Grand Rounds: MVD for Trigeminal Neuralgia and Hemifacial Spasm: Pearls and Pitfalls
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- My name is Steven Giannotta and I'm Chairman of Neurological Surgery at Keck USC School of Medicine. And today Aaron Cohen-Gadol has asked me to discuss with you, microvascular decompression for both trigeminal neuralgia and hemifacial spasm, and I'm honored to do so. First trigeminal neuralgia, it's important, probably the most important thing about trigemial neuralgia is making the diagnosis. And of all the components that go into making the diagnosis, obviously the patient's description of their pain is probably the most critical. And the thing that I look for and ask about is the electrical nature of the pain. If the patient describes something that is fleeting, sharp or stabbing, or I'm always listening for the keyword, namely electric shock. If I hear that, then I think we're probably 90% on our way to establishing the diagnosis. Obviously the pain is fleeting, it's not constant, it can occur in any of the three or all of the three divisions of the trigeminal nerve. Probably the second most important component of the patient's description of their pain is trigger phenomena. If a patient walks in to the office and is describing their pain and they're holding their hand against their face, that's probably a good sign that you're dealing with some other form of pain, perhaps some atypical facial pain that may very well not be a trigeminal neuralgia. At least from the association of a vascular compression. Not all patients will have pain free intervals, but a pain free interval is not a factor that would preclude the diagnosis of trigeminal neuralgia. The causes of trigeminal neuralgia, obviously the cause that we're most interested in and the most common cause that we see as surgeons is vascular compression. Clearly patients can present with trigeminal neuralgia with associated tumors. Most commonly these are probably meningiomas at the petrotentorial junction, less commonly trigeminal tumors, frankly most tumors in this area do not cause typical trigeminal neuralgia symptoms. They cause hypalgias or some other dysfunction of the trigeminal nerve. However, tumors can cause classic trigeminal neuralgia and frequently do so because they actually cause the vascular compression by compressing the artery between the tumor and the nerve. You will frequently find that when operating on these people to remove the tumor. We've seen arteriovenous malformations, small ones, especially of the brainstem that can actually cause vascular compression. And rather than a cause of trigeminal neuralgia, more an association trigeminal neuralgia causes multiple sclerosis. Rarely do these people have a vascular compression syndrome, but if you see enough patients with multiple sclerosis with trigeminal symptoms, every once in a while you will find someone who has a vascular compression phenomenon as a cause of their trigeminal neuralgia. Treatment I tend to divide the treatment categories into destructive and non-destructive. Virtually everything on the left side of the slide is in some way, shape or form destructive. Rhyzotomies, radiofrequency, nerve avulsions, that usually refers to local nerve avulsion. Like for instance, the inferior cerebellar compression or decompression, glycerol, and of course, radiosurgery using any one of a number of methodologies. The most common one, and the one that we use most frequently is Gamma Knife. Of the non-destructive MVD of course, is the classic. And with neuro, I put nerve stimulator on there. Rarely do we use the nerve, peripheral nerve stimulator for trigeminal neuralgia, more commonly it's used for atypical facial pain. Along with the classic symptoms to help us establish the diagnosis, or I should say to establish a cause, some form of a complimentary imaging is extremely helpful. And now with a sophisticated MRI and fusion techniques, one can use these techniques to our advantage. And in many instances, not only identify the offending vessel, but where the contact is and how compressive the, or how distorting the contact is. As far as surgical technique, I usually use a relatively small S-shaped incision. I try to position it at the junction of the sigmoid and the lateral sinus using some external landmarks. Once the craniotomy has done a C-shaped dural incision, usually the most helpful with, at the beginning of some retraction on the dorsolateral aspect of the cerebellar hemisphere. Once you get a little bit of room, a retractors thereafter rarely needed. This trigeminal cisterns open spinal fluid is allowed to egress. The petrosal veins, we'll see some pictures, but there are various ways of dealing with the petrosal vein. Certainly branches of the petrosal cistern can be sacrificed with relative impunity. And certainly there's no reason to leave petrosal vein branches in your way, if there in any way gonna compromise your ability to identify the nerve root entry zone. We monitor hearing on all of our cases and I'll go over some statistics on what our experience has been using hearing monitoring during the procedure. So an S-shaped incision behind the mastoid. We try to use landmarks to identify where we think the lateral sinus is going to be and try to position a little craniectomy at the junction of the lateral and sigmoid sinuses. The craniectomy doesn't have to be large. You'll see in this instance, the partially exposed lateral sinus and the total craniectomy width is about just a little over two centimeters. And you can see here, the trigeminal nerve is exposed. We are on the right side. Here's some arachnoid covering over the origin of the supracerebellar artery, which you can see is looping down and underneath the trigeminal nerve and then it loops back up and here you see the arachnoid still intact over the eighth nerve. I use this as in effect a safety measure to ensure that we don't stretch the eighth nerve and compromise hearing during the procedure. The typical retrosigmoid approach is shown here. This is in effect what we try to avoid during the microvascular decompression for trigeminal neuralgia, namely that lateral retraction of cerebellar hemisphere. We know from a monitoring studies that can put traction on the eighth nerve and can be responsible for hearing loss. We thus try to restrict any retraction that may be necessary to a more superiorly at the junction of the tentorium and petrous bone, supposedly on the dorsolateral aspect of the cerebellar hemisphere. In this drawing, you can see how we emphasize that whatever retraction is necessary, a small two millimeter retractor can be used to depress the dorsolateral aspect of the cerebellar hemisphere, get you started. And then the rest of the procedure almost always can be performed without the use of much in the way of retraction. The reason we need a little bit of retraction as you saw in the initial slides, the craniectomy is relatively small. And with this approach, one does not have access easily to the cistern magna. So you need to really coax the cerebellum down a little bit in order to get the type of exposure that you need without the ability to empty the cisterns of spinal fluid. So the technique checklist is the following. We need a precisely placed opening in order to keep it at relatively limited and a relatively small exposure, minimal retraction, just enough to get you started and get you into the trigeminal cistern. The direction of retraction is key, so as not to put undo stretch on the eighth nerve. And then in an effort to maintain as little traction over the eighth nerve as possible, we try to maintain the arachnoid over the eighth nerve. Now with such a tiny craniectomy or craniotomy, there's a relatively small bone flap. I have not been in the habit of putting that back in there, I think it forms a potential virus for infections. So we just use a titanium plate, that's one of an array of prefabricated plates that we use in order to cover the craniectomy. And that I think personally reduces the possibility for any postoperative infection and the closure is relatively straightforward. So this is a video that will show a typical use of both the pledget and the glue, which I think most of us use for maintaining the vessel out of contact with the nerve. So here you can see we're on the left side, you can see the supracerebellar artery being advanced away from the trigeminal nerve, use of a fluffy pledget of Teflon felt and you'll see me taking pains to try to keep the Teflon felt away from the nerve and also to try to keep the Tisseel glue from coming in contact with the nerve. I'm not sure that that is always necessary, but you'll see here an effort to glue the Teflon up to the tentorium and keep it away from the trigeminal nerve so that any potential toxicity and or distortion of the nerve by either the Teflon or the glue is obviated. Remember where we are. The supracerebellar artery may be at a place where it's starting to bifurcate. In which case, one may have to decompressed two branches from underneath the nerve, as this video will show. You can see an indentation in the nerve from the underlying vessel. Here's petrosal vein. And the eighth nerve is under some arachnoid to the left of the screen. You can see the SCA looping down, and as we deliver the SCA from underneath the trigeminal nerve, you can see that we're actually at the branch point of the SCA causing us to have to in effect, move two vessels instead of one. And as it's typical, try as you might to maintain the vessel away from the nerve without any form of buttressing, many of these vessels with their memory will reinsert themself and compress the nerve. Here you can see the Teflon again being glued up to the tentorium and trying to decompress the nerve as much as possible. So the use of Teflon is probably, the Tisseel is used really to keep the Teflon from contacting or distorting the nerve. I know that not all surgeons take the pains to do that, but I think that adds to the results that we see. I think that I have seen some toxicity from the Tisseel, and I'll talk about that in the results of the series that we have recently published. About petrosal veins, they not infrequently obscure the surgical field. Frequently there are a number of branches in the petrosal system and by taking one or two of the branches and then moving the, what the residual branch out of the way, one can get as much exposure as is necessary. However, it's not infrequent that the entire venous complex has to be coagulated in order to get appropriate access to the nerve of exit or correction, the nerve root entry zone. The trigeminal nerve. And here again, you can see part of the trigeminal, part of the petrosal system is intact. And again, you can see the classic indentation of the supracerebellar artery underneath the trigeminal nerve at the nerve root entry zone. This is still pictures from videos at my residents had made and they use this for prepping themselves for the relevant surgical anatomy. Here you can see a retractor on the cerebellum. The point that they're making with this slide is the relative depth of the eighth nerve relative to the fifth nerve as a point of identification of the nerve. And in this slide, you'll see actually the eighth nerve above the trigeminal nerve here and bending supracerebellar vessel that has been basically insinuated itself within the fibers of the trigeminal nerve. We usually don't think of the trigeminal nerve having a number of fibers, but with the steady pulsation of the supracerebellar artery within the substance of the nerve. The nerve as you can see, is now fanned out into individual branches and not uncommon phenomenon the more of these that you do. Another example of a very distorted trigeminal nerve from an offending supracerebellar artery. Once the vessel has started being moved, you can see that the nerve actually assumes not only a relaxed and decompressed architecture, but even in effect what looks to be an apple core from probably from some local atrophy from the long-standing compression. And here you see again, the Tisseel and a Teflon felt glued up against the tentorium as a methodology to maintain the vessel in a decompressed attitude. Not uncommonly you may see open artery and the vein. In this circumstance, we're looking at the trigeminal nerve here being distorted by the supracerebellar artery looping down from above. Now that the artery has been transposed to our left on the screen, you can see another fairly large vein coursing behind the trigeminal nerve path, nerve root entry zone, providing another source of compression for the nerve. And if the vein is mobile, which it frequently is not, one can then use the Teflon to hold not only the artery, but also the vein away from the now decompressed trigeminal nerve. This is another image that was taken after we discovered that there was a combination of both venous and arterial compression. Here's the mobilized, the supracerebellar artery that had compressed the nerve. In this area, you can see the discoloration in indentation, and we now know that the artery was compressing the nerve against a vein that looped completely behind the nerve. And then you can see the size of that vein. It's served as a counterforce against which the artery pulsated suggesting that both venous and arterio compression was the offending physiology. Here's an interesting finding. This is the petrosal venous system with a fairly sizeable varicosity that had indented itself within the nerve. And by moving that varicosity the out of the way you can see the distortion that the varicosity had caused on the trigeminal nerve. In general, in patients with appropriate indications and good selection criteria, one should be able to get at least 90% initial relief of pain with a microvascular decompression, with a relatively low failure rate and an even lower a major recurrence rate. In an effort to look at complications related to microvascular decompression, we analyzed some data of my cases and looked at the surgical technique as an index of safety. And this is what we found. One of the issues that we always discuss with patients, the possibility of hearing loss from this operation. This is a very long list of reports in the literature. And as you can see the incidents of hearing loss with this operation ranges from almost 20% down to nothing. So the key is to try to identify those issues that might reduce the hearing loss rate is to as little as possible. So my team reviewed the outpatient records, notes, the neurophysiology recorded during the surgical procedure. We sent questionnaires to all of our patients that hadn't been followed up in the clinic in the last few months and did phone interviews with the rest. We had 106 patients, got follow up on all of them. You can see the breakdown in age, in sex and so on and so forth. Those who was not a pristine group, there were patients who had had previous procedures for their syndrome, including radiosurgery. Seven cases had previously been operated on, some had the radiofrequency ablation and glycerol rhizotomies. Our operative findings, as we all recognized the supracerebellar artery alone was the offending agent in greater than half of these patients. And in conjunction with the anterior inferior cerebellar artery or vascular artery in another 10% of patients. Interestingly in 13% of the patients, there was venous compression only, and in 8% of the patients, there was no compression found at all. In those cases, a compressive operation was usually performed. I have not done many at all, rhizotomies. Outcome measures are based on the BNI pain score, which everyone is quite familiar with, in the immediate post-operative clinic visit a BNI score of one was enjoyed by 83% of the patients. And basically 93% of the patients got some acceptable pain relief. Looking at a longer-term follow-up, a BNI score of one that was maintained in 72% of the patients. In 91% of the patients had a reasonable control of the pain with or without medications. Those cases with only venous compression, 11 out of the 14 enjoyed a BNI score of one, which frankly was surprising to me, but heartening none the less. In those patients that had a compressive operation because no vessel was found, only 63% maintained a BNI score of one, in probably in keeping with what we know about other compressive and, or partially in various procedures such as stamina. Looking at our hearing results, we reviewed all of the electrophysiologic monitoring during the cases and looked at changes in wave five latency, the mean change, as you can see from this slide is 0.28 milliseconds with a maximum of 1.24 milliseconds. Two patients had a change in their latency greater than one millisecond. One was associated with increased anesthesia with no other mention of an intraoperative event and no patients of the 106 experience the hearing loss. 64 patients had recordings and as you can see, 58 of them had reproducible data that we can analyze. So that's the good news. What's the bad news? Well the bad news, of course there are complications. The surprising thing to me was, and again this highlights the fact that you've got to do your own data mining, that we actually had complications involving the wound more often than we had neurological complications. There was no hearing loss. There was a tangent fourth nerve palsy, and I think that frankly, this may have been my getting the Tisseel glue adjacent to the fourth nerve. One patient with transient nystagmus, no hearing loss. And the rest of the complications in my series were unfortunately related to the wound. Either a CSF leak requiring a lumbar drain or something to do with the wound edges themselves. Remember where this wound is, it's behind the ear, it's under hair and unfortunately the patients lay on it. So I think one has to expect the occasional complications related to the closure. Hemifacial spasm. Let's look at a video of microvascular decompression for hemifacial spasm. This is a much less common entity in my practice. Here you can see there on the left side, you can see the lower cranial nerves to our left, arachnoid being opened over the ninth cranial nerve. Here is the eighth nerve being pulled slightly superiorly. This vessel was adjacent to the eighth, to the seventh nerve but wasn't causing the compression. One had to look by moving the choroid plexus out of the way and look at the nerve exit zone in order to find the offending compression. As far as the closure is concerned, you can see a continuous closure with an underlay graft of a DuraGen in order to effect a watertight closure in what is a fairly small dural incision. Here is some intra-operative photographs showing the classic compression of the eighth cranial nerve. Mostly in my experience by the PICA artery, as you can see the tenth and the ninth nerves flocculus is slightly retracted away, and here's a loop of PICA. You can just see in the lower part of the screen, the eighth nerve. By moving the eighth nerve slightly. one can see the changing color of the seventh nerve, which is another one of the many ways to differentiate the seventh nerve from the eighth nerve. And here's a loop of PICA indenting the seventh nerve at the nerve's exit zone. And once the vessel is decompressed, you can see the classic indentation that the vessel leaves on the facial nerve. And here again, you can see the PICA artery chromatically pulled away from the nerve root exits on the seventh and along with Teflon, Tisseel glue is used to glue the Teflon to the dura of petrous bottom so that we keep the glue away from the compressed nerve. The sling technique. One can use the Teflon felt and form a rope, if you will loop the rope around the offending vessel and then with glue, or some people use various other techniques to tack if you will, the loop of a Teflon up to the adjacent dura of the petrous bone, to maintain the vessel in a manner in a location will not recontact the nerve. And in this case you can see that we used Tisseel glue to glue the loop up to the petrous bone. I think it's important not to be confused about what vessels are actually causing the compression. Here we're looking at again on the left side, you can see the lower cranial nerves to the left. Here's a looping PICA coming up. Here's a branch of AICA, which clearly contacts the eighth nerve and may very well contact the seventh nerve behind it. But remember where the pathology and the pathophysiology comes from, it comes from a vessel that contacts the nerve where it exits onto the facial nerve. That would clearly be underneath the flocculus, which you can see here. And more likely would be from the PICA artery. And I would not do much at all with this vessel for fear of, number one, not dealing with the vessel that's causing the pathophysiology. And number two, possibly affecting the hearing. So in, as we would have thought, clearly the PICA artery has indented the facial nerve at it's exit zone. And now is identified to be the offending vessel and would be moved away. And again, with the loop technique, kept away with a loop of Teflon felt and Tisseel glue. Large vessel compression is a difficult thing to treat in certain circumstances. However, the large vessel on imaging may not infrequently only be an index of compression of the nerve and the large vessel. In this case, the vertebral artery may actually not be the offending vessel. The offending vessel is in this case is frequently the junction of the PICA artery as it emerges from a medially placed of vertebral artery. And it's the PICA loop that actually does the compression. You'll see in this next video, me struggling with a very large vertebral artery that I really had almost no options in terms of moving or in terms of decompressing from the nerve other than to start inferiorly below the tenth nerve and progressively buttress the vertebral artery away from the brainstem by using large thick pledgets and between the brainstem and the artery itself. Not ideal technique. You heard about situations where the vessel can be pulled away with for instance, aneurysm clips and so forth, but that proximal on the vertebral artery, very little options in terms of moving the vessel.
- Dr. Giannotta, I wanna thank you for your very thoughtful comments. I really like the method of using the Teflon and the Tisseel because it really decompresses the nerve nicely. You just don't leave the Teflon between the artery and the nerve and still have a chance for the Teflon to touch the nerve. At the same time, you don't make the procedure very complex, by putting sutures into the tentorium to sling things and potentially increase the risk of the procedure. So I think that's a very neat technique. And personally, I gonna try that. I wanted to sort of run through a couple of, actually three cases where I have had myself issues with handling challenging moments in surgery, and get your expert opinion. I think you already pointed out the difficulty of thyla-ectatic arteries in terms of compressing the cranial nerves. This is a case of an elderly gentlemen who underwent two percutaneous procedures that I did, one glycerol and one a radiofrequency rhizotomy continued to have disabling pain and has a very torturous basilar artery. You can see it definitely deforms the trigeminal nerve and on the Satish sagittal images. It's really a very, very large artery. This is a patient who has an extremely disabling pain has a difficult time eating, has a failed already two needle procedures. What's your thoughts for the next step? I don't think radiosurgery has improved at all here. What would you do next?
- Well first of all, I would always consider the potential for radiosurgery. However in the case that you described, there may be two reasons why radiosurgery wouldn't even be feasible. One is that you may not ever actually be able to image the trigeminal nerve on your imaging studies because of the distortion of the larger artery. Secondly, in a patient that's had a longstanding compression from a large artery like that, and several needle procedures, the nerve itself may actually have such a small caliber as to be very difficult to target with radiosurgery. So although we like to rely on a less invasive technique like that, as you point out, it may not actually even be feasible or certainly not effective in a patient like this. I admire your courage in trying to mobilize these vessels. I find it a difficult procedure. And although I have not done many of them. I haven't had a major complication, but I know of very good surgeons, nationally recognized surgeons who attempted to move some of these larger arteries and have experienced a disabling complications. So I think if one understand what the potential risks are, then one can try to mobilize the vessel. Remembering that you don't have to move the vessel very much at all. In fact, it would probably be difficult to even identify the displacement of the vessel on a postoperative imaging. You simply need to decompress the nerve. And in this circumstance, it may very well be the better part of valor to simply go ahead and not move the vessel, but just put a Teflon buttress between the vessel and the nerve assuming that you can actually identify the compressive area. I've watched a Dr. Janetta do that. And it certainly works in his hands. So I think it's a definitely worth considering.
- That's exactly what we did, and obviously your thoughts are very well taken. The other issue is the fact that there's not much space for the sling technique, even if there was some between the tentorium or any of the dural sleeves. This specialist probably so calcified, if you get too aggressive with it, you're going to end up putting the patient in harm's way. So let's go ahead and sort of review what we found in surgery or what I've found. As you can see here, this is a very highly calcified vessel. And more importantly, you can see the seven and eight is almost where five should be. And the fifth cranial nerve is a level above the tentorial. This is how much have deformation this artery had caused. And here is what exactly you mentioned that the nerve is so thinned out, we can't mobilize it in any way. Being aggressive is risky. Just like you mentioned, I put a piece of Teflon patch and then really massage the nerve. To do a very sort of aggressive rhizotomy, hoping that this guy will not come back in early future because I really don't have any other options. Would you do anything else different looking at this video?
- No, I agree. If you could put a buttress between that nerve and the vessel, I think that's a major step forward. And I think massaging the nerve is definitely a tried and true technique. We use it not infrequently in patients that we find do not have vascular compression. So I agree completely with your technique.
- Thank you, and here is the massage technique I think of using that sort of, here it is right there trying to tweak the nerve and sort of put it under a little bit of stress and put that piece of shredded Teflon and hope for the best for this guy. Luckily he did very well. He's about four years out from this procedure and has not had any more recurrence of pain. Do you ever consider partial transection of the nerve? The bottom 2/3?
- I've definitely considered it. I've probably only done it a couple of times in my practice. I think that stroking the nerve like you showed, or sometimes just compressing it without forces. Like the kinds of forces that you would exert if we were going to do, let's say a balloon compression, is almost always effective. But there, one needs to have a menu of techniques at their disposal because there's a fair amount of differential among patients in terms of what pathology you're going to see when you get in there.
- Thanks again for your valuable comments. Let's go ahead and if you don't mind, I would like to show you a video of a redo MVD. This is a problem we run into. We have that patient who's younger, in their fifties, sixties sort of have many years ahead of them and they are about five years out, they had the MVD by somebody very competent. The vessel was found. They come to you with pain recurrence. How, what is your threshold in doing redo MVDs? What are the perils? And I'm going to start the video and have you sort of talk over the video as I will show one of those. But before we start the video, how aggressive are you in terms of redoing MVD versus doing a needle?
- First of all, if the patient had classic trigeminal pain, let's say for the sake of argument that I did not do the original procedure. Patient has classic trigeminal pain is number, is my first critical question of the patient. The second critical question is, did the original operative decompression cause your pain to go away? If they say, "yes," if they've gotten a dramatic amount of relief, especially if it was a fairly prolonged release, such as the case that you described, I would have very little hesitation in terms of at least imaging the nerve in anticipation of perhaps another microvascular decompression. If I did the original operative procedure, then obviously I would review my operative note, I'd try to review any followup imaging. And if there was any sense that whatever we put in there such as Teflon or a sling had perhaps come loose or become dislodged, I would have a very low threshold for going back. Now if patients had any atypicality in their pain to begin with, if they did not get any relief from a microvascular decompression that either I did or another surgeon did, I would have a much higher threshold for re-exploring that. And then we'd probably use alternative methods such as radiosurgery.
- Thanks very much. This is a patient who had a right sided in the procedure, a very young man. I think he was 45 years old when he had his own VB by competent surgeon in our state. And he was pain free for about five or six years, came back very classic V2, V3, trigeminal neuralgia, Where you open his incision, you can see the scar that you have to go through. You can see the seven and eight cranial nerves on the right side of the video. And we're trying to sort of remove, this is again the seven and eight cranial nerves removing this Teflon to see around it, to see if there's a compression by these branches. Again, this is the root entry zone of the fifth nerve. Can you tell us what you think as you go through the dissecting the Teflon. Do you believe in Teflon granuloma? Often you injure this nerve by removing the Teflon, as you can see here. And is that the reason why the patient had pain even after surgery?
- Well I've definitely seen cases of so-called Teflon, granuloma, very difficult. The cases that I've seen if you can believe it, are maybe even more adherent and scar causing than you're seeing here. I think for the viewers, I think one of the impressive things when you do a redo is to see that in the absence of the so-called granuloma or scarring that the Teflon is almost pristine in terms of its color and its consistency from the day it was put in there unless it's been reinforced with Tisseel glue. And I think that one of the reasons why I try to keep the Tisseel from touching the nerve is this very situation. 'Cause if you glue the Tisseel, if you glue the Teflon to the nerve with Tisseel, then you've got even a more difficult situation. Again, showing your technique for sharp dissection of trying to decompress the nerve actually from the Teflon itself. So these are difficult cases. I don't enjoy them at all. They're not very satisfying. And I probably have to say that in my experience doing this operation that you're doing with this amount of contact and scar, I bet you my results would probably only 50% satisfactory.
- Yeah, I would say that's a very honest appraisal of sort of this surgery in general, with your technique of using Tisseel and holding everything away from the nerve. Probably the chance of such a recurrence is smaller. Don't you agree? Because you really keep everything away from the nerve. It's not even Teflon compressing on that. Do you agree or not?
- Well I, you know, I haven't done thousands of these, like our heroes, like Dr. Janetta and perhaps Dr. Toon and so forth, but frankly of the redoes that I've done, the overwhelming majority have been in patients that I didn't originally operate on. So I would say that my recurrence rate is relatively small. And I think that as you say, it may very well be to try to keep anything from touching the nerve at all costs.
- The last short video is something that you have very eloquently mentioned about venous conflict. Do you believe in venous conflict? Obviously it depends what you've seen in the operating room. I'm going to show a short video of a venous conflict that I think it is very impressive and convinced me that venous conflict. This is a left sided retromastoid craniotomy, large number of vessels that varicosity you mentioned very well of the superior petrosal vein. And I think in this case, the veins do make a difference in terms of cause of conflict. If you see just this man alone, let's say right here and not this vein compressing, would you just coagulate and cut the vein or would you decompress the vein? Just like you do it? Or would you do the rhizotomy?
- So if I see a vein that actually is mobilizable such as perhaps the one we're seeing in this video, I may very well try to move it away and perhaps hold it away. And that would be usually in the context of another potential offending vessel, either an artery or another vein, like you're showing in this video, where to get completely definitive decompression, I may have to coagulate the vein. Most of the cases of venous compression that I've done, I've actually coagulated the veins or at least the one that I thought was the offending vein. Clearly there's enough venous collateral so that you're probably not going to compromise the venous drainage of that area of the brainstem. I've been able to get away with it, back to your original question about, do I believe in venous compression? I must say that the thing that influenced me to have more confidence in the concept of venous compression is actually when I did my own analysis of my own patients. Because I was somewhat dubious, but when my physician's assistant and one of our two medical students that helped to get all this data, presented the outcomes, it was clear that these patients did reasonably well. And not only did they do reasonably well in the short run, but they did reasonably well in long-term follow-up. So I agree that there is definitely something to venous compression.
- Well Dr. Giannotta, I want to really thank you for a very, very worthwhile session. I personally learned a lot, and again, we will look forward to having you again with us, if it's possible central. Thank you.
- Thank you, Aaron.
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