Transcript

- Hello, ladies and gentlemen, and thank you for joining us for another session of the Virtual Operating Room from the Neurosurgical Add Class. Our guest today's Dr. Roberts Spetzler from Barrow Neurological Institute. He is among our very few guests who requires absolutely no introduction. He's pioneering work in cerebrovascular surgery is internationally known. Today, he's going to talk to us about vascular malformation of the spinal cord. His work is also pioneering both in the arena of resection of spinal cord, malformations and the sub peel technique that am sure he'll talk about as well as cavernous malformations among many others. Dr. Spetzler, thank you for being with us and I'm very much looking forward to learning from your take outs, please go ahead.

- Thank you, Aaron. It's a pleasure to be talking about, one of my favorite topic, it is not a very common lesion, but it is one that has truly made a difference as to how we treat it and how our patients do. So it is basically a classification. We can't really start talking about these unless we separate apples and oranges. So I've divided these vascular lesions in the spinal cord into neoplastic, which are the hemangioblastomas and the cavernous malformations. And the reason they're in there is because hemangioblastomas have frequently been misdiagnosed as AVM, and an angiogram was performed, and you could see this incredible blush. And they occur sporadically and they occur familiarly, and very similar cavernous malformations who outwardly exist with the endothelial cell. But otherwise, they're very much like hemangioblastomas except you can't see them in angiography, but they also occur sporadically in families. And then we go to the arteriovenous lesions, and there are really two types here, and those are the fistulas and the arteriovenous malformations. So I want to just give very briefly the neoplastic cases as an example. This is a 27 year old male, presents with minimal myelopothy, he has a thoracic lesion and the approach was through a Costotransversectomy. If we look at the lesion, you can see why it's often misinterpreted as an AVM. They are fast flowing. They have spectacular vascularity, but here on this MRI scan, you can really already tell that this is a mass lesion and it's distorting the spinal cord. When we look at pictures of the lesion, we see this incredible vascularity that is around the lesion. You can see it here after the lesion has been identified. And the important part about hemangioblastomas is that they have to be treated like AVMs. And by that, I mean, you have to go around the lesion, not through the lesion. So here's a very nice example, we're seeing the MRI scans and the lesion. You can again see the vascularity, and then you see this beautiful fluorescent orange color that is absolutely classic of the arteriovenous component of the hemangioblastoma. So now, we're very carefully separating the lesion from the spinal cord. We're underneath the spinal cord, because as you recall, this was anterior and there we are, and taking the lesion out. And post-op shows the lesion entirely gone. This patient had no change in the neurological examination. So when we talk about cavernous malformations, this is really, a entity that has taught us an enormous amount because these lesions occur everywhere in the spinal cord, in the CNS. And they have forced us as a specialty to find new routes, to very difficult locations. And the same really exists for the spinal cord. If we look at cavernous malformations, we basically have three approaches, one through the midline, one through the dorsal nerve root entry zone and one between the nerve roots. And I will show you an example of each. So we have this one, we have this one and we have this one. We don't want to come in from the front because when you come in from the front, you have the circumflex vessels that have to be sacrificed, which can result in permanent neurological deficit. So we want to come posteriorly, keeping the anterior spinal circulation intact. So these are basically the three avenues shown in this little cartoon that we can enter into the spinal cord and medulla. Here is a perfect example of a cavernous malformation. The reason this picture is there is because, this young man, was the son of this man. And it was a family that I already knew. They had cavernous malformations, familial cavernous malformation, and dad and son, of their multiple cavernous malformation had one in exactly the same location, which was right here. We followed these because they were asymptomatic. And then the young man suddenly presented to another hospital with a devastating event, became really paralyzed, quadriplegic, was rushed over to our institution, he still had some sensation in his legs. So we operated on him immediately took out the large, extra lesional clot, a occurrence that does not happen very often with cavernous malformations as they usually bleed into themselves. But in this case it was extra lesional hemorrhage. He had some mild recovery, but you can see from the smile on his face that he has, he was just a terrific attitude, and he was an inspiration to everyone around him. Well, his dad, after about eight weeks after this happened, insisted that his cavernous malformation be taken out. So we have several things. First you'll notice the vascularity with the veins. These are venous lesions, there's no doubt in my mind. They look like little mulberries. And this one is obviously posterior in the midline. So taking it out was very straightforward, preserving all the vascularity that was not part of the cavernous malformation. More difficult is a lesion like this. This one here is, not in the midline, it's off to the side. So how do we get there? Well, in this case, the best approach would be this way. And so, when we approach this, what you're seeing in this video is a lateral approach. Here is the dorsal nerve root, we're going right next to the dorsal nerve root. We spread the fibers, come right down on the cavernous malformation. And then with tiny little forceps, sharp dissection, whatever is required, we take out the entire lesion. It is very important to spend quite bit of time at the end of taking it out and inspecting the bed and removing every little white fascicle that there is, I used to say, "Never bipolar in the spinal cord or brainstem", and I've obviously changed my mind. So once that lesion is out, we go on to the next case, and this is somebody with repeated small hemorrhages and presented with this cavernous malformation. We see it's an anterior lesion, but it's a lateral lesion. So we want to come in like this. So we're going to go from a posterior lateral approach. And this time, what we do is we really go between the nerve roots. Going to make that, there we go. So here you see the dorsal nerve root, you see the dentate ligament. So dorsal nerve root, ventral is below it. So we're going below the dorsal nerve root, just like I showed on that little cartoon, find the lesion and take it out. One step at a time, and we just gently, and you can see the different ages, the consistency of the cavernous malformation where it reflects when they bled and here you see postoperatively, the lesion nicely gone, and he's been free of symptoms for that time. So now we get to these complex lesions, which really require putting them in their appropriate baskets. So you have the fistulas, there are two types. There's the extradural, which is one that is almost always being taken care of endovascularly without any trouble. And then there's the intradural fistula. For the intradural fistula, there are two variations, the much, much more common dorsal and the less common anterior spinal ventral lesion. Then we have true arteriovenous malformations, that means they have tinnitus with multiple feeders and multiple drainers. And you have the extra intradural one, and we'll go through each one of these separately. And then the intradural arteriovenous malformations, and they're divided into intramedullary, two variations, a compact and a diffuse and the Conus AVM. So here they are pictured, here's the extradural fistula. It may frequently cause symptoms by its large extradural mass through compression. You have the dorsal arteriovenous fistula, which is the very common one that occurs here. And then the ventral one, which is always fed by the anterior spinal artery. So here we have the extra-intradural arteriovenous malformations, these are the metameric lesions, the juvenile AVMs, they can be associated with syndromes, but they do not respect any orders. They can be intramedullary in the dura, in the bone, extramedullary, then you have the intramedullary AVM, the diffuse type which tends to be laterally and then invading the spinal cord. And then you have the compact one, not very common, but they are the ones that are fed by the anterior spinal artery, almost exclusively. And then you have the Conus AVM, which is a separate entity, which is a combination of diffuse and compact because of the anatomy that exists there, the basket of the anterior spinal and posterior spinal arteries, unique in its anatomic location. So I said already, there are two types of intradural AVM, the dorsal and the ventral. Even today, there are people that believe that this fistula exists in the dura as opposed to being actually intradural, I hope to convince you otherwise. And then the other one, which is straight forward, ventral. And if you look at the pathophysiology of the dorsal intradural fistula, it is venous hypertension, and that is the culprit, and that's what needs to be diagnosed to avoid progressive neurologic deficit. Rarely do they hemorrhage, I have seen one. Imaging, I'll show you but it's very straight forward. Slow flow on angiography is mandatory, explaining the high venous pressure. The presentation is progressive myelopathy. Old nomenclature was type one or long dorsal. So let's take an example of one. This is a 38 year old female, progressive paraparesis, lower extremity pain. She underwent the laminoplasty. This is the study beforehand, the classic coiling. Also, you can see the edema in the spinal cord, that's from the venous congestion. And then this is very slow flow. You see an artery coming up, coming down, and then you see all these coiled vessels. So, in the old days, and Yasuda was one of these individuals that would do a laminectomy from the top to bottom, take out all these coiled vessels in the expectations of curing the patient, when in fact these are nothing more than draining veins. When we look at the lesion and I've done a lot of exploration, so this is extradural and what you see here is really a plethora of vessels all over them being recruited to the fistula side. When you look intradural, right here, you see one vessel coming out and that is the fistula. And this here is nothing more than all the veins. So if we look at it anatomically, and we've done this repeatedly, you have the artery here and here, you're going from artery to vein, same thing here. All we need to do is cut this, occlude it and you have a negative angiogram, and the patient will slowly improve. There are cases where you see more than one feeder and here's another 41 year old female, progressive paraparesis. And what we want to do here, is this here. You can see why individuals thought that this was the problem because you have all these vessels but that's the extradural recruitment, this here is the fistula. There it goes, from artery to vein. Two levels lower, we also see feeding, but if we look at this closely, we see that this here is exactly the same as over here. So this here is nothing more than an artery that connects to the other artery. It's just a recruitment, just like all of these vessels to the recruitment. And sure enough, I've turned the operative picture, so it's in line with what I just showed you. And again, we go from artery to vein and this here is the vessel from down lower, joining the one here, and this here, right here is the fistula's point. So how, with this lesion, do we get this progressive venous pathology? When you think about the fact that they're very slow flowing, why would a slow flowing fistula cause venous hypertension? In comparison, if you have a hemangioblastoma, an arterial venous malformation, you have a lot, lot, lot faster flow. Well, the problem is this here. When you measure the pressures inside the vessels, you can measure the draining vein while the fistula's open, and it can be as high as 60 millimeters of mercury. But think about that, 60 millimeters, that's approaching arterial pressure. When you close the fistula, it goes down significantly, but it does not go as low as the veins into which it drains. These are the epidural veins and if you remember, the intraspinal vasculature drains into the epidural vein. So if we measure all these pressures for this, this is what comes up. Well, what's the explanation? Well, the explanation is very similar to the dural arteriovenous fistula you have up in the head that are related to venous occlusions. So this, I think, is what happens, is we have the fistula, you compromise the venous outflow and you get these incredibly gorgeous vessels. These lesions are important to diagnose because you can make a huge difference in the prognosis of your patient. So I will include just one extradural arterio, I mean, one dural arteriovenous malformation that's higher, and that's this sort of a dramatic example of a patient with this lesion. If you look at the MRI scan, you see edema in the entire cord, significant trouble with mobilization. This is one that my colleague, my endovascular colleague, Dr. McDougall was not able to embolize, probably would be able to today. And, it's a nice example of what you need to look for. Here we are in the posterior fossa, and we're looking at this massive vessels where the vertebral artery and PICA come out. All it requires is occlusion of the fistula, but here's PICA now, still filling. And all we've done is we've kept intact, the vertebral artery and PICA and occluded just the fistula's point. All we need, just like in the head, is one clip. Post-op, angiogram is completely normal. This is pre-op, remember all the edema, this is one year post-op, fortunately he was able to recover virtually back to normal. Now, when we go to the, pathophysiology of these lesions, which is the anterior fistula, this is a lesion that was separated into three types by Merlot, and we kept that small, medium, and large. Imaging is straight forward. These do present with hemorrhage. They can also present with progressive myelopathy. And here is a nice example. This is a little 15 year old. She's had several episodes of transient paraplegia, was brought in and she has this, so you have the Artery of Adamkiewicz coming up. Here's the fistula and venous drainage up and venous drainage down, went through a transthoracic approach. Dr. Dickman helped me with this exposure. And then here, we are anterior, we see the Artery of Adamkiewicz coming up. We see the fistula, we see an aneurysm, that had obviously bled some and it's causing the problem, and, we take it out. Again like, here, you can see the Artery of Adamkiewicz coming up, and then the anterior spinal artery continuing on Once the appropriate exposure, the procedure itself was easy, and here we see, no longer any fistula, normal anatomy. Type C is the large type, same sort of thing, but here, it was progressive paraparesis because of the large coil vessels, here, you see the size of these vessels to come, dramatic at surgery. Look at these venous aneurysm, looks absolutely awful. Here is the anterior spinal artery, here is the fistula going into, this is looking anteriorly from the side, secret is finding this point. All it required is this one clip, and this is what happened, from red to slowly turning dark, angiogram, negative. Extra-intradural AVMs, fortunately are very uncommon because they can be quite problematic and they can cause trouble with compressions, still hemorrhage, progressive myelopathy, pain. They used to be called Juvenile AVMs, Metameric AVMs or Type three. I call them extra-intradural AVMs. Here's a classic case of an eight year old. You can see what's been done beforehand, three previous operations. This is what she had. I went up to the end of vascular suite, stole all the glue that was available, injected it directly into the muscle, after I had separated the AVM from the dura, and we were able to cure this lesion, that's not always possible. Here's one that's a little more interesting. You can see the component, where it is extradural compressing the spinal cord, and that really was the cause of her symptoms. When we look at angiography, we see this here, we see partially involving in this spinal cord and I'll show you that on the surgical, angiogram. So I count on my colleagues, a great deal to obliterate as much of this as at all possible. And here's the post, after they have embolized rather successfully, and then we come to surgery. So here, the dura is open, so that I can inspect the inside and you can see the component of the intradural arteriovenous malformation. The secret here naturally is, here's the portion intradural, the secret is to preserve the nerve that is surrounded, and I wasn't sure whether I was going to be able to do that or not but I started off with that. So I'm going extradural, I want to get all the feeders, I want to get the drainers, and I just keep going around identifying the nerve root at some point, which is right, caught underneath here, and these bipolars are godsend for this nonstick. And here we go, we get the intradural component. Can you go onto the next slide, please? There we go. And here was the pre-op, and here's the post-op. This lesion is gone. The spinal cord is no longer compressed as you can see here. So she improved immediately because naturally her problem was one of compression. Conus AVMs, these are fascinating lesions and they really came about, we identify these and published it in 2002 is because, they are unique, and they are unique because of their anatomic locations. They are peri and intramedullary in location. They have multiple feeders, ventral, and dorsal, and their unique angioarchitecture is based on the fact that this is the basket of spinal artery connections of the posterior and anterior spinal artery. And this has all been published, but you can see the presentation, weakness, bladder, bowel, seizure, but really pretty much of everything, prior hemorrhage, 30%, myeloradiculopathy, 63%. Some present only with radiculopathy, if it only involves the nerve roots, 75% were ambulatory. This is what they look like at surgery. So they can present with everything, venous hypertension, compression, or a hemorrhage. They're easily diagnosed because they're are so location specific. So here's a classic case. This patient presented with a subarachnoid hemorrhage. She was a professor in Texas and her intracranial workup was negative because she presented with a subarachnoid hemorrhage, they thought she had a intracranial aneurysm, and that's obviously one that you have to keep in the back of your mind, that a subarachnoid hemorrhage can occur from lesions in the spinal cord and even from tumors. So she was at this point, neurologically intact. This is what her angiogram looked like. And this is what our surgery was. There was a very little embolization that could be done, but here's the secret. So we want to do is we want to go right along the Pia, bipolar, trying to keep the normal vascularity of the nerve roots intact, so we're right at the Conus going down to the nerve roots, separating it between the nerve roots, sharp dissection, light at sucker, the non-stick bipolars made by Stryker, and then sharp dissection, making every effort to preserve the nerve roots. We may traumatize some of the nerve roots, but as long as we keep their vascularity intact, they will certainly recover. And so we just really keep going to take the lesion out. And we cut the final terminally. Doing ICG, there's no longer any fistula's component. And we still see lighting up of the nerve roots. And the next one, this is her post-op angiogram. She was full strength, but she had mild lower sacral root anesthesia. She had urinary retention requiring straight cath for a couple of days. She was discharged home on post-op day four, and then came back for a repeat angiogram in six weeks. And, it was also negative. And then by then her urinary symptoms had resolved. Anesthesia was improving, and she ended up doing very, very well. So when we look at the Conus AVMs, we recognize that they are a distinct entity, symptomatic patients are best treated with a multi-modality approach, and results are encouraging, 88% cure, 43% stable, 43 neurological improvement. Of the cured patients, all ambulatory patients remained ambulatory, of the non-ambulatory patients, 75% became ambulatory, and we published this back in 2012. So the last entity that I'm going to discuss is, the actual arteriovenous malformation. Remember we divided them into two types, the compact and the diffuse. And this has also been published for 20 patients during this time period, and this is how they presented paraparesis, parasthesia, myelopathy, et cetera, all the way down before. Embolization was attempted in 100% and was helpful in 60%. Morbidity, angiographic obliteration, functional status, these patients did very well. I want to show you just a few cases. This is a compact AVM. If you look at the lateral, you see the AVM, you see a large venous aneurysm, in the, AP projection, you see the anterior spinal artery, again, the aneurysm and the AVM. So in this case, you really have to come in midline, and here we are opening the median raphe, gently coming down, we're going to be facing the aneurysm before the AVM, unfortunately, so we have to be particularly careful. Here's aneurysm and AVMs. I don't use these peel sutures anymore. That was a old case, coming all the way down to the anterior raphe. So here, underneath this arachnoid is the anterior spinal artery, just so slowly go along, separating all the feeders and then just lifting the lesion up. And here is the lesion cavity and post-op, and fortunately she ended up doing very well. Next. More difficult are these, this here, is an AVM that you can see intraspinal, patient became very symptomatic with an event, clearly intradural, but if you look at this cut, you can see that most of this lesion within the capability of the resolution of the MRI scan is lateral. And if you look at the angiogram, you see the anterior spinal artery and you see that almost all the lesion is off to the side. This could not be embolized because when they did a challenge test, the patient became quadriplegic. So this one is, we're looking at the lesion now, and you can sort of see the ICG briefly. And so what's the secret with these lesions? Here, we see the dorsal nerve roots. What we discovered that we can do with these lesions is to go along the edge of the arteriovenous malformation. There obviously are vessels going further intramedullary, and what we're doing is we're cutting really across the AVM, why that is possible in the spinal cord, whereas we can't do it in the brain, it's still not entirely clear, but obviously there are a lot of U-fibers that go in and out. And so the whole secret here is to separate these lesions, get them out, leave the normal vascularity intact, ICG shows, no longer any flow. And if you look at the post-op, completely gone and the patient had no change in the neuro exam. This is a patient that had been embolized twice in Paris by a famous endovascular surgeon. This young woman is from Norway and they stopped with a third embolization because she became worse during the procedure. And here is what is left. So this is the arteriovenous malformation. Here, you see it, here, you see it, again on the MRI scan, notice that there's a good portion of it that is lateral, that's what we're banking on. And so when you look at these angiograms, these are actually videos. There we go. You can see the diffuseness, but again, coming off to the side. Here we go, lateral in the gutter. So what we want to do with this here is basically the same approach. Next. And, Oops. When you look at this, you see lots and lots and lots of vessels, but the same practice of staying right at the edge of the spinal cord. And again, I can't overemphasize how important with these little fragile vessels it is to have non-sticking bipolars, and, we just work between the nerve roots, along the dentate ligament, cutting it, and give it more mobility for the spinal cord. And we can always, and that's the dentate ligament we're cutting right there. We can always rotate to get to the anterior portion, and there's the lesion, and there, it comes out. Important, as awkward as this looks, we don't want to do anything to it. We don't, we see it all filling, but we don't see any shunting, that's the important part. Here she is, this is with permission. A very, very happy patient, indeed. And if you look at the angiograms, you see that the lesion is gone. I'm going to show you one last case, which fortunately, came after I'd had quite a bit of experience with these lesions, because I don't think I would have tackled this the first time. This is a woman that came in, in a wheelchair devastated by this lesion. And when you look at it, you just, it's just hard to imagine that there's any spinal cord that you can really preserve. Giant lesion intradurally. You look at the MRI scan, it becomes even more intimidating, really takes up the entire AP ratio of the spinal cord, huge draining veins over to the other side, she was desperate to have something done. Left thyrocervical injection, everything was feeding it. And then we see, the embolization, post embolization, very nice job, really helps. Even when you can't obliterate a lot, just having this onyx in there helps you at the time of surgery, with knowing where you are and Dr. Albuquerque here did just a beautiful job. So here we are at surgery. You see the shunting that continues, we're looking down at this formidable lesion, but just like before, we recognize how far the spinal cord has been moved over to the other side, and we do exactly what we did with the smaller AVMs, we go along the spinal cord and remove all the feeders, all the vessels that are going into the spinal cord, here, you can see, the black is the onyx that Dr. Albuquerque put in there, and just keep going. ICG is so helpful because it helps me to direct my attention to where there is still a fistula's component. And then just ever so slowly, bipolaring all the vessels, bipolar cut onyx, and here's the lesion out. Now, you see this big empty space where the AVM was before. And when we look at the post-ops, we are gratified that there's nothing feeding. And in fact, she came back a year later, with negative angiogram, walking into the office. This is one of the most grateful patients I've ever encountered. And I'm delighted every time I see her or her pictures. So, why is it possible to be able to do this, to cut across an AVM in the spinal cord when we can't do it in the brain? And it must have to do with so many of these fibers going in and going out, maybe the vascularity is just different enough from the intercranial one to allow us to get away with this. So in conclusion for spinal vascular lesions, I think, microsurgery and embolization remain the gold standard for intramedullary AVMs. I did not address radiation and I do not recommend it, but recognizing the ability for obliteration without complete resection, I think has important implications for treatment and really allows us to do things that we thought previously were impossible. I thank every one of you for your attention and hope that you can help future patients with these fascinating lesions. Thank you.

- Thank you so much, Dr. Spetzer, really incredible contribution. This area of spinal cord vascular malformation is such a great example of your personal, incredible contribution to neurosurgery as a pioneer for diseases that really previous to that, did not have a treatment. I think arteriovenous malformation of the spinal cord, just that patient you mentioned with that large AVM, that was quadriplegic and walked out a year later in your office, extremely satisfied, truly exemplifies your legacy in neurosurgery, and that's just so huge. I think one of the things that I have learned about these AVMs is really, again, preserving those PO membranes, staying epithelial and remaining courageous and believing that you can remove the lesion and cut through it without really getting into trouble, as long as the trunk of the spinal cord and the vascularity of the spinal cord itself remains intact, I think the patient does well. Do you have any closing comments about technical expertise required in operating on these lesions?

- One of my main tenets when I teach and you do very complex cases is that the patient and family are always prepared that it may take more than one stage. And when the patient and family are prepared for that, it is not a big deal for them to go back to surgery. What that comes down to is that when you're in a situation where you're not sure whether you should do the next step, maybe sacrificing a vessel or something, and you're not sure whether that's going to have negatives equally, the beauty is to be able to stop, reassess with imaging, reassess the neurological condition and come back the next day. I think one of the big mistakes we make when we're very young is we sort of feel the urgency to finish what we started when in fact is, the only thing we really should be concerned about is the best outcome for the people that put their hands in our care.

- That is so well said, and that goes back to the first principle of medicine, which is primo no che, in other words, do no harm first, and I think that's so extremely important. I have become, routinely performing intraoperative angiography for these vascular lesions, spinal cord, wire popliteal stick, or, putting a sheaf in before surgery to do that, and that you can do in an angiogram in surgery rather than after surgery and gauge how much further you need to go. Do you do routinely intraoperative angiography or you don't feel that's necessary?

- No, I don't. Actually. I used to early on, I've gotten so comfortable with ICG for my decision-making and then no matter how good your inter-operative angiography is, it is never as good as it is when it's up in the room where you have the angiographer really being able to use every possible mode for the best result, and so since resolution is very common. However, what I have done is when I'm worried that there's still residual and I'm not set up for inter-operative angiography, I keep the patient asleep, pick him up one floor, get the angiogram done, patient and family knows about this, and if there's any residual, bring them back down. I think having inter-operative angiography is perfectly all right. There's more than one road that leads to Rome and you have to use the road that you're most comfortable on.

- Makes great sense, and lastly, I want to ask you, do you routinely use motor evoked potentials? I assume you use somatosensory evoked potentials. What kind of monitoring do you routinely use?

- I use both motor, I use sensory and I use anesthesia that allows you to get burst decompression in order to increase the length of time for temporary ischemia. So tolerance, temporary ischemia by getting down to the bursts decompression, we could all go way back to the basement, we produced produce barbiturate anesthesia, which has sort of disappeared. The other thing that that metric does is it decreases blood volume, which gives you more room.

- I got you. And very last comment is on these AVMs, I do routinely monitor, just like you mentioned. However, there at times that the motor evoked potentials drop, I avoid the retraction I'm doing, I leave everything alone. I irrigate, I bring the blood pressure up. We do all the routine stuff that I'm sure you do and everybody does. Still the motor evoked may be declined. I usually continue removing unless I have a complete loss because I've been so surprised when in the beginning, I, because of the epi peel or sub peel technique, the drop looks like there's significance, 80% drop on the evoked potentials, but the patient wake up with minor weakness and they dramatically improve, and there could be residual dural disease. So in fact, they can be misleading even though the patient is going to eventually do well. So unless I completely lose the evoked potentials, as long as there is some evoke potentials remaining, I get more evokes, I continue doing the operation. Have you been doing anything different?

- No, you answered it much, much better than I could have. I agree 100%. I would go even so far as if the motor potential disappears for me, it's sort of like a drop in the blood pressure. You stop, you look at, your operation, see if there's a problem that needs to be addressed, but if everything else checks out okay, I have seen a lot of absent motor evokes that have had absolutely no deficit after surgery. So I think it's just one more thing to keep in the back of your mind, it triggers, stopping, looking, assessing, and then making a decision on whether to proceed or not based on what you'd see.

- So in other words, it's just one piece of the puzzle. You cannot make a decision based on that to see the whole picture. So what I'm hearing from you is that even if you lose the entire potentials, if you feel like everything to you looks good, blood pressure as well increased, you don't see any inter-operative disasters of huge hemorrhage or significant sacrifice of the vascular church of the spinal cord, you still continue, but it will be a piece of information that would include in your overall decision-making. Am I correct in understanding that?

- Yup, that is the objective algorithm.

- Okay. Well, I cannot thank you enough for your incredible technical pearls. We all have been your students either in your OR or outside of the OR, and you have been an incredible innovator, teacher, neurosurgeon, athlete. And, in many, I don't know what to say. The multidimensional aspect of your career is essentially not only unique, but just one, is second to none. So I want to thank you again for being our guest, and as I'm sure you know, I'm going to harass you again for another one soon. So it's an honor to have you.

- My pleasure. You have a great day.

- Thank you, you too, sir.

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