Transcript

- Okay, well, I want to first thank Aaron Cohen-Gadol for asking me to participate. What I'm going to do is I'm going to spend the next period of time talking about awake craniotomy for glioma resection. I'm going to introduce the topic and talk about the basic strategy concepts that led up to the technique. And then we're going to talk about the technique itself, and then eventually we're going to look at how the technique can be applied in various different situations for glioma resections. So I'm gonna start first with the process by which I had to go through to develop the awake mapping technique that would enhance ability to maximize extended resection and minimize morbidity. And in my background, I came from a training program in UCSF where my cherish Charlie Wilson was very aggressive in terms of achieving a maximum extent of resection, but yet the morbidity profile was not as clearly delineated in terms of avoidance of those problems. When I went to the University of Washington, I started working with George Ojemann who taught me the number of the techniques to do functional mapping for tumor resections. He, of course, was an epilepsy surgeon, but a lot of these techniques could be translated into the glioma realm and I found this to be very useful. So therefore I combine the concept of maximum extent of resection with minimal morbidity. So I wanna take you through this process. Now in the beginning, prior to when I started doing this, there wasn't a lot in the literature about how to use functional mapping for enhancing resection of gliomas. And one of the interesting things about this early on was that it was clearly, this was primarily a strategy to identify critical sets of localization, but it didn't have all of the important components to try and decide how and when to remove subcortical regions so as to not disrupt subcortical tracts. So this was the first big problem that I encountered and obviously this had to be dealt with primarily through the understanding of these pathways. So there were other sources to draw from, and these were the cognitive neuroscientists. Norman Geschwind was a good example of an individual neurologist. How did a neuroscientist could looked at language localization before he even had imaging? So these were done basically on autopsy studies and his principles that he discovered then are very much in play now. And that is that there are connectivity systems, subcortically, that link one area to the other. These are potentially pathways that can be discovered and identified it with mapping. And the other thing that he alerted us to with his early work was the potential for plasticity to exist in the brain, especially if the lesion was more chronic. So we'll come back to this later, in terms of plasticity. Now from a neurosurgical point of view, Penfield was really the pioneer in developing what we now know of today as low frequency bipolar stimulation mapping. This was done principally to identify cortical sites of localization for language, principally naming and reading, as well as the motor system. But where Penfield's technique fell short was in identifying the connectivity systems that Geschwind had described earlier, that resulted in a number of the clinical, aphasia syndromes that we often see in patients who have pre-operatively post-operatively. Now going back to the basic tenant here. This is the concept for both low grade and high grade gliomas that extent a resection really significantly impacts outcome. And we know this to be the case. The question really is how to facilitate an aggressive resection without causing morbidity. And this really went hand in hand with the principles that I've practiced throughout my career in terms of patient safety. To me, maximum extent of resection was meaningless unless it could be done safely or with the very, very minimum amount of risk. And that's what the mapping movement really brought to the glioma resection field was to basically minimize who were admitted in profile. Now, as time has gone on, certainly in my career we've adapted and developed a number of strategies and techniques that are very useful for removing tumors, but probably when it's all said and done the most important advance really comes with functional localization. In other words, we don't stop based on the anatomy, we stop the resection based on function, and it's the functional considerations that are much more important than the anatomical wounds. And of course, the process of interrogating function, both cortically and subcotically, comes under the certain composite effort that we know as the physiological monitoring or brain mapping, where we're gonna map different functions, depending upon the location. Now, early on, as I started to do this, one of the things I learned, and this has shaped my approach to these types of tumors is the fact that there's tremendous individual variability in terms of localization of language. In other words, there are none two people alike, we map where we find the same language pathways. You can't use functional imaging to identify significant areas that if resected are going to result in a post-operative deficit. They only give us an idea in a very surrogate way as to whether or not a given area is potentially leaned to function. But what we've learned through the years is that there's individual variability and that's why mapping has to be done for every patient, and every stage when we see these issues. If we know that they're going to be anywhere near areas that can be functional, that's pretty much anywhere from the back end into the frontal lobe all the way through most of the parietal lobe into the temporal lobe, of course, all the subcortical pathways that subserve those sites. The other critical aspect of this, was as a tumor surgeon coming at this from a tumor surgeon point of view, it was clear to me that I would often have to operate on more than one patient a day. And so I needed to focus my resections down to a significant degree, which meant that at times early on, when I did this, I would get negative mapping results. In other words, I would map the surface and I wouldn't see anything positive. And in that setting it took a while to really feel comfortable removing a negative site, when I didn't have a positive site. It's very easy to remove a negative site if you have positives sites, but if you don't have a positive control, there's a concern. So early on, this was a very daunting issue, but as it turns out, as you'll see, it's very clear that negative stimulation blocking without a positive control is perfectly acceptable to proceed with a reception strategy. This was a study that I published recently, and it, again, I put it in here because it emphasizes the fact that as time has gone on we've collected hundreds of cases, and we saved all those functional wounds with navigation, taken intraoperate photos, reconstructed those maps into the probability to find new functions, such as naming or reading versus the variable. You can see that in the red zones, you have a highly probable likelihood of finding, for example, over the left, speech areas, but in the green zones, in the yellow rooms zones, there is great deal of variability. So you might find that as well for both naming and reading. So, because of that, variability, we really need to map everybody. We can't use a composite series of maps and predict where language is gonna be for every individual. This was the paper that we published several years ago, which very nicely showed that we could rely on negative mapping data to guide the resection. And basically what this showed us is that if we had a very focused exposure and all of the sites that I mapped were negative, and I removed those sites, being careful to map subcotically, that negative language mapping was perfectly fine as a guide to start on the cortex, remove that disease and then pick it up again, subcorticaly make sure we're not injuring that. So negative mapping became pretty much the standard for me. And when I looked at the outcomes in doing that, I realized that even though sometimes we see transient deficits within a few weeks, or certainly within a month, by three months we're pretty much by there, meaning by three months we're gonna see all the deficits, we're gonna see the permanent risk is still under 3%. And so this is a very safe strategy to do a resection based on negative mapping. The other thing that was uncertain to me early on in my mapping career or doing these on the cases was whether or not the right side was functionally wired the same way as the last one, as I did more and more right sided cases in way for left hand patients that I knew had language on the right side, we learned that there's really no difference in localization. There's not any peculiar pattern on the right side. Therefore, the type out messages, you have to map the right side, awake in patients who are left-handed or who your demonstrate through some other means whether it's in the side or motor test, that there's language over on the one side. Now, when these resections are done, I think the other really important message that I've learned is that the early postoperative condition is not always pretty. And what I mean by that is postoperative patients don't really perform well because you're coming very close to these sites. If you have a positive site, you're living those in place, You're not interrupting any. If you find subcortical pathways, you're leaving them in place. But as you get closer because of transient ischemia or swelling or manipulation, the patients don't look very good early on. So you can see within a few days post surgery, that they all look pretty bad, but by one month, as you now know, from the other data presented, most of those patients returned to baseline, no matter what function you tested. And so the overarching message with mapping is that when we look at every paper everywhere about resecting gliomas , and if you'd look at those done with stimulation mapping, versus those done without stimulation mapping, you can reduce the morbidity profile by 50%, if stimulation mapping, brain mapping is used to identify the function of interest, whether it's language, lower visual, et cetera. But we now know that this really has become the standard of care for the glioma surgeon. Well, let's talk about the awake mapping technique. I think this is really the most relevant protocol that I've used from a mapping point of view on a daily basis in surgery. I'm also gonna cover the role of sleep motor mapping, because I think it still has a role. But basically I'm dealing with over 2000 cases that I've done awake for glioma resections, both at the University of Washington and the UCSF. And in essence the procedure has changed to evolve a number of things that are now fairly constant. So for example, the anesthetic regimen, it's a combination of remifentanil, propofol, dexmedetomidine in various different renditions, but we always find that combination works best. We have conversations with patients where we talk to them and tell them what's gonna happen and tell them how they're going to be positioned, indicate what's gonna be painful, how we're going to take care of their pain. When a patient is having a resection that's done deep near the sub-cortical pathway, we talk to them about becoming more awake again during the procedure to have subcortical stimulation. So sometimes we start with them asleep, we wake them up, we map and we put them down again, bring them back up. And so we have to go through this and prep the patient very well. We have a routine where we use local anesthesia, lidocain and marcaine just around the incision. And as you now know, we can focus the exposures, because negative mapping is falling and we take this mapping both into the cortical and subcortical area, again, depending on the function of the tissue. So these things haven't changed. I think what's changed a little bit is the fact that sometimes I will do patients where they go to sleep, they stay awake and I keep them awake for the sub-cortical mapping. The variation of the theme is that they're asleep, they wake up for the cortical mapping, and then I keep them awake as I go down into the subcortical system, keep them awake and get all the way to end. And the reason that that varies, it just depends, if I'm in an area that I know I'm gonna DTI and is away from the sub-cortical system entries, I'm gonna put that patient back to sleep, finish that up for a while in the resection, then bring them back, wake them up and test when I get closer to the DTI tracks, which I have in my navigation system, just as a means to tell me what I think I'm gonna cause. So this is gonna vary a little bit, and as I mentioned, the anesthetic regimen really relies on three drugs, propofol, remifentanyl, dexmedetomidine. But sometimes up to 42% of the time, I'll change that regimen. And the way I do this is I put the patient asleep, I watch the patient in the operating room and make sure they're comfortable. Some patients get very disinhibited on this regimen, and then we have to back off one drug or the other, but this is all worked out before the skin incision. So by the time the skin incision is made, we have the anesthetic regimen that we're going to use for that patient. Could be dex and remi, could be propofol and remi, it could be just remifentanil, it just depends what they tolerate, we have to be flexible in this regard. Now, in my experience in this population of patients, even though this series was well before I hit the 2000 patient mark, the late neurological deficit rate has not changed. It's still between 2 or 3%. Using these standard strategies of mapping cortical and sub-cortical, all the testing paradigms that you see. So that's good news. The good news is that if you follow this regimen, once you get up to the speed of it, you will stay on this plateau and continue to be on plateau. That's very, very acceptable. And as you'll see from other publications, that's not always the case. Now, there are times when in the post-operative period, we get concerned about the recovery pattern of patients. And so when I have a patient with a deficit, what I like to do now is get post-operative DTI. That gives me really good information as to whether or not I've come close to the tracts or even transected the tracts. What's interesting about this as I've learned, is that not every spoke or part of the TTI tract is functional. So a lot of times we're down in there, we map, we don't see the tracts. We map, we don't see any deficits, we resect. Postoperatively the patient has a deficit, we do the postoperative DTI, and we can see some of the pathways can be transected. The fact that we didn't find them during the mapping just indicates that not all of these spokes of the subcortical pathway are accurate, right? This is a DTI. This is not a functional image. It's a DTI. So why don't we see a significant deficit that is permanent? We can get a sense of which part of the tract is injured and then going forward we know exactly when to do the post-operative DTI, if we're concerned that the deficit is not resolved in a timely fashion. But take on messages that I find the post-operative DTI is very useful as a welcome strategy. So for example, in a case like this, this is a study that's about to be published in Journal of Neurosurgery. And what this study represents is a perfect example of where the cortex is silent, but it's the sub-cortical path where it is important. But what I mean by that, when you have a slow growing tumor in a region like this, oftentimes, I can just go back, Often times the cortical region is silent, meaning, it's been reorganized. And for that reason, we don't find any function stimulated in cortex, but where you can get into trouble in these cases, in other words, if you say, why don't we do mapping? Where you're getting into trouble was on the deep end, on the subcortical system, where we're looking for these pathways, like the SLF or the arcuate fasciculus. And in this study, we show very nicely that even though the cortical pathway is negative, we can activate subcortical pathways. Once we activate them, we don't go in further, we leave them alone, as long as we don't injure them, these patients don't have a deficit. All of these deficits were resolved. So look at what happened. We find the pathway, we leave it alone, no deficit. We find the pathway. Sometimes we don't find the pathway. The patients have a post-operative deficit, but because when we find the pathway, we leave that alone, they're not going to have a permanent deficit. And if we don't find it, we just do the resection, we're not concerned about it because anything we're gonna see is transient. And it's gonna be from swelling or transient ischemia or manipulation. The bottom line is, if we find function subcortically we stop, 'cause plasticity in the subcortical white matter is definitely not as likely impossible as when removing the cortex. Now, if you wanna look more about the awake technique, this is a review we did colleagues all over the country and North American, in Toronto, spearheaded this effort and what we basically looked at was every article ever written, so that, ever written, so that we could get an idea of what the likelihood of the deficits were in the literature. Now coming back to this, in this study, because this was a study that we published, on our experience, using these modalities the we mapped, with language, motor function, visual fields, et cetera. And then went back and looked at the literature and looked at the stimulation induced seizure rate and permanent deficit. So if you want to say to yourself, "Well, where should I be at your stage? And doing these cases, when you have learned the technique, if you're using the technique that we're talking about here today, then the likelihood of a permanent deficit is very low, 3%, anything more than that is just simply too high. So again, this, the only thing I could say based on this talk is if you use these strategies, use stimulation parameters, this is what you can expect. And when we have intraoperative seizures, even though we still see them a couple percent of the time, they're very transient. We can abort them with cold water, irrigation and I'll show you an example of that later. Okay, from a technical point of view, what does it look like in terms of the organization of what we do? Well, this is our basic set up, with us being in this location. The nurse here, navigation here, the electrocorticography unit is over here, the technicians are here working with us on the scopes, and we put the stimulator over here, and our physiologist is behind the drape, as is the anesthesiologist. This is a really basic setup for us. On the left side, you can just reverse it for the right side. And we'll do this in both this direction and over 180 degrees for the other side, we very well. Now these are the basic tests that we use, object painting and reading. And I think this works very well. And the reason why we use this is because years ago Penfield showed that if you look at postoperative deficits in naming and reading, then it turns out that these are the most reliable ways to predict who's going to have a permanent deficit. So object painting and reading is critical. When you get underneath the surface, you need a different strategy. Well, of course we always test for naming and reading, when we get under the surface of the subcortical system. But depending on where we are, we do different tests. So let's tease this out. There were two basic subcortical systems. One is the ventral pathway, which is represented primarily by the IFOF and the ILF. And the second is the dorsal pathway, which is principally related to the arcuate fasciculus and the different portions of the superior longitudinal fasciculus. We published a paper showing that we could use two mapping paradigms, to find these patterns pathways. So the first was picture-word interference. So if we show this slide to a patient and we say "We want you to read the word that's related to this picture here" So these are two animals. This is an animal and fruit. So if you look at this and the patient sees it and they're told to read the word that's related to this, and they say rabbit, while I'm stimulating, it passed the word interference test. It's your word interference test. If I'm not doing this, and I'm just before I get to this point and I'm stimulating along the way, and I start to see semantic paraphasias, I know that I'm getting close, if not in the ventral stream with the IFOF and ILF. if I'm in the posterior stream, the dorsal stream, looking at the arcuate fasciculus or the SLF, while I'm stimulating white matter, I can have the patient's name and I can look for stimulation induced phonological paraphasias. If I want to test for this during a white matter dissection as well, I can have them do sentence generation where if they can tell me upon looking at this picture that she is writing a letter, then I know that this white matter pathway is intact. This is where we do the sub-cortical language mapping. And we're stimulating in one hand, we're using the Cavitron in the other hand, this could be done with both monopolar bipolar stimulation. There are another, there are other devices now that stimulate monopolar through the Cavitron, stimulate monopolar through a suction device. I prefer to do this one because I like to use the Cavitron to remove the tissue. And I just wanted to point out that there are a lot of different strategies to do the subcortical mapping and the cortical mapping. So in my experience I told you I use naming, reading, picture-word interference, sentence generation, combination of those things, cortically and subcortically. In other experiences, such as like my colleague Hugues Daffau, he likes to use multiple different tests for different locations. So he'll know all of his cases and the right and left side awake, he will look for based on the location he's at, he'll look for different stimulation induced deficits in a number of these functions like reading or naming or comprehension in the sub-cortical system. He will look in the left and the right side for different functions based on locations here. And again, this can be very extensive. I don't go to this extent, not that it's not important, it's just that I'm perfectly fine, as are the patients I've talked to with very subtle processing deficit. That's the occasional perception issues in spatial orientation. Things that allow them to perform 95, 90% perfectly fine. But if I extensively map, I might be able to find some other functions that got them to the hundred percent phase, but they're not phased on this. And I think this is a major difference in some of us who do a lot of this type of surgeries, and I'm willing to definitely use the basic strategies that I've explained here to get me to a point where patient speech is perfectly preserved, they're able to do their work, they may not be as proficient and may take a little bit more time, but I'm just trying to do everything I can to get as much of this tumor out and if there's a bit of a trade-off, I'm perfectly fine with that as long as it's a very small, minor trade-off in that setting. You'll have to pick and choose as you go along as to what you think is important. And it's important to also talk to your patients to make sure that all of you are on the same page. Okay. So if you want to learn more about this, this is the paper that we published. It very nicely shows where the cortical and subcortical localization may be. And I think that this can be very useful before you start doing sub-cortical mapping. They're just trying to understand what these pathways do, what functions this subserve. Now there's another strategy that you can use, which has to do with connectivity map. So preoperatively you can use functional MRI, you've can used magnetic source imaging and you can present paradigms to patients and you can look for an activity networks in these patients. And I find this to be somewhat useful in the sense that if I get a map like this where I know that there are low levels of connectivity in blue, high levels of connectivity for a given function in orange then I'm more likely to begin to interrogate this with subcortical mapping sooner than I would do this, in other words if I got negative mapping here, I might continue to go through the subcortical system quite extensively before I begin my subcortical mapping. If I get through this and I get anywhere close to a highly connected area that I saw preoperatively, I might subcortically map that sooner. Why? Because if you look at some of these tests, some of these tests have shown us that if certain degrees of resection are obtained, then of course, you know, you're going to have certain deficits there. And so you have to stay under these if you're going to be careful. So again, the take home message here is I'll use preoperative functional connectivity maps to tell me when I should begin my subcortical mapping. Based upon these tests, which we use preoperative before we use connectivity maps, I won't go into that much more. Okay. So I'm just going to begin to go through the indications for awake craniotomy. And I wanna just emphasize the fact that this can be done on the left side, it can be on the right side, essentially anywhere you want to go down to the thalamus, the spinal cord to the cortical spinal tract, it's up to you to develop your interest in this. I do wanna talk about motor mapping and the sleep techniques before I get into some videos here. In motor mapping strategy, I found to be very beneficial when you're working in motor cortex or around it. And the beauty of this is you can do it asleep. And when we do it asleep, we put in EMG responses or EMG electrodes to look at muscle responses and that's very, very useful. In fact, this is the technique that I described years ago, sub-cortical motor mapping, very effective. You see how this works with the bipolar low frequency stimulation. Now, when I went back and looked at my outcomes two or three years ago in over 700 cases using this strategy, I was a little disappointed to see that with the low frequency stimulation technique if I found both the cortical stream and the subcortical pathway, and I had about a 4% risk using a low frequency technique of having a permanent deficit. And to me, that was unacceptably high. What did that tell me? It told me that the bifunctional mapping strategy with bipolar stimulation, 60 Hertz, 1 million of phase duration, that current density was greatest between the electrodes and what that told me was that I got too close to these pathways and I needed a more worldwide strategy to send the current up further, define the pathway before I got close to it. So recently we published the study with a new technique called triple motor mapping. Triple motor mapping uses the bipolar stimulation low frequency, but also uses the Bello, the Lorenzo Bello technique, where we use the monopolar electrode, high frequency stimulation, very high frequency stimulation, where in this setting the current spread is one millimeter per 1 million. And then in addition, we use either electrodes in the scalp over the motor cortex or stripping it through to get either transcranial or direct cortical stimulation to interrogate the cortical respond in term. These three strategies, monopolar high-frequency, bipolar low frequency in TMS or direct cortical stimulation, I think has turned this whole morbidity profile around. And now using these parameters, we're seeing at least in the first experience with the first 60 patients we've done, we only saw one deficit and this was four plus over five awake deficits. So basically the morbidity profile is about a half percent or under, and it was a very mild deficit. Why? Because we're able to send the current out, tell us when we're getting close. Once I get 10 millimeters away, five millimeters away I'd walked down with the bipolar stimulation mapping. But turns out that the monopolar mapping is really the best way to interrogate that white matter, and again, as close as you can and activate a response, the bipolar stimulation doesn't do. You get close enough. In fact, it gets so close that you can injure the pathway. And that's exactly what happened. And this just confirms that the distance is about one millimeter per one millimiter very reliable. And this just shows you with the first few patients that we did, there were 60 in this series and when we looked at the permanent neurological deficits is a monopolar stimulation as well, that these were very mild and they resolved in many cases, and they were only permanent in a few cases. So very, very useful. If you want to know more about the monopolar technique, this is Lorenzo's work published, looking at both cortical and subcortical stimulation, using monopolar. He very nicely compares to the world's literature, including papers with asleep versus a awake motor mapping, and when to use it when not to use. It in essence for me right now, I like to use motor mapping asleep. I find those very reliable now that I have a triple motor mapping technique. Okay, well, we're going to continue now with the heart of this discussion as to where the way craniotomy can be used in all the different applications of the technique for things other than fairly straightforward tumors that need to be approached for the awake strategy. This is just kind of an overview that sets the stage, showing that tumors located anywhere in the frontal lobe is close to the Sylvian fissure or near the motor cortex, can be done with mapping, of course, in the temporal lobe, front, mid posterior portion, parietal lobe certainly as one gets more toward the inferior to middle parietal lobule that's where you want to invoke these techniques. And then of course, in complicated areas, and we'll come back to this in an instant. let's start with just a zone one insular tumor. This is the Berger-Sanai classification. Then it's a brief video, which again, shows you that we're gonna first map the cortex, we're going to identify areas that are not functional and then we're going to proceed with the approach I like to take, which is a transcortical approach to the insult. So we're gonna go transcortical through the silent superior temporal gyrus and we're going to go transcortical, then the super Sylvian region through the silent operculum and then we're going to continue to stimulate and map, until we joined those two cavities through the uncinate fasciculus which goes underneath the fissure and above the lenticular stronger vessels. You can see them through there very nicely, see the middle cerebral vessels skeleton and flow seal put into the cavity. And then we can take a look at what be achieved with a transcortical approach. So you could see the lesion on the left, post-operative scale on the right shows you the access points, access points, for example, going through the operculum to get to this region of the zone one, and so we're too to go down along the cerebral vessel in front of them and behind it, continue that trajectory all the way back until we get a very nice resection of the lesion. So that's a pretty good example of an awake resection, where we use mapping to define the cortical function, work around the cortical function, few silent zones, to do a transcortical approach to the two. Let's get into sleep motor mapping cases. You see tumor in the supplementary motor area, and you see the DTI tract put in here, so we're not in the motor system, we're just in front of it. So how would we deal with something like that? Well, once again, we're gonna start with mapping the motor cortex behind the lesion, which is back here, we're then going to correlate this negative region here, cortically, done sleep and we're going to work down through this area, identify the faults, and then continue to resect and putting in the electrodes. Or I should say the stimulator in this case, if we're gonna use bipolar low frequency stimulation or in this cases we could use monopolar high-frequency stimulation to achieve the same degree of assurance that we're not getting near the motor system. So that's how I would do the sleep motor map in case. And that's what it looks like going all the way up to the motor cortex, but most importantly, in this area preventing any injury to the descending motor tracts, here's the postoperative scan, showing them all the way back. Let's go back and take a look at that, all the way back to the motor cortex here and you're through the MSA down to the motor cortex and all the way down to the singular sulcus. Now we have a study coming out that's going to redefine the supplementary motor area syndrome, but I wanted to put this in because I think it's important to keep in mind that there still is some controversy as to what needs the transient nature of a supplementary motor area syndrome. There was some speculation for awhile that it's disruption of the Aslant tract. This is a case report where you see very nicely the preoperative as them tracked through the tumor, how we transected the Aslant tract postoperatively, and the patient did not have a supplementary motor area syndrome, which is very nice. If anything had a bit of a hesitancy for just a few days, but this resolved pretty dramatically quickly, despite the fact that the Aslant tract has been dissected. So the is not the only component of the SMA syndrome. It's also a combination of the degree and the resection back to the premotor sulcus and the compounding factor in this oftentimes is singular resection. So if you stand above the single jars, you come back to the premotor sulcus, the degree of the SMA syndrome is not as great as if you continue to take the singular charms and you go back to the pre motor sulcus. Now let's go into the phase of this talk, where I show you how you can use the mapping technique to do other things that are critical for a gliomas surgeon. Certainly first one has to do a trajectory into the tumor. I like to think of this as a standard approach, where we're going to basically define the equator of any tumor in any dimension. Then we're going to draw the distance between the point on the surface to the equator and that's the shortest distance. And then we're going to go transcortical into that lesion. So I like to call this the transcortical equatorial approach for gliomas. So in this case, there are lots of different ways to come at a tumor like this in the mesial temporal lobe. I prefer to map this area. You choose the distance that's shorter between the surface and the equator, and I come directly at that area to do my resection. That's my general approach to all interactive gliomas, anywhere in the brain, as you see in some other slides. So this is a very nice animation, this is a tumor, for example, underneath the surface, we're trying to figure out how best to get there. I want to go straight down to the equator at the point closest to the surface, in order to do that I have to map the cortex to avoid injury to any of the language fields or the motor system. This gets me to the equator. I then map out into the periphery so that, if I find any sub-cortical tracts, I can stop at that point and then continue to do this until I've done a complete resection. And you'll also notice that I don't use a retractor system. I don't use the tubular system because I like to manipulate the cabin with my left hand, with the instrument in my left hand, which is typically the bipolar. I don't like to cover up or distort any of the anatomy because I'm still using my navigation strategy. So here's a perfectly good example of a lesion that I would use the transcortical material approach into the center of this lesion. And because this is on the left side, I'm going to map awake the sensory cortex. I'm going to map language pathways and it turns out there are no cortical sites in the inferior parietal lobe. There's one site in the superior temporal gyrus at the termination of the Sylvian fissure. It's critical for language. Now we're going to do a transcortical exposure and map all the way down to avoid injury to the subcortical pathway. Here, you see the delineation of the internal capsule, which allows me to do a very nice resection into the tumor trans cortically leaving a little bit of tumor on this side, which stimulated out to cause motor responses right here toward posterior capsule. So this is very, very nice and a nice way to do it, which is an untraditional way to go transcortical equatorial and to do something like this awake. But this is the best strategy from my point of view, using mapping to expedite the shortest distance into the center of luci. There are other difficult to reach lesions. I think probably the best example of this is the insular region. The insular region is complex for lots of reasons, not the least of which is the decision-making process. So do you go transylvian or transcortical, your work in between the vessels, like the two branches. Are you able to take the perforating branches into the insular system? How do you expedite this if you don't go train someone? The other thing to keep in mind is the lenticulostriate, turns out that the lenticulostriate vessels are typically not in the tumor, but as you can see by this graphic, they're pushed easily. And this particular striate branch is typically the lateral, is typically those branches that we can very nicely see with a peel bank around them. They're shiny because in addition to the pia, there is some arachnoid space primarily that has CSF on it. So just if we're not sure this is a lenticulostriate artery, we can take the suction device gently stroke the pia arachnoid interface here and if you see a drop of CSF that leaks out, no, this is not a tumor vessel, It's a lenticulostriate that's exactly where you stop. And don't go deep to that area because these branches get smaller and smaller as you go deeper and deeper. We tend to classify the insular tumors based upon classification system that we developed several years ago and anatomically on imaging we divide this so I can go back to the slide into zone 1, 2, 3, and 4 tumors based upon lesions above the Sylvian fissure one and two, lesions in front of the foramen Monro zones one and four, versus behind the foramen Monro. And as you see the reason for doing this is it gives me a pretty good idea to predict extent of resection before we even get into the awkward route We've also looked at the process of transcortical versus transylvian approaches. And in my experience with all the technology that microscopy, the, the issues that have to do with the Cavitron stimulation devices, et cetera, I actually find that I have better access into the insular through the transcortical approach. And I've shown that very nicely in the number of videos that we've done throughout the years. This is an animation of the video. Again, showing the technical principles of removing the front arm curriculum. After you map that it's silent, now, going through two branches in between, this is what we call the window technique, we're going in between opening the windows between these empty branches, then defining the lenticular strides and mapping the posterior limited internal capsule, which would be here creating a nice connection under the two branches and three branches behind the M3 branch is showing very nicely. I think the definition of the uncinate fasciculus which can only be seen, if you can join the super sylvian cavity the applying the lenticulostriate into the infra-sylvian cavity that defines the uncinate fasciculus. Now there are times where the trans-sylvian we approach works very nicely. This is a, the section that I did with Michael Lawton when he was with me, very, very nice to suction, not triviality. Even in somebody like his hands, it takes a good 30, 45 minutes to do this, but it gives you very nice exposure to some of these very smaller lesions. Then you have to just gradually dissect, move the Sylvian vein to one side or the other. You see it above the fissure here, and then you can gradually open it up by quite getting in these branches and defining the insular. Now the problem with that is if you have large extensions of tumor deep underneath the middle temporal gyrus, or underneath the front out with turbulent, you're not going to be able to use the transylvian approach to get that out of there. So in that setting, it's not unusual that I'll actually have the patient come into the operating room, do the exposure asleep, wake them up to do the mapping, put them to sleep again, do the transylvian split, do the resection and if, and now need to do any dissection transcortically, I now have a good critical map, and I know where I can do the candidate. So that's a another approach. And I don't make that decision until I get into the operating room as to whether to go transport or transylvian unless I know to begin with like this, it's a very small tumor. Well, as I said, most of the tumors we see in the insular system, they go well beyond the insular, they go up underneath your periculum behind the motor face cortex down underneath the middle temporal gyrus, and that requires transcortical opening. And on the dominant side, you really need to know that there's no language that's going to be transected without approach. Okay, this is the second of the part two series showing the approach to insular tumors. And again, the reason for making this so classification based on radiology imaging preoperatively is to be able to predict extent of resection of the insular tumors. And this is really stood the test, test of time, very nicely I've been able to show very nicely that even in the latter part of the series, now the series gets very close to 400 cases. We now have the same degrees of extent of resection really has a very significant degree. This is when I wrote the compendium article for colleague Shawn Jumper in the anniversary issue in 2018. Now 2021, we're up to nearly 400 insular tumors the same strategies, same transcortical approach, unless these are small tumors, the same use of mapping cortical and subcortical during process Plasticity I alluded to this earlier with some of the work that Geschwind did early on, and I have to really thank to Hugues Daffau for constantly reminding me that brain plasticity can and does occur in patients with chronic lesions, such as low grade tumors. And he encouraged me to go back to my population of patients, where I was able to show in low grade glioma patients that I had re operated on that plasticity does exist. So for example, in a case like this, we first define two regions in the back of the frontal lobe that are critical for speech, production and naming, 32 months later when the tumor recurs, I now remap the area and I did not find those same areas. So really very interesting in the sense that function moves in this case. And in fact, in 40% of all these examples, and I went back and read map, I saw function that move away. I rarely defend it, maybe one time saw function that moved into previous big resected site. So there is clearly the ability to lose function via reorganization from sites previously functional. And there's not a great likelihood of gaining function in sites that were not functional. Then you just map close to, or involving proximity than resection cabinet. There are ways in which we're trying to look at predicting plasticity in tumors in follow-ups. So for example, if we see a lesion and we don't want to resect it because we find function at the initial operation, the question is, when does reorganization occur? We don't often know the answer. We're trying to get the answer through network connectivity, maps, your MSI, or MNG studies with transcranial magnetic stimulation. And we think indeed that TMS or transcranial magnetic stimulation could give us that information as to when we're starting to see reorganization based upon those preoperative localization maps superimposed onto the MRI scan in the recurrent seven. The other thing that TMS does, which I think is very useful is it helps expedited gross total resection. And again, defines the functional system superimposable onto the MRI scan before you go into the operative. So not only can improve grocer resection rates with TMS, like we can do with other adjuncts such as intraoperative MRI, but we can also use TMS to hopefully begin to project when we're starting to see plasticity. So let me give you an example of it. This is a case that I did, where when I did the initial procedure, I found that there was an area that had had tumor in it that resulted in stimulation induced motor sensory responses that I did not want to compromise at that point. So I left that area. I watched the patient, we began to see on the TMS that there was an increased distance between the residual tumor and the motor side. So we're beginning to see a reorganization over a two year period of time. This is what it looked like initially. And now when we stimulated, we didn't see much in the way of motor function over the tumor that I left previously. So now I went back remapped that area, found that the motor system, which was previously located here had moved forward. And this allowed me now to come up to that area, extended my resection to the point of now being able to achieve the kind of resection that I wanted to get, being able to resect this era. So TMS was very important in telling me when plasticity what's going to occur, wasn't occurring in a real-time fashion. And it was very useful in allowing me to go back in and operate. Now, another area now I think mapping has helped me to find is it's really proved to me how viable it is in terms of being able to define operability. A lot of times we as neurosurgeons go into a clinic, we look at a scan and we say to ourselves, gee, I don't think this is surgical. I don't think this is operable. I think it's eloquent issue. And I've been surprised so many times in my career when I get into the operating room and find out that the preoperative imaging does not correspond to the intraoperative stimulation. So I wanted to go back and prove that that was the case. And so I took cases that were sent to me by surgeons who felt that the lesions were inoperable, We conversed before the patient was sent to discuss the fact that these were cases that we think they were inoperable based upon imaging, but we were going to go in and prove that. And indeed the skip to the end point of this study, we found that in those so-called inoperable cases, if I used mapping, I was able to achieve a mean extended resection of 84%. So again, there was no question that in that setting, I knew that I could go back in because things were really not functional at that point in time, even though the preoperative imaging was worse, but we relied on intraoperative stimulation mapping. And that worked out very, very nicely. I was able to go in and do the resection in areas that I was able to document there's no function. So for example, in this case, you know, show you what the issue was here. If you look at it, we saw two lesions and a multicentric GBM. And when I saw the patient that came with this FSRI map, which showed these hotspots of activation on FMLA, I said, look, I don't know whether these are real or not. You can see them super close here. So let's go in and let's map it. I did go in and map it. And indeed this was a previous biopsy site. Patient was told they had an inoperable multicentric glioma. I went in and map both of these sites to take out both of these areas of churn up. There was no functional finding there at any stage of the mapping. So I was able to then achieve the resection of both multi centered focus on, whereas before the patient was told this was inoperable based upon functional imaging. So I think it's a really, really lesson to learn for all of us. That mapping is really what the defines functionality. And you can't assume based on functional imaging, that the patient has an inoperable tumor until you go in the OR and map it. Now we can also use this technique to take us in the areas that we didn't think were possible, such as Broca's area, you know, forever we Were taught in medical school and during residency, that Broca's area initiates motor speech. So we can't go into that area. And so for that reason, I think we went back and we started looking at cases we had resected in the frontal curriculum, and I was actually surprised to see that the morbidity profile was very, very low. In fact, the only people who had morbidity afterwards were people who had morbidity preoperatively. It got worse a little bit. It wasn't significantly made worse with a permanent fashion. Most of those deficits did resolve to baseline and that there was really only one or two patients that had a new deficit afterwards. And I think that was probably because I was doing it in a time where I really did not have the right strategy for subcortical language mapping using both high frequency and low frequency stimulation. So based on that, we started looking at Broca's area and this is a perfectly good example of where you would expect to find Broca's area. This resulted in stimulation to speech arrest. This is a strip collector identifying the motor cortex and sure enough, we're able to resect this area completely, including the area that resulted in speechless Broca's area. This is what the patient looks like afterwards. You can see that they're able to open their mouth and articulate very, very nicely. So they don't have speech over this, they're disoriented, they have a facial group, but they're able to count and say very staccato based sayings like today's a sunny day in San Francisco. So when we looked into this and I must say that recently, we have a paper submitted with the combined experience of myself and it changed one of our residents, John Andrews. And we're looking at this where we show very nicely that we can resect areas that result in stimulation is speechless without pharyngeal movement. In other words, Broca's area. We can resect this very confidently because as it turns out Broca's area is a speech planning region. So we had published previously showing that we created recordings that what happens in this setting, when you show a very straightforward verb generation task to the patient, when they hear the word ball, they're told to speak what they would do with it, you can see exactly what happens in course, about 2000 milliseconds where they hear it in the auditory cortex, thinking of what the say Broca's area is activated first, and then the face motor cortex in Broca's area is silent. So Broca's area is a planning station for motor speech versus the face motor cortex, which is activated when Broca's area is silent. Then you see very nicely with the grid recordings, how this varies where when the STG activation occurs, Broca's area is just beginning to become activated. And then when we see motor activation of the motor cortex to say the word kick the ball Broca's area is now silent. Having been activated just before the board chip is stated, which is all proceeded by activation of the auditory cortex, which has the STG overlying. So it's a very, very nice, I think, depiction of how this whole system works. Now, I'm going to stop at this point. I think I'll come back at another point in this lecture series. And we'll talk about extended resection and outcome. This is not really a well-versed for technical video, because basically what we need to do is review the data that's associated with standard resection and outcome. The preceding lectures were really geared to identify the role of maximal resection under the auspices of mechanisms to improve safety and minimize morbidity associated with achieving maximum resection. The next phase of these discussions we'll get into the issue of why standard resection is important for global survival, but I'll stop at that point. And again, I wanna thank Dr. Cohen-Gadol, for allowing me to give this talk on the hope to come back and give you some other thoughts as well. Thank you very much.

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