0:36
be able to start here. That's the beginning. We talked about that. So when we recorded people will know that's the history of several vascular neurosurgery,
0:47
a paper which was written as you can see, it was in 1946.
0:54
And if you have a chance, you should pick this paper up It's
0:59
in the journal brain, you should be able to get it online. Volume 69, Part 2. And it was written by these two people, Dr. Charles Kubic and Raymond D. Adams, they were neurologists and Mass
1:11
General at that
1:19
time. And this is a time when there was not very much technology There's a message here. And when I show you the paper, you'll see what the message is, okay? This is what they did. They were two
1:33
neurologists. And they had a large number of patients. This starts in 1940s. So this is the history starting in 1940s. I had a large number of patients who came to them with symptoms that they
1:47
thought were related to the brain stem. Brain stem. And so they followed these people and they had the clinical record. All these things you can do. And then when the patients died, they
1:60
autopsied them. And then they sectioned the brains As you can see here on the left side of the screen, at multiple levels. Multiple levels. And then what they did is they related the areas of
2:14
damage in the brain to the patient's symptoms.
2:19
So it sounds like a very simple thing to do. It's a very fundamental, basic experiment. That's what what Jorge wants to talk to you about is.
2:33
The question they were asking is, I've got to let this man in. So I'm going to stop here, man. Is to, is, what is the cause of these symptoms in these patients?
2:48
And, and so there were a hypothesis was, I think they're related to something in the brain stem. And then they decided, well, we're going to do a study. And then in a study, we're going to,
3:01
we're going to follow these people. And after we follow these people, we're going to do autopsies and we're going to relate their symptoms to what's in the brief. That's basically what Dr. Lassar
3:14
of wants to talk to you about, which is how do you ask a question and how do you form an answer to the question? Because you're going to find many things in medicine that are going to be puzzling
3:25
that people don't know. Most of the things we, we're treating, we don't know much about, frankly. And so that's what they did here. And they had some, I think, 20 or 30 patients. And what
3:40
they found, as they've autopsied these people, and you see they took out the circulation, you see the
3:49
circulation on the base of the brain there. You see what they found, they found an occlusion of the basilar artery, and you can see in the medulla, you can see in the pons, you can see in the
3:60
membrane You can see that these people had different lesions in different locations. And then what they said is the following. They said they've caused
4:15
that to -
4:19
Two causes of stroke they could find. One is thrombosis, which you saw right here. And the other was emboline. So it came from some other place. a small embolism and went up to the circulation
4:32
and it blocked a blood vessel, getting a stroke. The problem is that they found that there were some people who had no problems, no lesions they could find in the percolation. And as I present the
4:47
history over the next 80 years, you can see how that becomes very clear. And actually 20 years from this people began to find out about this So this was a very important study. The reason I tell
5:00
you, I think it's worthwhile reading is because you look at the high-income countries and you say, we don't have all this equipment, we can't do this. And the answer to that is that's not true.
5:14
They asked some fundamental questions they use what they had in their intelligence. They came up with one of the best papers in the literature in 80 years because they were smart and they were
5:26
listening. You could do this today. using CT scans or MR scans. So there are lots of different ways to do this that people haven't done. So that's just a message from neighbors. Not only about
5:42
neurology or neurosurgery, it is about medicine and research and how you do this. Now, there were two more people, neurosurgery, two more neurologists who came and those neurologists were
5:57
militant and secret. And they followed patients who had similar symptoms. And those symptoms were people who had evidence of a brainstem disease. And
6:14
so what they said is they had symptoms of motor or sensory or cranial nerve deficits or problems with balance These are all things that we think
6:26
of. They call this vertebral basilar insufficiency, VBI. That's a word you read in the textbooks. You'll see it a lot. And they didn't do as many patients as the first people did. But they asked
6:40
the same question. So, well, can't we do something to treat these people? Why don't we study it and learn about it? So they on top see to maybe 15 of their people that they had and in one of them,
6:54
one of them, they found a blood clot that was what they call laminated. In other words, there are successive levels of blood clot and they said, well, my gosh, if that's true, maybe this is a
7:08
disease caused by clotting of the blood. And so they had a drug at the time called Coumadin. Coumadin was
7:17
a drug that was available then and probably has a different name. In Baghdad, a it's drug that, you can take by pill, they give by injection, it's a blood thinner, and they found that the
7:30
mortality of the group of people that were following went from 43 from those symptoms, all the way down to 14.
7:40
Now, what's the second lesson from this? Here are some people who did not, again, they didn't do randomized controlled studies. They used their brain, they used, they thought about the people
7:52
who came to them, they wondered how they caused it, they looked into the pathology, they asked some questions, they said, well, it looks like a clot is causing us, they gave them the drug, I
8:03
was to see if it would blood thinner would work, and it worked. Now, today, if you published the study, people would say, well, it's not a randomized controlled study, and it's a small series
8:15
where it came from Iraq, so we don't have to pay attention to it because people in Iraq don't know anything, because they don't understand the people in Iraq or very smart, and that's today's world.
8:28
But don't buy that. Don't agree with that, because you can do this also. And so they treated these people with high degree of success, and this treatment is used today, 80 years later, based on
8:43
their work and the work of the first paper I showed you. That just is with a simple amount of things that you have with you. You don't need a lot of complicated things. To brain, you need to ask
8:55
questions, you need to solve problems. Well, what else? So now, what happens is,
9:03
people then ask some more
9:07
questions, and the questions they asked here, can you see the signers are cut off? We didn't see it. You see it I got to see. Yeah.
9:17
So. So what happened is they asked some questions. They said, well, why don't we try to use angiography to see if
9:27
we can
9:29
demonstrate this disease without having to look at it after people have died. Well, angiography was started, as you know, by a Spanish doctor at Gasmoniz in the '30s,
9:39
1930s. They began to become more used in this circulation, the vertebral circulation. It didn't occur until the '40s,
9:50
or this period of time, the '40s to the '60s, as you see here. And what happened is you could do a vertebral artery puncture. Well, you do that by putting a needle into the vertebral artery from
10:03
the neck. You can imagine that's not easy. They had a risk of 25 because you could put the artery or injure the artery. Or you could expose a brachial artery at the elbow and you didn't check
10:16
retrograde, I did that. That worked, so you have to just put it under high pressure so it gets into the brain, it's diluted, but you can see something, it was better than nothing. You can
10:26
puncture the subclavian artery. You have to avoid puncturing the lung. That was done, but all of these things, including trans-femoral angiography, which you do now routinely, was introduced and
10:41
over this period of time, but the risks were too high So the neurologist who basically took care of the D, said, Oh, it's riskist UI. Can't use angiography. Risk for surgery, they tried to do
10:54
an inartorectomy of the vertebral artery. The risk of that was failed almost half of the time. And so what they decided then, as well, the only thing we can't do much for these people. So what
11:08
happened next is people asked a question. This is from the '50s to the '60s And that question was, the question was, let me go back.
11:18
The question is where are these lesions
11:23
occurring? The lesions were occurring. I'm going to have to let this man in here. Okay. The lesions were occurring. They sampled people after they died. They took out the whole vertebral system
11:38
from the origins all the way to the end cranial, which they hadn't done in the first series, I told you. And this now gives you a whole exposure to the vertebral basilar system. And what they did
11:49
is they looked for the plaques, and
11:52
they found that they had plaques that were going from the origin, and then they went up to the high vertebral artery where they had more plaques there, which skipped areas. Then it went just when
12:04
the artery went into a dural, then it was in the basilar artery, and then it was in the posterior cerebral artery. So the question is, why is it in certain location? Nobody has answered question.
12:15
Yeah. So. That's something you can work on. Why does that happen? Nobody knows what it happens. Okay. And they found that there are atherosclerotic plaques and most of the people they had in 10
12:29
of them had
12:31
embolite. So embolite become a small part of these people. They found that there was collateral circulation through the posterior communicating arteries at autopsy. And they also found that they
12:44
found patients who had symptoms in the brainstem. And they could have lesions anywhere. They all worked in one location. Well, that's a problem because I neurologists used to use their examination
13:00
to find where the lesion was. You could find it. You don't know where the pathology is.
13:09
Don't relate to the pathology, okay? So they found also that if you include one vertebral artery,
13:17
that that's not very good because sometimes, and I'll show you in just a minute, you don't have enough collateral circulation. And then they found that the distribution of lesions in the vertebral
13:28
basilar system, the posterior circulation was different than the anterior circulation in the carotidaries. Why is that? Nobody knows that either. So there are many questions today, we still don't
13:39
know the answers to. Well, a man began to ask some questions again in the 1960s was a neurologist Martin Rivet, she was in Philadelphia at the time, and he was making the hypothesis. He made the
13:53
hypothesis that the symptoms are not just related to the atheroma, or to
14:01
the plaque, or to the emboli, but symptoms can be caused by changes in flow. Nobody, remember I showed you the very first paper, I said they found patience. and they had symptoms, but they had
14:16
no lesions. And that was true in the second paper. And so now here's a paper that's investigating that question. The flow can cause symptoms. Well, why? Because both circulations are connected.
14:31
And so he began to do a study on a syndrome they called the Subclavian Steel Syndrome. I'll show you what it means. First of all, this is a patient they had A nation presented with headaches in the
14:44
exceptional region for six months. They were worse with exercise. Okay, this is how you get into the mystery of medicine. So now he's got headaches that made worse by exercise. He gets on and off
14:58
paralysis of the left arm. He had it four times in one year. Was admitted to the hospital. They checked the blood pressure. Simple thing to do in the left arm it was 85 over 75 the right arm, 120
15:10
over 80. So obviously there's a difference in pressures. Why is that? The retinal pressures they were checking in the eyes was the same. But what they then did is put an EGEG leads on the head,
15:25
press the carotid artery and the brainwave slowed. And they slowed on both sides of the brain. And then the patient became tingling in all four extremities and then lost consciousness. What does
15:40
that mean? Well, it means that just by compressing the carotid artery they did, they put this patient into unconsciousness. And so the assumption here is that they weren't getting enough flow to
15:54
the brain. And so they did angiography at that time. They found what I'm going to show you here is they found this picture. They found over here, you can see in the circle, a stenosis of the
16:06
subclavian artery. And you know the vertebral artery takes off after that. And they found that the circulation and look on the other side. goes up and we've outlined it in pencil here, it goes up
16:16
on the right vertebral, it goes up and crosses over and comes down the left vertebral and it goes down into the arm. Well that explained several things. It explained why the blood pressure was low
16:30
in the left arm and it was higher in the right arm. It also explained that there must be, there's obviously an occlusion here or stenosis leading to one of the vertebral arteries and it also
16:44
explained that there must be some compromise in the circulation to the brain if I compress the carotid. So what they did is they went to the laboratory and they tried it in animals. They had four
16:53
dogs and they measured they exposed the carotid and vertebral arteries. You can see on the chart there with under no occlusion internal carotid artery right. That was the flow they measured. Left
17:07
was the flow they measured 22. Retievable artery flow on the right was 27. And the left it was 43. Usually the left vertebral artery is bigger than the right. Okay. And the total flow is 106
17:21
millimeters a minute going to the brain. Well, wait a minute. Now they went ahead and occluded the subclavian artery on the left side of the dog. The flow in the right side and the carotid artery
17:34
stayed the same. The flow in the left carotid stayed the same. The right vertebral went up See that it went up, almost doubled. And in the left vertebral artery, it reversed.
17:48
So it wasn't going into the brain. It was coming out of the brain. So in essence, the amount of blood going to the brain was almost 40 less. It was 63 milliliters per minute. So what did you
18:05
prove by this experiment? What they proved is that if you have an occlusion of a blood vessel, that's not even in the brain. You can cause the flow to change. You can cause a reversal of flow.
18:18
You can show a compromise of flow that can lead to symptoms. And when they shut off the carotid artery, that meant that only the only circulation they were getting was going up one vertebral. It
18:30
probably wasn't going up enough
18:34
to go through the collateral into the brain And we don't know about the other carotid, probably was okay. But his whole brain was based on one carotid artery. And that's why the symptoms occurred.
18:45
So now I'm going to add some more complication to it. If you do a study and you want to check the circle of Willis, which you all know, in the brain, that's the arteries on the base of the brain.
18:57
The circle of Willis is abnormal in 50 of the people. So every, if you turn around and look to the person on the right and left, There's a chance that the person on your left. 50 chance, their
19:08
circulation in the brain is normal. And there's an absent posterior communicating arteries in anywhere from 31 to 70 of the case, that's large. So if you add that to this patient or the dog they
19:22
were looking at or the patients they were seeing, they had already compromised circulation of the brain and at least half of the patients.
19:32
So these are things that are now building on what people know about stroke. So we've got stroke due to aethroma, we have stroke due to the MLI, we have stroke now due to blood flow, but nobody
19:45
knew how to measure blood flow. So the neurologists were still treating the stroke in the 70s 'cause surgery was still too risky. And the only things they could treat the patient with were aspirin
19:57
and Coumadin. They didn't want to angiogram people because they thought it was too risky And so in the end, they had very little offer these patients.
20:07
Now, if you compare where you are today to where they were, and this is now 50 years ago, your way ahead, but this is where they were, and they were working to see what they can do better. Well,
20:19
at that time, some advances happened. We had the microscope coming into neurosurgery. You see that in Dr. Hose's lab. Neurosurgeons became very interested because they could see the blood vessels
20:30
in the brain. They could see them everywhere. They got the radiologists to do detailed angiography, which they could use, now people are interested because you had something to treat. And so this
20:42
began the change in neurosurgeons becoming involved in stroke. Now what was happening in the 80s at the time was coronary bypass surgery was becoming very common. It started actually in South
20:56
America, I think it started in Argentina
20:59
or Brazil. Yes, in Argentina, in Honolulu, yeah. Right, in 1952, I think, or some, in the early 50s, right? So anyway, coronary bypass surgery was taking hold and people said, well, why
21:12
don't we do bypass surgery to the brain? So many people began to do this. And then the governments who had to pay for this said, well, wait, this gonna be a cost just a lot of money. But let me
21:23
tell you first what happened. So now I'm gonna show you some of the circulation in the back of the brain. This
21:32
is a vertebral artery. You see at the bottom V1, which is where it comes off, the subclavian artery goes into the intervertebral foramen at C6. And then the second portion of the vertebral artery
21:42
goes from C6 to about C2. Comes out of the frame in there. It comes outside, goes around C1, and then goes into the dura, into the base of the brain. So that's V2, just when it goes from C6 to
21:57
C2 is the second portion of the vertebral. Third is when it comes around C2, goes into C1 and
22:06
V4 is when it's comes around the the atlas here and is about to penetrate the brain. Those are the first parts of the vertebral artery. That's going to relate to this. So people then began to do
22:20
angiography in detail. This is a case in all of these people I'm going to show you at the same symptoms. They had vertebral basilar symptoms. They basically had been treated and failed treatment.
22:28
They failed treatment. Nobody knew what to do. They came to us. We did an angiogram and it showed in this patient that the
22:40
vertebral artery was occluded on the right side in the proximal portion. You can see the artery is reconstructed on the left side of the picture here and what we then did is operation to expose that
22:52
and connected that stump into the carotid vessel and now the vertebral artery is filling the intracranial circulation. So that was surgery that could be done for for that kind of disease. And I
23:05
already told you that if you have an absent vertebral artery from the pathology studies, that's not good. And if your collateral circulation is compromised, that's not good either. That's 50 of
23:17
these people. What about the second portion of the vertebral artery from C6 to C2? Again, you can see up on the cut A, you can see a reconstruction of the external artery territory And what
23:34
was done there, you can see how it's reconstructed by collateral's off the subclavian artery. And so that was disconnected and connected into the carotid artery. And that patient's symptoms went
23:44
away. And here are some other things you can do from V2 from V6, from the second portion of the vertebral artery, from the sixth vertebral to the second. Sometimes you get an osteophyte, you see
23:58
it on the left picture, pressing on the vertebral artery there. Other kinds of treatments people had as used in the occipital artery to connect to the artery as it goes around C1. So it's an
24:10
occipital to C3 or C1 and astomosis. If you unroof the artery, you can do it to C3. Okay, so that's another treatment. What about the intercranial portion? Well, we have trouble here. I told
24:23
you that the periods where the atherosclerosis occur are at the
24:28
origin, they're up at the, where the artery penetrates the dura, then the basilar artery, the posterior cerebral artery, and people get an atheroma, why? I don't know, up at the area where the
24:40
artery penetrates the dura.
24:43
And they get a stenosis, they can even get an
24:46
occlusion there. So there were several people who worked on this and they did an intercranial vertebral endoderectomy. We did six cases. We were only successful in two of the 60 others So I'm going
24:59
to remain strong boast. And this is for Sammer, this is an idea. You could do this Sammer. What we didn't do at the time is we didn't know much about using antiplatelet aegis after surgery or
25:14
before surgery. And the second thing you could do, and this was done by one of the people in Spetsler's group, is to put a patch graph. Because if you enter to rectumize this portion, this is
25:28
just for Sammer, what happens when you sew it up there and it becomes smaller. So if you have that problem, Sammer, or you can get people who have that problem, try to do a patch graph, put them
25:40
on aspirin or a percent or whatever the anti-platelet agents are, it may work. I don't know if anybody's, they did that as a paper out of Spetsler's group in Barrow. I don't, I think they did
25:53
some impatience, I don't know. That was one, okay. So now here's what I've shown you. I've shown you that no matter where you have a lesion in the vertebral artery, that there was a surgical
26:05
procedure, I've listed them here, most of them I discussed, which you can do to overcome that lesion. So there's a surgical treatment now, this is in the 1980s and 70s, that's available to treat
26:20
a disease that we could only diagnose clinically in the 1940s and 50s and no treatment for, and most of these patients I've told you about failed treatment, this was the only thing they got to have
26:33
done. And if it's a treatment, that works. Okay, that sounds good. What about the posterior circulation? Well, you can do bypasses there too. And here's a bypass that essentially you see down
26:44
here in the screen that comes off the base of the skull and goes in and it's connected to the posterior inferior cerebellar. You see the base lardary with circulation and filming his share of both.
26:58
That's an acceptable artery to pike up bypass. Here's one, you have to look at the left side of the picture, I've got to let Fatima in here. I'm
27:10
not sure I can do that, no, yeah, I can do it this way. Here,
27:15
I'll let her in, now let's start back. Okay, and so if you look on the left picture, there's an artery that goes off the page, that really comes in, goes to the base artery, that's an
27:28
acceptable artery that I could bypass. This is, that's an AP and that's a lot of them. So there are different kinds of things you can do for people with these symptoms. Well, we took all the
27:37
patients, we did bypass this together, we put them all together. There were 75 or 85 patients here. And we found that if you put them all together, we put them into two groups. Again, this is
27:48
something you can do in Baghdad. This is not that you don't need any fancy machines for this. Okay, you just need a brand.
27:57
And we found that the cases that came where the symptoms were basically maybe occurred very infrequently.
28:05
If we took those and put them in a group, we were almost 80 of them. We could help their symptoms go away at a mortality of 5, morbidity of 7 and it occurred in 10. Now, these are people who
28:18
failed treatment. So they failed treatment, they either died or continued to have symptoms without surgery If we took this unstable cases, what you can see, we were only able to help less than
28:31
about 50 or less than 50. Mortality went up, morbidity went up and the symptoms occurred. What does that tell you? Well, neurologists like to keep the patients, they don't want to refer to the
28:43
surgeons that are trying to protect the patient, they're worried that we're going to do something to them. And so anyway, what it tells you, you can't do that. if you're gonna treat it and see if
28:55
you've got to treat it early, which you all know anyway, from the parts of medicine. If you wait till it gets to be bad, the chances of treating it are very, are low. Okay. So this is what the
29:07
surgical treatment was in the 1980s. My past studies were not randomized. We didn't do any randomized studies. They were performed on people who failed treatment. They were unstable, excellent
29:20
results Intracradially, if you got people in time and 70 of the cases and in 95 with they had extracranial disease in the vertebral artery, there was no medical or surgical treatment that was
29:35
randomized. The symptoms basically were not understood except through endiography. They were hemodynamic, which means they were flow or they were embolite, okay, or theerytheroma Neurologists are
29:48
still reluctant to offer an angiography and the bypass. I bypassed came out about that time. And we'll let 15 appear, okay. So here's the story at this time. Now the bypass study came out. This
30:06
was a study they said,
30:08
Why don't we spend it worried that they're gonna spenda lot of money on this? This is another lesson. And you get the government into something, be careful. You know this very well. You get the
30:19
government into something, can screw it up So here what they did is they did a study. I was involved in a study. They said they studied about 1, 377 patients. They divided them into two groups.
30:32
They said they're randomized. But the problem was, they weren't getting enough patients. So they kept adding patients at the end who didn't have symptoms for months. Okay, that didn't come out
30:43
too much in the study. But the conclusions were, as you see on the bottom, the conclusions. Now this is how you make a conclusion for observation Study failed to confirm the hype. hypothesis that
30:54
bypass is effective in preventing cerebral ischemia in patients with atherosclerotic disease in the carotid and middle cerebral arteries.
31:11
Is that a fair conclusion? Well, I think I would, it's pretty good. I would say in this study, from the patients that we examined, in the manner in which they were entered into this study, we
31:27
found no difference between bypass surgery and medical treatment,
31:33
in trying to resolve the symptoms of stroke, predominantly in the anterior circulation.
31:42
What did they come out and tell everybody? They said that bypass surgery is of no value for stroke, and that's in what people have believed for years. Now, that's not a fair conclusion. It is the
31:58
wrong conclusion. They didn't study the posterior circulation. They had no idea about that, But they say stroke, that means everybody. and you'll see what the effect of that was. Well, the
32:12
neurosurgical society in America was upset about this. They sent three wise men up to the center in Canada and they found, what did they find? They found that over 2, 000 patients were operated on
32:30
outside the study. Well, wait a minute, that means the study wasn't done the way it should have been done That means the surgeon would say, I want to operate on this patient, or I'm going to put
32:40
him in the study. So there was a selection bias.
32:47
And then they said that you can't make the conclusion they made and they were trying to discontinue Medicare payments because they said the conclusions are too sweeping because the evidence is limited.
33:00
Now they made a fundamental scientific flaw
33:06
and there were a lot of scientists there. and the government was involved. You would think that somebody in that room would stand up and say, look, this is wrong. We didn't do this. We should
33:17
have made a better conclusion at the end. It didn't change. Why?
33:25
So what happened is we criticized the study. It wasn't a study of posterior circulation disease. That's true. It was a biased sample, that's true They had a lot of people in there who basically
33:39
had accommodated to whatever occlusion they had. And this conclusions were study incorrect, but it has become an accepted study for the last 40 years. It
33:55
was a first randomized control surgical procedure.
33:60
Now, when they sent the experts up there, the experts said, well, let me see the data They couldn't reproduce the data. they went back another time. They couldn't reproduce the data. So now
34:12
you've got somebody who does the study, doesn't report the conclusions that are true. You go and ask them for the data, they can't give it to you or they give you different data. You go back a
34:22
third time, they give you different data. And what would you do? You'd say, well, you can't do any more, how many more grants?
34:29
It was a corrupt study. And all involved were corrupt, including the government. Well, you can't make that statement because we're gonna persecute you. And the person who was ahead of the study
34:40
was a very prominent neurologist. And the neurologists were intimidated that if they criticized the study, they wouldn't get grants. And so were the neurosurgeons, so money. Well, after this,
34:53
neurosurgeons became devastated. They lost interest in several vascular surgery. They were still interested in aneurysms. And for the, almost for the next 30 years, neurosurgeons have been on the
35:05
periphery. of study of cerebral vascular disease. That's how it happened. Now, Sam are very aggressive, and he's asking questions, and he's doing these things, and he doesn't have people who
35:18
are trying to impede him.
35:22
At the same time, what was happening in a neurosurgery, we had coiling coming in for aneurysms. So neurosurgeons now are losing stroke back
35:32
to the neurologist. They were gonna be loose They were beginning going to lose some of
35:40
another part of their specialty to interventional neurologists. ADMs were being treated by radiosurgery.
35:48
Interventional treatment was tried that only were successful, I'll tell you about that. Cardiologists were stenting carotid lesions. It didn't matter if they had symptoms or not, but yet they
35:59
criticized neurosurgeons only for operating on symptoms And we're very careful that they have to be - 60 stenotic or something. And
36:08
so then what we had is all these people working independently, and this is another principle that's gonna come out of this. We're all working at the same disease. Now this is for you young people
36:21
who wanna change the world. If I tried to do it, it couldn't do it. I wrote this paper about the death of aneurysm surgery, and I never got invited to another vascular meeting.
36:32
Because I said that aneurysm surgery is gonna be overtaken by interventional treatment. And we had a very famous interventionalist who was working for us. In fact, he became a member of our
36:43
department, 'cause it didn't make sense to me that we were working on aneurysms. He should be in another department. I should be in another department and we'd compete with each other. That made
36:55
no sense to me. So I said, we have to be together. And so what the message is for you in the future And then in the next alone. the rest of the 21st century is we have compartmentalized. We put
37:10
into different groups, everybody who's treating a thermometer's disease. That doesn't make any sense. The cardiologists do
37:19
that, the vascular surgeons do that, the neurosurgeons do it, the neurologists do that. Where is the group that works on this all as a disease together? It don't exist, why don't they exist?
37:32
Because there are certain roles that say you have to have a department of neurosurgery and neurology and we have residents who are raised in neurosurgery and raised in neurology. Well, how does that
37:41
make sense? In Mexico, Mexico, we visited some of the best centers in the world. Mexico, they have a neurology and neurosurgery institute in Mexico City. One of the best institutes I've ever
37:56
seen in the world. They had it also in Chile And
38:03
they headwood in Spain. And these were integrated systems in which everybody would work together on the same disease. Very, very good thinking. No, what are you thinking about it today? Because
38:19
everybody's protecting
38:22
their own interests. That's what the young people need to work on. You wanna change the world? Try it, start. I tried was not successful. I hope you are Okay, here's a man who came to us just
38:36
to give you an idea. So we had some other ideas. What about, can we use interventional treatment for aneurysms? Here, if you look on the left side, you see a vertebral injection. It goes up and
38:47
it stops. And if you look at the picture next to it right here, it goes beyond what's a stenosis and fills the rest of the basal artery. But what happened? Well, we put a catheter up there. You
38:58
can see the catheter of the picture on top And we infused some thrombolytic agent.
39:07
I can't remember the name of it now, but it's wrong with the medication. Okay, urokinase, streptokinase, they're not used now.
39:13
And we opened the artery up so there was flow. You could see it in the picture below. You could see the artery, but there's a stenosis. That's why the patient had the stroke. And we went ahead
39:24
and did a bypass. And the patient did well. So that was done in 1990. That's 30 years ago
39:35
Okay, now from 1985 to 2015, I say we have a lost period in cerebral vascular disease. Why? Well, when people did mostly neurologists, 'cause neurologists and we're losing stroke patients to
39:50
neurosurgeons, they didn't like that. And so now the neurosurgeons became dissatisfied. They didn't wanna treat the patients. They wanted to go do something else. So the neurologist got into this
40:02
and you'll see the same story. They said, Well, let's get a group of patients together. We'll make a registry. We'll study these people. And that was done. Well, the problem is the registry
40:14
where you get people from all over was wind up wound up being a biased sample of the universe of people with vertebral basilar disease. It's predominantly white people. It doesn't matter to me if
40:28
white, black, whatever it is, but in that sample, it wasn't a sample of the population demographics of the United States They use CT and MR imaging, which don't show vessels smaller than three or
40:40
two millimeters in size. The blood vessel you do a bypass is one millimeter. So it's inadequate, those studies that are inadequate to evaluate cerebrovascular disease. You can't do that. But that
40:54
became the mainstay of all the evaluations of vascular disease at that point, okay? So that's another problem. So they based drug studies on this. And obviously, those studies are invalid. They
41:09
tried interventional treatments, but they weren't very effective. Okay.
41:15
They only, maybe for basilar stenosis, we'll get
41:24
to that. And surgical treatment was totally ignored on the basis of a flawed, incorrect, corrupt study that also didn't consider the previous work that was successful in the post-year circulation.
41:35
And this was done by a national organization, more intelligent people making another mistake.
41:42
And we have neurosurgeons and neurologists competing and everybody's competing. That makes no sense to me. I don't think it makes sense to you. Okay, that's a lost period of time. Any of the
41:54
studies during that time, to me, are basically of no value. So now we're up to 2010 to 2021.
42:02
There are some very significant things that have happened that'll influence stroke in the rest of this century. The first was a study that I'm gonna show you in a few minutes about advances in
42:12
imaging, which now are able to compute blood flow in the brain and show more detail that you get by an angiogram. We have other diseases that people don't even understand what you're working on in
42:24
your laboratory. And I gave you a paper from a man in Peru, who had worked on this subject. Why Peru? Why isn't he from Boston, Massachusetts? He's from Peru, and it tells you that smart people
42:39
are everywhere in the world. He worked with us in the lab. He was working on diseases of small vessels. We have people who are getting into the genetics of AVMs and aneurysms. And now there are
42:52
large studies of patients that are coming out of EGLE. So let me tell you about this. Okay, seven tests that I mentioned. most places in this country, United States don't have
43:05
it here. Don't feel badly about it. And it's going to reveal an enormous amount of information. I'll just show you an empty minimum. They had a man who came in with this and his visual field
43:16
deficits. They used a 05 Tesla, MR, an occipital infar, put him on antiplatelet drugs. Same story. Six months later began to have more symptoms, loss of consciousness. Now he had a 15 Tesla,
43:33
which showed lesions in the cerebellum, thalamus, and pons, which you couldn't do with the 5
43:40
millimeter lesion. Let hagger in here. Okay. And then they did anceography, which showed bilateral vertebral occlusions. You know what that means. You know what that means. That's, that's a
43:56
devastating problem. There's paid for, paid profusion of of the posterior communicating arteries in some of the circulation. So obviously the man has compromised circulation. And then they did a
44:11
seven-testile MR that did a specs scan, I'll show you about those show. This is it. See the angiogram in the upper left corner here with the arrow? You can barely see the little fragment of
44:22
posterior communicating area on both of those films, one right next to it OK, now if you go over to the seven Tesla MR in the right upper hand corner, you see the carotid artery, the big blobs up
44:36
and white in the front, and you see that corkscrew with that very curly Q artery going back from the carotid artery, eventually joining the basilar circulation. That you can visualize with seven
44:48
Tesla angiography. Seven Tesla - it's not done in this country routinely. This came out of Japan It's not done routinely there. just read a paper last week where they were using enhanced CT to show
45:02
more detail. So people aren't, they still act there.
45:08
And okay, we like somebody else too. So now that's where you go. If you look at the, go down to the lower left corner, you see on the MR angiogram seven tesla. Now you see that tentorial artery
45:22
in great detail
45:24
Okay, and you look at the, the, the scan, you can see resting. It's see the, there's perfusion around the brain. And when they, when they were, they used a cedical
45:41
clarithiside here, they did a diuretic agent essentially. You could see that there's less flow in the cerebellum and so forth. And then they went ahead and did a bypass in the last, to help this
45:53
man So here's an example. of how new technology will tell you new things that you don't know will change your pattern of what you do. And I've seen this, but if you look at the seven Tesla images
46:05
of the brain, you can see the vessels in the brain that are below a hundred, below a millimeter in size, there are
46:14
a hundred microns, and you'll be able to diagnose and treat diseases that are very complex that we don't know anything about today. All you have to do is have the machine That's where a machine
46:25
would be important. Okay, nobody's done that as far as I know. Okay, that's the future. You know that's gonna happen. Now, somebody else was at with our group, did something called
46:37
quantitative angiography. And what they did is they used the MR machine to measure blood flow in various arteries in the brain. They started with some 47 patients. They were had symptomatic with
46:50
vertebral basal disease. They followed them along They were going to look. to see if they had stroke or TIA after their study,
46:59
they all had quantitative magnetic resonance and geography, QMRA, all had 50 stenosis on their integrams. So the flows were, were, could it be compromised? They decided that if the flows were 75
47:18
to 80 of normal, they weren't 100 normal, they were gonna consider the meschemic. And they, they took the patients who had normal flow and they managed them medically with anticoagulants and anti
47:30
plate, platelet
47:33
antigens. And so the patients who had this normal flow had no more strokes in almost 100, almost 100 of the cases. But the patients who had low flow had, I had 50 to 75, 25 to 50 had had had
47:54
strokes.
47:56
and it was showing a significantly higher risk of recurrent ischemia.
48:01
So now what we have is a test that you can do if you get this, and most people have not picked up this technique, this is 2005, 15 years ago. Most people have not picked up this technique where
48:16
you can study patients and you can select those patients or the ones who have normal flow can go on and you saw that back almost now of 60 years ago where people had normal flow and they had it in the
48:31
pathology studies and the clinical studies, okay. And here are people who have normal flow who did well, but people who have low flow didn't do well. And those are the people you select for
48:44
treatment. So now we have a way of selecting people for treatment instead of saying, well, I think this person should or I think this person shouldn't or surgery is good or surgery is not good. So
48:54
this study's out there. Nobody's paying attention to it. And this is how they measured it. They measured it in all those little blue parts of the various arteries there. OK, here's the difference.
49:07
If you have normal flow, you can see that basically your survival is of almost about 100. You have low flow on the bottom. You don't do very well. But if you have low flow with treatment or
49:19
intervention, you do better, and you almost are like normal So that's, I would think, a good treatment, a good diagnostic test. We've got two tests, seven Tesla, and now we've got quantitative
49:33
flow. And I don't see it being used. So anyway, so I'm gonna go on to the small vessels. Now, there's another disease described very well, but this is a neurologist who did this Dr. C. Miller
49:47
Fisher. He had a paper in 1967 in archives of neurology, another outstanding paper. He wanted to find out about what causes lacunar strokes. These are the small strokes you see on the CT or MR
50:01
that little holes in the brain, the basal ganglion. He sectioned the brains of, I think, 10 or 11 patients. I think a thousand times, a thousand sections, a huge number of amount of work,
50:14
trying to find out where the lesion was. And he found out that the lesion, which he called the Charco-Bushard aneurysm, occurred within
50:23
a centimeter of its origin from the middle cerebral artery. So we now know, and that was 67, okay?
50:33
That's 50 years ago. Nobody's done anything.
50:39
Nobody's done anything. You're working on it in the laboratory. And so now we can, if we show these arteries, which you can buy angiography, and if you get a small enough catheter, You can
50:50
selectively catheterize those. I've seen it happen.
50:55
It was done up in Buffalo, New York, and
51:00
you can demonstrate the lesion. Well, now if you demonstrate the lesion, we're gonna be back where it's about. If you find the lesion surgeries too risky, what are you gonna do? So they did
51:08
nothing. Well, that's not true. We already been through that history 70 years ago. And the answer is you can think of some things to do. Maybe you inject some
51:21
vascular endothelial growth factor in the area and try to get more blood vessels. Maybe you put a small stent there. Maybe you can't put a stent there. Maybe you occlude one of the vessels and I'll
51:32
tell you why you can do that. And we'll show you in a minute. This is a study we did on a laboratory of Sammers working on this. And this is looking at, here's a, you can see the, over here you
51:43
can see the optic chiasm. Okay. And you see the anterior cerebral arteries on top of it, just underneath it here OK, the object is in some - or at least two stumps on time. And you see the
51:56
carotid artery, you can't see it coming up, but it leads to a blue part, which is a metal cerebral artery, proximal in the yellow part, which is just so. And the red part, which is the anterior
52:07
cerebral artery A1. And so we selected those in the laboratory selectively by tying off the other sections. You could do this in Baghdad. This is not rocket science. It just takes somebody smart
52:22
who's doing this Other people work on this. And this is what they find. I remember red is from the anterior cerebral, blue is proximal, middle cerebral, and yellow is just a middle cerebral. You
52:34
expect this distribution is gonna be similar. That's what the brain looks like. It's anything but similar. Remember, the yellow is the distal. You can bury seal it on the bottom here. It's only
52:46
a peripheral amount. And you see the red on this one side, It's almost already fed by the anterior cerebral. And the other side, it's almost blue fed by the metal syrup. So what does that mean?
52:57
If somebody has a stroke on one side in a middle cerebral, he could have a devastating basilar infarction, okay? But not much else, if he had the same thing on the right side, it wouldn't happen
53:10
or the opposite side. So it means clinically, and nobody knows this, clinically, the disease will present differently depending upon the collateral circulation You just learn something most people
53:23
don't know.
53:27
So the disease can present differently in different people even down to the micro level. That makes sense. Well, now they're doing something else. I told you about this in England. They have a
53:37
population of about 91, 000 people in Oxford. They were able to sample this population because apparently all these people came to the hospital there. And they were trying to compare the anterior
53:50
circulation the post-year circulation. And they found the posterior circulation disease had people had symptoms, but they were in classic. They weren't in the usual numbness or weakness of one side
54:02
of the body or double vision. Wasn't, it was just a mixture of symptoms. In the posterior circulation, 27 had symptoms and TIAs, and only 10 had symptoms in the anterior circulation. So they're
54:16
different. Well, you can understand that from the pathology, I showed you. The vessels are smaller They had more symptoms for TIAs in the posterior circulation, 22 versus 3 in the anterior
54:28
circulation. What does that mean? It means that the disease is more rapidly progressing, but we don't treat it that way. In fact, we ignore it.
54:38
Early recurrent TIAs in posterior circulation disease, almost half, brainstem symptoms. What are they? They were vertigo by themselves, or dysarthria by themselves, weakness or double vision,
54:51
not altogether, or by bilateral visual disturbance, they wouldn't come together. But right now the rules say in medicine, in order to have posterior circulation and ischemia, you have to have
55:04
multiple systems involved. Well, here is a disease that's presenting early, rapidly with isolated symptoms you're gonna miss.
55:14
And of that group, only 10 sought help from a doctor. So from the knowledge that's out in the public, they're not even gonna treat it So what does it mean? You're gonna have early, early
55:25
diagnosis, you gotta teach the public, you gotta come to the hospital early. When they come to the hospital, the doctors have to be informed of just what I'm telling you now. They have to be able
55:35
to triage them to a team of people we talked about so you can make early diagnosis and treatment. Well, we're getting into the early treatment, but I can still tell you that nobody knows what to do
55:46
from posterior circulation disease in the United States That's leftover from the bypass study that was corrupt.
55:55
Well, we did some other things that you can think about. Patient came in, was having symptoms had failed everything, had a thrombosis in the basilar artery, this is for interventional therapy.
56:05
So we opened the skull base, this is for you
56:09
to run. We went through the mouth, opened the base of the skull, opened the door, got down to the basilar artery, huge atherosia there. And we opened the basilar artery, we put a clamp distal
56:21
and proximal to the atheroma. And what do you think we found?
56:28
When we took the
56:30
atheroma, we found blood coming, flowing back into the basilar artery from the brain stem.
56:38
Well, wait a minute. That doesn't happen. These are end arteries. That's what the textbooks tell you. That's false. And the reason you know it's false is you've seen people who come in with
56:48
throwing emblest to the basal artery, they have very few symptoms. And that's because they have excellent collateral circulation. Again, something I showed you early. So basilar indirect to me,
57:00
but obviously the patient didn't do well. But it showed us our attempt to try to push, we've talked to the wife and she gave us permission. She understood that. We did all the things you wanted to
57:11
do. But what did we learn? Something that the textbooks keep telling you is wrong. We went to the lab and we transplanted middle cerebral artery bifurcations and trifurcations between animals,
57:25
transplants. To the work you've previously seen on reconstruction of the post-year circulation, in 1985
57:33
and 1986, we published work on reconstruction of the vessels in the anterior circulation. A paper in 1985 showed a variety of different approaches to reconstructing the. vessels with an occlusion
57:52
of the main branch of the metal-cerebral artery with intracerebral grafting and bypass surgery. In 1986, we published a paper on a patient who presented with a cerebral aneurysm with one of the A2
58:09
vessels coming off the dome of the aneurysm. In order to treat this patient, we had done work in the laboratory reconstructing the vessels in the anterior circulation in
58:23
all types of human brains. And the diagram shows multiple ways of treating this problem by eliminating the aneurysm.
58:33
The subsequent picture shows a pre-operative view of the aneurysm with the ACA taking off the aneurysm dome. And the subsequent view shows a side to side and an anastomosis of both anterior cereals,
58:47
vessels filling the anterior cerebral circulation. and the aneurysm was absent. This work led to other work 20 years later by Michael Lawton and Abla on using this in more detail and reconstructing
59:04
the circulation for complex aneurysms.
59:09
Now they're interventional treatments out. People who studied the genetics of AVMs and aneurysms that's been studied in Japan Radio surgery has been used again for AVMs to cause fibrosis in the
59:24
tissue around it in occlusion of the blood vessels. It also causes blood vessel proliferation. And now work's coming out of Japan showing that aneurysms are basically a result of inflammation
59:40
and now work is coming out which shows that atherosclerosis is an inflammatory disease
59:47
macrophages go into certain areas of the blood vessel. They absorb the lipids from the blood. They become swollen. They cause an atherosome and they keep swelling and they have rupture and they
59:58
have a plaque. People have tried to treat the disease with antibiotics that doesn't work at this point. Doesn't mean it's not going to work. This is a disease that's going to disappear in your
1:00:08
lifetime. So what's a neurosurgeon going to do? What's a neurologist going to do? What's going to happen if we treat eight aneurysms with genetic treatment, or AVMs with genetic treatment?
1:00:22
Some of these diseases are going to be disappeared. By the time you're my age, I'm 83 going in 84. OK.
1:00:32
What about today? Now we've gone through 80 years. We're off to today. So we've got complex cases that are left. Intervention we use,
1:00:42
but they're still for coiling them and yours is 25 failures. What happens to the failures? Well, Sam or knows because he's an intervention.
1:00:53
But if the interventionists are not working together with the neurosurgeons, they don't know. And they say, well, the neurosurgeon couldn't do anything about it, leave them alone. Well, that's
1:00:60
not true, we don't know that. They avoid treating posterior circulation disease 'cause there's obviously no treatment for it. I just told you that's not true.
1:01:10
If AVMs are treated with radio surgery, they don't all work, we know that. And now they're long-term complications with radio surgery. So what do we do for that? Where do you get those patients
1:01:21
back?
1:01:23
Why not? So,
1:01:28
we've gotten more specialized, we've gotten more competitive, basically, for the patient and for the money, it's in different, different countries. We have central control. You've seen what
1:01:38
happens to scientific studies when they're under central control and not where the practicing neurosurgeons don't have input into this central control better. You know the answer to that.
1:01:56
patients coming last. So what's the future?
1:02:02
In this anterior and posterior circulation diseases are different, I've shown you all the answers, all the reasons for that. And what I've also told you is the only answer to that is what you have
1:02:16
to do is develop teams that work together.
1:02:21
Atherosus discriminator disappear I've talked about the genetic things. You need to have disease management, multi-specialty groups that, so I'm working in atherosclerosis. And you all work
1:02:35
together and you solve this with the basic scientists. You find a way of compensating everybody. Then you're gonna be the leader in the world.
1:02:46
Should people come because they have a particular problem or go to disease centers? Think about that.
1:02:55
Ask the most important question in life is why? Why am I doing this?
1:03:02
Cerebral vascular disease is likely gonna be gone by the end of this, when you're 100 years old.
1:03:10
What am I talking about? I'm talking about change. You wanna change the world, I'm for it. But you're gonna have resistance. And the resistance isn't gonna be for me Resistance is gonna be from
1:03:24
your colleagues. It's gonna be from other people. You're gonna have to fight resistance. It's going on since man became civilized.
1:03:34
So that's your challenge. Principle in medicine. Principle in medicine is a patient comes first. Not the hospital, not the system, not the government, but not you. The patient's contract is
1:03:50
with you patient comes to you and says. I want you to treat my family. You have that contract. You have to make sure it's fulfilled. If you can't fulfill it, you tell the patient, right then, I
1:04:04
can't do this.
1:04:08
That's your contract. Okay. Thank you very much. If you want to see this paper, it's an SI, which you know is the internet journal we have Look it up in
1:04:23
SI on search, osmond, vertebral basilar disease. You find most of it in there. And I want to thank you for listening. If you want to write me, that's my email.
1:04:50
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1:05:05
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1:05:12
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