peripheral vestibular and cerebellum disorders with ... · canal, like, type of otitis externa....

MODULE fOUr TrANSCrIPT: PErIPhErAL VESTIbULAr DIAgNOSTIC | © 2016 fUNCTIONAL NEUrOLOgY SEMINArS LP | PAgE 1

PeriPheral Vestibular and Cerebellum disorders with aPPliCations (module Four)

transcript – diagnostic maneuvers for the Peripheral Vestibular system

Presentation by dr. brandon brock

Alright everybody. So it’s time to start doing some diagnostic procedures. Yesterday we talked about dif-ferential diagnosis between things like BPPV, neuronitis, labyrinthitis, our fistulas, our Ménière’s disease. Now it’s time to start doing some things to show you some hands-on. So we’re really going to… I’m going to try to lecture a little… just minimal off the slides, and go through as many hands-on procedures over on the other side of the stage, with a demonstration, so that you can have these to watch. I really think it’s important not just to talk about vestibular maneuvers, but to actually show you the diagnostic procedures, and then to go through and show you the treatment procedures.

So we have about an hour and a half to run through this section right here. And this is the diagnostic maneuvers, and then of course after this we’ll do the treatment applications, which go hand in hand with this. This is just really one continuous lecture with a break called lunch. And then after that we’re going to do cases. Dr. Kharrazian and I will both do cases, and you’ll see the two worlds merge together, his and mine, him being very chemical, mine being very structural. And then we’ll hopefully start getting the point across of, “Patient looks like this, what do you think?” “Patient looks like this, what do you think?” And I want you just to be able to very quickly go through it. And then you can watch these procedures over and over and over and do them.

Now, most of them are pretty easy. Some of them you know. Some of them are a little more complicated than you think. So, I’m going to spend a lot of my time with the canals, and the ways to challenge the canals, because a lot of my treatment is going to be: How do you treat these canals? How do you treat a posterior canal, or horizontal canal, and the anterior canal? How do you evaluate those, and then how do you treat them? What are the maneuvers? Alright? So, you can, of course, google these. You can – you know – look at them on YouTube, and then you can hopefully watch it on this. The reason why it might be okay on this video is because it’s going to sink in with what I’ve taught you for the rest of the weekend, alright? So there’s a little casualness, because there’s a little bit of manual labor involved in this, so I don’t want to be too – kind of – wrapped up.


Okay, so look. Here’s some things that we’re going to look at. We’re going to look at spontaneous eye movement and how to evaluate for it. We’re going to look at the provocative tests: body position, Hallpike, stuff like that. And then I’m going to show you some stuff that just kind of… bedside – and I say “bedside” meaning you don’t have to have sophisticated machinery – to look at things for unilateral weakness. So, when we look at some of the provocative tests, these are things that may look at an overactive canal.

But then when we do things like a head thrust, or a head shake, or visual acuity, it might look for the unilateral weakness. So I’ll show you those differences. Notice how they’re in a different color right here.

And then we have things like Valsalva, fistula testing where we’re going to actually do insufflation, noise induction. And then when we get into the central nervous system, we’ll have pursuits, saccades, and optokinetics. We have not enough time to do all that now, but we have plenty of time to do it later on. So itty bitty bits. That’s the way we’re doing it. In increments, okay?

Calorics, again, I’m making a video, because I just don’t… Number one, to do it here on stage would take shipping tons of material, and I would get to make somebody feel extremely bad, and you would probably go to sleep and never do one. Audiometric evaluation, I want you to find somebody.

Don’t forget all this stuff over here on the left side. Alright.

So, let’s get rolling here. This is your chart. Now, everybody’s like, “Oh God, this thing is crazy.” It’s not going to be that crazy when I’m done. You can simply use it and do something like this: Draw a line through it, like a maze. Okay? Or you can go vertigo, vertical, positional, torsional, upbeat, BPPV, canal, nystagmus, less than sixty, repositioning maneuver. So it’s not… It looks like a bunch of scattered boxes, but if you just follow one box to the other to the other, it actually will help you. So, we’re going to look at things like fixation suppression and nystagmus. So, with the peripheral examination, we always want to start out with things like looking at fixation and the ability… Like, just look. Do they have nystagmus or not? And I showed you that yesterday, and we went over first-, second- and third-degree. And I’ll review that.

But what we’re going to look at today is tests to look for, again, spontaneous eye movement, BPPV, neuronitis, otosclerosis, Ménière’s, labyrinthitis, fistula, all the way down the list here. Now, some of these have more tests that we can do here on the stage than others. And some of them I will focus more on than others. Okay?

Alright. So, first things first. This is a great picture, because right here, number one, this is the external canal. So, the very first thing – and I’ve got one tool up here, other… I’m not calling you a tool – let’s say this is an otoscope. It’s really a tuning fork, okay? A lot of people… You know, the first thing I want you to do is, whenever we’re looking at some of these positioning maneuvers is, I want you just to look in the ear. And I think it’s important that we talk about how to look into the ear real quick. A lot of people want to do this kind of thing, where – you guys can go ahead and zoom in up here. Just, if you want – where I’m just kind of sitting here like this, and if I do it like this, and she moves, we now bump heads, both have a concussion, and I rupture her tympanic membrane. In other words, there’s nothing stabilizing the instrument to her head. Turn it upside down, place your hand against her head. That way no matter however she moves, this is going to move with her head, so it’s nice and safe.


Grab the tragus, or the – I’m sorry – the back of the ear, and then really pull it in a direction… and a lot of times you’ll say: adults, you want to pull up, kids you want to pull down. That’s just not always true. You need to pull in the direction that allows you to see what’s inside of there: the tympanic membrane. Now, if you start pulling on that, and it starts hurting really bad, you need to inspect the outer part of the ear and say: Is there infection? Or do they have and external – you know – like an external auditory, like, canal, like, type of otitis externa. Alright? So you look in there, and with otitis externa, you may see fungal growth, you may see irritation in the lining. But I want to look at that tympanic membrane and see how vascularized it is, see if it’s clear, see if there’s scars through it, see if there’s holes in it, and I really want to check those things out. That’s number one. And then, I like to go ahead and insufflate. And I’ll show you about insufflation when we get to fistulas. I’m not going to do it right now.

So, that’s one of the first things that we do is, just look in the ear. I told a lot of people Friday night, if that ear is really impacted with dark, amber-colored cerumen, and you can’t see into that canal, they’re not going to be able to hear good, and they’re probably going to have conductive hearing loss, where Weber will lateralize over to this side, and I’ll show you those tests in a second. But you want to get this out, and I suggest that you don’t use a cerumen spoon, or a pick, on older deposits. What I suggest you do is, use Debrox. You can get it over the counter. Get it soft, and then high-pressure syringe it out if the tympanic membrane is intact. And then most of the time, what you’ll get is this giant chunk of stuff that just comes out, and the person feels like their life has changed. Alright?

So, we have to go through: one, like we just did; two, if this right here is filled full of fluid, we’ll see it as a fluid line. We’ll see it as a fluid line, while we’re looking in the ear. So, otitis media. And there’s adults that get this. It’s not just kids. There’s adults that get it, okay? We can’t really see the ossicles, but we can test them in a little bit. And then of course, we’ve got cochlear tests, and we’ve got canal tests, and we have neuronitis, all the way up. So really a nice picture to kind of get going.

So, right out of the gate, we have these canals, we’ve got to test them. We’re not going to do too much utricular and saccular testing today, because it’s a little bit more difficult to do. We’re going to stick to some of the basics. And I’m going to show you how to run through these canals, and give you tests that will look at one canal versus the other versus the other. And we have to know eye movements, and we have to know how the canals hook together with these eyes. So we’re going to show you that here in just one second, okay?

So really, the first thing is, is there a descriptive term for the symptoms? And I told you: Is it disequilibrium? Is it dizziness? Is it vertigo? Is it syncope? Is it… you know, what exactly is the patient experiencing? Is there any eye, body or limb movements? Do they have nystagmus? Do they have myoclonus? Do they have a tremor? Do they have a jerk? Are they falling down? Are they falling to one side? Those things are all still in play as they’re walking up and sitting down right here.

[10.02]

Can you associate any spontaneous eye movements with what’s going on? That is the most important thing. Okay? So, real quick: We’ve got to look at number one, and that is spontaneous movement right here. Now, this has now turned into a way to evaluate your eyes. Okay? So we have otoscopes, we have all these different types of scopes. Now I’m going to have an ophthalmoscope, and I’m going to look into


her eye. So, I’ve looked in her ear, and now I’m going to look into her eye. Let me teach you a really easy way to do… Because remember, I told you, with benign paroxysmal positional… or peripheral vestibular pathologies, you need to have the ability to do what? Fixation suppression. So in other words, you put them in the dark, they don’t have something to fixate in, the nystagmus all of a sudden jumps out at you. So, I’ll look at you and say, “Alright, I don’t see nystagmus,” or, “I do see nystagmus,” or, “I don’t see an oscillation,” or, “I do see an oscillation.” Does that make sense? But then I’m going to… I’m like, “I don’t really know. I don’t have Frenzel lenses. I don’t have a hundred million dollar VNG machine. I’ve just kind of got me and her hands, and my ophthalmoscope.

So go and cover your left eye. Now look straight ahead.

Now, as soon as I look into her eye, she can’t fixate on anything any more. So I’m using my ophthalmoscope to look into her eye, and then I look at the back of the eye, and watch it move. Now, caution: the back of the eye moves opposite whenever it comes to nystagmus. So here’s what I suggest you do. You cover, lift this up a little bit, shine the light right on their eye, and then just watch the eye move. And then go in and look fundoscopically. Okay? The only one that doesn’t change direction is torsion. But if you’re looking at nystagmus, here’s the back of the eye; here’s the front of the eye. You can see how the beat is opposite direction. So I hate to tell you: Hey, learn nystagmus fast-phase this way, but then just learn how to do the opposite way by looking at the fundus. So, you can use your green lamp, your green color, or your blue color, and you can hold it on there, and not blast their eye out. You don’t want to hold your white light on their pupil for a long period of time, especially if you do this and you start seeing hippus on the eye, the pupil is bouncing, and then it just fatigues and blows out. Okay? Even though I know you’re trying to do everything you can to say, “Which way is it beating?” But that’s one way to do it. Okay?

So, I want to be able to say this: Is there a first-degree nystagmus? So that means this: “You just have to look straight ahead. You can move your hand. So, look straight ahead.” Now, I don’t want to get in their field of view. I don’t want to get right here. Because a lot of times they’ll converge into my nose, and you… they won’t… you won’t see the nystagmus as well. It’ll tighten up. So just look off and you just watch. And a lot of times I’ll just kind of pull their forehead up a little bit. And remember, with first-degree nystagmus, you don’t see anything centrally. Then I’ll cover, “cover,” look, and I’m like, “Oh wait a minute. I see a little nystagmus now. Uncover that.” Now, it’s beating to the right. It’s beating to the right. So, it’s going like this. Okay. I’m sorry, it’s beating to the right. Mistake number one of many. Okay.

So if it’s beating to the right, which side is weak? Unilateral weakness. Remember, the vestibular system, this side pushes this way; this way pushes this way. So if it’s beating to the right, it’s physiologically going which way slowly? To the left? So which side would be weak, in a weak system? Left. Okay, so here she has this nystagmus. It’s beating to the right, her eyes are going to the left, and I see that when I do my cover, and I do my funduscopic stuff, but I don’t see it in central gaze with fixation. So what degree is it right now? First degree. So what am I going to do to try to bring it out? Have her look in both directions. Which way would I automatically make her look to try to bring it out? The direction in the fast phase, which would be what? To the right side. That’s Alexander’s Law. Okay? So that’s fixation. And when you do all these provocative tests, with peripheral vestibular pathologies, you want to suppless fixation or else you won’t see the beautiful findings that you want, like, “Hey, look at the nystagmus from the provocation,” or, “Hey look at the torsion from the provocation.” The only thing you may get is subjective complaints like, “Wow, I don’t feel good,” or, “Ooh, I’m dizzy.” Okay?


So, as we do that, let’s review this real quick. Which canal? Left horizontal. Which way does that reflexogeni-cally really want to push the eyes with a VOR response? To the right. Okay, so in this side, which muscle is being activated? Left medial rectus, and the right lateral rectus. Which cerebellum tends to integrate into this? Left. All left canals are the same sided cerebellum. Now, real quick, what’s this canal? Right horizontal canal. So now which eye muscle here? Medial rectus, and the lateral rectus. Which cranial nerve? Ooh, 3. Which cranial nerve? 6. Which part of the brainstem? Mesencephalon. Where’s 6? Pons. That’s how you do this exercise.

Now watch. Turn the head horizontally, then bring it down. Which canal am I activating? Now remember, the canals are like this: anterior, and anterior. They’re like horns sticking off in these directions. I want to get them in this vertical plain to activate them. So, it’s not this. Take it, drop it down. Which canal am I activating? Right anterior. Now, the best way to do this is…

You just find a spot and fixate on it. Yep.

So if I turn her this way, and then drop her head down this way, and she keeps her eyes fixated on that point, which way is she technically looking? Up and to the right. Now, which muscle’s being activated in this right eye? Right superior rectus. If it’s a right… If it’s a superior muscle on this side, it has to be inferior over here. If it’s the rectus over here, it has to be an oblique over here. So it’s the superior rectus on this side, and what on this side? Left inferior oblique. Perfecto. Now, this right anterior canal’s in line. Which one is back here being sort of deactivated? Left posterior. Okay. You guys getting the exercise? Alright. Which canal? Right posterior.

Now, so here’s a general rule. All the anterior canals make you look up; all the posterior canals make you look down. All superior muscles are intorters, all inferior muscles are extorters. All superior muscles will be on the same side you activate.

So watch this. Which canal? So, rotate right, take it back. Which canal? Right posterior canal. There has to be what on the right side being activated? It has to be a superior muscle. I told you that the side you’re activating always has a superior muscle in the vertical plane. So, she’s looking down this way. The obliques do what? Opposite of what they say they’re going to do. So there’s a superior oblique here. Remember, the superior rectus goes up here, superior oblique here. So if it’s a superior oblique here, what’s being activated on the other side? It has to be the two opposite words: Inferior rectus. Good. The superior oblique is innervated by which cranial nerve? 4. Where is it? In the floor of the mesencephalon. So what’s being activated over here? Left inferior rectus, right? So the inferior rectus – let me ask you about this – where does it come from? 3. Ipsilaterally. Alright?

So, these are just a few things. And you see how quick we can run through this. So, which canal? Right anterior. Which canal? Left posterior. Why do I care that you know this and the eye movements? Because the direction of nystagmus that you see instantaneously is going to give you the answer of which canal that you treat. And if you don’t know it, you’re going to have a really rough time with these procedures. You may be able to see it and say there’s something wrong, but you’ll have no idea which direction to go. And I promise you, people say they know it, and they don’t. Or some do. I don’t want to say that everybody doesn’t.

So, we’ve got to kind of continue to run through this. So here we go. Ready?


[19.59]

Person has vertigo. They’ve got nystagmus. It’s horizontal. It’s spontaneous. Well, we don’t know what that means until we go off in different directions, but in order to see that, we have to do our fixation suppression sometimes. Sometimes we don’t. With really bad neuronitis, you don’t need fixation suppression. It’s just there. Sometimes it’s not as bad, especially as they start to get used to it – okay? – and their body starts to kind of recalibrate.

So, this is really what we look at when we look at fixation, okay? So, we did it fundoscopically. You can get Frenzel lenses. You can VNG or ENG; one’s video, one’s – you know – not video, but VNG’s kind of the standard now, even though ENG is probably more reliable. But the Frenzel lenses are definitely cheaper, okay? I don’t really advocate any particular brand.

So, real quick, lets just talk about what you see here. If it will play.

Hmm. What did you see? How many of you say it’s an oscillation? How many of you say it’s nystagmus? There’s no clear fast phase. They were both fast phases. This is a person with a centrally mediated issue, and they’re trying to fixate, and it’s worse. I threw that in there as a little bit of a trick.

Let’s look at this one now.

Okay. Which way is it beating? Ah, it’s gone now. We didn’t get a chance to sit there and look at it a million times. That is how quick you have, okay? So watch it again. Okay, now they’re being laid down right there, so boomp, boomp, boomp. It’s beating up, and the eyes are doing… And it may go a little bit left, because their head’s being rotated in one direction, but this is a person being laid down in a Hallpike, and they have BPPV. What did you really notice? What jumped out at you? Watch the torsion. Watch that right eye. The top pole is beating which direction? The top pole is beating right. So we call that, it’s geotropic. Like if it’s right BPPV, and that pole, the eyes go in, and then as it comes back up the top pole goes blink! down towards the ground. So I’ll show you that in a minute. But you see how you didn’t have much time to look at that, right?

So demonstration number one. We just did the fixation, and we looked at: Is there any nystagmus? Is there any oscillation? We did that with fixation suppression. Can we identify a fast phase? It’s not always that easy, especially when we’re doing these provocative maneuvers, because they fatigue. As you lie down, and if otoconia’s causing it, it might go to its position, not have… You may only see five or six beats, and so you need to determine how many beats of nystagmus it really takes before you can say, “Hey man, that’s this, that, or the other.” Because if you can’t… And by the way, the more you do it, the less you’ll see it. So practice makes perfect, okay? Is it purely vertical, or horizontal, or does it have both horizontal and torsion? Now, what did the last on have that we showed you? Verticality and torsion, and it had a little bit of horizontal movement because, as they were going back into the Hallpike, they were being turned into one direction. As they were being… and you saw the eyes go a little bit left? Well, it’s because they were probably being turned back to the right and then brought back like that, so the eyes came over in this direction. And then you saw it beat up a little bit like this, and the eyes were torting like that. Okay.

So, real quick, that was just sort of that. Now, let’s get into this BPPV, and let’s get into what it really looks like. This is what we’re going to look at: our provocative tests, our Hallpikes. So now, just watch. We have


vertigo, meaning the person’s like, “I’m dizzy.” And so you ask them: “Hey, when does it happen?” “When I move quickly, look up, look down, look sideways.” Now, the posterior canals, which movement do you think would make them feel the worst? Looking side to side, or up and down? Yeah, looking back in like this. These are the people that, you know, they bend over to garden, and they sit up, and they fall down. Or they’re looking up to get something and they get dizzy and they fall down. If it’s horizontal, it may be just a rapid head movement, and all of a sudden they feel, like, unstable for a second or two.

So what I’m saying is, it’s nystagmus that doesn’t typically last very long, but it comes on quick with head movements or body movements, and then goes away. So they have vertigo, they have dizziness, they have nystagmus, and you have to provoke it. So let’s say it’s vertical, and let’s say that fixation makes it go away, but when you put them in the dark, or put Frenzel lenses on, you can see it better. And let’s say that it’s positional. So now the person says, “Look, it only happens when I move in a certain direction or lay down in bed or roll over. And as soon as I lay down it comes on; when I sit still it goes away. When I roll left, when I roll right, it comes back.” Now, would you ask them if they have any hearing loss? Yes, and they say no. Would you ask them if they have any pressure in their ear? And they say no. You ask them if they had any infections, and they say no. You ask them if they’ve had any barotrauma: “Have you been up in a plane? Have you been scuba diving? Have you been sneezing? Have you been coughing?” And they say no. They say no to everything else. What does that start making you think? This is related to position. And this is benign, and it’s paroxysmal.

Now, what is your main goal after that? Figure out which canal it’s in, okay? So, you say, “Wow, it’s when they look up or down, so that’s the provocation, is position.” The test is a Hallpike I’m going to show you in a minute. Posterior canal BPPV is when the symptoms are… They show up the way we’re going to show you in a second. And we have to determine if it’s the cupula or the canal; the canal, the nystagmus… When the debris is stuck on the cupula, which is the receptor in there, right? In the ampulla. If it just lasts longer than sixty seconds and won’t go away, a lot of times it’s hung on there, and I’ll show you the procedure to get it off in a second. If it’s less than that, it’s just good old-fashioned canal, so it’s dragging through, alright? So we have to do these repositioning maneuvers, okay? This is about twenty percent of all patients with dizziness. Very, very common, can occur after head trauma, because you knock otoconia loose. Sometimes it’s idiopathic in the elderly, and the answer is, the central calibrator doesn’t calibrate the canal that’s now being distorted. Maybe it’s been distorted for years, but it’s just now becoming symptomatic because the cerebellum finally said, “You know what? I’m not going to cover for you any more, man. I’m going to let the vestibular nuclei do whatever they want. I’m not going to keep recalibrating them. Okay?”

So, these otoconia, they’re dislodged, they go into the canal, they may stick on the cupula, a change in posi-tion makes it worse, and now we have to really go through and say, “Okay.” We have to be able to describe these procedures. So if you look at this, when I lay somebody back, a lot of times the debris will slide away from the actual cupula, and then drag it that way. So picture yourself like a boat floating by, like a buoy – or buoy – and then you see it kind of drag that way with it. As this drags down, it pulls the receptor with it. Or sometimes the stuff just gets stuck or hung. Let me ask you a question: No matter which situation, is the actual… Is this perilymph or endolymph right here? It’s endolymph. There’s no receptors surrounded by perilymph. Perilymph is the shock absorber, okay? Is the endolymph going to be… Is the receptor going to be activated the same in both of these situations? Yes, it is, okay? So, here it is. We decided they had nystagmus. We decided that it’s vertical. We decided that fixation suppression makes it come out better. We decided it’s positional. We provoked it. We did a Hallpike, which I’m going to show you in a second.


We determined it’s upbeat. So which canal is involved? The anterior or the posterior canals? So, upbeat means the slow phase is which direction? Down or up? Down. How do I make the eyes go down? Make the head go back. So if this is upbeat, it’s what? The posterior canals. So now you just say, “Wow. Which one is it? Canal or cupula? We’ll time it, and then we’ll actually to the repositioning maneuver a little bit later.”

So now, real quick, before we get going, what do you see here?

[30.0]

It’s not an… Look, look at this right here. The person’s lying down, with which canal being activated? The right posterior canal. How many of you saw upbeat nystagmus? Now, here’s the thing. Why did it look like it was just oscillating? Because it was fast. It was that aggressive of nystagmus. But here’s the deal: And oscillation doesn’t gradually ramp up and then ramp down. It’s just there. Sometimes it may get worse with fixation. But with this, you notice… Let’s watch it again. We lay the person down, and what’s… There’s not much going on, right? So the debris is just now starting to move. Watch the left eye. Boomp boomp boomp boomp boomp boomp boomp. It’s moving up. It’s beating upward really badly. Now, what does it start to do? Now it starts to settle down a little bit. That is paroxysmal. So, how many of you can see this? Okay.

Tell me what you see. How many of you notice it’s beating up? Now there’s torsion. Good. Just another video to see if you can see it.

Now, watch this. I’m going to play this several times. You have this video. You can notice that this is what? Anterior canal, posterior canal, horizontal canal. The blue stuff represents the debris, okay? So, some debris has come out of the vestibule. Why is the posterior canal so prone? Because it only takes a little bit to get over this hump, then it’s like boom! To get up and over this, much harder. Okay? So just watch. Sorry. It helps when I push the play button. Head to the right, and back. Now, look at that debris floating down towards the top of that canal. Now, what do you think? See, this is the degree of nystagmus they have. It’s up, up, up, and then as it goes down and settles, the nystagmus right here starts to slow down. Now, what do you think’s going to happen when they come back up to the nystagmus? It’s going to reverse. So now they come back up, and now the eyes start beating down, because the debris is now going back towards the other direction. So it reverses. Everybody comprende?

So your goal is to say, “Okay, cool. This is here. I’ve identified the canal. Let me get you up, around, and back home. Let me send you back home.” Is this a situation where the receptor is overactive or underactive? Overactive. Do you think that there’s been any central adaptation to this if it’s been there a long time? Hopefully, okay? Hopefully.

So we’ve got to do a demonstration now. So, as we do this demonstration, we still do everything we’ve done. We go and we observe for spontaneous eye movements right now, okay? Because – you know – if they have oscillations and stuff like that, and it doesn’t look like BPPV, there may not be a need for these maneuvers. You may not want to do them on every single person, okay? So, what I like to start out and do is, just a seated head evaluation. It’s not so aggressive. A lot of people just want to roll right into a Hallpike, okay? But I like to do things like, “Okay, let me just bring your head back.” Now, I’m not talking about the horizontal canals yet, so just hang on, because you’ll see something different with them. But I like to lean back, and then I’ll stand off to the side, and then pull the eye open. And I’ll kind of come back a little bit


more, and then usually I’ll start to get nystagmus, especially with the BPPV. Because what am I starting to engage? I’m starting to engage the posterior canal. So what will I start to see? A little bit of vertical nystagmus. Now, if you’re good enough to watch the top pole of the eyes, you may see the top pole beating in one direction or the other, so you can kind of decipher which one of these it is. But if you can’t It’s okay. You take the head back, and then you can just rotate it a little bit one way, and then rotate it a little bit the other way, and see which one makes it worse.

Do you see how this is just nice and friendly to the patient? And if they start feeling a whole lot of symptoms, you can stop and bring them back up a little bit. Some people that are really, really sensitive and sick, if you just lay them straight down, I promise you… How many of you have done it to somebody who was really sensitive? They start throwing punches, they jump off the table, and they start screaming at you. It’s not the best thing, okay? And you can also pitch them forward and see if they have symptoms as well, because a lot of times that will cause symptoms at the same time.

Now, when you do this right here, you want to look and make sure they nystagmus is not beating the other direction. Alright? At the same time, as I do this, the person’s like, “Man, I’m getting lightheaded.” And then I’ll say, “Okay, I need you to say the alphabet, or count from a hundred down to zero by fives.” And they start doing that, and they start slurring their speech. Okay.

Now, turn this way just a little bit.

The vasculature, especially the vertebral artery system, it runs up, and then it goes this way a little bit, and then it comes back like this, and then goes up. So there’s a little bit of way to put some tension on it.

So, turn back this way.

As I bring this back, and I start having those symptoms, I will take their occiput, and translate it forward. You see what I’m going there? When you do that, you’re taking that piece, and you’re stretching it, and making the lumen more narrow. And that increases the symptoms. And when that happens, you stop, and you say, “I don’t like this. Let’s do some diagnostics to see if there’s any vascular problems.” Is that cool? Now, if you start doing this stuff, and you’re just barely pressing their carotids every now and then, one of the things that people will say when they have carotid insufficiency is it feels like somebody’s a closing a blind over their eye. And that’s different than having a central scotoma versus – you know – bitemporal or quadrantanopial types of problems, okay? So, I’ve just done a simple test. I’ve done this. I’ve done a vascular test. I can come over here and I can now feel… If you go right above the clavicle, and you feel the SCM. There’s a divot here. There’s the vasculature in there. You can go just outside of here, and you can feel the scalenes and their tightness. You can feel the SCM and their tightness. You can come right in here and you can kind of compress in a little bit, and they’re like, “Whoa, my arm gets numb,” and thoracic outlet type findings. You can come over here, push down a little bit, and maybe feel a rib that shouldn’t be there. You can come over here, feel the AC joint, come down a little bit, press on the pec minor tendon, and sometimes the brachial plexus will get compressed underneath that tendon, and that will create symptoms.

As I bring their head back, and I rotate, and they’re like, “Ah, that doesn’t give me too many problems,” you can go ahead and stick your thumb in here just a little bit, and give a push down, and they’re like, “Oh my


God, my arm’s like… you’re… serious stuff’s zapping down my arm.” When that happens, that’s a foraminal compression test. You’re making the neuro foramina more narrow.

Now, as you go forward, there’s one thing that you can do also. So you’re going forward, you’re checking all these head positions and everything, okay? As you go forward, they’re like, “I’m feeling pretty good, you know? I feel maybe a little bit of tingling in my feet.” Take your elbows right here, take your head, scoop it in, bring their chin down, and it will apply a little stretch on their cord, and it will go vvipp, and it will zip, and that’s a Lhermitte’s sign, or a chin-to-chest if they’re lying down. It’s like subtle Hall test. But just bending forward doesn’t do it, because it will stretch all the way down to their thoracic spine, but if you block them with your chest, and then tuck that chin down and push, boom! It will become very positive. When you’re looking at the vasculature, if you translate the occiput, it will become much more positive. When you come over this way, and you just push down and block the segment, it will become much more positive.

So the reason why I throw those in there is because people will say things like, “My arm’s numb,” or, “My neck hurts,” or, “My feet tingle,” and you’re just looking at their eyes, going, “I’m just trying to find some BPPV, man.” And I’m throwing that in there so that you’ll get those things, and that they’re on video for you. So let’s just say that we did this, and she’s like, “Whoa, I feel terrible,” and you say, “Man, there’s all this upbeat nystagmus.” And you do this, and you think, “I think it’s the right posterior canal.” Does everybody follow me?

So, now let’s do a Hallpike maneuver.

Yep, so I want you just to turn your feet this way. Now, sit up. Scoot back a little bit.

Okay now, one of the things you want to realize is, you’re fixing to take somebody to hell. And do you want to be nice about it. A lot of people say, “You slam them down as hard as you can like a wrestler.” You already know what’s positive. And I’m going to tell you: Stand like this.

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Don’t stand like this. You’re going to get punched in the junk. I don’t know what else to say. I mean, if you have junk, it’s going to get punched. So be careful. Stand to the side. Get in nice and close so that they don’t feel very, very uncomfortable, and just say, “Look, you’re going to be okay. You’re not going to fly off the planet. We’re going to be good.” And then take them down about this fast. Now, what I want is for their forehead to be lower than their chin. And I want their head to be rotated at about a forty-five. So, what am I really engaging right now? A posterior canal or an anterior canal? A posterior canal. Right or left? Right. How did I know that to begin with? I already did my little subtle checks, and I already know.

So, bring it back. And now, if she has Frenzel lenses on, I’m looking. If she has VNG goggles on, I’m looking at the screen. Whatever. And I’m just going to time how long it takes, how long it lasts, and when it goes away, and I’m going to note it… kind of note it in my head, and them I’m going to say, “Okay, we’re going to come back up.” Now, if they’re really fragile, “Grab ahold to my arm.” Come up, stop, look straight ahead, and then you’ll see the nystagmus probably temporarily reverse directions. If that happens, you’re like, “We’re going to make this day much better for you.”


You okay with that? Good.

That’s what you can hope for. Remember, about twenty percent of your dizzy cases are going to be this: BPPV. The vast majority of BPPV is this canal. So do you guys got that?

Now, we’re going to look for spontaneous eye movements. We do the seated head evaluation. We look for the canal. We look for the vascular. We look for the orthopedic. And then once we do all this stuff, we go ahead and we do the Hallpike maneuver, if we think it’s truly that, to confirm it. Is everybody cool with that? Real simple.

Now, the next lecture will be, “What do I do if I get a positive Hallpike?” We’ll reposition her, and then we’ll do some exercises, and I’ll show you both. But right now I just want to kind of run through that. So…

Let’s talk about another horizontal canal, because that canal can be affected as well. Now, when I say “horizontal canal,” the eyes, instead of moving up and down, which way are they moving now? Side to side. This gets a little more confusing, so pay close attention here.

So now we’ve looked at spontaneous eye movement. We’re in the second part of BPPV. Again, we’re doing a provocative test. Now, just watch. We have vertigo. We have nystagmus. It’s horizontal. Fixation suppres-sion makes it worse. It’s positional. It’s either going to be geo- or a- or apogeotropic. Everybody got that? So in other words, it’s either going to be down toward the ground, or away from the ground. There’s two different procedures to treat both. We need to know them. Okay? I’ll show you that in the next hour. But right now, I just need to get you in the ballpark. Like, which one of these is it? Okay?

So, let’s run through it. We’ll do the repositioning maneuver after provocation, and body and head stuff. So, here’s what I want you to look at. Now, geotropic means that as you do the provocative maneuver, it’s beating towards the Earth, which means the ground. So if I turn my head to the right side, and this canal’s overactive, and it’s driving the eyes to the left, which way would it be beating? Back towards the affected side, which is towards the ground, not towards the up ear, which is what? Is that geotropic or ageo… or apogeotropic? It’s geotropic. If it’s the other way, which is less frequent, it’s apo- or ageotropic, okay? So let’s just watch a video real quick.

Now, is that horizontal or vertical? It’s horizontal. Which way was it beating? Right. Now which way is it beating? Left. It’s reversed directions with head movement. Their head is left; it’s beating towards the ground. Now their head is right; it’s beating towards the ground. Oh, no, now it’s beating left. So you saw it kind of switch a little bit.

So what’ll happen is, as you… The most affected side wins. So you lay it down towards the right, and it’s pushing, and it’s, like, beating like this, and then you may turn it to the other side, and it may beat the other direction, okay? So this horizontal canal is just like your Hallpike maneuver. When you come up, and you reverse directions, you may see things change a little bit. That’s what’s great about provocative maneuvers. It takes time to get them to go, they go, they stop, you go back the other direction, they reverse, they go, they stop. There’s nothing more diagnostic than that.


Now, here’s apogeotropic, which means it’s just beating now towards the other direction, and we treat it a little bit differently. So, I’m going to show you what we do with head, and now she’s just lying on her back. You see a little bit of a… beating a little bit… well, you can’t tell if it’s a little bit left. Now which way is it beating there? Beating right. Now it’s beating left. So the head’s turned right, and it’s beating left. Is it beating down towards the planet? Pretend I’m lying down. I’ve got my head turned right, and it’s beating that way. Is it beating towards the Earth? No, it’s beating towards outer space. That’s ageotropic, okay?

Here’s another person. Again, is it horizontal or vertical? Well, they’re blinking. Boom, boom, boom. Which way is that beating? It’s beating left, yeah. It’s pretty easy to see, huh? One of the things you’re going to do repeatedly: “Stop blinking. Stop blinking. Stop blinking.” What do people do when they get scared and they start having dizziness? They want to close their eyes, but they realize that makes them worse, so they open their eyes. Then then close, and then they open them. So they start blinking, over and over and over, and you’re like, “I can’t see your eyes. Quit blinking.” So tell them right out of the gate: “Try not to blink your eyes while I’m doing this test.” I’m just giving you some friendly advice from things.

Now, here’s what we really need to understand. Nystagmus really is pathological if it changes directions in any head position, or if it’s present in at least three, or if it’s intermittent at all for them. We can record these things. But the best thing to do is just look at these. So, one of the things we can do is just screen with a head tilt. Now remember, I told you a second ago…

Go ahead and face this way.

…that we were going to do a test where we brought the head back, and we brought the head forward – right? – to see if the eyes were beating up or beating down, to look for anterior and posterior canal pathology. Well, it might be possible that as I go back, or as I go down, what happens? It beats horizontally instead. So do you see how important it is to be able to do just this test right here, just sitting up, and be able to say, “Is it vertical or horizontal?” Because if you get it wrong, you’re going to do a repositioning maneuver, they’ll get no better, or you’ll eject the debris into one canal into another canal, and they get worse.

So, as you look right here, with canal… we’re just sitting here. Canalithiasis, meaning there’s just debris in the canal. It’s not stuck to the cupula. How much nystagmus do they have? That little line represents no nystagmus. Now, a lot of people are like, “I don’t know what this jagged thing means right here.” Okay. So you see the slope? Hold your arm up. Which arm relates to the slope? Huh? My left. I hold my left arm up. It’s beating left. There you go. Which way is this one beating? It’s beating right. Which way is this one beating? It’s beating left. Which way is this one beating? Right. How about this one? Left. So in these things right here, here’s the deal: If it sticks to the cupula, everything goes backwards, and it becomes ageotropic. If it’s just in the canal, it becomes geotropic. Alright?

So, right here, there is nothing stuck to the cupula, so the person’s like, “I feel pretty good.” As soon as they move, they’re like, “Oh, ah, oh, that doesn’t feel good.” But if they’ve got debris hanging on the cupula… Remember, these canals are not sitting perfect. They’re at about a thirty-degree angle, so even with the head at this angle, there’s going to be some beats. So they many naturally put their head in a certain position to kind of start to get rid of the nystagmus. Okay?


So in this person right here, neutral, you don’t see anything. With a heavy cupula, you can see on the left side, on the left side right there, that little arrow’s pointing toward her left side affected. What does the heavy cupula show that it’s beating? Okay, so it’s hanging on the receptor, so now the left side is just being activated for no reason. Which way is it slowly being moved then? To the right. Which way is it beating then? To the left. Okay? And then with a light cupula, that means the debris is on the other side of the receptor.

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So, you may see it beat the opposite direction. So now you’re right here, and you’re like, “Okay, let’s just hang your head forward. Now, you still want to be like this. Looking right here, and all of a sudden instead of seeing this, you start to see this. You’re like, “Oh crap, her eye’s beating side to side.” And you look at it, and you’re like, “Hmm. Is it beating left, or is it beating right?” You still don’t know which ear’s affected at this point. You just know that it’s a horizontal canal. Does everybody understand? Okay. So now you bring the head back, and now you’ll see it reverse, at A3. Okay? So a light cupula does the same thing as the canal. But remember, the canal is just doing this. It’s just, like, activating that canal. So if it’s the right canal being activated, it’s going to drive the eyes left, and it’s going to beat towards that side. As I come back, it’s reversing. So as I come down, it activates the canal, so it beats in the direction that it typically would beat if you’re activating that canal. Then when you bring it back, it just goes the opposite direction. So when I come down, and it actually beats left, and then I come back, and it actually beats right, and it’s canalithiasis, you’re like, “Wow, looks like the left side’s being activated.” You can kind of say that, at that point. Okay?

So, we’ve gone through this. We’ve done this test, and we’re like, “Wow, this looks like posterior canal BPPV or anterior canal BPPV,” or we’ve done this, “Looks like anterior canal or posterior canal,” or we’ve done these tests back and forth and it looks horizontally trajecting. So let’s say that we’ve ruled out posterior or anterior canal BPPV right now, okay? And it’s horizontal.

I need you to lie on your back. Okay.

She’s going to lie nice and flat. And you can see her lying nice and flat right here. And with just good old-fashioned canalithiasis, it doesn’t do much, just like it doesn’t do much here, just looking straight ahead. This is the least of the worries, right? But now, as soon as you turn head right or head left, you’re going to start having symptoms. So, right here, we’re just going to look straight ahead. Now, I’m going to turn the head, and you’ll start to look for nystagmus. Now, if the nystagmus is doing this, which way is it beating? It’s beating left, and it’s beating geotropically. You can see it right up here. Typical canalithiasis. Or, a little bit of light cupula. But if it’s heavy cupula, it’ll just beat the other direction, okay?

Now, if you do this, and it’s beating the other direction… You know, a lot of times what you’ll do with cupula is, you’ll just shake the head, or vibrate on the mastoid, to try to get the otoconia to come off of the cupula. Same thing when you do – whenever I show you the repositioning maneuver next hour, then what we’ll do is, I’ll show you how to get rid of a cupulolithiasis. Okay? So we do this, and wham! everything gets really bad. We come over here, we see nystagmus. Now, as we look the other direction, what happens to the canalithiasis? It reverses, right? Why would it reverse? It’s flowing the other direction. It’s just like the Hallpike. But they’re like, “That’s not near as bad as the other side.” So you say, “Wow, this is the affected ear. It’s geotropic. It’s left horizontal. That’s what we’re going to treat.” And we’re going to barbecue-roll


her in about an hour. Right? On the other one we’re going to do an Epley maneuver. Or we have other maneuvers if it’s ageotropic, that are much more simple, actually. Okay?

So, that’s just horizontal stuff. Now, if I turn her head this way, and her eyes are now beating to her right, so they slowly go down and they beat to the right, is that geotropic or not? It’s ageotropic, right? Some people use apo-, some use a-. Ageotropic, okay? So now we have to start thinking, “Man, is that, like, a heavy cupula? Is it something different? Is the debris on the other side of the receptor? Do we have to do a different maneuver?” I’m going to show you a different maneuver in a little bit to get rid of both. Okay?

Now, those are just real simple tests. But now, did I purely isolate the horizontal canal just then? No. Why? Because I rotated the neck. What if the afferent barrage from the neck that matches the information from the canals is incorrect and mismatched, and now the neck might be involved in some of the nystagmus? Watch.

Turn your whole body.

Now what am I purely activating? This is pure canal. Now, if this gives you the same symptoms, you can say this: “Man, your canal is definitely involved.” If there’s no symptoms now, but there is in the other one, you’ve got to go back and say, “There could be an etiology of cervicogenicity in your vertigo.” You dig? Okay. So, that is called body down, or a supine test. Head left, head right, body left, body right. I base that off my seated head-forward, head-back.

Sit back up.

My head-forward and my head-back, I’m looking for nystagmus to be vertical or horizontal, to give me an idea of which thing I need to go into next: a Hallpike or a supine body-left body-right, head-left head-right. Everybody catching me on that? It’s so important that you get that, because you need to know which canal you’re treating. Yeah, I keep repeating myself, and I’m sorry about that, but again, just important that you actually kind of grab that, okay?

Okay, so how we doing? You doing alright over hear? “Yeah, I’m great.” Perfect.

Alright. So, demonstration number three. That’s what we just did.

Anterior canal. Well, there’s really… There is no special testing for anterior canal. What we notice is, is that when we do things that engage the posterior canal, what we see is nystagmus that’s opposite. The repositioning maneuver will be different though. So we’ll have four repositioning maneuvers: an anterior canal, a posterior canal, and two for the horizontal canal, if it’s geotropic or ageotropic. One’s a barbecue-roll, another one is… We have a different procedure that we’ll show you. Okay?

So, there is our BPPVs. We know that we did the provocative tests. We know we did a Hallpike. We know we did body position with head rotation and without head rotation. Do you see how this chart right here just gives you what you need? Am I worried about any unilateral peripheral vestibular weakness right now? Weakness. Weakness. In an isolated environment, where there’s no other dual conditions. The answer’s no, guys. I’m worried about what? An overactive canal because of debris. That’s a receptor that’s being


overactivated. This is not neuronitis, where the nerve is dying and now it’s unilaterally weak, okay? But we’re going to get to that.

So with vertigo, nystagmus, vertical, fixation suppression, positional, provocation, Hallpike, torsional downbeat… Torsional downbeat, so the eyes are where? Being driven up and then beating which direc-tion? Down. Does that look like the traditional positive Hallpike for the posterior canals? No. That is what? Upbeat. So now we have this torsional downbeat, anterior canal, repositioning maneuver. You can just draw a line right through, and it’ll just show you right where to go. Okay.

Tell me what you see right here. This is really pretty cool. Now, by the way, I put these videos in your files so you can look at them. You’re like, “I don’t understand what this means.” But just go back and watch it. So now we’ve got this poor gal. Now, let me ask you something real quick. Are you going to activate the anterior canals when you go back this far? If you do a deep Hallpike, or go straight back? So, if I’m doing head-forward and head-backwards, and I’m seeing a little bit of stuff that makes me think it’s the anterior canals, I’m going to do a different… I’ll show you the test here in just a second, but I’m going to do a head-hang test. Okay, there she is. Which way is it beating? It’s beating down. That’s not BP… That’s not posterior canal BPPV, is it? So let me show you something here. You do these little tests, these little seated tests, and you think, “Man, there’s some verticality in this, but I think it’s the anterior canal.”

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And remember, that anterior canal, it’s not like the posterior canal were it’s like, got just this little short little hump and it drops down real fast, so it doesn’t take much to engage it when you go backwards. It’ll allow the debris to slope up. That anterior canal has more verticality on it. So in order to get it to activate, I have to now get more decline. So I’m going to do a Hallpike, but I’m going to modify it for a second.

Turn around.

So, now I’m like this: Forget body-left, body-right, head-right, head-left. I don’t think it’s horizontal canal. I don’t even think it’s posterior canal BPPV. I think it’s anterior canal. I want this to be pointed towards the floor as much as I can. So watch. Here, hanging. Now you’re going to get that debris to go mnnnh up to the top, and you’re going to start to see that nystagmus that’s doing this: It’s beating towards you. You’re looking at it, and their eyes are going dnt, dnt, dnt, like they’re beating at you. You come back up, what happens? It reverses. Cool? The repositioning maneuver for this is so easy it’s unbelievable. Okay? I’ll show you after lunch. I’m trying to separate the diagnostics from the treatment, because I feel like if I don’t, it… I’ll go back and quickly show you the diagnostic, and then quickly do the treatment procedure again.

So, how many of you can kind of sit here and say…

Turn around.

I’m going to do just some simple stuff. I’m going to tilt the head forward, I’m going to tild the head back, look for the nystagmus, see if I think it’s anterior, posterior canal. I’m going to tilt the head back, or forward and back, and do horizontal, and determine if it’s horizontal canal. I’m going to go ahead and feel some lymph nodes. I’m going to feel the thyroid. I’m going to do some orthopedic tests. I’m going to do some vascular


tests. And I’m going to do all this stuff real quick, just like this, right behind the patient, as long as they’re comfortable with you being back here, like I am behind you. Don’t worry about it, okay?

So you can do all these things. And then from there you can say, “Look, I think it’s X, Y, or Z.” Because if you start putting them through all of the provocative tests, you run the possibility of moving debris around, or reducing the effects so you don’t see it for the rest of the visit. Because their brain may start to sort of habituate. So, do you kind of catch that? That’s all the provocative maneuvers. That’s really pretty fun stuff. When you do about maybe ten of these, you get a whole lot better, and you don’t feel like, “Oh my gosh, this is – you know – this person is so belligerent.” Most of these people are pretty belligerent. They’re out of control. They feel terrible. They feel like they’re going to fly off the planet when you lay them down. And so you have to learn that you have trash cans on both sides, and when you’re doing these provocative tests you stay in nice and snug. But the biggest thing you can do is, give them instructions before you go. “Look, we’re going to… What you’re experiencing is just false perception. You’re not going to fall off the planet; you’re not going to roll off the table. You’re going to feel very uncomfortable, but there’s a good chance that it’s going to start and then stop, and you know that. And if it starts and stops, then I can probably fix it. And if I can do some stuff to make it to where it does start and stop, I can fix it easier, especially if it’s cupulolithiasis.” Okay?

Those are your positional things. Does she have any hearing loss? And a pure singular condition. Does BPPV affect the cochlea? No. Does it affect the cochlear nerve? No. Is there any cranial nerve damage? No. Is there any cognitive changes? No. In other words, this is positional. It’s vertigo. It comes, it goes, and there’s nothing else associated with it, okay?

So, those are the important things that you need to know about those three canal positions that I think is really going to be necessary for you. And that’s your demonstration.

So, do you know, in summarization – and I just added this in, so you don’t have this slide – but in sum-marization, can you really sit there and discuss the difference between the three canal types: the anterior, the posterior, and the horizontal? Well, you know by looking at nystagmus. That helps. And the provocative tests. That helps. And of course, by seeing a demonstration, you can go back and review those things. And I promise you, the next time somebody walks in…

How many of you have now learned more about BPPV than you did before when you started? Hopefully everybody. Especially when you start doing just those simple head… seated head tests that are not so aggressive, and you can start seeing some symptoms. Now, it’s not always easy to see, as you can see on the videos. A lot of people are like, “I don’t know which way it’s beating.” That’s why you kind of have to practice seeing videos, then practice seeing patients, and then you’ll attract more patients, and then you’ll get better at it, and hopefully all will be well. Okay.

Neuronitis. So now we’re out of the what? Positional things. And now we’re into the inflammatory condi-tions. So let’s check this off right here. Okay. With neuronitis, she’s sitting right there. Is she going to have any nystagmus? Probably. So it’s not quite like BPPV. Now, with BPPV, could she have some nystagmus sitting here? Yeah, if it’s stuck to the cupula and it’s really bad, she may have a little bit. What makes it worse? Position, right? Head movement. Rapid movement. Well, does rapid movement make neuronitis worse? It actually does. Is there any hearing loss with this? Not typically. Because remember, there’s the


cochlear nerve, and then there’s the vestibular nerve that has a superior and an inferior division on it, so what happens is, this is the portion getting damaged, not this portion or the rest of the labyrinth. It’s just this nerve. Okay? But what does the person tell you? “It doesn’t matter what I’m doing, man. This stuff is killing me. It’s been around for hours.” BPPV is usually paroxysmal. They’ll find a position where it’ll kind of go away. They can’t find any position on this that makes it go away. As a matter of fact, if they lie towards the weak side, a lot of times it gets worse, okay?

So you’ve got this neuronitis, and it’s got spontaneous eye movements. Provocative tests are not my best tests now. I’ve got to go down here and look for a decrease in vestibular output of one side. So now I’ve got to do things like my head thrust, head shake, and visual acuity tests. So, picture it like this. With BPPV, what was going on is, the canal was overactive. Now we have a nerve that, due to viral inflammation or some sort of other inflammatory response, the nerve is not working well. So let’s say it’s on the right side, and this side now has neuronitis. Which way is the nystagmus going to be beating? Okay guys, this side drives the eyes which direction? To the left. So if this side is no longer there, which way do the eyes want to go? To the weak side, so it beats which direction? Left. So you look at it, and you’re like, “You’ve got a left-beating nystagmus. It just started after an infection. You’ve been sick.” If it’s beating left, then I know it’s probably which side weak? The right side, okay? So you say, “Wow, that’s cool. Let’s do some stuff.”

Now, remember that as I activate the canal, the eye should do what? Equal and opposite reactions. Okay? So this person, if they have really bad nystagmus, these tests right here don’t matter. Or at least the first one does; the head-thrust test. So I’m going to go to the head-shake test. Okay? What am I doing right now, besides shaking her head? Left, right, left, right, left, right. Information’s coming in, it’s going into the velocity storage mechanism, and it’s building up, up, up, up, up, up, up, up, up. And if everybody has equal information coming in, it builds up and decays symmetrically. So you don’t see any post head-shake nystagmus. If this side is damaged, and this side is okay, how is it going up? Like this, and then you stop, and it decays, boom! And after you do head-shake, what happens to the nystagmus? It gets even worse, and you’re like, “Whoa, post head-shake nystagmus gets even worse?” There’s nothing going into the velocity storage mechanism, because this sides’ putting information in, this side isn’t, so it’s decaying much more rapidly, and it’s asymmetric. Okay?

But what happens if I do this, and I do head-thrust testing? Which way should the eyes go? So let’s say I’m standing in front of her, but I’m not going to get in front of her right now for the purpose of viewing. Okay? So she looks at a target, and she goes, chink. Or you move her head. Her eyes should do what? Equal and opposite go the other direction. So which way with a right-sided unilateral peripheral vestibular weakness are her eyes tonically wanting to deviate? Follow me now. Which way are they wanting to go? They’re wanting to go to the right, because the left side’s pushing it over there. So you do this, and the eyes go… like that.

[1:10.02]

So watch. Did you see the decrease in the VOR? And then you go like this: You turn them to the left, and the eyes are like, “Hell yeah, we want to go to the right every time.” Boom, tcch. It’s right on. In fact, a lot of times what it does is, as you go to this direction, the side that’s good, the eyes will actually go past their target and have to have a refixation saccade to catch back up and get to the target, because it goes past it. Because there’s nystagmus there. Cool?


Now, how do I know if this is resolved? Neuronitis. Now the nystagmus is completely gone, but I do my head thrust, and it’s still slow. And that’s still normal… I’m sorry, that’s still slow, and that’s still normal. If the VOR has not returned, and has not recalibrated, the vestibular nuclei have not shifted, and there has not been a reestablishment of a normal VOR side-to-side. So it’s chronic, but not recovered. That’s where your rehabilitation comes into place, and I’m going to talk about that next time. Okay? All neuronitis will probably resolve, because what will happen? The viral titers will go down, the inflammation will go down. This may last a week or two, and if it does, what are you going to start to build? Let’s say this side is down, this side isn’t, and you’re going to start to build plasticity? Which way would the head want to tonically start to rotate if this side is weak? If this side is weak, which way are the eyes going to want to bias? This way, and the head may want to bias this way. Now, do you think she could have postural distortion after this bout of neuronitis? Of course she could. Do you think it might behoove you to reduce that? That is going to be the rehab that you do that makes you different than everybody else. Otherwise, this is treated with steroids and antivirals. Prednisone and acyclovir. Some people are now using antibiotics a little bit, maybe. Okay?

Boy, I jumped ahead. So, we have vertigo, nystagmus, fixation, doesn’t… It may make it a little bit better, but it’s horizontal. It’s spontaneous. First-degree, second-degree, whatever. It’s a peripheral vestibular pathology. There’s no hearing loss. Exacerbated by head movements. Neuronitis. Did you see how we just flowed right through? Pretty cool. Okay.

So, let’s take a look at this right here. Which way is it beating? Left. Okay. Right now, take about ten seconds. If that’s beating left, and it’s neuronitis, which side is jacked up? Don’t say it, write it. Write it down. If you’re at home, you can say it, because nobody’s listening, except for maybe whoever’s in your house. Which way is it beating? How many say left? Okay, where’s the medial canthus? It’s right there. It’s beating left. Okay? You look to the right, it goes away. Go to the left, what happens. Comes back. What is that called? Alexander’s law. You can see this in central gaze, and then you see it when you look towards the direction of the fast phase. What degree nystagmus is this? Second-degree. Almost all of your acute neuronitis patients will come in second degree. The ones that are starting to recover will come in first-degree. So if it’s beating to the left, which side is deficient? The eyes are slowly wanting to go to the person’s right, which means the right side is deficient, because it’s not pushing against it, right? Okay. Cool.

Second most common: inflammation of the nerve. Causes rotational vertigo. Does it cause horizontal or vertical rotational vertigo? Horizontal, because the eyes are going this way. They’re not going this way. So a lot of times with BPPV, somebody will look up, and they’re feel like the room or the floor is spinning up towards their head or the other direction. Usually within seventy-two hours, the terrible stuff has gone away. Complete recovery may take six weeks. How come it may take six weeks? All of those central nuclei have to regain secondary plastic changes, because the nerve will do this: The nerve will be damaged, and it will come back, but it will only come back about eighty percent, or maybe seventy percent, or maybe fifty percent. How do you determine the percentage of loss? You do a caloric. And the caloric will measure the amplitude and degree of nystagmus, and compare one side to the other, and it will say this: “Dude, you had neuronitis, and it was damaged, and it came back, but it’s only fifty percent of what it was.” But then you do your head-thrust tests, and the eyes are equal, so all your VOR responses are okay. What has happened?

Well, the rest of your brain said, “It’s cool. There’s only fifty percent as much coming in, but what we’re going to do is, we’re going to recalibrate the output of these vestibular nuclei to where they change their threshold compared to the other side, so now, no matter what’s coming in, the response is still the same.


That’s how you know you’ve made it when you’re rehabbing somebody like this. Are you starting to kind of understand this a little bit now? Now I’m taking it beyond the “just kind of understand the difference between this and that,” and I’m taking you to a point where it’s like, “This is what it looks like early, this is what it looks like later, this is how you know if you got it better or not.”

Okay. So now there’s three tests that we’re going to do here. Or two tests. I’m going to test hearing. Most people already kind of know how to do this, but I’m going to do it anyway. Because what’s the difference between labyrinthitis and neuronitis, really? One of the big differences. Okay, so let’s say you have dizziness and hearing loss, and you’ve had a bacterial infection. Are you worried about neuronitis or labyrinthitis? Labyrinthitis. Let’s say there’s no hearing loss, you had a viral infection, and you have those symptoms. What are you worried about? Neuronitis. What happens if you just have hearing loss, and some occasional vertigo, but it’s not really constant, but you’re a forty-six-year-old female with estrogen problems and you have conductive hearing loss? Now what are you worried about? Otosclerosis. It all boils down to how you use this, okay?

This is a two fifty… This is – yeah, one twenty-eight, I believe. Anyway, this is your bigger tuning fork. So, let’s do this. Interpretation of Rinne – Rinne, whatever – and Weber test. So, we want to determine if there’s conductive loss, meaning anything from out here into where the actual cochlea is, where the nerve is. Sensory neural is everything from the cochlea into the brain. Right? So, conductive loss could be, “I’ve got a roach stuck in my ear,” “I’ve got cerumen stuck in my ear,” “I’ve got a ruptured tympanic membrane,” “I’ve got an infection in my middle ear,” “I’ve got otosclerosis.” There’s some sort of conductive hearing loss. Sensory neural hearing loss could be anything from the actual receptor organ all the way into the central nervous system – right? – which is central hearing loss. Okay?

So, what we find here is, we have Weber and then we have Rinne. We have to really determine: “Which side do you not hear out of?” Like, some people will say, “I can’t hear out of my right ear.” Some people will say, “I can’t hear out of my left ear.” Some people will say, “I can’t hear anything.” Some people will say this: “I have auditory discrimination issues.” They don’t know right from left. Okay? You can do simple tests, like, “Tell me when you hear this.”

Do you hear it? Okay. Tell me when you hear this. Okay.

So, let’s exaggerate a little bit, and say she heard it out here, and then she heard this one right in here. These are really rough tests. These are finger-rub tests. So you’re like, “Wow, maybe she doesn’t hear well here. I don’t know.” And then you take this tuning fork, and you go… some people put it here, some people put it in the middle, some people put it over the nose, some people put it under the nose. What you’re doing is, you’re just conducting, okay?

Now, with conductive hearing loss, which way does this lateralize? The noise, which way does it lateralize? Toward the affected ear, right? If it’s sensory neural hearing loss, it’ll lateralize the other direction. One way to do it is just stick your finger in your ear and go, “Mmmmm… Which side do you hear better?” You hear the plugged side better, because there’s no ambient noise coming in, or outside noise coming in. So when you look at this, whenever you have normal findings, Weber is equal in both sides, and your Rinne tests – or your Rinne tests – you come over hear, you put this on the mastoid, and then they say… And


you’re just like, “Hey, tell me when you don’t hear this any more, and they’re like, “Okay, I don’t hear it.” And then you go like this, and you’re like, “Do you hear it?” And they’re like, “Yes.”

[1:20.07]

So, air conduction is greater than bone conduction. That’s normal. Okay? So what happens is, with normal findings, Weber is equal in both ears, and then when you do your Rinne test, air conduction is greater than bone conduction. That’s normal. Okay?

Now, you still don’t know if there’s a little bit of loss in one ear versus the other. You can just say this: It’s not asymmetric, okay? But let’s say that your Weber test lateralizes to the deaf ear greater than the good ear. And your bone conduction is greater than air conduction on the side that the deaf ear’s on. Well, that’s conductive hearing loss, right? Well, then you come over here, and you look at sensory neural deafness. It actually… Weber test lateralizes to the good ear, and air conduction is greater than bone conduction. So whenever you look at this, this is just one little chart that’ll help you interpret it.

Here’s another one. Hearing; Weber; hearing from both ears; conductive, lateralizes sound to the affected ear; sensory neural, best heard by the non-involved ear. This is just looking at the Weber test. The Rinne test helps you determine if you have conduction greater than air. It’s not as accurate as the Weber test. It’s really nice just to know this: Which side doesn’t work well? And does it lateralize to that side when you do Weber?

Now, it may lateralize over here with conductive loss, but then you don’t… Then you have bone conduction greater than air conduction over here, and you may end up with, like, sensory neural hearing loss on one side and conductive hearing loss on the other. Or, maybe you just have bilateral bone conduction greater than air conduction, and you’re just losing hearing on both sides. Presbycusis. Okay?

This is another chart that is really, really easy to use, and I didn’t… I’m going to throw… I’ll throw these charts up for you, okay? But this right here just summarizes everything I just said. Sensory neural hearing loss, mixed hearing loss, conductive loss, and you can see right here, conductive loss. It lateralizes to the affected ear. Sensory neural loss lateralizes to the unaffected ear. Mixed, you may lateralize to the unaffected ear away from the affected ear, meaning you have bone greater than air on one side, but conductive to the other. So you have a mixed presentation. Okay?

I just taught you that because some people don’t even understand that. They’re like, “ I don’t know what conductive loss means,” and I want you to understand that when you have labyrinthitis, that might be sensory neural hearing loss. If you have otosclerosis, that might be conductive hearing loss. And that is the one thing, ladies and gentlemen, that helps you to understand the difference between the freaking two. Everything’s out of the external auditory canal. The tympanic membrane looks good, but there’s conductive hearing loss in a female at that age with hormones – I’m giving you the perfect scenario – and it’s conduc-tive hearing loss. It’s clear. Then you might start thinking, “Man, there’s some otosclerosis here. Okay?” Whereas, if it’s labyrinthitis, or if it’s an acoustic neuroma, and you have hearing loss, that’s sensory neural.

So, understanding this lateralization actually means more than people think, and I very seldomly see anybody in the neurology world do these tests, trying to differentially diagnose peripheral vestibular pathologies.


So, when we have something like, you know, any of these things – neuronitis, labyrinthitis – we have to do head thrust tests to see if we have what? Unilateral weakness. And then we have to do head shake, and stop to see if we have post-head-shake nystagmus by the decay in the velocity storage mechanism.

And then we do one other test that’s really cool. Watch this. So it’s, like, you know your little Snellen chart, and your eye charts? When somebody’s reading their chart, find the line that they can read, have them go up two lines, and just say this: Can you read it? And guess what’ll happen to them whenever they have a loss in their VOR in one side versus the other? They lose at least one to two lines of reading. Why? Because their retina, or their fovea, is slipping because their VOR is gone. And then you can do this: “Tell me if you can read this one like this.” What am I doing? Activating the left side. They’re like, “Yeah, that’s not too bad.” “Now tell me about this one.” “Oh man, that one gets blurry.” Boom, right there. That’s a whole lot better than going zztt – “Did I see it?”

You see how easy it is? I mean, you can teach your staff to do this. It’s so easy. It’s just like, “Tell me about your visual acuity here,” and they’re like, “It’s not good.” “Tell me about your visual acuity here.” “Oh, it’s not that bad. It’s actually better.” Okay? That’s your visual acuity, man. And then hearing tests, which is what I just showed you. Sideline may make it worse. This is neuronitis. Okay? So, typically neither. What is the difference between BPPV and neuronitis? Neither one of them… I’ll summarize these in just a second, but you have this slide.

Labyrinthitis… Guys, it’s basically what? Infection. CBC may show a nigh neutrophil count. It may show a high white count. They may say, “My ear freaking hurts!” Sometimes you can contuse the labyrinth from a car accident. “Bam! I hit my head. The whole freaking thing is swollen up.” So no matter what you do, they have all the canals messed up, everything’s irritated, and it looks… it feels terrible, and there’s hearing loss, and there’s ringing in the ear. So when we do this test, we have to actually test for hearing. We’ve got to maybe sometimes look for pharmacological intervention. We’ve got to look for all the things that look for a unilateral vestibular weakness.

So here we go. Ready? Vertigo. Nystagmus. Fixation. Horizontal. Spontaneous. First- or second-degree, it doesn’t matter. Goes to peripheral vestibular pathology. There’s hearing loss. There’s no aural fullness. It’s labyrinthitis. What would happen if there was aural fullness? Meaning pressure in the ear? “Augh!” And they have these events that are… where they just fall down, and they have these events where they have hearing loss and it comes back? That’s what? Ménière’s. So cool.

So, these people. Same thing as neuronitis. Okay? It’s associated with nausea and nystagmus, terrible dizziness, gait instability, and positional provocation. Trauma and infection that goes beyond the vestibular portion of the nerve sometimes. It has hearing changes. Neuronitis doesn’t. Guys, look. Send them out to get audiometric tests. They’ll just map it right out and say, “You know what? They’ve got hearing loss thirty percent on this side.” Cool? A little audiogram. Okay.

So, it’s the same practicum. It’s a head thrust test. It’s head shake test. It’s visual acuity. And then it’s hearing. How do you diagnose really neuronitis versus labyrinthitis? That last test. Hearing, and then labs. Virus, very common in neuronitis. Bacteria, very common in labyrinthitis. Trauma, very common. You can contuse the labyrinth.


Otosclerosis. I just want to read a couple things to you. So now, we have vertigo, nystagmus, horizontal with some… maybe some mixed torsional. Spontaneous first-degree, maybe second-degree. Hearing loss. There’s no barotrauma. It’s not labyrinthitis. They haven’t had an infection. It’s not as easy to get the nystagmus. It’s not like neuronitis. They just pretty much start losing their hearing. The nystagmus is not as great as the hearing loss. With neuronitis and labyrinthitis, the nystagmus is greater than the hearing loss. That’s the two. You see the two big differences? Okay.

Almost done here.

That’s otosclerosis, familial disposition, bone and metabolism disorders, and you can start to see these ossicles start to have problems. Now, this is your viral history and your bacterial. This is just a repeat slide of what Dr. Kharrazian already kind of gave you. So we know the difference between neuronitis, labyrinthitis, and otosclerosis. We just went through those. Very, very important we understand those.

Now, last thing is Ménière’s disease, and fistulas. So, let me just talk about fistulas. Fistula and dehiscence is where the top of the posterior canal blows off. The round or the oval window blows out. Now, could I have pressure coming in that makes them implosive? Yes. Could I go ppllt and hold in a sneeze and make it – phhw – explosive? Get your otoscope and your insufflation bulb, and stick that in there, and make a seal, and pump air, and you start seeing torsional nystagmus, and they start feeling bad. Guys, that’s pathognomonic for fistula. And then say, “Hey, bear down and do a Valsalva.” And they’re like, “Ooh, no. That’s not good for me at all.”

And then you start asking questions. “Have you been lifting weights? Have you been straining? Have you been constipated? Have you been sneezing?”

[1:30]

So when you do these things, you need to understand that with Ménière’s disease, they’re going to have these unilateral vestibular weaknesses, they’re going to have hearing loss that’s high-frequency and low-frequency. So if you think it’s Ménière’s disease, and they have all these things… And let me kind of trace through what I think Ménière’s disease looks like for you, okay?

Ménière’s disease, ready? Vertigo, nystagmus, there, spontaneous, episodic, hearing loss, aural fullness. They need this, they have tinnitus. It’s hydrops. So let me just show you something real quick. This right here expands. Dr. Kharrazian showed you a video of that. But what’s really cool is, this criteria – I just want to show you something real quick; this is just repeat – this criteria right here. If they have episodic vertigo, maybe. Definite, like, episode with some audiometric changes and tinnitus and fullness in the ear, yes. Certain is histopathologic. But definitive is two or more episodes of at least twenty minutes, audiometric testing that shows it, ringing in the ear with the fullness. That’s definite Ménière’s disease. And yes, they’ll have all the unilateral vestibular weakness whenever they have their episodes.

We’re rounding third base here, okay?

So, you do your head-thrust tests, you do your head-shake test, you do… Let me show you an easy way to test for a fistula. Just get your hand, put it over the ear, and just do pressure. You see I’m making pressure


in your ear? And if they have it, they’ll go, “Oh, oh.” You don’t have to have the insufflation bulb. You can just do a pumping compression like this. Okay?

With Ménière’s there really is nothing. It’s: Do the audiometric testing, and the audiologist will say, “This looks like a Ménière’s presentation.” That’s exactly what they’re going to say. And then you’re going to use your criteria. For a fistula, you’re going to use your pressure tests. Okay? I had a fistula. I used to be a professional stunt man, and I was a platform diver, and I smacked my head on the water, and it blew out all the membranes all the way in one ear, okay? So I had to go through treatment for that.

And these are your fistulas. I just want to go through them real quick. Again, we did the Valsalva, and we do the Hennebert’s test, and we look for these little leaks in the perilymph, and we do these provocative tests. Now, you can also get a noise inducer, that’s like deeeee, that makes a high-frequency noise, and you put it near them, and they may pass out. So pressure and noises. That’s called a Tullio effect. And they hate it.

So, I have a noise device that puts a loud noise in their ear, and they start getting nystagmus; a Tulliometer. And then there’s another device that is just your otoscope with pressure. That starts to create nystagmus and problems. And look: Vertigo. Nystagmus. All the way through spontaneous maybe, peripheral vestibular pathology, hearing loss, barotrauma, fistula or dehiscence. Barotrauma meaning Valsalva, a diving accident, something happened, there was… They’re like this: “Dude, I got off an airplane; now I have dizziness.” Okay? They may have a patulous Eustachian tube with that.

Fistulas are common. You may break the round or oval windows. There may be barotrauma. Absence of the bone over the superior canal: that’s dehiscence. That’s where you hear the clicking in your eyes. So, that’s this part up here that’s been broken. It pops off so the perilymph leaks out, so now every time you do something in your head, it conducts into the labyrinthine system and you hear it, so you hear your own voice – autophony – or you actually hear your eyes clicking, and that is when you know the difference between superior canal dehiscence and an actual fistula of the round or oval windows down here. And this just describes the round and oval windows breaking, and that loud noises and pressure on the ear makes the eyes jump or have nystagmus, and it’s pretty rare. This guy right here: A perfect candidate for one. You can see him straining. And can be aggravated by loud noises. Again, often present with dizziness; worse with pressure changes. And these people, they can’t lift weights any more. Okay? It’s in the horizontal plane, described as sensation of oscillopsia, where they eyes are jumping up and down. So when you lose your VOR, as you walk your eyes will do opposite of what you’re body’s doing, so it looks like the room is moving like this, because your eyes aren’t moving the same speed as your body. So you get perception changes.

And that, ladies and gentlemen, as we do this, there’s your Tullio phenomenon and your Valsalva. Really rounds the corner of everything that we would do, between fistulas, hydrop, neuronitis, labyrinthitis, and BPPV.

Summary. Can you do positional tests? Can you do hearing tests? Can you look for unilateral weakness? That’s the things that we want to know. And then can you say this? “Can I do some labs to look for bacteria, to look for viruses, to look for white blood cell counts?” And then, “Can I do imaging?” “Can I do imaging?” Okay.


So, as we go into the next module, or the next part of the module, after lunch, I’m going to jump into the treatment of some of these. Like, how do I treat all those positional pathologies? And how do I treat fixation problems? And then how do we start to progress through helping some of these people get better, not just identify them? Hopefully you’re getting to the point where you can identify these a little bit better. How many of you can identify these a little bit better? Good. The canals, they get trickier than people think. Cool?

So now we have lunch ’til – I don’t know – one thirty, right? Okay. Everybody enjoy your lunch. Thank you.

Thank you so much. “Thank you.”

[1:36.25]

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