PeriPheral Vestibular and Cerebellum disorders with ... filevertigo and dizziness, but sometimes people have dysfunction of the vestibular system, and that might change their core

MODULE FOUR TRANSCRIPT: NEURO INTEGRATION VESTIBULAR | COPyRIGhT © 2016 FUNCTIONAL NEUROLOGy SEMINARS LP | PAGE 1

PeriPheral Vestibular and Cerebellum disorders with aPPliCations (module Four)

transcript – neurological integration of the Vestibular system

Presentation by dr. datis Kharrazian

Okay, if you guys are ready, let’s get into this next section. So, as we go through the material this weekend, what we’re going to review right now is just the pathways involved with the vestibular system: neurological integration of the system. So, what I’m going to cover is how the vestibular system fires into autonomic centers, how the vestibular system fires into centers for eye movement, how the vestibular system fires into vestibulospinal tracts for postural tone, and these… If you know your pathways, then you can use vestibular therapy for spinal stability, or you can do vestibular therapy to fire into the cortex, or to help with somatosensory integration, or to understand autonomics.

So, a lot of people that have vestibular disorders, first of all, they don’t always have to have dizziness, right? So we tend to focus on dizziness because we’re going to go over a bunch of diff-dis that are associated with vertigo and dizziness, but sometimes people have dysfunction of the vestibular system, and that might change their core stability, and they have neck and chronic back pain. Or the have vestibular disorders impacting their eye position, so they have chronic neck pain. Or they have vestibular disorders that are spontaneously firing into autonomic centers, so they have anxiety and nervousness, especially around movement and motion and crowded places. So it’s really common for people who have vestibular disorders to come in with symptoms that you may not even think are vestibular based.

So, the anxiety scenario is really a common thing. So lots of people that have anxiety, they feel like they have anxiety when they go to crowded places. Any time someone tells you they get anxiety when they go to crowded places, or things where a lot of things are going on, you should always consider they have a vestibular problem, because as people walk into their visual fields, and things are moving, and the brain’s trying to readjust to where they are, there could be a vestibular problem. So a lot of chronic anxiety disorders, many times, are vestibular.

We know that lots of chronic cases of nausea have a vestibular component, because projections from the vestibulocerebellum fire right into the pontine areas where you have vagal activity.

We know that a lot of people that, again, have chronic neck, back weaknesses, tightnesses, they tend to come in and have vestibular disorders. So, the chief complaint to you may be chronic neck pain no one’s


been able to help. Chronic headaches that come from neck tightness. Anxiety. Chronic nausea. Those are all very common symptoms that people may have, unrelated to dizziness. So as we go through the pathways and you understand them, then you can learn how to use the vestibular system to treat them, and also to evaluate the vestibular system to know if those pathways are involved. Okay?

So, here’s an example of what I mean. If someone comes into your office and they have anxiety, and they tell you that they have anxiety when they’re around crowded environments or things are moving, what if you put them on a pulse-ox, measure the heart rate, then you try to rotate them in a chair a few times, and their heart rate goes up fifteen points? What did you just find out? Their vestibular system is firing into their autonomic centers. What if you turn them a few times and their blood pressure, their heart rate just goes down? Well, they’re firing into their pontine centers more, which are going to have a parasympathetic effect. So you have projections sometimes that are sympathetic, you have some symptoms… projections that are sometimes parasympathetic as they go into the pontine areas, but I’ll show you all those different types of pathways, right? You can sometimes just have a person move their eye to one side and they can tell you that their neck tightness is getting much worse, and they have, let’s say, chronic right-sided neck tightness.

So, like everything else, if you understand the pathways, then you can go through and figure these things out. So we’ll go into applications of those as we go over the pathways.

So, we’re going to go into neurological integration of the vestibular system, and then after my… after this presentation we’ll have a break, and then Dr. Brock is going to go into how to diff-di each one of these associ-ated with dizziness. But what I want to do is, not really focus so much on the dizziness, but the pathways, and then some of the clinical patterns that happen involving these pathways that have nothing to do with dizziness. So you kind of see the whole approach to how we look at the vestibular system.

So, this is the vestibular apparatus. You guys are all familiar with this. Remember, you have the canals, and then you have the otolith, which includes the utricle and the saccule, and then the vestibular nerve and the cochlea. So the snail-shaped structure is the cochlea; that’s involved with the auditory nerve for sound perception. And then you have the canals which are involved with rotation, and then you have the utricles and saccules involved with translation.

I’m just going to review everything, assuming you’ve never heard this before, just to make sure everyone’s on the same page. Okay? So, translation forward and back, translation to the side, or translation up and down, is all involving the otolith. The otolith are your saccules and utricles. Your saccules go up and they go down. Translation this way, that sense, because of the position of their structures, their receptors, as you go up and down, that’s involving the saccule. So what happens with people that have symptoms when they’re in an elevator? Now, what kind of symptoms could they have? If their saccular and their vestibular integration is off, let’s say they go to an elevator that stops quickly, or they go up, or even people that fly in a plane, as they go up.

But as you get in that translation, the body up or down, or they watch a movie, and the movie, there’s something bouncing, going up and down like that, and they have some symptoms, then you know that there’s a utricle involvement. So when you see people that have vertical translation symptoms, you know there’s something going on with the utricles. Okay?


Now, their symptoms may not be dizziness. Now, sometimes they’ll just say disorientation, so on the questionnaire form, one of the questions is, you know, “Do you notice any symptoms going up and down in translation, like an elevator?” So we have a lot of these things screened for you so you know where they are, as Dr. Brock was in the form for you.

But just so you understand the basic concepts, if you’re going up and down like that, that’s involving the saccule. Okay?

Now, some of the symptoms could just be they have a vascular phenomenon. Because as we look in the vestibular system, the vestibular system fires right into the autonomics. Now, here’s how this works. The vestibular system fires to the areas of the midbrain which create a sympathetic response – which I’ll show you some diagrams – and they fire to areas of the pontine area where you have a parasympathetic response, and the balance of that temporal summation of how they’re firing into each of these centers, and the pontine areas, and to the midbrain areas, they have to be integrated at the same timing to have proper autonomics.

When people have vestibular disorders, vestibulocerebellum disorders, they can be off. So someone can go up in an elevator like this, and get nausea, and someone else can go up an elevator like this and get a saccule response, and then they have actual dizziness, and someone else can go up and they get anxiety. So you always have one of the side effects of the vestibular escape, or vestibular cerebellum integration issue, autonomic symptoms. It’s really common. There’s a lot of dysautonomias promoted by vestibulocerebellum pathways. The reason is, is because your vestibular apparatus and your movements fire into autonomic centers, so you properly shunt blood flow, have proper amounts of vasoconstriction, vasodilation, so you don’t pass out, you don’t fall. So the vestibular system has a direct input into autonomics. So when it’s not functioning well, certain positions or movements can give you clues of what you… of which part of the vestibular system is involved. So, any time you guys here some kind of symptomology, autonomic, or dizziness because of rotation up and down, you’re going to be thinking about the saccules, and then your therapy should be what? Oriented towards the saccules. Okay?

Now, sometimes people have utricle translation issues. So, utricles are involved with forward and back, and side to side. So, what if someone has symptoms when someone stops the car suddenly? So they put on the brakes quickly, and they get vertigo, or they get anxiety, or they get flushing, or they get a vascular phenomenon, or they get nausea. That means their utricle integration is off. Right? So either forward or back, and also side to side. Okay? So if someone’s going side to side, which is not as common. But some-times… You guys, remember: Sometimes people watching shows, they’ll see these things. The movement that… movies that come out where they’re in the ocean, and waves are hitting, and things are moving, that make people sick, you know that that’s pretty much vestibular based, okay?

So, those are the movements. Up and down, saccule; utricle, anterior and posterior translation and side to side. So, one of the things you… It’s always a clue to you if someone says, “Yeah, I get dizziness.” “What causes your dizziness?” And they tell you, “You know, I hate the way my husband drives. I always get dizzy.” “Why?” “Because he just puts on the brakes, and I get symptoms.” That’s utricle. Right? So this is the first thing to understand about the anatomy and the orientation. Okay. So, there’s your utricle and saccule. Those are part of the otolith. Those are considered the otolith glands.


And then you have the anterior canal, posterior canal, and horizontal canal. And these are… Everything that we’re talking about, with these receptors, they’re completely involved with your head moving. So these are receptors that are perceiving where your head is in space, right? Whether it’s translation or rotation. So, rotation to the left, left horizontal canal; rotation to the right, right horizontal canal; rotation this way, left anterior canal; right anterior canal; left posterior canal; and right posterior canal. Right? So those are the things. And listen: If you bend forward, like this, you’re getting, at the same time, bilateral and anterior canal, and you’re getting utricle.

[10.00]

If you bring your head back, you’re getting bilateral posterior canal and utricle activity. Some of it is rotation, some of it is translation. So they do have integration between each of their two, because those are the key things with it. So, when you look at these canals, these become important.

Now, if someone comes in and tells you they have dizziness or vertigo, or… So, if you see someone move to one side… Like, you can have patients that have dizziness and vertigo and go, “Hey, just… I want you to visualize spinning to the left. How do you feel?” They might just tell you, they get dizzy or disoriented. “Visualize moving to the right.” Because as you visualize it, you actually activate some of those receptors. You have people on VNG goggles, and you have them visualize it; you actually see some nystagmus take place. Okay.

So, it’s always important to know, as you dissect these canals, from an integration point of view, if their symptoms are rotational, going forward, going back, up or down, to know what part of the vestibular system may have some issues in it. Just the basic concept point of view. Okay? One of the most common non-dizziness symptoms of vestibular disorders are dysautonomias, either in parasympathetic or sympathetic. Okay? So don’t always fix it on dizziness. This module is not just on dizziness. It’s about understanding the vestibular system.

I’m going to show you guys a video that has a really cool illustration of how these fluid exchanges and hair cells and otoconia all work. Just make sure you can see it in animation. Ready?

The human ear is divided into three compartments: the external ear, middle ear, and inner ear. The inner ear contains the spiral-shaped cochlea, where soundwaves are transduced into neural signals, and the vestibular complex, which contains the receptors for our sense of equilibrium. The central egg-shaped cavity is the vestibule, which contains a pair of membranous sacs: the saccule and the utricle. Inside the utricle and saccule are hair cells similar to those in the organ of Corti. The hairs are clustered in the macula, where their processes are embedded in a gelatinous mass, and lie under a thin layer of crystals called otoliths. When the head tilts, gravity moves the crystal mass, and distorts the stereocilia of the hair cells. This is how the saccule and utricle provide information about position with respect to gravity. Behind the vestibule is the third portion of the bony labyrinth known as the semicircular canals. The canals project from the posterior region of the vestibule, and are responsible for the detection of head motion in three spatial planes. The anterior ducts senses forward and backward motion. The posterior duct detects moving up and down. The lateral duct senses moving left to right. Each canal contains a membranous semicircular


duct, where angular momentum is sensed. At the base of each duct is an expansion called the ampulla. Within the ampulla, long stereocilia of hair cells are embedded in the cupula, which sticks out into the endolymph. When your head moves, the endolymph moves the cupula, and stimulates the stereocilia.

Okay? It’s nice to see an illustration. Let me show you another one. So, let me go back here. You know, one of the things here is if you look at the utricle and saccule, the vestibule, the otolith system, this is where they have the… they’re weighted down. These hair cells don’t have fluid that’s really in the canal that’s moving them; they have those crystals on top, and those crystals weigh them down so as you move, those things translate it. It’s those crystals that can break off and go into the posterior canal, that then cause benign positional vertigo, right? In the canals, you have these ampullas where you have the hair cells, where fluid then starts to move them, either to excite them or to inhibit them as you go one way or the other.

So, let me show you some illustrations of that. So, here you can see illustration of head rotation, and then what’s happening to the stereocilia, the hair cells, as a person moves. Okay? One more time. This is the horizontal canal. You can see…

Now, when you turn your head to the left, you turn on your left horizontal canal, because the fluid move displaces the hair cells this way. But on the right, the way the fluids move, they move the hair cells in an opposite direction and you inhibit. Because you excite one canal, you inhibit the other. So you can see this counterbalancing. So this person’s illustration, rotating to the right. So the right side gets activated, left side gets inhibited. Okay? Show you one more time. Okay.

Now, as we move on, here’s an illustration of the utricles and saccules. So, these have these heavy crystals on top of the hair cells, so as they translate up and down, you can see some activity. So let’s watch this. One more time. Okay. These are angular, but more of a pure vertical would have some effect. Okay.

So that’s just the basic review of the receptors. Everybody okay with that? You have canals that are involved with rotation, and you have utricles for translation forward and back, up and down. Right? Very simple. And patient symptoms could be in one of those specific regions, and those are the receptors that are involved. This is primarily with the head. It has nothing to do with the rest of the limbs and the body. These peripheral receptors in the vestibular apparatus then have an effect on the cortex, primarily on the right side. The parietal insular vestibular cortex. We’ll go over that. But then this area coordinates information from your parietal lobes about your somatosensory cortex, from your cerebellum integration, and then from your visual pathways, to then let you know where you are in space. Okay?

Most of the input from these peripheral vestibular receptors, even though they have bilateral projections, have their effect on the right side. This is just like hemineglect. Hemineglect, or injuries to the right brain, impact central perception, loss of visual perception, the hemineglect pattern. Lesions of the right brain also cause injury, especially in the parietal temporal region, to the vestibular cortex in a sense. So you can have disintegration of your vestibular system that’s really cortical based instead of being cerebellar and vestibular based. So we’ll go through all the different pathways involved.

Before we go any further, let’s go… We’ve gone from the receptor; you guys understand utricles and sac-cules, semicircular canals. Let’s now go into the vestibular nuclei.


So when you look in the brainstem, as you look through here, you can see what’s cut here are the cerebellar peduncles, so the cerebellar peduncles are cut. You can see the brainstem here, and this is the posterior brainstem. And one of the things that you’ll see is that there are four vestibular nuclei: superior vestibular nuclei, lateral vestibular nuclei, medial vestibular nuclei, and inferior vestibular nuclei. So input from the semicircular canals, from the utricles, from the saccules, they integrate into these vestibular nuclei. Okay? The vestibular nuclei then have projections. The vestibular nuclei have projections into a pathway called the medial longitudinal fasciculus, which is involved with the vestibulo-ocular reflex, and conjugate eye movement. So if you move your eye one way, you have equal movement between your left and right eye at the same speed, so you don’t have disconjugate gaze. Okay? So you don’t end up with double vision. Your medial longitudinal fasciculus So, your vestibular ocular reflex means, when you turn your head to one side, the eyes go to the opposite side, right? So if I turn my eye and head to the right, I activate my right medial rectus – right? – and my left lateral rectus. When I bring my head back in a right posterior canal position, I activate my right superior oblique, left inferior rectus. If I turn my head right, to this position here (right anterior canal) – right? – I’m going to get my right superior rectus and my left inferior oblique.

So, those are the basic muscles that are involved with this vestibulo-ocular reflex. If you didn’t have those muscles integrating properly through this medial longitudinal fasciculus, you would have double vision. And some people do. When people have injury or compromise to the medial longitudinal fasciculus, which is a common area of lesions in multiple sclerosis, people will get disconjugate eye movements with that.

So, these vestibular nuclei project up as a tract to the medial longitudinal fasciculus, to help with eye muscle coordination for conjugate eye movement, and there’s also a descending pathway, called the lateral vestibulospinal tract, and the descending medial longitudinal fasciculus.

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The descending medial longitudinal fasciculus is also in textbooks as the medial vestibulospinal tract. Okay? It’s just the area of it. The descending medial longitudinal fasciculus, or the… also known a the medial vestibulospinal tract, is what controls intrinsic muscles of the neck. The lateral spinal tract –lateral vestibu-lospinal tract – controls your intrinsic spinal tone all the way down your spine, and even has impacts on your legs and even your arms as you rotate. Okay? So if you turn your head to the right, and you activate your right vestibular system, you get projections into your vestibulospinal tracts, which activates extensors and muscles so you don’t fall over. Right? So your head positions have immediate impact on it. And sometimes you can even just put your hands here and just move your eyes to… Just put your hands on your right side, okay? And then move your eyes to the left. Do you feel those muscles contract? This is why a lot of times we’ll do eye therapy to activate vestibulospinal integration. Okay? So if you’re going to rotate your head to the right, which way should your eyes move? Left. So put your hands on the right, move your eyes to the left. Move your eyes to the right. And if you put your hands and move to the opposite side, you can feel those muscles contract. Right? So, there’s this integration between these pathways with eye movements, and then intrinsic spinal tone, which are important for us.

Now, I’m going to show you each of these in detail, and then make it a little bit more clinical. So, here’s an illustration. Here you can see ocular motor nuclei, trochlear nuclei, abducens nuclei. So these are the… So, the trochlear nuclei innervates superior oblique, abducens the lateral rectus, ocular motor all the other eye muscles, right? So here we go.


Here’s a nice illustration. You see input coming from the vestibulospinal tract, they hit each of these eye muscle nuclei, and they go all the way up to control integration, and then eventually to the thalamus. There’s projections from the vestibular nuclei to the thalamus, to the parietal insular vestibular cortex too, but we’re just talking about the vestibulo-ocular reflex itself.

So, here’s a scenario. You check someone’s… You check someone in a Romberg position, right? And then we did this in the workshop the other night. But you check someone in Romberg’s position. Then you put them in a tandem Romberg, and you see if they have any sway. Now, you can check the integrity of their vestibular system by putting them in different head positions, right? So you put someone in a right posterior canal, or horizontal, or anterior, they may totally shift. So they may be like this, and then you put them in anterior canal and they start to get worse. Or you put them in posterior canal, and they get worse. Or, they’re totally off, and you put them in one position and they get better. So if they had imbalances and you put on a position and they get better, maybe that’s the area you rehab. If it’s an area that it gets worse, maybe that’s the area that you rehab. So you have to figure out which one is involved. And then the only way you know how appropriate it is, is if you try some stimulation in the area, so maybe you do some head tilts in one direction, and then see if it makes their balance improve or get worse, and that will dictate what you need to do for rehabilitation.

So, we can use those in the clinical model to see what’s going on. Okay?

Now, there’s also the vestibular integration to eye movements, which we talked about. So let me show you this here. So, the vestibular projections come in, they go into the vestibular nuclei, and the brainstem, and then these go up to the medial longitudinal fasciculus, where they coordinate eye movements.

And this the illustration of what’s happening with the canals. The canals fire into the vestibular nuclei, the vestibular nuclei fires to the medial longitudinal fasciculus, which then excites or inhibits muscles, so you have proper vestibulo-ocular reflexes.

So, one of the things, like, you know, you can do clinically is, you look at someone, take someone’s head, and when you move them to the right, what should happen to the eyes? Left. And then you go the other way, you should… What happens when you put them in the posterior canal? The eyes should go down and out. You put them this way, the eyes should go down and out. You bring them to the anterior canal, they should go up to the same side, and up to the same side. So you can actually evaluate their vestibular system, cerebral ocular reflexes, just by having them, as you check their eye movements. Right? It’s better if you have VNG goggles, because then they’re in darkness, and you can actually see them; they’re not fixating on anything. But you don’t necessarily have to have it to see the… to do it. So here’s an illustration of that. Just muscles being turned on and turned off in a sequence for conjugate eye activity.

Alright. Now, one of the things you’ll see when people have vestibulo-ocular reflex issues is, when they turn their head, they get double vision. That’s potentially an MLF problem, Okay? I want to show you an illustration of vestibulo-ocular reflex that’s normal. So, here’s an ice skater, and here’s what you’re going to see. She’s going to start to spin herself to the left, over and over and over and over again. She’s just going to spin. She’s going to keep spinning to the left. So, as she does that, what happens to the fluid in her ear? And with her canal, which canal? Horizontal canal, because she’s rotating in a plane, is going to get activated. And the left one’s going to get activated; what’s going to happen to the right? It’s going to get


inhibited, just from the direction of how these hair cells are moving from the fluids, right? So she does that for a while, and then she stops, and then she looks in the camera, and you’re going to see her nystagmus develop, which is normal. This is what should happen – okay? – when you get that much activation. So when she stops, the fluid in her ear canals are still going, even though she’s stopped. That’s why you see that nystagmus beating, because the fluid’s still there activating this medial longitudinal fasciculus, through this vestibulo-ocular reflex, and causing that change.

Now, remember that when you activate the left vestibular system, the eyes go which way? They shift to the right. Right? And just so you have gaze, when you turn your head you want to make sure you don’t lose your vision. And then that’s a slow phase, and then the fast phase would be what? It would be the frontal eye fields pushing back over. So you’re there, boom. Pushing back over. So she spins to the left, and then she stops, what should you see? You should see a left or right fast-beat nystagmus? You should see a left fast-beat nystagmus. So that’s the side that you have increased activity for. Okay? So take a look.

Completely normal. You would expect to see that.

Right? Okay. I’ll show you another example. Now, here’s the situation with this one. This person’s holding a camera, and they’re spinning to the right. Okay? They’re going to do it for a while, and they’re going to stop. And once they stop, the same thing happens. Fluid’s still going, so which side should the fast-beat nystagmus be? So they’re moving, so it’s going to be to the right side, because he’s activated that, so you’re going to see the fast-beat-to-the-right component. Okay?

Now if this is making you dizzy, that’s also diagnostic that you probably have a vestibular problem; vestibu-locerebellar integration issue. Or if it’s making you nauseous. Or if it’s giving you anxiety, because this is the projections that take place. You guys see that? So, in any plane, if you keep moving them, fluid keeps moving, and you have those changes.

So just remember: The vestibular system pushes eyes slowly to the opposite side, and then comes back in a fast beat. The side where the fast beat is coming to is the side where you have the activity taking place; there’s an increased activity to that vestibular apparatus. Okay?

And this is, you know, vestibulo-ocular reflex tests. What he’s going to do is, he’s going to put this patient in all the different canal positions and look at her eyes. As she puts the head in positions, the eyes should go in the correct opposite directions, right?

I want you to look at the point right at the very distant part of that wall. Keep focused right there and don’t move your eyes. Keep focused. I’m going to turn your head quickly, but you keep looking over there.

This is the head thrust test.

Now up and down. [?]

So you could do this specific for each canal, right? Okay.


Now, the other thing you could do is, you can just take people and you can have them close their eyes and put them in each canal position and see if they get any symptoms. Because you take out their visual input; they’re really counting on their vestibular system to determine where they area.

Now, another test that is commonly used to assess the integrity of the vestibular system and integrity of the brainstem is the caloric test. Right? So you basically take warm or cold water – this is an illustration of cold water – and then, cold water inhibits the same side; warm water stimulates it. So here’s how this works. As you put cold… Now, I have a caloric machine in my office, but it’s not water. I have one with air, because I don’t want the mess. So I have this machine to go in there, and I put something in the ear, and it can put out hot air or cold air, the exact temperatures I need, and then I can assess the vestibular system. So you can do it with, you know, a five-dollar plastic syringe for calorics, that you can get anywhere – right? – Amazon, even, and then you can do your caloric testing that way. You’ve just got to make sure you have the right temperature for those, actually warm, actually cold, right? And then you can check the system out.

So, as you get temperature, the cold or warm water hit the eardrum, the eardrum changes its temperature, and then so do the fluids behind the ear.

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Cold decreases nerve conduction, and warm increases nerve conduction. So if you put cold water, let’s say in this example, on the right ear, what should happen? Well, I’m putting cold water in, and that’s going to change the temperature of my eardrum and the fluids behind it, and it’s going to decrease nerve conductance. So then this side is now dominant; becomes overactive. So then this side’s going to push the eyes away, and then it’s going to come back fast. So I’m going to see a fast beat on the left side when I inhibit this. Okay? Alright.

Now, I’ve got to show you this video. It’s so funny. It’s an actual person doing a caloric test on themselves, with his buddies, and he’s experiencing the… going through the experience. Now, if you guys have never done caloric testing on yourselves, it can totally mess you up. Just so you know. I remember the first time I had it done to me, I was off balance and weird for like a day or two, and I usually always have pretty good balance. So, what they’re doing in this video is, they’re putting cold water in their right ear. Since they’re having guys do it to each other, and torture each other, and throw up, and get dizzy and nausea for a few days… Just watch what happens to a person going through it. Okay?

So. “No, that’s fine. Aw, that’s done straight. That’s good.” Let’s see. I don’t know what…”

They have music

“Oh, it’s painful.” That’s a great song. “It does hurt.” Can you put your head straight? Look up. “I might fall out. Oh shit, I feel dizzy.” Good. “Oh my God. Do… I actually do, I feel dizzy.” Can you look… put your head like this? “Yeah. Okay, I feel a lot more dizzy when I look straight. And my eyes are going. There we go. Eyes… Oh shit! Oh God, I can’t!” What? “This is really weird.” Your eyes are going, I think. “I feel like… I feel as if…” Is that nystagmus showing? “I need to…” Yeah, that’s nystagmus. “I feel as if I’m spinning. Oh my God. Which way am I spinning? I feel like…” Yeah, you’ve got some wicked nystagmus then. “I feel like


everything’s going that way. It’s really weird.” Yeah. Oh, massive! Sick! “Oh my God! I feel like everything’s, like, scanning.” Yeah man, your eyes are just going mental. “Really?” Yeah. “Okay. Shall we let this settle down? And do the second part of the experiment?” Yeah. “Which is the warm water.” So… “Holy shit.” … first phase is… “Okay, so it’s worse if I… okay, now I’ll just try it. Someone do a…” Yeah, yeah. So… “Okay, so it’s gone now. I feel like I can control, because that’s what I mean to aim at.” What have you got… now come back this way. “It’s gone… slightly less nystagmus.” It’s gone. “It’s gone. But did you catch which way it went?” Yeah. Yeah. Well, we’ve got a kind of a…

When he goes in the fast phase, Alexander’s law, you can see it. He goes slow, phase two,

[unintelligible] “Go to my extremes.” Okay, yeah.

You can see it there. Okay. Though, anyway, I thought that was so funny, I wanted to share it with you. But that actually is what it’s like. Because when you… If you haven’t done it to yourself, and you want to try it, go for it. You’ll have the same experience. All of a sudden you’ll just see spinning, and you can see how the… at first you have tearing. So as the vestibular system gets activated, fires into the brainstem areas – right? – so you hit your inferior and superior salivatory nuclei, so you can get mouth production of saliva, you can start to have your eyes tearing, and then you start to turn. You can get autonomics, you can get anxiety, your body feels like it’s moving all over the place; that’s the caloric test.

Now, you can use it as therapy. So a lot of times, when you’re trying to activate a vestibular system, it’s not just diagnostic. You can use cold or warm water for therapy, but you’ve really got to make sure that’s what you need to do, because it’s very, very powerful stimulation. Okay? And one of the worst things you can do to a dizzy patient is to do this on them, because they will completely fall apart. I mean, they’re already fragile, and we start inhibiting, exciting pathways this aggressively, they can be in bed with dizziness and vertigo and disorientation for, I mean, several days afterwards; even a week or two, depending how compromised they are in their ability to recalibrate and integrate. Okay? So be careful with the test, but we use it for stimulation all the time.

You can use… You know, some people have always taken things like – if they want to do warm calorics – they have people get, like, a hair dryer, and then put a straw and a funnel into it, so they can put some warm water in their own ear. But you’ve got to be careful of those types of things. But they do work, as a way to get some activation to the vestibular system. Okay.

So, let’s talk about this tone pathway. So, you guys are all familiar… you guys all understand the vestibulo-ocular reflex, calorics, movement move to the opposite side, you can test the different ways.

Let’s get into this illustration here. So remember: These are descending pathways. So as vestibular pathways fire into the medial lateral vestibular nuclei, you get the medial and lateral vestibulospinal tract. They go all the way down, and what they do is, they activate the intrinsic spinal muscles. So again, these are the medial and lateral vestibular nuclei; they go down to projections, the medial mostly for neck muscles, the lateral all the way down to the spinal cord, and they increase the activity of the intrinsic spinal muscles.


So this is why, in a functional neurology approach, using vestibular therapies and treatments, and eye movements, and calorics, can be used many times to stabilize the spine. Okay? So when people have chronic postural instability – like that one video of that guy that you guys saw that had arm swing, and it kept getting worse all over the place, he was stooped over – he definitely needs some vestibulospinal activity to try to improve his tone. A lot of times, when you activate the vestibular system, people will just feel like they can stand up straighter, and they feel better.

So when you see people hunched over and… Even if you guys have – those of you that do manipulation – do manipulation, sometimes they’ll stand up more erect. That manipulation caused muscle spindle, Golgi tendon and activation, proprioception, hits the spinocerebellar pathways, goes to the cerebellum, fires to the vestibular nuclei; vestibular nuclei has the vestibulospinal tract, fires down to these intrinsic spinal muscles, and then improves their posture and tone. So that’s why it’s really common to see people who get any type of vestibular activity or manipulation, all of a sudden they feel like they’re more stable, and their straight, because of this projection. Okay?

Now, here’s something to look at. I’ve got another funny video for you to watch. I don’t know why these parents thought this was funny, but they did. So they take their child, they spin him in a chair, and their activating the vestibulospinal system, and then what you’ll see is, he has trunk… his trunk muscles pull him to one side.

Alright, get out. Alright, get out. Here we go. There we go. [laughter]

So you guys, every ride at an amusement park is totally based on manipulating your vestibular apparatus. Right? You go loops, things are moving, images, three-dimensional, you’re moving back and forth. It’s all there to get your vestibular system going. But as you fire your vestibular system, your brain is trying to not fall, so your autonomics go crazy, you get an adrenaline rush, and then you’re done, you go, “Wow! I feel great!” Because you had this huge adrenaline rush, because your vestibular system is trying to tell your brain, like, you’re dying and falling and all these things, and then you get that endorphin rush. So, you know, I mean if you spin yourself for a while, that’s kind of fun, and then you get dizzy, and you know, you can get some of that. But that’s really the whole point, is to have the activities in these areas of the brain, but that can help you.

Now, could this vestibulospinal defect be dysfunctional? So you’d have abnormal vestibular input, or asymmetry in a vestibular input from your right to your left vestibulospinal tract that can lead to scoliosis? Really? Is it published? That means it’s just, like, a theoretical thing? Yeah, you guys. It’s published. It’s been published for years. It has nothing to do with the chiropractic neurology world. This is well-known stuff for years. So, asymmetry of the vestibular system can cause different types of change.

So, they took… This is what I picked as a paper. There’s many papers, but I picked this one because you can actually see some really interesting images here. So, they go in here, and they have a control group, they leave their semicircular canals alone. They come in this group, they cause a lesion in the vestibulospinal system, and then they look at their spinal torsion. The one they left untouched, no change in their spine. The one they injured, their vestibular system, you see this torsional… this scoliosis start to develop. And then they imaged it. You can see control group, those that get their vestibular apparatus lesion. You can see that asymmetry of their vestibulospinal control, that starts to change their spinal system. So this was


the one that they can do in an animal study, because they can actually injure it. You can never do that in a human study, to do an asymmetrical lesion to one side, because no IRB would approve it.

[39.51]

But there have been other types of studies done, with actual humans, and kids that have idiopathic scoliosis, and you have this paper in your notes. But basically what it showed is that patients that have adolescent idiopathic scoliosis, they found without question that they have vestibular integration disorders. So this is another application of the vestibular system unrelated to dizziness. So whenever you see a patient come in that is complaining of scoliosis that’s unrelated to a hemivertebra or a bony abnormality, but just from postural tone, you want to get in there and really do a kick-butt job evaluating the vestibular system, and trying to integrate it and making it as efficient as possible, because that can impact those. Or, if you have someone that has chronically intrinsic spinal muscle tightness of one side or neck, tightness one side, these applications between the vestibular system are useful for that too, alright? Not just – again – dizziness. Okay.

Now, we’ve covered the vestibular apparatus firing into the intrinsic spinal muscles. We’ve covered going into the vestibulo-ocular reflex. Let’s talk about vestibular projections into the cerebellum. So, here you go. Here’s some illustrations. So, here’s the vestibular apparatus, goes into the vestibular nuclei, and then it fires into the cerebellum. Now, vestibular imbalances, peripheral vestibular disorders, are going to be more clinically pronounced, based on how healthy a person’s cerebellum is. So if someone has benign positional vertigo and has an otolithic crystal, or someone has some kind of vestibular neuritis that sends abnormal input to the cerebellum, if the cerebellum is really healthy, it can match and accommodate and calibrate for that, and there’s not that many symptoms. So you can have people that have a vestibular injury or some kind of peripheral vestibular compromise – maybe they have a perilymphatic fistula, or they have a hole; maybe they have benign positional vertigo; maybe they have Ménière’s – and they have these hydrops that pop every now and then that cause symptoms. So their recovery, and how well they do with the vestibular disorder has a lot to do with their cerebellum integrity. Okay?

So, with vestibular disorders, we still like to look at the cerebellum and try to improve function there. And when you look at the cerebellum, we have different parts of the cerebellum involved with different parts of balance and function. So, you guys see this red area? The midline vermis? And then you guys see the nodule? So, this is the flocculonodular vermal areas of the cerebellum. Those are the pathways that are directly involved with the vestibular nuclei. Okay? And when you take a look at this illustration, here you see the vestibular apparatus. It comes in, it fires into the vestibular nuclei, the vestibular nuclei fire into the midline cerebellum vermal areas, flocculonodular areas, and then input gets calibrated, interpreted, and then goes back to here. Now what’s also coming into the cerebellum? You have input from your cortex. You have input from your cortex going down your frontal pontine projections, so remember the pons has that big belly where you have all those pontine nuclei. So cortical projections go to the pontine nuclei, which then goes to the brachium pontis, into the cerebellum, and you have this integration happening all the time to cerebellum. At the same time, you have projections that are called spino-olivary projections. Projections from the spinal cord area coming up to the inferior olivary complex in the medulla. That inferior olivary complex is projecting into the cerebellum, so your cerebellum is constantly getting feedback from your spinal cord projections, from your cortical projections, and then trying to match it with the vestibular and trying to calibrate things that are working efficiently. Okay?


Now, when you look at the cerebellum, this midline area’s really important. Now, what you see here is this fastigial nucleus, this midline cerebellar nuclei. Okay? It projects to pontine reticular formations, and these pontine reticular formations is where you have the sympathetic chain, changes that take place. So as you move, as you do things, you have to fire autonomics to have both [?]constriction and vasoconstriction in a way so you pass out and shunt blood the wrong way. So, these autonomic connections also explain why people who have vestibular disorders get dysautonomias. Their heart rate goes up, they get skin changes, they get pupil dilations, they get anxiety, they get chronic GI issues, they get variable… they have their bowels move very quickly. Right? Those are all these projections into these pontine areas. So that’s one of the key things.

Now, the way we have been building our information up to make sure we can have a model people don’t miss anything is, we broke down the cerebellum into the vestibulocerebellum, and we gave you symptoms of loss of activity, seizure activity or epileptiform activity, with both the… You have your form that screens for these symptoms, and then you have exam findings, and you have the applications. But that’s very specific to that vestibular cerebellum.

Now, when you look at the dentate nuclei, out here, the dentate nuclei and the hemispheres of the cerebellum are not so much involved directly with the vestibular system; they’re involved with calibrating fine motor cortical activity to muscles turning on and off. Okay? So, if you take a look here, you can see the dentate nuclei, which are the more lateral, large nuclei, and they fire into the thalamus, and to the cortex, so you have this projection from the cerebellum there, and you also get projections to the red nucleus, which then have spinocerebellar types of projections too.

So here’s the thing: If you have someone that touches their nose, and they have a kinetic termination tremor, is that vestibulocerebellum? Or is that the lateral cerebrocerebellum? That’s the lateral cerebro-cerebellum. Okay? Now, at the end of the day, when you activate the cerebellum, you’re going to have activation integration of all those areas. And if you activate the cerebellum, guess what? You’re going to shunt blood to all these other areas too. So if you remember the arterial system, the posterior inferior cerebellar artery, and the anterior inferior cerebellar artery, and the superior cerebellar artery, they don’t go to one specific region. They kind of just circulate the top part, the bottom part, or surround it. So any time you do any kind of cerebellar activity, whether it’s vestibulospinal or cerebrocerebellum activity, you’re going to actually get blood flow and circulation to the entire cerebellum. You’re going to get some activity throughout the whole region. Plus, those areas all integrate for movement and motion anyway.

So, we went into the questionnaire form. Again, we went and have these symptoms screened for you in the brain region localization form, and then we have the spinocerebellum which is this blue area here, and the blue area has the interposed nuclei that’s very much controlled with your overall extensor muscles, your hip and shoulder, to kind of keep you stable as you function.

So, vestibular input has an impact on those too. So when you do any kind of vestibular therapy, you can have some change in your other cerebellar findings. So if someone has a little bit of a termination tremor, or they have dysdiadochokinesia on one side, you can do vestibular therapy, and vestibular therapy – remember – the vestibular system fires to the ipsilateral cerebellum. So if I have right dysdiadochokinesia, and I can’t… and I touch my nose, I’ve got dysmetric movement, if I wanted to activate my right cerebellum, I could do


vestibular activity, like right anterior canal, or right horizontal, right posterior, and see if it changes it. So I’m getting blood flow to that area indirectly. Okay? And co-activation through these other nuclei as well.

So, those are the cortical region vestibular pathways there. Now, the other thing that the cerebellar projects to… So, let me recap, put this all together for you before I move on. So you have, you guys, you have these vestibular nuclei… I mean, I’m sorry: You have the vestibular receptors. You have the canals – anterior canal, posterior canal, and horizontal canal on both left and right side – involved with rotation of your head. You have your utricle and saccule: saccule for up and down translation; utricles for forward-and-back, side-to-side translation. They then fire to your vestibular nuclei. You have a superior and inferior medial lateral vestibular nuclei. These vestibular nuclei project upward to the medial longitudinal fasciculus, so you have coordinated conjugate eye movements, opposite of the head movement that you’re going with. Horizontals, down and out for the posterior and to the same side with the anterior canal. Right? That conjugate eye movement. That’s there to make sure you have integrity of your visual pathways; you don’t have double vision when you move your head. Then these vestibulospinal, these vestibular nuclei have descending projections that control the intrinsic spinal muscles. Okay? That’s the key part of the review that we went over.

Then the vestibular nuclei also fire right into the cerebellum, so you can get other changes of cerebellar functions because of collateral shunting of blood flow, and because as you move, you have to engage your cerebellar system, and your vestibular integration between those two systems. Okay? And then the other key concept that we went over is, your vestibular system has to fire into your autonomic centers for vent shunting. That’s why you get some of these autonomic symptoms. Okay?

Now, the information of your vestibular system also projects to the thalamus, and to the cortex as well. So there is cortical interpretation of movement and motion that’s also involved. And one of the things that Dr. Brock will go over with you that is, is how to differentially diagnose central versus peripheral vestibular disorders. So, central vestibular disorders can involve the cerebellum, or they can involve the parietal insular vestibular cortex, which I’ll show you right here.

[50.07]

So, the cerebellum also projects… I mean, the vestibular system also projects from the nuclei all the way up to thalamic projections, and then to areas of the cortex. The temporoparietal regions of the cortex are associated with vestibular integration. So here’s a key concept: Subjective experiences of self-location in relation to the environment is an aspect of cortical function. So, one of the common questions that’s done in a diff-di is, “If you have disorientation or dizziness, do you feel like the world is moving? Or do you feel like you’re moving?” So people who feel like they’re moving, it’s their perception, that’s usually involving the parietal insular vestibular cortex. If the world is moving but not them, that’s the vestibular, more likely peripheral vestibular systems. Okay? So you’re trying to distinguish where your treatment applications are going to be. Okay?

Now, what about people that have out-of-body experiences? They feel like they’re floating around? They’re about to die, and they float outside their body, and they think… Well, they’re getting lack of blood flow and spontaneous firing of their parietal insular vestibular cortex. And people feel like they’re… People may even come in and tell you when this area of the brain’s degenerating, or injured, that they’re flying around,


they’re floating outside their body, sometimes. That’s activity – epileptiform activity – maybe from an injury or degenerative change, or even tumor of the parietal insular vestibular cortex.

So it’s really, really important as you do your workups and you try to look at these integration centers, do they have autonomic changes? Do they have symptoms? Do they feel like the world is moving? Do they feel like they’re moving? Because it tells you where they are. Is there a difference between if they move forward or back, or up and down, or rotate to the left, or rotate to the right, or something moves in their left field or their right field? As you kind of pinpoint those questions, you can then narrow it down to what area of the peripheral or central vestibular system is not working well. Once again, and as you go through that process, that’s when you smile when someone comes in with a chief complaint of dizziness. Because like, “Oh, there’s only so many things that could be. And I know my flow chart, I’m going to figure this out right now.” Okay?

So, this is a summary of the paper that you guys have in your notes. “Altogether these experimental stud-ies imply that by integrating multisensory – visual, vestibular, somatosensory, motor – signals, the brain generates a coherent spatial representation of body parts, the body as a whole, and the body as related to the external world.”

So when you look at cortical perception of movement and where your space is into movement, it involves the temporoparietal junction. Now, the temporoparietal junction has different centers that are involved. You have the PIVC, parietal insular vestibular cortex; you have the VIP, ventral intraparietal cortex; and then the MST, the medial superior temporal region. Okay? Now, these have… The vestibular system projects bilater-ally, but for the most part the function exists on the right brain. So it’s really usually, like, when right-brain injuries cause hemineglect, the left-brain injuries cause language, it’s usually right-brain injuries that really impact vestibular sensory perception, because majority of – even though it’s bilateral – the majority of the function of integration takes place on the right side of the brain. Okay?

Or, to say it differently, if someone tells you that they feel like their body’s moving and floating around, it’s a greater probability that it’s not peripheral, that it’s central, and involves the right brain at the temporal parietal junction. Okay?

So when you look at these different regions, in your notes, under key concepts, I summarized these things for you, each of these regions and the central processing, so just to make it easier to take it all in and understand it. But let me review some of these key concepts.

The PIVC is really considered the main cortical region for perceiving all these different sensory, auditory, visual inputs, and understanding where you are in relation to space and how your vestibular system activates and integrates those. So the PIVC’s a major input area for encoding vestibular signals contributing to self-location and first-person perspective. Where you are. Where your brain is. Where your head position is. Okay?

Now, the ventral intraparietal neurons integrate spatial information from different sensory modalities – visual, auditory, somatosensory – into common body-centered areas. So if you look at where it’s located, it’s located right next to what? The post-central somatosensory cortex. So the somatosensory cortex gets input,


and then you have input from auditory and visual. They all come in, and that integration with, really most of your somatosensory parietal cortex then projects to your PIVC, to then interprest where you are in space.

And then you have your medial superior temporal region, which processes the visual output flow in addition to vestibular signals, and it comes into the PIVC.

So here’s a summary way of looking at this. For the most part, vestibular projections from the thalamus through your utricles, saccules, and semicircular canals, fire into the PIVC. Input coming in to integrate with your somatosensory, from your parietal lobe homuncular map, come in and integrate in the VIP. Visual input comes in to the MST, they all integrate in this region here, which then really allows you to know where you are in space in relation to the world. Okay?

Now, information to the PIVC is coming from cerebellar projection, from the vestibular apparatus directly, and all those things integrate so you know where you are in space. So when people get injury to their right – you know – temporoparietal areas here, it can cause them to feel like they’re floating, disoriented, can’t feel in place, and it becomes very serious stuff. And those are not to be confused with peripheral vestibular disorders. Okay?

Now… So here’s the thing. If you do optokinetic… You know how you guys do optokinetics? If you go to, you know, the left or right, you’re supposed to have different impacts, different cortical regions. Some people will learn that. You go to the left, you activate the left parietal and left frontal. Guess what? You always activate the right posterior inferior vestibular cortex. Always. You’re always getting a right-brain effect. Motion and movement of vestibular system always has a right-brain effect. Even if you’re theoretically thinking it’s just going left, it’s not. Okay? So there’s that dominance of your vestibular input going to the right brain, there’s a dominance of your language going on the left. There’s a dominance of your parietal somatosensory perception on the right brain. Okay?

Here’s the other thing. Oh by… So, let me show you this interesting study. “Out-of-body experiences in some neurological patients were caused by damage, dysfunction, or electrical stimulation of the right temporoparietal junction. So if they go on there and do electrical activity there, people have out-of-body experiences. Okay?

This is from a paper that you have in your notes, but read this: “Vestibular input activates PIVC and simulta-neously deactivates the parieto-occipital region. Optokinetic stimulation…” – that’s the red and white flag people used to use – “… on the other hand, would activate parieto-occipital region, and simultaneously deactivate the PIVC.” Sometimes, when you guys do, like… Have you guys ever seen those red and white strips, optokinetics? If you have someone who’s got a PIVC injury, and you do optokinetics – doesn’t matter which way you go: right, left, up, down – and immediately feels to them like they’re floating, and they’re out of… they can’t coordinate with their bodies in space, it’s a strong sign that you have an injury there. Because the optokinetics shut that system down. If it’s already not integrating, it gets work. So as a clinical pearl, if you do optokinetics, it doesn’t matter which direction you go, and they totally feel like they’re out-of-body experience, or they can’t tell where their body is, or they feel disoriented, that is a strong clinical sign that they have a PIVC cortical sensory integration problem. Okay?


Now, if you take someone like a red and white strip that moves, makes a person feel like they’re spinning to one side or the other, you go to one side, only one side causes symptoms, that could be more diagnostic to which vestibular cerebellar integration that’s involved. But it’s any of them will inhibit that PIVC pathway and cause some symptoms.

Now, if you guys want to read a great paper in your notes, this is a good one. And it goes into vestibular pathways involved with cognition, and it just summarizes all the main research of how the right posterior… the right temporoparietal junctions impact different perceptions of activities. So just as an example, how important would it be to an athlete? Do you see all these movements here that are involved with it? So you guys, you can take a world-class athlete, and they seem like better than everyone else, and they won’t have the edge. You can almost always find something to do with their cerebellar or vestibular system, to even make it more efficient. The more efficient they become, the less balls they hit, if they’re missing tennis, or the more efficient they can judge and cut if they’re running or doing something.

[1:00]

And that’s what makes some of them world-class athletes. But even with world-class athletes, they may have decreased integration between their anterior versus their posterior canal, or their left versus right, and if you can make both of them as efficient as possible, compared to themselves but not to other people, they even become better athletes than where they’re at. So again, this vestibular application is not just for dizziness, but you can also apply it to improving athletic performance. But the ability to tell self versus object motion or body motion related to the vestibule or to the head, these are all involved with this vestibular pathway there. Okay?

And then as you look here, you can see the projections from the vestibular apparatus up into different cortical areas. These are mostly parietal somatosensory areas of the brain, and these are just some of the pathways that you guys can read about in that paper. Okay.

I want to take a minute and go into autonomics, okay? So, in session one we talked about brain autonomics. And with brain autonomics, we know we have multiple areas of our brain involved with central processing of autonomics that are bilateral. We have insular cortexes, we have anterior cingulate gyruses, we have areas throughout or even our occipital lobe; they’re all integrating to control autonomics, but we have the ipsilateral projection, the hypothalamal spinal tract, which has activity there. The pontomedullary reticular formation is an autonomic pathway that’s used in instantaneous movement and motion, exclusively for the vestibular system. Most… pretty much for the vestibular system. So the fastigial nuclei fires into these areas, so as you have movement, you shunt blood properly in perfect regions. The pontomedullary reticular formation tract is not an ongoing how-healthy-your-brain-is activates [?] IML. That’s not it. The PMRF is the pathway used by your activation of movement, mostly through your vestibular system, to cause instantaneous change in autonomics to look at blood flow, circulation, and shunting. Okay?

So, this is a great paper. You guys have this in your notes. The vestibulosympathetic response. So, what you see in this diagram is activation of vestibulospinal pathways, and it hits the reticular formation, which then hits the rostral ventrolateral medulla, which then activates the IML, and that’s done in such a way where you have shunting. Okay?


Now, I also want to show you this diagram here. Let me show you this one here. So, do you remember this is the area of the midbrain, and then this region over here, you have your cuneiform nucleus and cerebellar projections, vestibular projections fire to the cuneiform nucleus, which then fires to the rostral ventrolateral medulla, which then activates the sympathetic IML response. So one of the things that you want to do is, you want to really look at… Let’s talk about sympathetic tone first.

So, vestibular inputs can fire right into sympathetic centers. And if you have patients coming in that have arrhythmias, people that have no cardiopathology, they just have their heart rate spike up all of a sudden, no one knows why, and they’ve had extensive workups, they can’t figure out what’s going on… You have people that have – like we talked about earlier – anxiety and nervousness, and just feel tense all the time, they could have vestibular escape to the sympathetic center. Okay? So the way you assess that, one of the ways you can check that, is basically, you can do some vestibular stimulation with them, and see if you see autonomic changes with them – okay? – that are exaggerated. So an example I gave you earlier is, you can have someone, for example, you put them in a swivel chair… You guys should all have a swivel chair in your office, just so you can test the vestibular system. So I have a nice swivel chair that goes up high enough where most people’s legs can hang freely. I mean, you always get the huge, tall, six-foot person, you go, “Ahh! Keep your legs up!” But for most people, if you have them scoot all the way back you can sit there and you can put them in canal positions, you can test their – you know – their utricles back and forth. And if you have a flexible enough release, you can go up and down and kind of see what’s going on. I like to put them on VNGs and look at their eye movements as I’m doing it, to kind of see what’s going on. But you can do it different ways too.

Now, if you take someone and you put pulse-ox on their fingers, that’ll give you their tissue saturation and also give you their heart rate, right? So if you put them there, and you do… So, like, here’s a scenario. Patient comes in, and they walk like this. You guys ready? I’ll just do it here. What does that tell you right away? Swaying right, something going on with the vestibular system right. They tell you they have anxiety, and the anxiety is worse when they’re in a crowded environment and so forth. So you take them to the chair. Which vestibular system is not working as well? The right. So you can literally, like, turn them to the right a few times, and then check the heart rate, and if it goes up… Like, it shouldn’t go up for most people. It just goes up, and they start sweating, you know you have a vestibular-origin sympathetic-promoting pattern. Now, It could also be the same thing with people who have arrhythmias.

Now, the other thing you can do is, you can also just look at pupils. You can take a look at their pupil and see how dilated they are, turn them a few times, look at their pupil again and see if it dilates. Those things are happening, they’re pretty exaggerated. Now, assuming you’re not whaaa! like, spinning them like crazy, and aggressively, but – you know – some fairly not-so-aggressive turns, and you see pupils completely dilate. You can even see some of them go onto sweating palm reaction or heart rate changes. Those are clue to you that they have vestibular disorganization, or vestibular integration problems, which probably involve vestibulocerebellum integration issues that are firing to sympathetic centers. Everybody okay with that? Okay.

Now, you can also have… So here’s the illustration of what I was trying to show you. Cerebellar input comes in, in this scenario, through vestibular nuclei. Vestibular nuclei fires into the cerebellum. The cerebellum is going to process that information, but the cerebellum is also going to inhibit it, because it has to gate the amount of input that comes into the brain. It’s like a filter. There’s so much muscle spindle Golgi tendon


vestibular input coming in, the cerebellum has to gate it. Okay? Now, input from the vestibular system also directly goes to projections in the rostral ventrolateral medulla, where you have sympathetic chain, but either through cerebellar projections or through the direct vestibular activity, you activate this midbrain, lower medulla, rostral ventrolateral medulla region, that activates the sympathetic chain, you get a heart rate, get anxiety, get your metabolic rate that goes up, and those people are also really prone to have blood sugar drops.

So any time you get someone who’s got a vestibular-related issue, unrelated to dizziness, some of them fire into these sympathetic areas, and their heart rate goes up, on an ongoing basis, meaning, like, listen, they’ll drive and a car goes by quickly, and they get a sympathetic response. May not be very significant, but it could be subtle, but they’ll get one, and they notice it, right? So they’ve kind of got some anxiety. Just like if you have a negative thought of something, what happens? Get a little bit of anxiety. But that’s happening to them all the time, throughout the day. So it’s not like it’s totally taking them out, but it’s making them feel anxious and uncomfortable all day. As they get their heart rate up, they’re going to burn off all their sugars, and then the blood sugar drops, so now they get shaky, lightheaded, irritable; they have changes in energy. So you’re going to see most of these people that have sympathetic responses are prone to being clinically functional hypoglycemics. So they’re going to come in and have those symptoms as well, and they’ll have a vestibular issue, and they’ll have their dizziness and their anxiety, and they can’t handle movement. For some patients, you can literally do this: “Look at my finger. How do you feel?” “I don’t like it.” Okay.

You can also go into your… have them sitting in your chair while you’re doing history, and then you ask them what happens. If they say, “I feel a little anxious,” or, “I feel my head is throbbing,” what’s that? That’s the vascular phenomenon. So you can have some of your vascular migraines and headaches be vestibular in origin, because as you do some vestibular input, they tell you they feel constriction in their head. You hear that, you’re going, “Cool. I can fix your vestibular system, maybe get rid of your migraine, your headaches, or these chronic vascular throbbing patterns you have.”

So, how you challenge the vestibular system and what kind of symptoms they get are really, really critical. When you put someone in a Romberg, or you put someone in a chair and you move them, or you move their head, you always want to know what symptoms they have, so you can understand their case better. So a lot of people have projections into their sympathetic system, okay? So anyways, when you take this person and you start to move them, and you see vascular change, or heart rate change, or sweating changes, you know that component’s there. What you’ll have to do next is figure out how to dampen that. We’ll go over treatment and modalities and different things to see if that stops, okay?

Now, the other projection is to the pontine areas, to the brainstem areas. So you have people that have activation of projections from their vestibular system to their pontine… pontomedullary areas, where they have a parasympathetic effect.

[1:10.08]

You guys, which cranial nerves are in the pons? 5, 7, 9, 10. Right? And those are all your parasympathetic nuclei. Your nucleus ambiguous – right? – your superior inferior salivatory nuclei, those are all pontine autonomic parasympathetic nuclei. So when the cerebellar system fires into that area, you can have people that constantly complain of saliva production, or tearing – their eyes are always tearing – and you can ask


some people the same things. You can put them in a rotational chair, and you can move them a few times, and you can see their eyes get really wet. So you know they’re having a parasympathetic response. But the most common one is that they get nausea. So when you put them in the chair and you move them, and all of a sudden they get nausea, you know you’re getting activation of the vestibular system to that vagal area.

Now, those people usually have chronic gut problems, because one of the constant inputs the vagus nerve needs is input from the vestibular system. So as you see people that have vestibular imbalances, you see many of them have chronic GI issues because they’re not getting that proper, you know, ongoing temporal spatial summation to that vagal nuclei, so they have various types of GI issues. Now, one of your clues that’s happening is, when you do anything to vestibular cerebellum, they tell you they have nausea. Okay?

So, let me give you a few examples. You guys ready? I’m a patient. I’m standing right here. You go like this, you ask me to close my eyes. I close my eyes, and I go, “Oooh.” First of all, let’s say I don’t really move. So I close my eyes, and I don’t really have a major shift or move. But you go, “How did you feel?”

Here’s one: “I felt like… I felt like I was just floating.” Where do you think the problem is? Cortex, probably right cortex, most likely parietal insular vestibular cortex, right? You challenge the entire system, and that couldn’t keep up, that spontaneously fires. Something happened where you saw symptoms there. Okay?

So, same thing: They do it. There’s no interchange, but you go, “What happens?” He goes, “Man, I’ve got this throbbing pressure after that.” What’s that? It’s autonomic, most likely sympathetic. Someone else does it, they go, “Oh, I don’t like that.” “Why?” “I get some nausea.” What’s that? That’s to the pontine areas.

So where they go can explain some of their symptoms. Because you could have a patient… Here’s the thing. You don’t even… They’re just coming in for chronic GI issues, or just anxiety, or nervousness, or hypoglycemia no one can figure out, and you’re just going through your tests, and all of a sudden you do your routine neurological exam, and they tell you, like, “Oh my God, I have nausea,” or, “Now I have anxiety and I’m sweating.” Now you know their component of whatever their chief complain is could have a vestibular origin, because you understand these autonomics. Make sense? Okay.

Now, here’s another scenario. So they stand here, they get up: “Oh, I felt off.” “What did you feel like?” “Um… I felt like… um… I felt like I was here and then I wasn’t…” Sometimes they kind of go into that pattern like that. They can’t even explain what’s going on. So you kind of have this integration issue. Now, you can also have these types of responses, whether it’s anxiety or disorientation, or floating, or vagal responses, from anything you do in your exam that causes vestibular…

Oh man. Music next door. This always happens here.

So you can have all that happen from the vestibular input. That’s why it’s so important to ask the question. To me, asking the question is as important as seeing what I visibly see with the patient. You understand? Because they can tell you things that sometimes you can’t clinically see, like they’re having a little bit of anxiety, or a little bit of throbbing in their blood vessel or their arteries there. Okay.

Now, let’s say we do this: You put them in a position to balance, to change out their balance. Now you see them kind of shaking forward, back, like that more. Do you think it’s more of a utricle, or a canal? Well, it


could be that they’ve lost core stability of their vestibular cerebellum, but what if you just see their head more? That could be a utricle issue. What if they just go to one side? You go to the side of their canal inefficiency, because their canal stem’s integrating, but this one isn’t, so they start to fall into it. Okay? Or forward. So whatever sways they have can help you understand which canals they are, which then you can use for therapy. Okay.

When you do vestibular therapy, just because of these projections, you should be very careful because you can activate autonomics and totally make a person crash, too. Okay. So anyways, this is what you see here as an illustration for that. Okay.

So, when you look at this vestibular pattern here, this neurological integration center, this is input that you have. Now, what we’re going to do tomorrow morning… So, tomorrow we’ll go right into treatment. So after we finish… After I finish with this, we’re going to take a little break, and then Dr. Brock is going to go in there and diff-di all of the other peripheral vestibular issues for you, and then you’re going to immediately know by following certain rules where the different lesions are, whether it’s inflammatory or vascular or structural or peri- or endolymph or autoimmune or so forth. And then tomorrow what we’re going to do is, I’m going to go into pathways like this. I’m going to go over the neurochemistry of dizziness and vestibular disorders – okay? – followed by canal repositioning and all those things. But right now, the goal for you, is just to make sure you guys understand all the pathways and all the projections and all the different integration issues. Okay?

So, what you see in this diagram here, just to also improve this input, is, you have motion taking place, whether it’s active or it’s passive, and then you have input coming into the vestibular input, visual input, and somatosensory input. So, let me ask you a question. If I’m standing here, and I do a Romberg’s, and I turn my head, or a practitioner turns my head, what’s the difference in the input to the brain? So, let’s say you want to challenge each canal in each position, in a Romberg’s, maybe with their eyes closed, or in a pointed Romberg’s, tandem Romberg, with their eyes open. Okay?

What’s the difference neurologically whether they do it or you do it for them? So, one is cortical, right? So if you say, “Turn your head to the left, what you just did is, you actually initially activated executive function in the premotor areas, which then fire down corticospinal tracts, which then immediately fires input from the corticopontine areas to the vestibular cerebellar system, and you decrease the tests being as much vestibular, because you asked them to move their head to the left, versus you have them say, “I’m going to move your head in different positions; just try to relax,” and then you move their head. The faster you move their head determines how much input you get. The faster you go, what happens to the fluid hitting the hair cells? They become more aggressive. So you have to also be consistent of how fast you’re moving each position, versus this to that. Because if you go really aggressively to one canal, and slower to one canal, you can misinterpret how it impacts their balance. Okay? So, the amplitude and how you activate things are important. So passive motion versus active is also critical when you test individuals. Okay? The head positions.

So what you’re seeing here is that vestibular input, visual input, somatosensory input comes in; you get sensory integration, and the sensory integration that you see in this diagram takes place where? Vestibular visual input that take place in the temporal parietal regions bilaterally, but for the most part, mostly on the right side. Okay? This sensory integration comes in, and then there is control with neural storage centers,


so you have visual motor discharge centers that are integrating with the vestibular system to move your eyes in a conjugate pattern with the right amount of amplitude so you don’t have any discharge. And then there’s always this input of all these different vestibular, visual, and somatosensory input centers to see if you have proper combining and… Here’s what I mean by this: proper integration.

So if you’re moving… Let’s put it this way: If you put some kind of object in your shoes, like a rock, or you put a heel lift in one side versus another – okay? – and you go on a moving balance board, that’s going to completely change your brain. Because all of a sudden you just change the amount of input coming into your feet in a different rate, and now you’re vestibular and parietal areas have to integrate with that, and then your visual system, and if you close your eyes you’re having all these different inputs. If you get dizzy from that, what you’ve just accomplished is a mismatch. The brain couldn’t adapt with the somatosensory input coming in as well as your visual and vestibular reflex are going, so you got a mismatch, and now you got dizzy. Okay? So those are mismatch patterns.

So, when people have an injury, or anything that involves input coming n through the large-diameter fibers, or the parietal lobe, or the vestibular system, or the cerebellum at an abnormal rate compared to before, and they get symptoms of disorientation and vertigo, that’s called a vestibular mismatch, or sensory mismatch pattern. Okay?

[1:20.03]

So you’ve got to make sure you don’t have any mismatched patterns, and then if everything is working, everything is cool, and then there’s no symptoms. But in this illustration it shows for motion sickness, it abnormally fires to the vomiting centers, which is your vagal motor nuclei, and you get symptoms that way. So anyways, that was just kind of a review of this.

Now, this is a good paper, because it shows you which receptors are involved, and now different anti-dizzy medications work, through which pathways. So if you always wanted to know which medications are used for dizziness and vertigo, this is a great paper you have in your notes, and it breaks down the mechanisms and which receptors and which pathways they work at. So it would be good, useful if you’re wanting to know more about that.

So, let’s talk about this integration summary as we finish up here. So, this illustration is showing the vestibular sensory pathways. They’re coming in, they’re firing to the vestibular nuclei, The vestibular nuclei is also getting input from your neck proprioceptors. So this is also important too. Now, your neck… Your proprioceptors and your muscle spindle Golgi tendon and mechanoreceptor inputs are also, in addition to firing to the parietal cortex, having some input into the vestibular system. So some people that have movements and head rotations have cervicogenic mechanisms of dizziness, because you have inputs from your neck into your vestibular system, to know where your head position is. Right? So one of the things that you usually do is, like for example, if you keep someone’s head still and you just have them on a swivel chair, turning their body, and they get dizziness or symptoms, you know it’s not coming from the canals, because the canals aren’t being activated, because you’re keeping the head still, but it’s coming from their neck. Okay?


So, this is the neck proprioceptors, and then you have cortical input to the vestibular nuclei, visual input, cerebellar inputs going to the vestibular nuclei, and then these fire to descending pathways, to control your vestibular posture and balance, to your eyes, to have no development of diplopia – double vision – because your eyes are conjugate moving when they move, and then estimation of where you are in space. So this is also a good paper if you guys want to read something. Okay?

So remember that you have these different nuclei. So, I’m going to summarize everything in the last few minutes very quickly, okay? Now, when you see this diagram here… Whoops. Okay.

If I wanted to activate my left anterior canal, what could you do clinically? If you want to activate someone’s left anterior canal? You could have them turn their head and do this activity, right? You can have them visualize doing a roll, falling on the floor. If you wanted to activate the left horizontal canal, what could you do? Turn the head, spin them, have them go in circles, making sure – you know – again, doesn’t exceed either threshold. You could have them visualize spinning to one side. You want to activate the posterior canal, what could you do? You could have them bring their head back, right? And it’s always back to rotate and then extend, when you do these. So you could have them do those activities, or you could have them feel like they’re falling back to the left. You could activate that system that way. Just some general rules.

How could you activate the utricles? Forward or backwards. You could have people in a swivel chair and you could have them walk… push back, and then turn, and then push back, right? That’s an easy way to get things going posteriorally… posterior translation, which a lot of people have problems with. Or you could have to have someone push him forward, and then turn him slowly, and then push him forward, and turn him slowly, then push him forward. And then those things can add to be the translation, or you can get someone in the swivel chair and go side to side, whatever you need to do for those types of therapies. You can have people shift side to side, or do up and down movements as a rate that doesn’t make them have symptoms of dizziness. So if someone comes in and tells you that when they get in an elevator they stop so quickly they get nauseous, and they have GI symptoms and headaches if it’s too severe, you could literally have them do some squats. It would be better passively if you could figure out a way to do it with a chair that goes up and down, but you could have them do those at a rate that doesn’t make them sick, and then over time they get healthier and integrate, and then it goes away. Okay?

So that’s why it’s important to know which of these these things are.

Now, on the questionnaire form Dr. Brock will go into more of the diff-di interpretation, we ask questions like, “Do you notice any symptoms when you’re in a car, when you go in an elevator, if you rotate right, rotate left,” because you’re trying to figure out which parts of this are involved.

Now, this is a summary. Remember, the vestibular nuclei fire in, you have four of these nuclei, they go up, control vestibulo-ocular reflexes, they go down to control the intrinsic spinal muscles. And this diagram here, as a review, shows that the vestibular apparatus fires to the vestibular nuclei, specifically the fastigial nuclei, and it goes back. That’s your midline flocculonodular lobe.

The key thing is that it goes to these autonomic centers. And one of the points that I was trying to make is that many of these vestibular disorders are not going to come in with any chief complaints of dizziness. So as part of your neurological workup, you should always evaluate a complete neurological exam and do head


positioning and movements, and Romberg’s, and gait, and everything. The things that we talked about for the sympathetic system, easiest thing to look at is heart rate and pupil dilation, but the parasympathetic system most common thing you’re going to look for is tearing or increased fluid in their eyes, and symptoms of nausea. And you guys, some people have both. Some people you’ll spin them, their heart rate goes up, followed by a parasympathetic response, or a parasympathetic response followed by a sympathetic response, and so forth.

And then this is the dentate nuclei, and these are the major regions. These are the major regions that are involved with the brain.

So remember that your parietal information comes in… So, let me ask you a question. Or, let me go through… Let’s go through a case example to help. If someone comes in, and they tell you that they feel at times that their body is moving… So they tell you they have dizziness, and they have disorientation. And then you ask them, “Does the world move, or do you move?” And they go, “No, it’s for sure I move.” So you know it’s mostly central based. So now you know it’s the parietal insular vestibular cortex. So now, what do you do? You’ve got to figure out which pathways are sending abnormal information there, or is this itself degenerated and injured? You guys understand? Okay.

Just for the sake of an exercise, which blood supply can shunt blood there? Which artery? Well, the middle cerebral artery is definitely going to be the artery that projects into that area, right? So you know that if you do any activity that activates the right MCA, and get some blood flow there, in general, that can change some of your symptoms of disorientation even though it doesn’t make sense. So, you can basically take a pic… Here’s the thing. You might even not know it. They tell you they have dizziness and some vertigo symptoms, and you go, “Well, I’m good with my neurological exams.” So then you start checking temperature sensation, and light touch, and pinwheel sensations, and you go back, and they go, “Hey, I feel better.” Your vestibular input increased blood flow to that area, so now they’re going, “I feel better,” and you didn’t actually do anything directly for that. Okay?

But any time you see that someone has any central-based disorders, you’ve got to go through – like we talked about – check dorsal column, peripheral neuropathy issues, check parietal lobe issues, see if you have any parietal lobe loss in certain regions. And if you had parietal lobe issues, what would you do? You would do things in your brain compilation form. You could do TENS unit, you could put Icy-Hot on the area, you could have them visualize movement, visualize their hand that they have problems with, and those are all parietal. Right? If it’s vestibular, you’ve got to figure out: Is it the otoliths? Is it the canals? Is it the anterior canal, posterior canal? Do you work with that? If it’s cerebellar, do you have cerebellar issues? Is it lateral cerebellum, and then do you do balance exercises? Do you do movement? And you can do it at a rate… And here’s the next question: How often would you do it?

So, you have someone who feels like they’re floating, and they’re going all over the place, and you find out when you do some parietal lobe testing, they have lost their ability to discriminate vibration and tempera-ture sensation just in their left arm. What area of the brain could be involved? The right somatosensory cortex may not be integrating, right? And which region? Superior, inferior, or parasagittal? Superior regions, right? So you know that’s there. And then they also tell you… they also, when they try to walk, they have some sway, okay? And you check out each vestibular canal, and the vestibular canal that isn’t as bad is the left posterior vestibular canal. You do some therapy for the left posterior vestibular canal, they get… they


have no change. You do some therapy for the left horizontal canal, left anterior canal, they get more stable. So now you’re going to do therapy… So now you might, with a patient like that, go, “I’m going to do some somatosensory touch. I want you to visualize your right forearm. I want you to put some Icy-Hot in that area where you can’t feel things. I want you to put a TENS unit there. I want you to visualize those areas of your system.” And you would do some anterior canal and horizontal canal, because that helped them. But how often? It depends on how many you do, and do they fall apart and get worse as you repeat it? And that will determine if you can do that first, or if you need to do metabolic stuff. Does that make sense? So those are the major concepts.

So hopefully you guys understand all these different projections. Know that when we look at the vestibular system it’s not all about dizziness; that the vestibular system does involve autonomics. And you understand between central and peripheral, understand the symptoms between utricle, saccule, and canal patterns, and that should help you in your workup.

Let’s take a break, and then Dr. Brock will go into diff-di patterns. Thank you.

[1:30.45]

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PeriPheral Vestibular and Cerebellum disorders with ... filevertigo and dizziness, but sometimes people have dysfunction of the vestibular system, and that might change their core