoscopic pituitary in which there are two aneurysms. There's a large tumor with aneurysms pointing into the tumor, making it particularly challenging. This is what the virtual reality shows, and here's what you see during the surgery. So on the left is what you see on the video screen, and on the right, you see this with the VR screen. And as you move the sucker around, it's updated automatically, so we sort of know ahead of time where we're gonna find the aneurysms to help us stay away from those as we go through the tumor. You can imagine this is useful in conferences, as you can see here. We do a lot of these virtually now. A lot of these are done on Zoom for resident and PA education, as well as throughout. I think I'm gonna stop here. I hope I've given a sense of how important I think the relationship is between the doctor side of things and the PA side of things. How that relationship can extend outside the operating room, in the operating room, and also to promote the use of advanced technologies. And I'd certainly be happy to answer questions or chat with you about it if you like. I would like to thank Holly. I don't know if you're still back there, Holly, but I really appreciate everything you've done for the presentation. Thank you all. Yes. Great question. For those who didn't hear, what's the downside of this cost, it's expensive, and convincing my hospital president this would help was not trivial. I think that's a disadvantage. Time and work, it takes time and work to prepare the case additional to the time and work that it would normally, and until the whole team learns to use it on a daily basis, you have to figure that that's a little bit extra time taken away from other things. One of the big questions is, what's the best time in your career to learn this? And I liken it to aviation. When you're a pilot, every new instrument you learn, you have to actually get certified on before you can use it during a flight. I think it's good to learn all this while you're coming up as a junior resident or during your first days as a PA on the service, rather than to learn the whole service first and then add it. But there can be some confusion because it's a whole new skill set, and it can be distracting. Sometimes so much technology just breaks down, and if you're not, if you don't remember how to do the surgery without it, you're dependent on it. So there certainly are some, you know, complications of it. Thank you for asking the question. Okay, well thank you very much.

trigeminal neuralgia

facial pain disorder

vascular compression

medications

surgery

pain alleviation

functional neurosurgery

stereotactic techniques

neurosurgeons

APPs

collaboration

treatment accuracy

surgical techniques

tandem occlusion

low-income countries