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Welcome to SNI Digital Innovations in Learning in association with UCLA Neurosurgery. Linda Liao, chairwoman and its faculty are pleased to bring you the UCLA Department of Neurosurgery 101
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lecture series on neurosurgery and clinical and basic neuroscience.
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This series of lectures are provided free to bring the advances in clinical and basic neuroscience to physicians and patients everywhere. One out of every five people in the world suffer from a
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neurologically related disease. The speaker is Jacques J. Marcos, professor and Department of Neurosurgery, University of Miami, Florida, United States of America, Director of Cerebral Bascular
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Surgery, Director of Scobase Surgery, and Director of the Fellowship Program.
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Okay, so I will proceed with the second talk, which is really reflects a paper that is in press right now and
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it's my experience with bypass surgery for Moya Moya and cerebral ischemia and some, I think interesting new concepts, at least that
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I learned looking at flow measurements. I have to give credit to the first author of the paper, Nick Khan, who was my fellow a year and a bit ago. And of course, a large group of residents, who
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looked at the data and all of my stroke neurologist. Of course, we are a good team at the University of Miami between neurology and neurosurgery.
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So this is a prospectively collected retrospectively analyzed data about 20 years. I was the only surgeon that I am excluding bypass for aneurysms and tumors I very rarely use purely indirect bypass.
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I, as you will see, almost exclusively use some form of direct anestomosis. And I'd like - in this paper, actually, I've introduced it in another paper we published - this simple nomenclature,
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how many donors and how many recipients. So I used three techniques. One donor, one recipient, that's a single anestomosis one donor, two recipient, meaning a side-to-side and an end-to-side
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using the same STA branch, that's one D, two R, and the so-called double barrel is two D, two R, two branches of the STAs and two separate recipients.
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I like to keep things simple, so I still follow the old technique of doing a relatively small craniotomy six centimeter above the external auditory canal. So, Moya Moya disease, you all know it,
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you have Anthony and others who do excellent work here, but this is give you a flavor, a 32
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year
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old patient who is a stroke unit nurse herself, African American, developed typical Moya Moya strokes. Here is her angiogram. You can see the stenosis of the distal ICA,
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proximal
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A1, M1. She is attempting to form collaterals from the posterior circulation to the anterior circulation. Here is her STA. The one lesson, I've learned many lessons over the years doing bypasses,
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one of them is do not be discouraged by the size of the STA on an angiogram. You have to dissect it, free it up from the skin and soft tissue around it. It will then be very robust in most cases
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and it will give you excellent flow. So don't try it off this STA by saying, Oh, very small STA, what am I gonna bypass with? You have to dissect it. We do a transcranial doppler with vasomotor
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reactivity Our neurologists have a nice slab with a couple of excellent technicians I've measured this on all my patients. You want a number that is 70 or higher normally. This patient had very low
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numbers, 27 on the right, 32 on the left. And I used to do SPECT with diemox. Nowadays, we do CT perfusion or MR perfusion, but she had clear-cut ischemia Here
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is, again, the dissection of the STA, the two branches in this case, craniotomy, distil-silvian fissure. And here is what is key, at least to me. And with the concept that Fadi-Sharbel at
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UIC pioneered is measuring flow, intra-op, in CC per minute. We're not talking velocity, we're talking quantitative flow This is the Charbel Probe. The company is called Transonic and I have
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no relations to it,
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you measure the flow. Then this little STA you saw on the angiogram, guess what? It has a flow of 60 cc per minute when you cut it.
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That's very substantial. So I proceed with the anastomosis. In this case, I use a running technique. Sometimes I use interrupted if I'm particularly training a fellow or a resident. I usually do
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interrupted in case we screw up with one stitch. It's easy to redo. I
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complete the anastomosis. I measure flow again. Remember the cut flow, meaning the maximum theoretical flow this artery can give was 60 cc per minute. When I finish my anastomosis, I measure the
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flow the bypass 64cc per minute. you know, it's within margin of error. It means that brain really needed every drop of blood flow it could get. That already, this index, CFI, bypass flow
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divided by cut flow, the closer it is to 100, the more you would feel good that actually the surgery was indicated. If you have a very low CFI, you should re-question whether the surgery was
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indicated So, and I can measure which way the flow divides, proximal distal, and I tabulated all this for, you know, since I've been in practice on every patient. And that's supposed to opt CTA.
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It's a nice patent flow, bypass. She goes home two days later, and then I bring her back a few weeks later to do the other side, and then I do an angiogram, one angiogram to get both sides and we
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have nice. patent bypasses on both sides.
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I don't think this is controversial. I mean, the technique may be controversial. How do you do it? Combine, not combine, direct, indirect for Moia Moia. That's not control, but nobody's
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arguing that Moia Moia should not be treated. Where the, of course, the controversy, maybe is a steno-occlusive disease. And I don't have time to go over the cost study of many years ago, some
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of the reservations, we had about it, and we've published as a group from the CV section, some reservations we had, and criticism, lots of details. I'm not gonna go into, just to summarize, I
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encourage you to, if you're interested, to go read those publications, to realize that it was an excellent study with excellent internal validity, but limited external validity meaning it really
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did not apply to the urgent patient. average time to randomizing a patient in that study was 72 days. We have patients who cannot wait 72 days who are about to have a stroke because every time they
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sit up in bed and that blood pressure falls, they get a TIA. So all of those patients are not part of the external validity of the study, which is why SMART well-informed stroke neurologist and
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cerebrovascular neurosurgeons know that the cost should not be a prescription that says never bypass
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SOD patient. And again, you will see in my series, I have about almost 50 of those. But this is such an example. At the time, a 76-year-old man with this classic watershed infarction on the
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right side who was having daily. And I mean daily. multiple TIAs of the right hemisphere, maximum medical treatment, dual antiplatelets, blood pressure management with a cervical carotid
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occlusion. The cost study would tell you it's unethical to bypass this patient because of the results of the costs. Well, I submit to you and I'm not the only one to say that, that is not the
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right conclusion. So I proceeded the to bypass this patient He has very poor collateral. He has a classic Type 2 ischemia with a specked, with diamox, with a steel from the right to the left
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hemisphere with diamox. His vasomotor reactivity is a
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miserable 19, very low. No wonder he was having daily
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TIS So I did a 1D1R bypass and to side.
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patent bypass. He lived 10 more years, not a single TIA. He died at age 86 from a heart attack. I follow them. I mean, like I've tried to follow, of course, all my patients long term. I have
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no question in my mind that this was the right operation. And of course, he is one of many well selected patients who will benefit from a bypass. By the way, the costs you may remember, the pet
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data in the surgical group showed clear improvement of their cerebrovascular physiology. It is only because the surgical morbidity was 15 that
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the trial failed was in favor of maximum medical therapy When the co-PI presented the data and reworked the number, they said had the surgical 30-day morbidity mortality been 8, not 15, 8 or less,
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the trial would have been positive in favor of bypass. So keep that in mind. So I'm going to skip some details because we started a little late. You can imagine, we looked at every piece of data
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we had, the severity of the disease, the donor, the degree of collateralization. I remind you, naturally, when we form collaterals,
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there are really three or four groups of collaterals. You can get transdual, you can get leptomine and giel, you can get retrograde flow through the pcom or
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crossover via the acom. That's it. Those are your three groups of natural collaterals. But we decided to also look at an interesting concept and see if it correlated with any of the outcomes. is
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completeness of collateralization, meaning when you look at an angiogram and you merge all the injections together, do you end up with a bare area? Is there an area that remains hypo-perfused in
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spite of the attempts at collateralization? And we divided the
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patients in two categories, either complete or incomplete collateralization It's a very qualitative measure just by analyzing the angiograms. It's nothing quantitative about it. And you will see in
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a few minutes what we did with this data. We looked, of course, at bypass patency, Matsushima grade for the Moyamoya cases. This is your typical mature bypass several years after surgery. This
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is another one. You can see the evolution pre-up at the top, Three months post-op. The bypass is patent and 11 years post-op remains patent and large and obviously well-utilized. This is one of
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the few where the bypass occluded acutely while they were still in the hospital No symptoms, just we lost the Doppler as the nurses measure, I mean bedside Doppler, every shift between one shift
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and the next, the Doppler disappeared. I mean the signal disappeared. You can see the bypass is occluded. I rushed him to the OR, revised it. I had had some technical difficulties with the
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recipient artery I chose another one and bypass was now patent and did not occlude long term.
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I, like others, like Fadi Sherbel particularly, are interested in delayed asymptomatic bypass occlusion. Why do some patients without turning a hair, without having any symptoms months or years
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later, gradually lose their bypass potency? Very curious phenomenon.
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The common thread is that they do this. They develop robust collateral This is such an example, a
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bypass that was patent early on, and then slowly occluded as it was being replaced by robust indirect
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collators.
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We looked at TCD-VMRs, as you know, in the COVID times, we equipment couldn't use TCD-VMR. We used like a simpler alternative, the breath-holding index with the transcranial Doppler. It's a
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formula, I'm not gonna bore you with a formula, It's a similar
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concept as to measure vasomotor reactivity. We looked at angiograms, and here are the results. 162 procedures, 124 patients. There was bilateral disease in 72. Clinical follow-up, almost three
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years mean, some up to 21 years. Angiographic follow-up a year and nine months mean, some up to 12 or 13 years. It's interesting, my referral base, like I divided it into three seven years
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period. The first seven years, I only did 14 surgeries. The next seven years, I did 41. And the third, the last seven years, I did 107. And this is in spite of costs. And so again, working
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with a group of neurologists who understand. the indications in select cases. This is detailed data, but to show you that I divided the series in three groups, Moyamoya disease, Moyamoya syndrome,
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and steno-occlusive disease. We looked at everything we could think of, gender, race, hemisphere, presenting symptom, comorbidities, modified rank and score, and so forth We, I'll come back
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to
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the angiographic analysis later. The mean VMR pre-op was low, as expected,
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29. The second lesson I learned from this is, and I had been aware of this reading other series, never expect the VMR to become normal, even if your bypass is patent, even if the patient has no
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more symptoms, It's impossible to get to. normal VMR. That is not necessarily the goal. So you can see here, the mean VMR post-op went up, but to 39
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specked and CT perfusion analysis. And we, of course, gathered all the intra-op information. So here is what it boils down to. What is the surgical morbidity at 30 days? Ischemic stroke only one
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case out of 162 cases? So that's 06. ICH five cases, that's 31. You add those two, that's 37, 30-day ischemia or ICH
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morbidity. Now you add
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subdural hematoma, 19, wound complications 13, respiratory failure, am I? If you add all these, you come up with 10, but the cost,
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15 was ischemia or ICH, I remind you. So that's 37. Now, of course, you cannot compare this with costs. Cost was pure SOD, I'm talking about Moyamoye, but just to give you an idea what the
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general morbidity, I think in experience hands, is when you lump all of those direct bypasses together. I'm not gonna show you the detailed complications, but just read what they are. There are
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six cases, as I said, in a hemorrhage, a stroke, five hemorrhages, and one stroke we analyzed in detail why this happened in each case. And it's tough to come up with a solid conclusion why that
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is, but that's part of what you'd expect. Now, here is a very interesting finding. Remember when I talked about the angiographic collateral formation pre-OP. If it was complete pre-OP, 36 of the
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bypasses occluded long-term, not acutely long-term,
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if it was incomplete collateral formation, only 4, statistically enormously different You might say, Ah, well that's, it means the complete collateralization cases should not have been operated.
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But I remind you, these were symptomatic patients whose physiologic studies showed stage 2 ischemia for the most part. So what this, the conclusion to be drawn from this is that those patients have
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the capacity to form collaterals more than the other group, so once you do surgery, you plug in a direct they have the capacity to grow more collaterals than the others. And then the bypass is not
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needed and gradually atrophies over time. That's the conclusion I draw from this. And this is to show you in graphic form, a huge difference in orange are the incompletely collateralized pre-op and
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in blue are the complete collateralization. There's a big difference between both groups
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Clinical outcomes at the end of the day. This is what matters. Who cares about what an angiogram looks like?
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MRS vastly improved. Look at the shift to the left. Orange is post-op, blue is pre-op. We're making patients better with this operation. Here is when you divide the groups into three techniques
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1D1R, 1D2R, and 2D2R.
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It's only trends. There were no statistical significance differences, perhaps with larger numbers it uncovered the trend was that you get to have more long-term paytancy the
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more anestomosis you do. However,
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now the average angiographic follow-up was a little longer in the 1D1R because I had been doing 1D1R for longer than I had been doing the others. So, time will tell if this is really important or
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not. You will see from one of the other publications I'll show you, I favor nowadays 1D2R when possible. I'll come to that a little later.
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We did univariate, multivariate analysis.
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There were only two factors that predicted delayed Long-term occlusion of the bypass. One of them that makes no sense to me whatsoever is Hispanic race. I don't know why. Of course, I live in
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Miami. Well, almost most of my patients are Hispanic and it doesn't make any sense. It could be one of those random errors when you do P values. But the other one, the only other factor that
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makes sense is completeness of collateral formation that I talked to you about.
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Off note, I'm gonna come back to that. Look at the CutFlow index, that CFI, by the way, on the mean CFI was 085. It did not correlate with long-term latency. I want you to remember this because
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I'm gonna show you the UIC, Charbel, SEPI, I mean Hanjani data that is in contrast to this and try to draw some conclusions.
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So 1D to our example,
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let's show you Let's show you a.
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A brief video of this
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It's a Moyamoya case,
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typical angiogram, puff of smoke, here is my incision, my bone flap,
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Colorado needle, it's very quick to get the STA
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and I'm using ICG just to visualize it and then I'm going to cut it and you can see the cut flow will be 50 cc per minute
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We're going to do the craniotomy. I opened the muscle in one of two ways, either as a C or as a T, depending how thick it is. And now I have two recipients. So my goal is to do two anastomosis,
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because it's a moia moia case, and the frontal and temporal circulation may not be cross-talking to each other. It's isolated circulations Again, my favorite way today of doing at least moia moia
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cases. So I'm going to do a side-to-side to one of these and an end-to-side to the other using only one STA branch.
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In this particular case, by the way, you saw the flow numbers of measuring with the transonic flow book.
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And I'm playing here with the contrast I was experimenting with this microscope that I'm using. What's the best contrast to put? So we're gonna mark this. In this particular case, I did the
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end-to-side first, but usually you should do it the other way around. You should do side-to-side first, if you know you need two anestomosis, because you don't want to occlude the flow while
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you're doing the second anestomosis. So here I think I was working with the fellow, so we're doing interrupted, both of us
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We do that.
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Then, we measure the flow. The flow is 43cc per minute. So now we do the second anastomosis. So here is
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end to side.
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Of course, what is, I mean, the obvious danger of this technique, if you screw up one anastomosis, you likely will lose both because it's the same donor Maybe in the lab, we can talk about
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technique, but the difference between a side to side and an end to side. But I like to do the 12 o'clock position first.
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And I am running the back wall with this 10 o' suture,
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sorry,
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it's a bit catchy, okay So we are running the back wall and
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you can see that. I finish the back wall and then I do the front wall.
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I release the clip, remember the bypass flow after the first one was
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43. Now I'm going to measure the flow, it's going to be, I forgot what the number is, but let's see, it's going to come up in a second, I think it's 60. Yeah, 60, remember the cut flow was 50,
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after the first bypass, it's 43, second bypass is 60. Makes sense As I will show you a little bit, some of the math later, math and physics later, but so I've, you know, that's, that's how a
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typical 1D 2R
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will look like.
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I can't find my mouse for some reason
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Oh, maybe here
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So, here is a summary table that I do on every case, cut flow, every step-by-step what the recipient flow was, how the bypass divided into the two different territories, and so forth. And here
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is putting the bone at the end, obviously don't strangle the STA with the muscle when you close or the skin for that matter And you can see both anastomosis on the lateral in a second are patent.
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You can see here, well anyway, here and here, both of them.
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So that's your typical
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1D2R. I'm going to skip this video for time. This is double barrel. You can imagine n2 side, 2 branches, 2 recipients. We'll skip that
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There are other examples, of STMCA all not was series the course.
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we had a group of vertebrobasular insufficiency with occipital to pica bypass. Maybe I can show you snippets of that video. Maybe I'll go to the middle here.
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This, this VBI can be called the orphan disease because it's under-treated.
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Kaplan in Boston, the famous stroke neurologist, really said that many patients with posterior circulation ischemia are totally neglected and put on medical therapy when there could be surgical
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treatment And of course, the very task study with CEPI, I mean, Hanjani, is a PI of, showed clearly, a five-time fold, five-fold increase in stroke when blood flow is low in the posterior
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circulation. So this is, I'm choosing the fourth segment of PICA as a recipient through a far lateral approach, and we're going to do occipital to PICA and to side bypass. It's all
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the same, suturing and to side. actually plenty of room to do it. Of course, it's deeper, but you can see how much space there is around to do it. And when it's done,
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by the way, of course, you know you want to be careful about where the perforators are taking off from, and then you do it distal to the perforators.
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And here there was a small leak, so I added an interrupted suture
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And at the end,
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here is a post-opanger. You can see nicely the anastomosis and how the occipital artery took care of the entire via posterior circulation.
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I'm gonna skip this case with a saphenous vein, very unusual bonnet bypass going from one side to the other because there was no STA on theipsilateral side. So I think I showed you at least in that
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group typical North American series versus Asian series of Moia Moia. I showed you the importance of incomplete collateralization.
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You could see that I actually only failed in one of 162 cases from constructing a bypass. When I was able to do the bypass, a bypass paytancy was 100 acutely, but 90 at long-term follow-up,
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meaning there was a 10 incidence of
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delayed asymptomatic occlusion. You can see that my median CFI is very good, 086. What that says is I was very selective. I truly chose patients who in
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retrospect really needed the operation, otherwise my CFI would have been very low
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The final bypass flow, a median of 52. CC per minute of augmented flow, which is a good number for the MCA distribution. You can see the range almost 200 CC per minute. So as Fadi Sherbel has
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said for many years, you don't want to call an STMCA bypass, a low flow bypass, everybody does this. It's wrong, you don't know what the flow is until you measure it. 200 CC per minute through
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an SDA is definitely not low flow Extremely high flow is probably too high in some cases.
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Now here is where I found it very interesting. So this is side to side comparison between UIC series published in 2019 and the current series. So I was very curious why you'll see in a second. They
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had 146 cases, we had 161. The floor ranges were very similar. There were two, well, primarily Sherbel, but also Sepi, there are two surgeons, I'm one surgeon.
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I did a little more 1D2R and 2D2R than they did percentage-wise, but in purple is, I think, the key significant difference. They used concomitant EDAS in 35 of the cases. I did, I don't, I only
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used it in one case, as I said. Keep that in mind Their angiographic follow-up is slightly longer than ours.
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So they end up with the long-term bypass patency of 76.
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Mine is between 90 and
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91. And more interesting than this, when you look at CFI, CFI was a huge predictor of bypass occlusion in their series But as you saw, it was not in mind. In mine, it didn't matter what the CFI
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was. The bypass occlusion was about 10 to 11 regardless. In their
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series, if their CFI was less than 05, their occlusion rate was 54. So I'm sure it's not technique difference because that would have reflected on acute bypass occlusion, not delayed The only
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difference I can
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ascribe these two is the concomitant use of EDAS. It means because they use EDAS on top of the direct bypass, those bypasses were
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less needed over time and regressed. That's the only thing that makes sense to me at least
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So again, to summarize in my series, 37
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very operative 30-day morbidity mortality. When you followed patient long-term, only 62 overall had ischemia or stroke post-op. I remind you, the natural history would have been a five-year
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cumulative stroke rate of 82. So there is no question that at least our selected surgical patients were appropriately operated on. There was one death, and actually it was an anesthetic
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complication of letting the patient wake up during the anastomosis resulting in malignant hypertension. That's a video I skipped. This was a bonnet bypass. That's the only death we had
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unfortunately.
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So that's a 10 delayed occlusion Now, the next very briefly part of the talk is I'm focusing on the 21 cases of 1D2R. We publish this if you want to look at the details in the,
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I don't know if it's a white or the red journal, but less than a year ago, it has a lot more details. This is the largest really reported 1D2R series. Fadi Sherbel had published the first one in
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2018, about eight or nine cases. And I followed up with this. I'm gonna skip, I don't have time. I love math and physics. I will torture you in the lab maybe, as I torture my residents with
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brain teasers all the time. But the point is, you really need to understand the Poisoy's law to make sense of all of these bypasses. It's
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very simple. You remember it from high school, from Omslow. It's like an electric circuit The three components are flow. pressure or voltage,
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by the way, flow or current pressure or voltage and resistance or resistance. So those are the three equivalent numbers.
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We've learned a lot from the cardiac surgery literature. We always in neurosurgery, we seem to be 10 years behind the, it's also true in endovascular with the cardiologist and cardiac surgeons I
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mean, they figure these things out with coronary bypasses
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and those of you interested in this topic, go read some of their literature on how do you construct a bypass, what's the ideal geometry, what's the ideal donor
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to recipient and diameter ratio and so forth. Just lots of data that I don't think today is the right day to share with you. But the interesting concept is this, it doesn't matter what bypass you
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construct species humans, you know. monkeys, dogs, each species has a constant and that each species wants a certain wall shear stress. So it doesn't matter what you start up with post-op, they
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will, the vessels will remodel, the flow will remodel to achieve a certain wall shear stress that's appropriate for that species. That's very interesting concept and it's different for different
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species Obviously, you want the length of your bypass to be as short as possible to maximize the flow. An ideal diameter, a donor to recipient ratio is about, if possible, 15 to two.
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You want to fishmouth the donor. And so, to remind you, the geometry is end to side. This is, well, if you do simple calculation with Pythagoras theorem, you will realize if you fishmouth the
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donor,
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that's four times the cross-sectional area than if you didn't fishmouth. It's very simple square relationship. If you do end-to-end of maximize your surface area by slanting your cut. And if you do
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side-to-side, there's only one way to do side-to-side. You do the back wall first and then the front wall. When I do side-to-side, I put my arteriotomies at
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130 and 1030, because it's a very good compromise between the 12 to 12 or 3 to 9. You can see and you can oppose very well by doing in between.
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You can read more details in those publications from last year that we put out.
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These are the natural, I already discussed with you the flow concept. Now, what are the steps of that? That's how it's going to look at the end, 1D, 2R, 2 anestomosis, 1 donor. I am going to
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skip the video, I already showed you one similar. These, remember from high school physics, if you add series in parallel, you decrease the resistance, and that's a formula, 1R, summation of
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1R.
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So, here are the steps. You lay out the STA, you prepare your two recipients, usually I do the side to side first, I measure flow, I then do end to side, I measure flow in the first one, and
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the third, and the second one, and the total flow. So, I'm going to have two measurements of the first anastomosis, at two different parts of the procedure,
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and one measurement of the second anastomosis. You're gonna see what I'm gonna do with those numbers later. So the results, not surprising, forget these demographics, the same as the larger
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series.
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The Cutflow index was 064 prior to the second anastomosis and rose to 094 after the second anastomosis.
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It means on average, I actually increased by 50 the flow
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by adding the second anastomosis. Here is
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a graphic summary of the data. This is a Cutflow, a mean of 57. I
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do the first anastomosis, the flow is 36. I do the second anastomosis, it goes up to 52, on average. It didn't matter if I did side-to-side first or end-to-side first, I tried it both ways. the
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final result ends up being the same. Clinical outcomes, like the larger series, the MRS is improved. You can see the shift to the left.
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In the supplementary material of the papers, you will see all the math and physics. And here is our wonderful medical illustrator, Roberto Suazo, tried
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to express what I wanted him to express And here is an equivalent electric circuit when you can take each segment and figure out what the resistor is. And you can actually calculate every parameter,
42:58
flow, vascular resistance,
43:05
what am I for? Delta P flow and the pressure gradient in each of the segments based on those simple arms low.
43:16
we did it for every case and so forth. I'm gonna skip that, the benefit of the second as well. So this is what I want to introduce and we put it in the paper.
43:26
So I am extending the CFI concept and since I
43:34
have two daughters, they're not called Sarah and Sassy, but it's pretty similar. So Sarah is second anastomosis relative augmentation, S-A-R-A. So I divided CFI final by CFI initial. So that
43:49
tells you how much a second anastomosis helped and then Sassy second anastomosis sync index tells you actually the ratio of the flow of the second anastomosis divided
44:02
by the total flow. So it's their related concepts, but if you get into the math of it, you'll see that they're slightly different, but they're both useful in that way Uh. This is a typical case
44:17
where the bypass is mature over time.
44:21
In the 21 cases, only one patient occluded long-term bilaterally. Again, it's anecdotal, but it shows you that it's clearly not technique. It's something with the milieu of the patients who are
44:38
able to develop indirect collaterals and the direct bypass regresses over time. And I'll show you what this patient did. At the top row is the right side. You can see the bypass was perfectly
44:54
patent, immediately post-op. Then at one year post-op, it's gone. And he has very good collaterals indirectly. I did the surgery on his left side. And the same thing happened again on the left
45:09
side Very good bypass left side, initially.
45:15
gradually disappearing to be replaced by indirect flow, indirect collateral at one year.
45:24
This is the summary of why do I like 1D2R?
45:30
Let me, instead of reading all this, let me just tell you, I think, I don't think it's a technique for the beginner because if you scroll up one anastomosis, you will occlude the entire vessel
45:42
and you lose both.
45:46
It is, there's no point doing it if the STA bifurcates about where your craniotomy is going to be because if you're there, you have both branches, might as well use both. The advantage, of course,
45:59
is you leave perfusion to the skin by not using the frontal branch. The few wound complications we had in the large series, they're more likely to occur when you sacrifice both branches. And of
46:12
course, it's a much shorter case deal with one STA branch rather than both. And it's obviously, you don't want to do 1D2R. If after you measure the flow in the cut flow, it's still low. You
46:26
might as well go and get the second branch and be safer that way. But otherwise, I highly recommend it. And it seems to make perfect hemodynamic sense to use it. Here is a summary of what I
46:42
already told you about the physics of it. We'll skip that.
46:48
Sarah and Sassy were good. So
46:51
I think I'm going to stop here. Thank you very much.
47:02
So fantastic lecture. It's wonderful to hear your thoughts and your approach to this. Again, from kind of a residency training standpoint, how do you teach this skill? Are you having your
47:13
residents do a course like the course that Anthony has set up today and you see that you watch them do it 10 times and they have to be in 10 cases with you and then you let them sit under the scope,
47:25
or how do you judge when somebody's ready to sit down and tie? I could do a better job by being more structured. And that's what you just said is ideal. Some other programs do this and are very
47:40
structured and you have to, Nick Kahn, the first author on those two, my former fellow, had done 500 and as to most, 500 before coming to his fellowship with me in the lab, I mean, on these
47:54
artificial vessels or rat
47:58
I I don't do it. I mean, yes, of course you need to go to the lab to do it. I judge by watching my chief or my fellow a few times and I can judge if they're ready to do it. I didn't train, to be
48:11
honest, I say go to the lab. I didn't do too much in the lab myself. I actually learned through my fellowship with Spatsler but that's not the right way. The right way is to go to the lab and do
48:21
it. There are many, there are
48:26
lab books with this step-wise with this step-wise approach. Actually, I have one and that's the right way to do it. You can use, what's the name of that scale described in
48:39
1977, where you grade the skill, oh my goodness, it's initials, I forgot what it is. You can actually score a resident on the tissue handling economy of motion and I'm blanking on the mnemonic of
48:57
it. and decide, hey, you're not doing a bypass till you cross whatever score it is. I don't do it this way, I'll just do it subjectively.
49:10
A question about the vasomotor reactivity. Why do you think it doesn't go up? Clearly, it's a sign, it's an important sign pre-op of the severity of disease, but then the patients do well and yet
49:22
they don't go out. Yeah, it's a very good question. I don't know if the people on Zoom can hear you So the question was, why does the VMR not go up in spite of what seems to be a very successful
49:32
surgery? Because you're only augmenting the flow in one part of the territory. And I think the way it's measured, it doesn't reflect the entire hemisphere. And I think that's the only way that it
49:47
makes sense to me. We're not giving the patient a new brain or a new hemisphere.
49:55
I don't have a very good answer to your question, but it is no question that patients are very happy and they do well and most of them don't have more strokes after that yet the number. It must be
50:08
that the way the formula is set up doesn't reflect the entire hemodynamics.
50:19
Wonderful, two lectures. So, just from an engineering standpoint, when you, for sales law, really only applies to lavender flow, which just you stated, but he's a mastermosis in the way
50:34
they're constructed. He only must make turbulent flow. And do you think that has an impact on its long-term latency that we're ignoring the effects of turbulent flow? Absolutely, so again, if
50:48
they didn't hear you, Marvin had a very, very important question, laminar flow versus turbulent flow in bypasses. Some of those papers are skipped, are exactly that. It actually maps for you
51:02
which part of the anastomosis, the heel, where the turbulent flow is, which is why it's recommended, the smaller the angle, the incidence angle, the better the laminar flow is. the 90 degree
51:16
angle that most of us end up putting is least favorable for avoidance of turbulent flow. So, which is why fish mouth thing, if you fish mouth by the diameter length, the same diameter as next,
51:31
you end up with a 45 degree angle. That's what I end up using most of the time. 30 degrees even better, 20 degrees better, but if you take it to the extreme, if it's zero degree, it never ends.
51:45
So you have to compromise technically too.
51:50
Yeah, no, you're right, but most of the flow is actually laminar. It was, a lot of the data is actually from the corona literature, which has even higher flow than what we're doing here.
52:04
The intracranial and extracranial vascular origins are different, but
52:12
intracranial vasculature has the ability to - former collateral with an extroderal, don't as much. Seeing that in the future that, you know, after you do this direct bypass, these extro cranial,
52:23
the intracranial collateral form, and that's sufficient enough to cause symptoms to go away. You think that the direct bypass is just tying the body over for these collateral to form, or is it
52:36
bringing in like vet Jeff and things to allow those products? Yeah, it's certainly facilitating the indirect flow. The question you might take and say, you say, well, then why do the direct
52:49
bypass just open and do indirect? As some centers have suggested, again, I didn't have time to refer to all that literature. I refer you to some good work by Peter Vashkosi from Berlin at Cherry
53:03
Tea Hospital. That showed obviously the quantitatively, the amount of flow you're giving with the direct bypass is a lot better, higher, and of course immediately available as opposed to waiting.
53:17
None of what I've said applies to children. I'm not, I'm an adult, cerebrovascular guy. In children, you know, most of the time you don't need any of this direct stuff. They have the capacity
53:29
with VGF and others to, so indirect bypasses are unless, you know, for some unusual reason a child needs the flow right now, immediately, you know, they're stroking or something But otherwise,
53:42
indirect is fine.
53:44
I don't know, we don't have the, I don't know why some groups have the capacity to grow those indirect and some others don't. When you said intracran, I mean, you know, as you know, trans-dural
53:56
collators are still coming from extra-duraling. I know Anthony, he can, I think, likes to add gherholes in different makes, you know, makes perfect sense If I had.
54:10
Bad results, I probably would change my technique, but I'm happy as I think the numbers speak for themselves. I think keeping it simple has worked for me. And this is actually one of the reasons I
54:21
looked at it said, Can I do better, achieve better, whatever results? So I'm not gonna change. You will see in the literature, particularly our Chinese and Japanese friends, they do a large
54:33
combined question mark flap. They throw everything at it. The muscle, double barrel I don't
54:41
see the need for it. Not through my data, at least.
54:46
For your steno-acclusive disease patients, I'm curious, hey, how did you build the volume with your neurologist? Because I don't see that many in practice, like these patients that are teeter up
54:56
and down. And then part two is how do you wrap in the possibility for intracranial stenting in some of those similar patients that kind of overlap. So since I do both, I'm often torn between which
55:07
might work because as you know, San Francisco is awesome. Yeah, you know, you know, who our stroke neurologists are, they often more aggressive than I am. I mean, they call me and say, I
55:18
think this patient is, I said, no, no, no, no, let's study. So, you know, I mean, they see the results. You asked me how you built. I mean, if I was killing every patient I was operating
55:31
on, I won't send me another one. So they follow the patients, you know, how it is at our place. So, I mean, you know, when they see somebody where daily TIA's stopped having TIA's, all
55:41
you need is a few cases and you get convinced what Negar Asdagi, one of my stroke neurologist on the paper, is very interested in is exactly predicting she's working on it right now on my data and
55:55
some other non-surgical data, looking at the predictive value of all those pre-op studies that we're doing, MR perfusion, try a CT perfusion, try to bring in some quantitative predictors of how
56:09
patients do. In this manuscript that's in press, I didn't have this data, it won't be in there, but she's working on that. What was your second question?
56:22
Sometimes the patient will have an MCA stenosis and having ongoing symptoms and really to flow, right? Not perforator strokes or something. And how do you stand by path three? No. Stand for, you
56:33
know, if my three endovascular colleagues say they can stand it now, I say you go first And if and I only end up I mean, I only have 48 or so in that series that are pure SOD. And, you know, we
56:49
see tons more. So really selected cases. And I didn't show the analysis, but the results are very similar with the SOD group compared to the Moya Moya group But
57:02
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