New Syndrome Etiology; (SSCD) Semicircular Canal Disturbance; Skull base Surgery

SNI Digital, Innovations and Learning,

in association with SNI, Surgical Neurology International,

are pleased to present

an SNI Digital interview with Clinical Neuroscience Leaders, another in the series, and this is with Isaac Yang, who will be talking about a largely unrecognized disease which presents with

patients who are totally disabled by hearing their heartbeat or their own voice with some other symptoms,

and up to now there has been no successful treatment for it

This is called superior semi-circular canal dehiscence.

And Dr. Yang is a professor in the Department of Neurosurgery. radiation oncology and head and neck surgery is also a principal investigator in the UCLA brain tumor program at the UCLA Johnson

Comprehensive Cancer Center, a director of medical student education in the Department of Neurosurgery, also a skull base surgeon, lead neurosurgeon in the UCLA acoustic neuroma center, and the

lead neurosurgeon in the UCLA superior semi-circular canal to his center,

all at the University of California in Los Angeles, in the David Geffen School of Medicine.

Dr. Yang's email address is listed on this slide. We're starting this today's video with Isaac Yang. Isaac has received his training at UCSF in San Francisco in neurosurgery. was there for a while

and came to UCLA's and the faculty's professor of neurosurgery. And what he's going to talk about is a subject that is growing, it's growing in significance, not a lot of people know about it,

although there are a lot of people with these kinds of symptoms around. But the problem is they're not as disabling as what you're going to tell us And so, why don't we start with there? You can

kind of start with how you got into it or however you want, and we'll go through this, okay? Super. Well, Professor Aussman, thank you so much for having me. I appreciate the opportunity. It's

really a delight and an honor to speak with you. And it's so amazing that SI and SI Digital is now international in talking to so many audiences all at once that we can all have this conversation.

And this disease and specific that we're going to talk about is semi-circular canal dehiscence, SSCD.

It's a mouthful and it's described with this acronym SSCD in short and quickly and I actually came to this very serendipitously, like a lot of things in science. As Professor Asman mentioned, I

trained at UCSF and I think I got good training and I thought it was a great residency and in full disclosure, I never saw SSCD in residency. It wasn't a big thing and it wasn't being treated

commonly and we didn't see many patients in I for whatever reasons during my six years of residency at UCSF. I just, I hadn't seen it and when I looked into the weeds of this, I realized why I

hadn't seen it is this disease was first discovered or named or coined by Lloyd Miner in 1998. He had a series of patients that had the disease of oil sclerosis. He at the thought, I thought they

were diagnosed with oleosis. So he did the surgery for oil sclerosis, and these patients did not get better. And around 1998, he was a professor at Hopkins at the time. That's when the CT scans

were getting high enough from resolution, because the superior semi-circuit canal is a very small organ. And to get a CT scan with high enough resolution, I think the late '90s, early 2000s, was

when the CT scans were getting high enough from resolution. And so he found that in these patients who had autophony, who had balance with sound issues, he found that they had a dehiscence, a hole

in their superior canal. And some people still refer to this disease as a minor syndrome, and do reference to Lloyd Minor. But otherwise, SSCD or SCDS. So there's an actual physical hole that

develops in the superior canal. So these patients developed in that way. Yes. Do you mind if I ask you questions along the way 'cause the audience is, I'm kind of representing the audience. Sure.

First of all, Professor Miner, he was a autologist or an otolaryngologist as his background. Yes, Dr. Miner was a neuro-autologist at Johns Hopkins. That was his background. He listened to his

patients. That's the thing I always wanna highlight about that story is that these patients have this disease He looked at it one way. They didn't get better. He listened to his patients, believe

them, because they were saying they hear their own voice. And I think a lot of people were dismissing that as psychiatric, but he believed his patients, got

the CT scan, and then did the surgery. He did a middle foster craniotomy, and the patients got better. He was a neuro-autologist. When he did that, did he

assume, he must have done more than assume We must have recognized there were some. defect that was affecting the semicircular canals he must have had some imaging at the time that led him to

support that and then what you also mentioned when you when you it's hearing your voice louder than it is and it's got a word for it yes so the word is autophany so he is hearing your internal body

sounds so hearing your voice hearing your heartbeat hearing your eyeballs move hearing blinking your footsteps bow sounds and these things when you first hear of them and I was not exposed to this

until 2010 I also did not know about this and when I first heard about this I thought I also thought this was psychiatric and not biologic it's not not a surprise I think many of us with common kind

of symptoms like this you're going to get into this later they're dismissed. Yeah I mean from a neurosurgical perspective hearing your heart rate to me was Lomas jugularitumor. You know, I was

thinking, okay, you hear your heartbeat. That must be a glomus. There's no glomus. And we get an MRI on every single one of our patients to rule out a glomus tumor. And we have found other kinds

of tumors. I mean, in geomas, gliomas, acoustics, zero for zero on glomus tumors in our over 600 SSCDs now. Okay, well, I interrupted you, but continue on with this story. 'Cause I think

it's interesting about finding a disease and your story about how you were persuaded to become involved

and understand this is a real entity. Yeah, so I just wanna give all the credit to Dr. Miner, 'cause he's the one who discovered the disease, found the dehistance on CT scan, and started that

courageous step of fixing those patients, and then those patients got better. And then me and my ignorance, and then my training, and I'm blaming it all on me and owning it, I didn't know

anything about it when I started my job in 2010 here at UCLA. I was very fortunate and very blessed. And I'm gonna give credit to my colleague and one of my very good friends here at UCLA. His name

is Dr. Quentin Gopin. And he was an otologist, neuroatologist who trained at UCLA. He did a fellowship in San Diego. And then he got his job at Harvard. So he was a neuroatologist at Harvard and

in Boston. And then ultimately his wife wanted to move back to California and he came back to UCLA. And we started two months from each other Like my certain day one and his day one were two months

off. And so we were both new faculty here. And that was a very fortuitous serendipitous blessing. And so we started doing the things that we do. We started doing acoustic neuromas. Our very first

case together was a facial schwandoma that we approached through a middle fossa. And a week or maybe a month later after that facial schwandoma, Dr. Gopin comes to me and goes, Isaac, can you do

a middle fossa crani? And I was like, of course I did. I just did you one And he said, Well, can you do this for this thing called? superior canal de essence and that was in my career, my life,

the first time I had ever even heard of the disease or heard of the symptoms of the disease and he told me briefly that people hear their own heartbeat and their voice and I in hindsight think that I

didn't believe him. I don't think I believed him and I was very skeptical of the report from the patient but I knew Dr. Gopin was a very good doctor and he said that at Harvard he had done about a

dozen of these cases and that they got better and he was a he's a diagnostician like master class genius kind of human being he really is and so he diagnosed as a CD he said the patient had a toffney

heard their own heartbeat and he said Isaac we do the middle fossa I will fix this and the patient will get better and I said okay I'm doing this because I trust you I saw I went to the PubMed there's

some literature I don't I'm not fully on board but I do know it's not harmful, it's safe. and I can do this, and you think it is, and the patient wants to undergo this. Let's all do this, and so

we did that first case, and I, to this day, will not forget the response that the patient had, and my shock that the patient got better. The patient woke up and said, I don't hear my heartbeat,

I don't hear my voice. And one of my very most memorable patients, she had come and she was getting depressed because no one was believing her. She was being bounced around from many doctors. And

for over a year, she was losing weight, getting depressed, hearing her heartbeat for some unknown reason. She saw Dr. Gopin and Dr. Gopin within, I think a minute of hearing her symptoms said,

This is what you have, this is what you need to do. We fixed her and she said, Dr. Gopin, you're essentially the messiah, like you're the insane geniusbecause within a minute you knew, You all

did the surgery and I got fixed and I got better. This was maybe about a dozen patients into the series where I was just shocked. And it's because I had never heard of this. I was thinking,

everyone should know about it. This is just almost miraculous that this is a disease I had not heard of. They come in with an exact set of symptoms, hearing your heartbeat, your voice and

dizziness. And then they got better almost like that after surgery. I had almost never seen anything like that because I think in neurosurgery, we see that with maybe back pain, ACDF, neck pain,

functional neurosurgery with a GBS and the fix is instantaneous. But for me, coming from the world of tumors, we are either feeding patients when they are very debilitated and we don't improve them.

We try to stop at debilitations or we're doing surgeries preventative. We clip an aneurysm before it ruptures or we do it after they've had bleed. We've taken it out in acoustic or a meningioma

before it becomes symptomatic and so I this was very different coming from tumors where this is an Almost immediate post-operatively in the

PACU room They would be so thankful and so grateful and saying look I don't hear those voices anymore It was one of the most life-changing surgeries that I had ever been able to participate in and

because I was so shocked I contacted Elaine Schmidt who's no longer here at UCLA But she runs story power and I said Elaine there's this disease There's this condition and we did the surgery she got

better and then she started broadcasting that into the doctors Good morning America readers digest And because of that a lot of patients saw that and started getting disease awareness and actually one

of the more rewarding parts of this I think someone in Boston saw our story. recognize the symptoms, diagnosed himself and went and got treated somewhere else. Well, I didn't even treat them, but

they got treated. And when I heard that, I was so

grateful. And I felt such a remarkable feeling to know that what we're doing is helping spread disease awareness, because there's a lot of patients who probably have this condition and are not being

diagnosed and no fault to the doctors. Remember, I want to own my ignorance and my naivetuses That this was on me that I wasn't trained. I went to UCLA med school, UCSF residency, and I didn't

know anything about this until my first year as an attendee. Well, I think something we talked about before is it was so disabling to this moment like this, that you just described that the

difference was immediate to her and was was a big relief. So our audience that's watching this is going to say, okay, tell me a little bit about how the symptoms are and. and how you decide,

because I see these people, I see people with dizziness and so forth. This is a hard category to deal with. How'd you do it? And what are your conclusions as to what do you, how do you screen

them?

The most common presentation is a coffin. And so that lady, the one that comes to mind, and I'm still in connections with her, and we're 15 years out, and she's still doing well. A topic for our

viewers and other countries means you're hearing your own voice, you're hearing your heartbeat, and it's all accentuated. I know I've seen people in the past who go to bed at night and hear their

heart bite, they can't sleep and so forth. You think it's something else 'cause I never knew about this either. That's exactly correct. So they hear their heartbeat all the time. They can't sleep

because they're heartbeat. And what's really irritating about it, and I don't have the symptoms, so I can only imagine what it's like to suffer with this, is if they get more excited, they get

nervous. They start working out. Anything that raises your heartbeat, then the heartbeat and their ears get louder. They don't want to speak. The particular patient who was getting depressed

because whenever they spoke, their voice was echoing like a broken speaker or a kazoo back in their ear. They didn't want to eat potato chips or ice chips, anything crunchy. They didn't want to be

in a room with noise. They could hear their eyeballs move. Every time you move your eyeballs, they could hear a, And I'm just relaying what hundreds of patients have now told me. That sounds like

a grading sound or like a rubber band squeaking as the eyeballs move. They can hear their neck muscles, neck bones, bowel sounds, every footstep. And so a lot of these patients start

pulling back and with drawing because the more they participate, the more they move, the more they eat, the more they speak, it's just becoming self.

it becomes like torture, it's bothering themselves. And so then that follows with depression and being involuted in. And so they wear sound canceling headphones, they wear earbuds, they're trying

to withdraw. And so it's remarkable to see patients who get better 'cause then they can come out and try to be normal again. And there's some other do they have loss of hearing or dizziness or some

vertigo to they have some other associated symptoms or is it just hearing your own voice? That's a predominant one, right? That's the most common one. And just like a lot of diseases, there's

probably subcategories. And now that Dr. Gopin and I have seen thousands of patients with SSCDs, I think that's the most common like type one SSCD, if you will. I think there's a subtype type two

and those patients predominantly present with balance issues. So they feel like the world is on a trampoline or a boat that's rocking side to side. This is not vertigo where the room is spinning

around you. SSCD, I don't think causes that. That's more like a vertigo scenario, PPPV. SSCD patients present as if the world is just rocking back and forth, or that they're on a trampoline or

on a boat. And that sounds make that feeling of disbalance, not vertigo, but disbalance That feeling of imbalanced gets worse with sound, and even sometimes internal sounds. And so they put in

earphones or head-canceling sounds because there's another kind of presenting. And then what became more apparent after we got into the - a few hundreds. After a few - we treated a few hundreds of

these patients. The third thing that actually became more identifiable, which was hard to recognize early, was something they call brain fog applications call it brain fog or slowing cognitive.

slowing cognition, and that patients were reporting after surgery, one of the things that they said was, Yeah, my sounds better, Tophne is better, my balance is better. But what I really like

most is that my thought clarity got better. And so a lot of patients present with brain fog or cognitive slowing, and my way of hypothesizing about why this occurs is the brain is just using so much

energy to try to block out the sounds of the heartbeat and the voice, and the brain is working so hard to try to stay upright and compensate for the balance issues that the brain is fatiguing. And

so these patients, a lot of them present with brain fog and after surgery, they see that their cognition has improved. Okay. So I'm again representing the audience and they're hearing that they

say, well, you know, I'm just like I told you, I've seen a patient who's got, here's a heartbeat all the time. You do an angiogram. You don't see anything You don't know what's, you don't

understand what's going on. We don't hear about it. And in hearing your voice and your sounds come back more often. I'm probably never even asked the question so I Can see that but nausea and dizzy

and I mean dizziness we see a lot of people who have that for a lot of different reasons and Do they have any disruption of the cranial nerve function or is it balance? principally is it's and I'm

sure you got to it. That's why this is semi circular function So many circular canal dysfunction. That's what you're talking about That's right. It's semi-se - it is a cranial nerve, but it's hard

to assess because Normally our balance testing is limited to a pronator drift rumburg You know standing up. This is really small high level Balance function and then it's not even there's three

semi-se-circuit canal superior lateral and posterior This is really just looking at the superior canal and so it's Balance dysfunction in one degree. And yes, so for these patients who hear their

own heartbeat, hear their own voice present with balanced problems, the most important imaging diagnostic intervention we can do is a high resolution temporal bone CT, which is what I think

happened in the late '90s and early 2000s,

is that the CT scans prior to that were not, they did not have high enough resolution to detect the disease, and now CT scans are getting better and better with higher resolution So a temporal bone

CT scan with, I would say, 06 millimeter in fine cuts will be at the resolution sufficient to diagnose a canal dehiscence. I put this image up for you, you can see it, can't you? I can see it,

yes. And we see a yellow area there, and there's the, we see the temporal bone, we see the error here, and we see error in the area, I assume, in the external canal, tell me if I'm wrong I'm

not sophisticated about this. what you're pointing to, what it looks like, almost a discontinuity in the floor of the middle fascia here, and it's very specific, and it leads into what is a very

mildly dense, or semi-dense, or less, I don't know

what the word for that is, but anyway, it leads into, and I'm assuming that semi-circular canals are right in here Again, I'm not an expert, maybe you can explain that. Sure, so I'm gonna

annotate your screen here, so you're right, so I'm gonna point an arrow. Sure, go ahead, I don't know if this is - I'm gonna annotate, sure, so this here. Well, good for you, I got it, yeah.

This area there, as you point out yourself, that's air. So if you stuck your finger into your ear, and the wear of the ear waxes, that arrow there indicates the air in the external ear. And if

you can see, you can actually see, I'm gonna try to highlight with my how you see that line, that's your tympanic membrane, that's your eardrum. So you can actually make out your eardrum on this

portion. And then it connects,

there's the maliolis, the inchus and the state piece. You don't really see those. Well, you can kind of see the inchus here maybe, that little white bone there. And it connects to the

oval window. And so the state piece will be right about here, connecting to the oval window and to the cochlea This area here, I'm going to mark with a V is the vestibule, and that's the junction

of the three semicircular canals. And this arrow is pointing exactly to where - and I like where that arrow is, it's a good arrow. It's pointing. You see this dark spot. There should be a white

cap over this area. And you and me and probably most people who do not have canal dehiscence, if we were to get a CT scan, you would see white over this dark line. And that's the superior canal

dehiscence. The way, you have a normal here, by the way, what it should look like is here. This here is your lateral canal. If you can see my arrow, this is your lateral canal, and you see how

there's a white bone that is covering that line right here. And so there's no lateral canal, the essence here. This is your lateral canal coming outside of the ways, and there's a white cap over

it,

and that's the normal superior canal. So superior lateral posterior canals all should look that way. There should be a dark line with endo lymph inside of it, and a white bony cap over all three

canals. But if you can see here where the yellow arrow is pointing, there's no white cap over that linear structure. There is just nothing there. And so that is the space where a white cap is now

eroded. As neural surgeons, we know what that white cap is. That white cap is the argument eminence. So the neurologists are looking at it from below, and they're saying, oh, that's the

superior canal, that superior canal is the essence And they're calling a tagman, which is the middle fossa floor here. There might be a dehiscence there too, but they're looking at it and calling

it a tagment dehiscence and a superior canal dehiscence. We're looking at it from above, 'cause we're normally coming from a middle fossa craniotomy and we see this as an arcuate eminence. And so

from a neurosurgical perspective, this same disease could be called an arcuate eminence erosion or an arcuate eminence dehiscence, but what's inside the arcuate eminence is a superior canal and

that's what causes all the disease functions And then yes, they call it a tagment dehiscence, but from our perspective, these are middle faucity hystences that can present with either meningus

seals or encephalus seals. Now this hypodence area here, which I thought might be fluid, but I'm probably wrong, that's not a canal, is it, or is that in, what is that? You just said that this

is the bony covering what you're seeing down here. What is this hypodence area here? So you're correct, it is fluid.

It is actually fluid. And that's the vestibule where all the semicircular canals join. And if we want to go into the exact medical terminology without losing anyone, it's actually the odic capsule.

So the odic capsule is a junction of the cochlea, the superior canal, the lateral canal, and the posterior canal, they all come together. And so this is the odic canal. And then all these areas,

let me erase my markings there because they're still there. All of those markings become, all those areas are actually filled with fluids. So you were correct. So CT scan, it is what it is you're

looking at this and you are a professor. So you say, look, it has fluid density. This is not air and you are absolutely correct. There's endolim, which is a cousin or a sister, a CSF. It's

very similar to CSF. And so there's a membrane inside these bony openings and there's fluid inside all of these canals. There's fluid in your cochlea. And this fluid inside the odic capsule is what

allows you to hear and allows you to have balance. So, in here in this diagram, what you guys outlined in, you have some red or superior canal, that's the apex, is that where this yellow arrow

is here and that's, so it's very close to that point or am I, am I wrong? That's absolutely correct. So this struct, this drawing here shows you the Odic capsule, the cochlea, the anterior apex

and posterior, and what we're trying to show, because we've now done over six hundred and fifteen superior canality hiscences, there are other questions to ask. It's not just, oh, there's a hole

in this bone and it's causing this disease to go fix it. Second question we asked is where on this arch, because the superior canal, as you can see on this, I'm trying to show you with my hands,

let me just draw this out, you can see it's an arch. I was just in St. Louis over the weekend at Wash U for a conference. You see it's like an arch, like the arch of St. Louis And so if the

superior canal is an arch, where can the whole form, can the whole, does the whole always form at the apex? can it form anterior or can it form posterior? And what we have found in our series of

600 patients is that it's most commonly anterior or apical. So the most common position is anterior apical or anterior apical. So it's a combination of those two. So the most common location, yes.

Very sensible, obviously all, everybody semicircular canals are not exactly in the same place in everybody So

there's obviously some changes and

the terrific explanation. And then what we are seeing there are the areas where there's a wider area and more fluid. And I think that's where this is. Okay, so now you got your yellow area and I

assume that's going to be close to this part here where it says apex, am I right? That's correct. But the problem is most of the people, it's normal and people normal. And we're going to come

back to that in a second You don't see. This is closed. What you're saying is when it thins, when it thins or is absent for whatever reason it is and you're going to tell us a little bit about that.

That means it bears the semi circular canal there's probably some door or some memory, but it's very close to do the CSF and so forth and so on. Is that right Yes, that's absolutely correct. And

so when that bone dissolves now you have endolimp and endolimp membrane directly contacting Dura which is filled with CSF and something about the heartbeat and the pulsation pulsation and the movement

of the dirt or the pressure induction between those two spaces when they should be separated contributes to The symptoms of sscd where they hear their heartbeat or they have imbalanced and their

imbalanced sometimes get worse when their blood pressure goes up the pressure in the brain goes up it's something about the pathologic contact. of Dura on endowment membrane. And pulsating brain and

CSF. I mean, I don't know. That's right. I'm just guessing, but it's closer to that. I must, would it set up some vibrations in the fluid in the semicircular canal? I'm just trying to figure

out how does this transmit it? That's absolutely correct. There's a defect there. And so two things that are going on is that sound normally goes in through the oval window and comes out the round

window And now because there's a third hole, sound can escape out of this superior canal defect. The second thing is bone conduction. Sound can get in faster because there's another hole

in which sound is transmitting through the vestibule to the cochlea and lastly you're correct. There must be pressure transmissions from the dura. As we all know as neurosurgeons, the brain is

mobile. There's pressure in the CSF space. That's being transmitted without fluid into the now endolympt cavity causing the diseases of SSCD. Well, it's a great explanation, a great teacher, but

let me ask you this 'cause it really gets back to the symptomatology, and that is everybody who walks in off the street with dizziness, does not have the disease. When you talked specifically, the

first patient you had, had a disabling, just totally disabling symptomatology. So my guess is that you're seeing this, you're seeing these large number of patients who come because I'm bothered by

this, and out of that, you've got to select the people you think are going to have the higher chance of operating on you to want to operate on somebody and having the same symptoms or worse. I mean,

I wouldn't do that, you wouldn't do that either. So you're going to select out the people who are, who are the most symptomatic, the most typically symptomatic. And those would be the ones I'm my

guessing, you're going to have the highest chance of helping. That's correct We are looking for patients who have a distinct clinical history. very, very important. You present with a history

that's going to lead you toward the disease. The second thing is getting these high-resolution CT scans that are 06 millimeters in resolution or thinner, because if you do the CT scan and they have

no superior canal dehiscence, there's no way I'm going to operate on this patient because there's no canal dehiscence. Firstly, some patients may have the canal dehiscence and their symptoms are

either mild or it's not too bad and so in those patients we will not do surgery. Now here tell us what you see in these two, these are two examples from like here's a high resolution CT of the

left-sided and this is another left-sided okay and you see the little defect here is that as much as you need to see but here it's obvious, I mean it's so obvious So how do you make that distinction?

So that's what you see. If you see what they're trying to show in this particular one, what I can see is on this image here, on the left, this is higher up than the last one that we saw right here.

This arrow is pointing to an SSD that's higher up, more towards the apex. And then this arrow here, on the right side of the screen, this is pointing towards an SSD that's more posterior. And you

can see, as we said, here's the normal. Here's a lateral canal at the apex And here, you really can't see the lateral canal all too well. But the lateral canal is just plugging in here. You can

kind of see the lateral canal right here.

They're moving backwards on the lateral canal and showing that this SSD is anterior at the apex and posteriorly. OK. So it turns out that the 610 of a millimeter - cots, is that right? Is that

what it is, 610 of a millimeter? So, you're talking about the thinness of the. You're talking about the your your tomographic cuts because somebody's gonna say yes Another part of the the world or

another part of the country. Well, I get tomograms of the middle middle there Maybe that'll tell me about it But but you're getting a finer cuts that people aren't used to getting is that right?

That's correct. So Normally if you get a trauma head CT or the head CT that we're used to in neurosurgery They're gonna be too wide you you may either see it in one slice or you'll miss it all

together Because the entire superior canal in its length is usually subsonometer and it's also oblique Just to get into the neuroanatomy of it

is that as you go from anterior to posterior the superior canal is actually not in a anterior posterior or or Ventral to dorsal orientation. It's actually oblique and so the superior canal as you go

from anterior to posterior Actually gets more medial. So the anterior portion is more lateral and the post your portions more medial. So not only do you have to get this tiny organ, you have to go

along its axis and it's not front to back. It's actually on a slight angle. And so given the fact that's usually subsonometer and also oblique, it's as if it's trying to hide from a, if you do

cuts this way, it's almost trying to hide. And so if you do centimeter

cuts, you'll definitely miss it And if you do

one millimeter cuts, you will probably catch it in one, one to three, maybe four scan cuts. And so our recommendation or my recommendation is to get submillimeter or 06 millimeter cuts, because

at that resolution, then you'll be able to, be able to see the SSCD. Well, I think it's important. I can relate this to something in vascular and people use a CT angiogram It's a little different

category, but I'm getting into the same message.

And the CT is, it can only define something at that, we're using that technique, that's three millimeters. You're talking about something that's far smaller than that, not routine. And so the

routine CT is much more broader. And if you get the slices small enough, then it's good enough. And I think you made a cut off. Some people said 04, some people said 05, and you're talking about

the defect there. Is that correct? Yeah, so we want the six millimeter CT scan that are high resolution. The thing about the 05 and 06 that we've published and that we looked at was coming along

later in the disease, which is me and Dr. Gopin had fixed and started treating a few hundred patients at that time. And this was maybe a year or two before the pandemic. Dr. Miner, Lloyd Miner,

Dr. Gopin and myself, we actually were able fortunate enough to meet here at UCLA. And then we had lunch, the three of us. And it was only the three of us, which was also really fun and

remarkable because we got to sit and just talk about the disease, what we talked about, other things, and got to know each other better. And he's a remarkable human being. And he's now the dean

of medicine at Stanford. And we discussed at that time, what's the cutting edge? And what's the next frontier for SSCD? And the three of us came to the conclusion or the thought at that lunch was

that maybe it's going to be thin SSCD. And his hypothesis, and I want to give him the credit for the idea, because I'm not that smart. I really wanted to make sure he gets credit, and he gets

credit, and Dr. Gopin gets credit, because like I said, I came in this very ignorant and naive, and I've learned a lot from them. And so he gets the credit. His hypothesis, which Gopin and I

both agree, is that this disease develops because you're born with thin bones in the middle faucet. So everyone's born with an archeoeminence, but if you develop SSCD, perhaps you're born with a

thinner bone over your archeoeminence. And then in a subset of those patients who are born with thin bone, that that bone erodes for whatever life factor, poor calcium intake, poor nutrition.

It's, there's a higher incidence of SSCD in women, perhaps trauma, trauma is also a subset of it. So people were born with thin bone, they are at a higher risk for developing SSCD. And then

those patients who end up having those lifestyle issues or factors, a subset of those develop SSCD. And our conversation at that lunch was, what if these patients have an actual hole and have these

symptoms, what's the next frontier? Well, the next frontier would be thin bones. So Dr. Meiner, Dr. Gopin, myself said, what about patients with thin bone? Because we were seeing patients

who had these symptoms, but they had a thin white bone crest. They had a thin cap on the superior canal, no frank dehiscence. And we didn't know what to do with them at the time. Should we

operate as surgery indicated? Is that the correct thing to do? And we said, then this is probably early presentation of the disease and that thinness will be the next frontier. And so we started

our project and our idea, well, we're gonna start treating thin bones and Hopkins started treating thin bones too at the same time and they're also a good place that does SSCD and that's where the

disease was discovered. Well, if you're gonna start treating thin bone, the question has to be, well, what's thin? And what's too thin? And so we started measuring that thinness in a lot of

patients. We measured normal and we measured thin and we measured normal and thin and we did it in all our SSCD patients 'cause we had normal controls in all these patients in high resolution scans

And what we have found, based on a Gaussian curve, Looking at what pathologic thinness is, is we think it's less than 05 millimeters. If there's a small cap or a small bony covering over the

superior canal, and if it's less than 05 millimeters, less than a millimeter, 05 millimeter, and I think the human hair is roughly 01 millimeters. So less than three

or four human hairs worth of thinness, those patients also present with this same disease with no clear hole. They no longer have SSCD dehiscence per se because they don't have the hole, but they

still have the syndrome, minor syndrome or SSCD syndrome because they still have the pathologic disease. And so the bone is thin because the things we talked about, the sound transmission, the

pressure transmission, it can still occur when the bone is so thin that pressure transmission either from the brain sound however you will. is still transmitting through a bone that's too thin.

Okay, you covered my next question 'cause I was gonna say, okay, you got me to the point of hearing my voice more or my pulse and you're showing me a defect. Now you're gonna show me somebody who

doesn't have much of the defect, but obviously you guys got together, looked at your patients and you found I still have some people who are clinically disabled symptomatically and what am I gonna

do? I've done it, I see a thin room, I'm not sure about it. I'm sure you guys are concerned initially, well let's try it, we're not gonna hurt 'em. I don't think we will. And if it worked and

you're back in your surprise phenomenon, right? Absolutely, the surprise of science. Yeah, welcome to the human body, right?

Now everybody wants to know what kind of a surgical procedure you're doing in these people I mean, you were talking about it. And I'm looking at it from a public point of view. You're gonna operate

on my skull and my brain. You're gonna fix this, wait a minute. What's the risk here?

And you can't guarantee me I'm gonna have any good results. So how did you do that? So what do you do? Sure. So back to that last surprise point. So we followed our thinness and we, I think we

just published or it's about to get published, thin patients. So we operate on the cohort of patients with just thin bone and to my surprise again, those patients actually are doing better than

people with frank dehiscences. And so we can go into that. There's a whole bunch of series of papers about big holes when the superior canal gets plugging, balance outcomes. But just to make it

concise and to the point, I think young people say TL, DR, too long, don't read. The bullet point is that with thin bone, our patients are actually having better recoveries,

and better outcomes than if you have a full hold. So that's why I think the hypothesis and the supposition that this is early disease recognition is correct. And I think what we added, which no one

else has added, which I'm proud of and Gopin and I have added, is if you're gonna operate on thin, thin is just too subjective. You're gonna end up operating on patients, too many patients and on

patients who don't warrant the disease. I think we have been very clear that if it's less than 05 millimeters, you're gonna be enough standard deviations out that you're gonna capture the true

disease and true essence of the disease. So, yes, Dr. Ausman, oh yeah. Can you briefly tell me what you do surgically? We've gone into how we select them and so forth and so on. I think that's

a key issue. What did you do surgically?

So when I first started in 2010, and we first started doing SSEDD surgery, we did a regular middle fossa, And, uh, Like I suggested or talked about earlier, me and Gopin did a facial schwannoma.

And so for that, I do a small mini reverse question mark and do a middle fascia 'cause we need to get deep. When we did our very first SSD together, we and I was thinking, I don't need to go as

medial. So I don't need the entire superior portion. So I wonder if I could do it through you. And so I did an inverted U over the ear from the zygoma up straight across and down to where the

transverse sigma. I didn't want to go below where the transverse sigma junction is. And so I did a U and did a craniotomy in that area, lifted up the temporal lobe and came down just on the

temporal bone to the SSD. And that worked because

the superior canal is more lateral than the IAC. It's more lateral than the cochlea. So we don't have to go as deep as we normally would for a Middle Phosphor, an acoustic neuroma. or a Kwasi's

approach for a cavernous sinus or a brainstem issue. And so we were going more later on. So I started with a U. And then what I found was I was slowly shrinking my crani. Sometimes the burhole

would be put too close to the transverse sigmoid junction. And there would be some venous bleeding from that. And that was just issues that we learned and that I learned from as we were developing

the surgery moving along And the craniotomy continued to shrink. And I realized that I didn't need the entire U. I could just do it through an L. So I lost the back half of it and got just an L.

And then I said, well, I wonder if I could do this with just a burhole. If I could just make a two centimeter burhole right over the external auditory canal, can we still get to the same spot?

And so we decided to try that. And that is to Dr. Gopin's credit. that he was willing to try to do the surgery through that hole, I still shave the entire you and said, if I get into trouble and

I get into epidural bleeding or venous bleeding and I can't control it, I'm going to just go back to the old you and just do this good old fashioned way. So we'd save the area for the whole you.

And then I made a about a two centimeter incision from the zygoma up and then the just the first part of the L so it wasn't even the full L of the U it was just the just the half of the transverse

portion and then I found the root of the zygoma which then led me to the external artery canal. We use brain neuro navigation and using that navigation we put a burhole about a centimeter above the

external artery canal and I just kept on marking those lines over and over again and out of just pure facetiousness I said this line above the external artery canal I'm going to call that the line of

gopin because you're the year guy and this line I'm going to draw from the root of the legoma transversely, I'm gonna call that the line a yang 'cause I'm the skull-based guy. And where those two

lines intersect, I'm gonna keep trying to put a burr hole right there and trying to do this. And what I learned over the first 12 patients is that putting a burr hole right there will put me into

air cells. And then I'm disoriented and we end up having a patient and this is just radical candor. We had a patient who had an abscess and infection who ended up needing the full middle faucet to

clean that out That for me was a really good learning experience in my first 12 cases because I thought, well, if you want to make this a small small small small, go directly where you want to go.

What I've learned from that case is actually I want to go five to eight millimeters above the external auditory now to find the dura, to be above the air cells and then to come down and garrison down

the air cells down to the middle faucet floor. And so that became our operating experience And so then that worked in our first 12 patients and ever since. then, we have now shrunk our incision.

Our incision now is about

13 to 15, I'm sorry, it's about an inch and a quarter, so 13 inches. So it's about

25 or 3 centimeters. It's a little bit over an inch long, our incision. And then the opening in the bone, we started at 2 centimeters, we shrunk it down to 17 centimeters. And when they put this

on the doctors, I took the dyeing because I looked it up on Wikipedia that a dyeing is 17 centimeters in diameter. And so I held up a diamond and said, our opening is 17 centimeters. And I think

that was maybe in like 2017 or 2018. Well, now in 2024, we're actually smaller than that. We're smaller than the American diamond. So our typical opening is about 12 to 14 centimeters. It's very,

very small and it's a burr hole. And once we make the burr hole, then it's just back to good old basic, you know, tackling and blocking and neurosurgery. We bring a microscope in. we stay

extra-dural, we find the middle fossa floor. It's like spine surgery, fine bone, we stay on bone. And so we look around the corner, we find the middle fossa floor, and then we just start doing

extra-dural dissection, sweeping side to side, saying extra-dural until you come to the arcuate eminence, and you come to the arcuate eminence, and that's the SSED. It's typically about 254

centimeters. It's about two, somewhere between 23 to 28 centimeters below the

temporal squamosa. So outside of the burrhole, if you measure from the phony opening down to how deep you need to go, we have a Rotten 6 or Rotten 7 that has a mark at the 25 mark, and we just use

math, geometry, neural navigation, and the microscope. We get down to the opening, we fix it. And if you do the whole surgery through a burrhole, and if you've done hundreds and hundreds, like

me and Gopin have done, we can do this whole surgery in about an hour now.

Now, did you mention neural navigation? Do you need to have it or basically what you described, it may make it a little faster, but you're gonna probably get there 100 with what you described.

I would say you need neural navigation. Okay, why?

For a few reasons. One, I think neural navigation is becoming more standard and more typical in the vast majority of cranial cases And I know you're going to hate that answer, Professor, because I

know you and you're always looking for the real need for it. But I do think

it's becoming more and more typical use in a lot of cranial cases. I would say in actual functional use, sometimes there's an arcua evidence and you're right. So if there's a clear arcua evidence,

you can use it. But a lot of times it's so flat, middle fossa is a anatomically it's a barren anatomic flat land. It's a wasteland of anatomy. And so you can't identify exactly, so even though

you measure 25, it's circumferential. So it's somewhere along this circumference at 25, but you don't know exactly where it is. And then the last point is

knowing that you put it, that you did your best to put it exactly where you want to put it. And that bring that reconfirms that we put our repair exactly where we want to put it. Because we've done

615 cases, and I would say less than 1, way less than 1, I would say there's one or two cases where we thought we put it, where we put it. We use a narrow navigation and maybe the navigation was

off, our perspective was off, and our repair was a little bit sub-optimal. And so I think that is one or two out of 600, so like a 03 rate of improvement. And I think it's worth that 03 to try to

optimize as much as possible. Two questions. One. Okay, now you get there, you find, you find, well, let's just say there's a dehiscence, you'll see it, you'll find the dehiscence, you'll

see it, how do you close it? So the recipe that we have our not so secret, secret sauce is published, it's in the red journal, and what we use is bone wax, we use heelostat, we use fibrin glue,

and then the last part of the recipe has changed since the pandemic, we used to use a bone chip, because we make a burhole, we had this bone chip, and we tried to put the bone chip right over the

superior canal and kind of mark where our repair was. What we found was one of our patients got COVID, they coughed a lot, they increased the intracranial pressure, that bone chip moved, the bone

chip dissolved, it wore down under the pressure, and so since the pandemic, we have now replaced that bone chip, the fourth part of that recipe, we change it with a titanium mesh, which Gopin

and I colloquially call the IQ don't, because these quinten, so we call it the IQ Dome. It's a little umbrella. It's just titanium mesh that's in your standard, plating system, and we use it to

curve and mold around the RQ Eminence, so it covers that SSD. And we've been doing that for the past four years, and it looks like that repair is more robust over the RQ Eminence. Do you have to

screw it in, or how do you get it to seat, or do you sew it in? No, you don't have to screw it in, so we put bone lacks into it And so, if you can imagine, there's cement and steel rebar inside

of the cement to make concrete, which is very, very strong. Our thinking is similar. We have bone wax, and inside the cement of bone wax, we put the steel rebar, which is the titanium mesh.

It's held in place by both the bone wax, and secondarily by the brain itself, is that once you let go, it holds down, and it's being held in place by the anatomy of the bone, the brain, the dura,

and the bone lax. The reason the neural navigation, this is very good for nerve and navigation, and I've thought about this for some time. It's the bone doesn't move. Yes, that's right in the

brain. The biggest problem is brain shift, but you don't have to worry about that. We do not. So you can take the image that you get, you put it in the microscope, and it's going to be exactly

where it should be 100 you're absolutely correct. There's no brain shift. There's no sagging. There's no CSF release. This is just operating on the bone at the junction of neurosurgery and otology.

We're in this overlapping space, and the bone doesn't move. And so the neural navigation is very helpful, especially because the bone doesn't move. I think it's very good for scope-based surgery.

So the next thing is everybody's going to want to know, okay, you've done the surgery. What are the risks, what are the complications, and how did they do?

So I think some of the risks, one of them I mentioned earlier is an infection. You can get a risk for infection, especially if you get into the air cells, we got one in that case. I'd say that

there's about a 1 infection rate, even with the burr hole procedure and the way we do it, we still have about 1 infection rate. And so we have to go back and remove the titanium plate that we put

in to cover the burr holes. I think infection risk is one. There's a small risk for some high frequency hearing loss No one has gone deaf, but when they have a really large hole, the superior

canal dehiscence is very large, the bone wax will actually go into the superior canal and plug those spaces. So there's no more fluid, no more fluid in the space and no more fluid in that area.

And we have found in those patients, those patients have a slightly higher rate of decreased high frequency hearing loss. I put that risk at less than 5 in our hands and no one has gone completely

deaf. but that is a risk of the surgery. I think the other risk that we have seen is some temporary transient facial weakness. We've seen this in about less than 1, maybe about half a dozen

patients, whether they had temporary facial weakness or frontalis weakness, even with our incision being small, it's either irritated or stretched and it's always temporary. We've seen it always

improve, but that's a risk of the surgery And then I think the biggest risk and the biggest component of this is non-improvement. You know, like you said, it's all game of patient selection. We

make sure the patients have a clear hole or a thinness that's within that area that the patient's history lines up with the disease. And yet our success rate is not 100. For the atophany and

sound-based symptoms, about 90. I'm trying to be a conservative, but accurate, about 90 of those patients will get better If you present with the subclass type 2, S-S-E-D, which is balance

symptoms, I'd say about 80 of our patients get symptom improvement. And so that means that there's a 10 to 20 chance that you will not get improvement. There's very, very, very rare patients who

are worse. I would say if you're in that 10 to 20, most of these patients do not get better and are no worse than they were before. And so for those patients, I feel like they feel that it was

worth the chance or the risk or the opportunity of surgery, however you will But there are a very select few patients who feel that they are worse after surgery. So that is a real risk of surgery

for sure. Okay. So we got everything covered except for let's say somebody comes in, you do a tomographic cuts and they've got dehiscence on both sides. Now they got bilateral potential,

bilateral disease, what do you do?

So two things history and normally in those patients they have one side that bothers them more. and we will lean towards that side of the surgery and lean towards fixing that side first. Some of

those patients will not be able to localize right or left. And so for those patients, we give them a vent test, vestibular testing, balanced testing to see which balance side is more affected and

that will help us lead us to doing surgery on that side. We normally only fix one side, not two sides at the same time. I've never done it. We will only fix one side And if that one side is enough,

then we're done. If that one side, they feel a lot better and they say, hey, fix the other side, then we get better and then we do the other side. If we fix that one side, they don't feel much

difference than we tried and we did and we leave the other side alone. We're trying to do the most effective and the least amount of surgery as possible. What I have been learning in the past few

years though, is that some of these patients, they'll get their sound symptoms improved when you fix one side, but their balance will not improve until both sides are fake. Oh my God. And so

that's something I've learned in the past few years, because I thought, look, your sounds symptoms are improved, but your balance isn't better. I don't know. Is it worth it to fix the other side?

And we had a few patients who are very courageous who understood the risks. We knew what we were going to. We all took that together. And what we have learned in our series of hundreds and hundreds

of patients is that if you have sound symptoms that improve on one side, but your balance is not improved, it may take fixing the superior canal on the other side to make your balance better. Yeah,

okay, I've done a great job explaining this. Is there anything, I'm gonna ask you one other question. Let's say, I don't live in Los Angeles.

I may live in San Diego. Maybe they don't do it. I may live in Chicago or St. Louis or may it be in London or Paris or Brussels Is this have to be done? you know, this is done everywhere in the

world or, or how do we approach this? Because I'm in another country, I got this patient coming into me. They, here's their heartbeat. I can't do anything for them. They're totally disabled.

What do they do?

I think it's going to become more and more of international recognition as a CT scans get better. And as there's more awareness of the disease,

people are going to hear about more and more, I would say 90 to 95 of our patients are coming from out of state or out of the country. We've had patients come in from Japan, Singapore, Dubai,

South Africa, Australia. Patients are flying in because internationally, I think you're seeing as you normally do, you're seeing 10, 15 years in the future. In the next decade or two, it's

going to become more and more prevalent internationally, not because its incidence is rising, but just because our diagnostic capability. disease awareness is going to go up. In the United States,

I think in my opinion, and I think the centers that have the most experience, that have done the most surgically, are going to be Hopkins and UCLA in no particular order. And because of that

experience, if you were my family member or my patient, I'd recommend one of those two centers, either Dr. Gopin at UCLA or Dr. Kerry at Hopkins, because that experience makes a big difference.

And that experience makes the best chance at good outcomes the first time you have surgery, because once you've had surgery, the second surgery, the odds of success with the second surgery, they

start diminishing. Now, that's a luxury that if you live close to Baltimore or Los Angeles or have the means to travel, but not everyone does. And so, if you don't, then I would try to find a

skull-based surgeon and and Neurotology team. that has the most experience doing other skull-based procedures because this is just a cousin to the normal skull-based procedures we normally do. And

so if you have a skull-based team that can do middle foster craniotomies and get to that area, I was just at Washew St. Louis, as I was mentioning, and I was talking to my colleague Dr. Albert

Kim, and he says he does a handful of these a year as well. And he's a good skull-based surgeon. He normally does brain tumors and that him and his otologist, they do them because they're patients

in that St. Louis area that cannot travel as well and go to him. And I'm sure they do just fine because he does a handful. And so I would try to find the skull-based team because this isn't unique

to me or us, even though Hopkins and UCLA have the most experience specifically with SSED. What you really want to look for or trying to build is skull-based expertise. And skull-based expertise,

particularly with the middle fossa approach between neurosurgery and neurotology. Excellent. Now, is there something we didn't cover for the audience that's watching or anything else you want to

say? Sure, sure. So this is not just neurosurgeons and neuroatology. There are two other ways that you can approach the superior canal dehiscence. This is well-diverse in the literature, and it

would be beyond it would be another few hours for us to discuss it. The other way to approach this space, if you can imagine, is that an autologist does it without a neurosurgeon They just do a

mastoid, and they do a mastoid approach. It's almost like a trans lab, but they don't trans the lab. They just do a mastoid. They identify the lateral canal, and then they drill into the

intracranial space from the side and reach over to the superior canal and fix the SSCD. This is not the typical way that we do at UCLA, and it's not the standard way they do it at Hopkins, but if

you don't have a neurosurgeon, and you're just approaching with an ENT-specific and anti-only approach, that's another way to do it. I think some of the literature suggests that it has a lower

success rate, but again, I'm biased because I do a middle foster craniotomy, but I don't think the success rate of this is so low that I would disregard it, that if you're in the area without the

resources and you are just having an otologist or an ENT approach to it, and you don't have an ICU and you're not going to do a craniotomy or a burr hole, then doing through a mastoid approach can

be a resource limited and yet fairly effective way to do this. And then the last way to do this, the way you could try to approach is something called a round window of repair. So you have sound

going in and it escapes out the third window and it escapes out the round window. A way to try to put a band-aid on this approach is just to occlude the round window. They take part of the skin and

the ear, I think. I don't do this so I'm just trying to figure out what they do and they patch up the round window. I think the literature and experience has suggested this has the lowest rate of

success. It may not be worth the risk and the investment of a treatment, unless you are, I would say, over 80. We published our series of surgery on the octogenarians and had found that the

thinness of the Dura, the stress of the surgery, the success rate starts falling. And so for our octogenarians plus, and again, we're using age right now as

a marker, but over 80 we do round window repair, under 80 we do surgery, but we just did surgery on an 81 year old, 81 year old a few months ago, because he was healthy. And so this 80 is

actually just a biomarker for frailty. So if you're frail, I would recommend a round window approach. If you're 81 and very healthy, then you're not frail, and I would recommend a middle fossa.

And we did that middle fossa on the 81, and he did fantastic. And so I would recommend a round window only for patients who are frail or sick. That's good. Well, you're talking to an 86 year old,

So you punch like a 56 year old, you punch like a 56 year old, and I bet if they put the frailty, you know, things on you, you'd come out, your telomeres are very long. That's what I had. I

would guess. Okay.

Thank you. Send me the bill.

Are you done? You're a great teacher and you did a great job, is there anything we missed? I don't think so. That was very thorough. Okay. Terrific Well,

I'm going to thank you very much for doing this and educating people around the world. And I think one of the fundamentals here is you're starting with something and imagine this is a history of

medicine and the history. This is something everybody passes by because it's just, you know, I don't can't understand it. I don't know it. Maybe it's psychological and then you wake up one day

and you find out, well, maybe I got the same problem or something. science advances and you're learning as you go. But the root from the beginning to now is not smooth and everybody is not there

saying what a wonderful job keep going. It's what the hell you're doing here. Absolutely. We got to keep learning. A hundred years ago, they thought germs and bacteria, they thought that was

absurdity. They thought microscopic bacteria and viruses that you can't see are causing these diseases. They thought you were crazy to think that. Look, really, you don't have to take my word for

Google this a hundred years ago. They really thought you were crazy for not saying these and we're just learning and I'm just learning and I continue to learn and I'm sure 20 years from now, they

will have learned from us and it just keeps getting better because things that we think are absurdities. Now, they're going to take it for fact in 20 years, because now no one takes I mean. some

people do, but no one takes the viruses and the bacteria as absurdities because these are things that we quote unquote know and we know for fact, but as recently as a hundred years ago, doctors and

very well-knowing human beings did not accept that theory and they thought it was an absurdity. And now we're in 2024 and I credit Dean Miner is that in 1998 he said there's a hole that we can barely

see that's causing this disease And I can only imagine where they're going to go in the future as the CTs and the MRIs become lower radiation, more precise, they're going to have computers and AI

that diagnose more holes, more defects, more integrations. They're going to have more biomarkers, blood, health, age from like maybe a hair sample that will detect my frailty and then determine

my probabilistic outcomes for which treatment path will be best for surgery, aneurysm, coiling, hernia repair, you know, all these things and Those things will then be taken for granted 20, 30

years from now. And today, in 2024, we're like, can a computer outthink us? You know, it's absurd to think that now, but in 20 or 30 years, that will probably become standard. Well, I think

you're absolutely right. And we're limited by the techniques we've developed to visualize what we're visualizing, right? Before the microscope, you may have some powerful glasses, or you may do

that, and you remember seeing, pushing in a surgery and an open operating without one lamp coming down in there, or somebody shining something over his shoulder. And it's true. And when we get to

seven tests, I'm an even finer cut CT, or even maybe some other modality, you

realize I'm Dummyore.

Justin, I mean, we're going with what we got, right? Yes, but we're still learning. And you are definitely pushing it, Dr. Osmo. Okay, terrific job. I appreciate it very much Thank you.

Okay, bye-bye.

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Superior Semicircular Canal Dehiscence (SSCD) ; Disabling Symptoms; Dr. Isaac Yang

James I. Ausman, MD, MA, PhD

Isaac Yang, MD

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Superior Semicircular Canal Dehiscence (SSCD) ; Disabling Symptoms; Dr. Isaac Yang

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