PeriPheral Vestibular and Cerebellum disorders with ... · cause dizziness and vertigo, we went over the vestibular pathologies, we talked about the pathways that integrate in the

MODULE fOUr TrANSCrIPT: KHArrAZIAN CASE STUDY | © 2016 fUNCTIONAL NEUrOLOGY SEMINArS LP | PAGE 1

PeriPheral Vestibular and Cerebellum disorders with aPPliCations (module Four)

transcript – Case study with dr. Kharrazian

Presentation by dr. datis Kharrazian

Alright. So, what the goal right now is, as we finish up the day, and there’s no more new information, it’s just there to chill out, relax, and just see the applications to some real cases. We’ll do some review, we’ll answer some questions, and hopefully this will – you know – start to come together for you if you’re new to it.

So, if you look at where we are, we talked about vasculature, we talked about the vascular syndromes that cause dizziness and vertigo, we went over the vestibular pathologies, we talked about the pathways that integrate in the vestibular system; that’s why you can see changes in autonomics, and changes in spine intrinsic function and stability, and we – you know – went through all the key things related to vestibular input to the cerebellum and to the cortex, and we’re going to then going to expand about those and really focus on the vestibular cerebellum and posterior… parietal-insular vestibular cortex next time, and really get into that central part of it. And then we talked about – this morning – neurochemical and nutritional applications. So, we went through each one of those and talked about how to address each one of those, and then Dr. Brock went over the diagnostic maneuvers, and then some treatment applications.

So, here’s what we’re going to do. I’m going to take you through the flow charts we have. I’m going to take you through the clinical decision-making tree. Like I’ve always said, we don’t want to give information out to people. The information is everywhere. What’s valuable is a clinical thought process. That’s what people have a hard time with. That’s where people fail with patients. That’s why people can’t build a practice, because if you don’t have a clinical thought process and explain it to the patient, and it’s thorough and it’s effective, patients don’t stick around. They really need to get at least an understanding, or outcomes, of what you’re trying to do and the things you’re going… and you’re going through.

So, we’re going to go with a vestibular case, and we’re going to go through and rule out, and rule in, every single condition, based on the patient’s history, and then talk about applications. Then I’ll show you what we did with them. Okay?


So, this is a case of a thirty-one-year-old single male professional skateboarder. He’s very generous; he allowed us to share his case. And he was, at the time of the injury, he was a halfpipe vert skater, and he was at the X Games ranked in the top ten. And basically, he was always in pain, so he always took Vicodin, acetaminophen, and he fell at a contest… and you know, these halfpipes are about twenty feet – fifteen, twenty feet – and the skateboard went all the way up another fifteen, twenty feet, he didn’t know where he was, and boom! landed on his head. So he had a jolt, a shock to his head. And after that shock and injury to his brain, over a period of time, he started to have these symptoms, and they started to progress, and started to progress, and started to progress. Okay?

So, he had disorientation, he had double vision, he had cloudy head thoughts. His symptoms worse with caffeine, which was a problem, because one of his sponsors was Red Bull, and… He went to see various people. I got to see him about a year and a half after his brain injury to help him – try to help him – and he was prescribed Klonopin, GABA agonists, to try to manage some of his SEPs sometimes, but nothing was really successful. So as he went to various people, he had dizziness, and he had double vision, so he got treated for cranial adjustment. Like, no diagnosis. I don’t know how to do that. “I think the cranial bones have been misplaced from the trauma, and we’re going to realign them.” Didn’t work.

So then he went to see an upper cervical guy. “Oh, that trauma must have subluxated your atlas. You need to adjust it.” No effect. He went to see some functional medicine people. They diagnosed him with methylation defect and heavy metal toxicity, and they put him on treatment for heavy metal toxicity. He kept trying different things. He then went to see some people that do esoteric muscle testing and started to introduce him [to] emotional disorder types of techniques. And then he finally got to an otoneurologist, and the otoneurologist was one of the two in San Diego, which I was telling you about, and he diagnosed him with benign positional vertigo. And he did an Epley maneuver; didn’t work. So then he had an Epley chair. He put him in the Epley chair over and over again, and over again. He got dizzy, got nausea, and that was it. Didn’t get better. Okay?

So, let’s go through this flow chart, and start with the patient’s chief complaints. So, his chief complaints are disorientation, double vision, unable to skateboard, cloudy head and thoughts. So, let’s talk about these symptoms. What part of the brain could be involved? Disorientation. What part of the… What areas in the brain cause disorientation? The vestibular system can cause disorientation, right? The cerebellum can cause disorientation. The parietal insular vestibular cortex injury can cause disorientation, right? He could have a crystal dislodge and cause him disorientation, right? The trauma may have ruptured his eardrum, or ruptured things, but unlikely. But, you know, it’s possible. And so those disorientation.

Now that fact that he has double vision means he’s got some pupil-related issues, right? So he’s got double vision, which means his eyes can’t have conjugate movement. So your eyes should move at the same speed in a conjugate pathway. So if this goes at this speed, this should go at this speed. And what’s happening with him, he’s not at the same speed, so when he looks in certain directions – and I’ll show you the direction in a second – he gets double vision. So which pathway could be that? Or could be involved? He didn’t have it prior. So, the vestibulocerebellum, because the vestibulocerebellum fires up, fires into the vestibular nuclei, and the vestibular nuclei fire into the medial longitudinal fasciculus, which will then cause conjugate eye movements. So now we have to figure out, “Wow, he may have a vestibular issue,” because here’s the thing: A posterior inferior vestibular cortex is not going to cause double vision and disconjugate eye movements. You guys understand? Peripheral nerve injuries are not going to cause a parietal lobe dysfunction; they’re


not going to cause that. So we’ve got some involvement of the yoking mechanism to his eye, which is for sure the MLF. Then the question is, what can impact the MLF? Right? And medial longitudinal fasciculus is tracks that cause conjugate movement. But we know the vestibular system is really the key pathway there.

So we go through, and next part of this is to localize the region with the general survey. So I’m just going to show you a picture of him, and I want you to see… pick up on what you see. Okay? So look at his posture, look at his head angulation, look at his joint angulation, look at his eye position. In this scenario he’s not going to speak, we’re just going to get a visual picture of him.

So, you have to have a process. Whether you go up-down, left-to-right, you have to have one. You can’t make it up every single time. You guys understand? If you make it up every single time, you are clinically inefficient. You need to go, “I’m looking at the patient, I’m looking at their eye position, now I’m looking at their forehead, I’m looking at their facial muscles, I’m looking for skew deviation, I’m looking for head rotation,” and you have to have your list. So you just go do-do-do-do-do-do. Right? So, that’s part of the reason why people take forever doing a complete neurological exam. They just go and reinvent it every single time. Of course you’re going to look at the face and head. What’s your process? Ch-ch-ch-ch-ch. And maybe, when you first learn it, you just put it on a form, and just go through a checklist, and get used to that. And then after a while, you won’t be even looking at your checklist; you’ll just go da-da-da-da and then just add it in. Right? So, create a system for initial survey. Go through and really look at what you’re going to look for with his joints, what are you going to look at his face.

Now, do you guys see a head rotation? Okay. And you’re going to see him moving around, so you’ll see this is not just a random picture that caught that, okay? When he moves around and talks, you’ll see his head’s rotating left the whole time. Now, what would cause the head to rotate to the left, from a vestibular model? Activation of which canal, or inhibition of which canal? So if he activates, now do you see an extension? Do you see any flexion? Or do you just see pure, lateral rotation, right? So you see pure lateral rotation to the left; you’re probably thinking his left horizontal canal is either firing too much – right? – or his right horizontal canal is not, or he’s getting increased vestibulospinal projection into his descending motor pathways, his medial longitudinal fasciculus. You don’t know yet, but you just know that’s there, and you’ve got to figure out what’s going on. Okay? It could be a compensation. It could be because he has double vision, and unless he moves his head to the left, he – you know – he won’t be able to have the one monocular view. Right?

So more than likely, when you guys see people with double vision, and you see their head position, you immediately can figure out which eye muscle it is. So if they come in with diplopia, and you see this, then what’s happening is, one of the muscles – either the lateral rectus or the medial rectus – is not firing. So they have to turn to stop the double vision. Because if they look straight, and have to look to the side, they’ll have problems. So they’ll reflexively start to do that. Then they get chronic neck pain, okay?

Now, if his head was tilted, you start to think of oblique muscles. Rotational muscles. Because you have to compensate for the rotation. Inferior oblique, inferior rectus.

[10.0]


I’m sorry, you’ll have to look forward. The rotational system the superior and inferior muscles, but not the medial lateral rectus, right? And just figure out which ones those are. So we see that in it.

Now, do you guys see facial paresis? Do you see any… Let’s start with the forehead. Do you see any facial paresis in his forehead? It’s a little difficult to see, but just go with what you have. Do you see anything? Do you see anything in the lower part of his face? Just a question right off the bat, without knowing which side it is. Does it look symmetrical left to right? Okay. So look at this this way, and then look at it this way. Which side looks older? Which slide looks more tired? If you saw him right now, would you think he was tired? Or if you saw him here you’d think he’s tired? Okay. Well, you have your own diagnosis. May be different than other people’s. But you do what you can when you do a neurological exam. Okay? Alright.

Now, let’s move on. So, what we get from the initial survey, and for me the assessment was left facial weakness, because this is just fatigue and tiredness there. You see the droop. And this is much more vital to me. Now you guys, when you look at facial stuff in pictures, it is harder. Okay? But it doesn’t matter. You just go through your own process, and maybe you’re right and maybe you’re wrong, but you keep adding up your exam findings and you go through it, okay? You’re not going to totally miss this guys case, because you can’t really tell if it’s one side or the other, as you look at the other factors. Okay.

So, we had a left compensatory head rotation was present, and he had a left lateral rectus strabismic amblyopia. So he had a weakness in his left muscle. So we take his head rotation out, and he looks to the left, he sees two images. Okay? So his eyes can’t track, and then he sees two there. Okay, left ptosis, initially noted during the examination, and left facial paresis. If this is accurate, assuming, let’s say, it is left, what part of the brain is going to cause a left ptosis and left facial paresis? Because remember, cranial nerve 7, if it’s injured, the entire [?], you get the entire face. But if it’s just the lower part, you know that you have those dorsal and ventral streams that only go into the lower, from the contralateral cortex. So, the initial impression is that he may have a right… decreased activity of his motor strip. And as we go through the process, we go in there and we add in some of the initial survey. Now, you’d be doing this in your office really quickly. This is just an exercise to go through a clinical decision-making tree.

So, now you’ve got to go and localize the region. And before I give you… Before you localize the region, I’ve got to give you the history, because I want you to do it from the history, okay? So in my practice, what I do is, I have a whole case review process, so that patients send me files, and I have all these questions asked on it, and usually when I get files, they’re very thick. And I go through it, and I screen them. My office staff first screens them as a candidate, and then if she’s okay with it, then I screen it, and we have certain criteria. Most of our criteria is that we can do something to help them. Right? We don’t… There’s patients we know from the very beginning we’re not going to have success with, so I don’t take them. Okay. So I got his history, and one of the things I ask in my forms, I go, “Give me a timeline of what happened.” Okay? So I’m going to read you is timeline. Okay? Ready?

“I hit my head skate… while skateboarding. The board dropped from approximately eighteen feet straight to the top of my head. I was wearing a helmet. Skated a contest in Phoenix. About five minutes before the end of practice, I started feeling a little weird. Didn’t think much of it since I was done for the day.” So he makes his life going to contests and getting points, and trying to get to get to, like, the Dew Tour and the X Games, and all those things, right? The higher he places, the more sponsors give him money, and he gets more sponsors, and that’s kind of the career – right? – of a professional skateboarder. So he skated a


contest in Phoenix; about five minutes before the end of practice he started feeling a little bit weird; didn’t think much of it since he was done for the day, and then on 9/2… So as we go through, let’s look at the head injury. It’s 8/22, and then about nine days later, he has noticed some symptoms after five minutes. And the very next day, “While skating the finals at a contest, started to feel really weird. My vision became weird. I had a hard time focusing, tracking with my eyes. I started seeing double, and things just felt very ‘off.’ I could barely get through my routine.”

Now, I want you to look at what happens to his fatigue and his endurance and all the things that are hap-pening. Now, in 9/4-5, he could skate for about forty, forty-five minutes before getting any symptoms… Let me see. Yeah. He could skate for about forty, forty-five minutes before getting any symptoms. He started seeing double, and everything felt ‘off’ again. The next day he’d wake up and feel fine, and about forty to forty-five minutes of skating, the symptoms would come back. So what does skateboarding do? It activates the vestibular system like crazy, right? It activates your utricles, your saccules, and all six of your canals, as you do different movements and tricks.

Now, on 9/7-16, as time goes on, a few more days, “I was in Mexico at the contest. I could skate for about thirty minutes before I started getting double vision and felt ‘off.’ First day was qualifying, second day was finals. I couldn’t practice, since I had about thirty minutes before I couldn’t skate any more, so I just waited for finals.” So what’s happening to his endurance? It was at forty-five minutes, and now it’s what? Went down to thirty. So you know, a lot of times people get head injury, they go, “You should grow out of it. You should recover. It’s just the inflammation and swelling.” But we here see a different pattern. And then on 9/11, just about four days later, “This week I started going to see people and getting some initial tests done. At this point I could skate for about twenty-five to thirty minutes before symptoms. The day after I would feel fine. I took a couple days off, but no change.”

And then three days later, “Drove down to the prelims for San Diego contest, skated for about five minutes before starting my symptoms. I left the contest and drove straight to the imaging center and did an MRI of my brain. After that stopped by urgent care to run some basic blood tests.” At this point it’s gotten bad enough that within the first five minutes he had symptoms, he’s getting disorientation, double vision, vertigo, and he’s scared. So he goes and gets worked up. MRI comes back, it’s totally normal. Okay?

And then on 9/19, “Went to the Dew Tour in Salt Lake City, mostly to see the medical staff, and just by entering the contest I get points, so I would be qualified for next year and in year-end rankings. Could not complete a full run.” A full run is two minutes. So his endurance keeps going down. So there could be an inflammatory cascade, there could be swelling, there could be a greater dislodge, there could be lack of adaptation. All these things are potentially possible, okay?

And then, end of September, “Right around here I would be able to skate for about ten to twenty minutes before symptoms, but the next day I would feel normal. One day around here, I don’t remember the exact date, I went skating and got the symptoms right away, and they didn’t disappear the next day. They became permanent all day long, every day.” So, as time went on, he suffered from his endurance going on, and then he had chronic, ongoing dizziness and disorientation from that date, at the end of September. So then about… a little over a month, he started to… maybe about five weeks, he completely declined and then never recovered. And then seventeen months later we get to see him, and during that time he’s seeing all those different treatments we talked about.


So, can you localize the region with the medical history and timeline? What are some possibilities? Because you may not get to one exact one, but what are some possibilities? So let’s go here, and as an exercise, let’s try to localize the region, and then let’s go through each one of these mechanisms. Is it inflammatory? Is it vascular? Is it structural? Is it endolymphatic? Is it the vestibular apparatus receptor damage from ototoxicity? Is it a central lesion? So what is it?

So, that’s what you want to do when you leave. Guys, what people do when they leave is, they go, “Oh, I don’t know what to do.” Because they don’t sit down and write down the clinical thought process. There’s certain forms you should just pull out, and when you see a patient, go through each one of them. And you should also rewrite the information we’re giving to you in your own words, so then it becomes yours. Then you own it. Maybe like in your recall and your memory. You explain things the way you understand it versus how it’s written. Okay? But have the process.

So, first question. Is it vestibular neuritis? Do you think it’s vestibular neuritis? Do you think it’s labyrinthitis? Do you think it’s autoimmune vestibulopathy? No symptoms whatsoever before a head trauma, and then he developed all these symptoms. Do you think it’s vestibular neuritis? Did you guys see a history of infec-tion and then he ended up getting dizzy after that? Did you see any hearing loss? No. So it’s not probably vestibular neuritis, it’s not labyrinthitis. Is it autoimmune vestibulopathy? Probably not. I mean, there are some cases published of people getting head trauma and developing autoimmunity. Actually, in animal models, they’ve shown that, so the autoimmune shift, but it doesn’t necessarily present that way.

So, I’m going to go through how I went through it, and my thought process. And it could be different than yours, and if it is, it’s okay, as long as we’re going through a process, right? So, I’m assuming it’s not inflammatory peripheral nerve issue. Now, he could have inflammation in his brain, and he probably has swelling and inflammation in his brain over time, but it’s not a peripheral inflammatory condition as far as my workup. Okay?

So then we go into vascular. Do you guys think it’s a brainstem stroke? Or a TIA? Or a migraine? Or dysau-tonomia? Well, it’s not a brainstem stroke, because he doesn’t have any other lateral medullary, lateral pontine symptoms, right? And he had it after a traumatic injury, like it’s not common to get an injury and stroke like that. It’s more likely that was the culprit. It’s probably not a TIA, because the symptoms what? They disappear after about twenty-four hours.

[20.0]

He may have some dysautonomia from his vestibular system, but for the most part, it’s not… it’s secondary. So we’re going to probably put that there.

Now, let’s talk about structural. Is it possible that he could have a fistula? Do you have any symptoms of fistula with him? Does he complain that when he bears down and… because he’s going to bear down when he pumps in the skateboarding. Does he have symptoms come on? Maybe you should ask. Maybe he does. Does he have any symptoms when he is straining, going to the bathroom? Or does loud noise make him have symptoms? So probably not. So… And some of these you leave into shades of gray, you don’t have to fully commit, but it’s probably not likely.


It’s probably not superior canal dehiscence. Doesn’t have the symptoms of that.

Could it be his tympanic membrane is damaged? Maybe, maybe not, but probably not, because he doesn’t have any hearing loss. If you damage your tympanic membrane, you’re going to have hearing loss.

Is it otosclerosis? No, because then he’d complain of hearing loss. So we’re just trying to diagnose from history. Now, you could do an exam and be wrong, but just from the history, not present in the history.

Is it acoustic neuroma? Probably not. You probably don’t have the timeline, and an event, and all of a sudden have a tumor. Right?

And is it potentially BPPV? Maybe. I mean, Dr. Brock showed… went through a case where we had… what I recall, he’s getting in a car, and fall, and injure his head, and he had dislodge of crystals. Maybe it’s a possibility that there could be some BPPV, that some of those crystals got off the otolith, and now in his posterior canal, and when he looks up and he skates, as he pumps up, he’s getting symptoms, right? And it’s getting more adaptive and worse. But we’re not really sure. So for me, the way I did it is, I said, “Mm, maybe I’m going to put my potential possibility here, but I’m not sure.”

Is it Ménière’s? Do you see tinnitus and pressure in his ear, and drop attacks, and vertigo associated with that? No. So it isn’t any of the clinical presentations of Ménière’s.

And then, is it potentially pharmaceutical ototoxicity or environmental toxins? Well, probably not from the onset, but listen, he’s on a lot of acetaminophen, and he’s been taking that for a very long time for chronic pain. So we have him with one of the drugs that may have some ototoxicity. Okay? So for me, I put that as a potential possibility.

And is it potentially central lesion or something of that kind? Could he have just damaged his vestibular? Could he have cerebellar contusion, and just damaged his brain from the injury? Absolutely. Right? So that’s a possibility too.

So when we’re done going through this process, now my list of diagnoses goes down. Now, for me, in my practice, I always do an exam, kind of figure out what’s going on, and then I rule everything else out. So I’m going to go in there and check his hearing. I’m going to go in there and check his eardrum. I’m going to go in there and put some goggles on him, and have him do a Valsalva, and see if he has any symptoms. I’m going to clap next to his ear and see if he has any symptoms associated with the fistula. Right? I’m going to see if he has any horizontal nystagmus associated with vestibular neuritis. I’m going to do my lab work, make sure I’m not missing something inflammatory, autoimmune that’s there. Right? I’m going to do my exam and make sure there’s no subtle transient stroke symptoms left over.

So, we still go through the exam and go through the same thing one more time, but I’m just going through the symptoms first. So usually you want to figure out what it is, and then rule out everything else. At least that’s how I do it. Okay?

Now, so what we’re left with is, it could be mixed central and peripheral. And the reason I say mixed central and peripheral; peripheral I mean he may have ototoxicity that the high dose of acetaminophen he’s been


taking for all these years may have caught up with him, especially if he’s had chronic inflammation and depleted his glutathione. And here’s the thing: His endurance is involved. So what does inflammation do to brain mitochondria? Inflammation uncouples it. And here’s how the brain works: When you injure the brain, you turn on glial cells. But the glial cells then turn on other glial cells, and the glial cells then turn on other glial cells, like a domino effect. So this is the entire mechanism of post-traumatic encephalopathy. You get a blow, and you promote an inflammatory cascade. And an inflammatory cascade promotes other inflammatory cascade. So, you know, I think he might have some central peripheral vestibulopathy, or vestibulocerebellar-related issues, and central, and also peripheral from the ototoxicity.

That was my thought process. You guys see how I’m going through it? I could be wrong, could be right. Doesn’t matter. As you go through your exercise, you would just kind of think about how to go through the process. Do not just jump to treatment. This is what the worst practitioners do, let me tell you. They jump to treatment to see if it helps them. Don’t do that. You’re going to make patients sick, you could make them worse. It means you’re a diagnostic… You need to be a diagnostic champion. Diagnose it, and know very clearly what it is, and then smile cheek-to-cheek, and then figure it out and then try some things and see if it makes a difference. Don’t go, “Oh, I just learned positional maneuver techniques. Let’s try that! I think you have nystagmus. Let’s turn you over here. Let’s turn you over here.” And then they get up and they throw up, and they go, “I hate you,” and all these things. Alright? Okay.

Now, so here he is. Some exam findings, more than one year after the injury. So I check blood pressure bilaterally simultaneously with electronic cuffs, and no major difference there. Now, if I saw some changes and shifts there, then I know as he stands up and changes positions, his vestibular system could be firing into his autonomic centers and causing massive change. So I’m not seeing that. But he’s also not really complaining of dysautonomia symptoms, okay?

So, we did some panoptics, we saw his pupils fatigue, and basically we went through and we look at the panoptic, we have him close his eyes and then we see a slight beat nystagmus. So he’s got some nystagmus, and sometimes when you are looking at someone, when you cover one eye and then a light shines in, you can’t fixate, so you see nystagmus. But the direction of nystagmus is switched, because of the lens. So if it’s beating right, it’s actually left. If it’s left it’s right, okay?

And then we looked at his palate, and… You know, for the most part, nothing serious going on there. We checked some pursuit issues, and he had some compensatory head rotations and diplopia, found it was the left lateral rectus muscle. We did a cover-uncover test; he had eye muscle weakness, especially with left lateral rectus. We went through and checked pinwheel face testing, and he had a little bit of difference or hyperalgesia on his right face, and that’s it.

So, I’m going to show you his exam, and I want you to try to figure out what’s going on. Okay? Now, when you look at his exam, what I’m doing is, I’m letting him play out with things over and over again. So I’m not just doing, for example, he’s going to do supination-pronation, I’m not just doing this, “Oh, got it!” I’m letting it go on for a while, and I want to see what happens. Because I want to do repeat testing to see if he’s got endurance issues. Right from his history, I’m a little worried about his endurance, because he’s getting worse over time. Right? So, here he is here.

Volume?


August 27, Mathias Ringstrom. Go ahead and move your hands back and forth as fast as you can, fast-fast-fast-fast-fast-fast-fast-fast-fast-fast-fast…

You see something…

…fast-fast-fast. Keep going.

You see the left side?

Now keep going.

Not moving as well?

Okay, and bring your elbows in.

See he still has the left side rotation?

Do the same thing. Elbows in like this. There you go. And as fast as you can, fast as you can, fast as you can. Okay. And go ahead and…

A little dyskinetic palm…

Slap palm fast as you can, fast as you can.

That’s dysrhythmia.

Okay. Hands out, and then go ahead and play the piano as fast as you can.

Watch what happens to his left hand.

Fast-fast-fast-fast-fast. Okay. That’s good.

It cramps.

And just relax.

It’s endurance.

And then what we’re going to do is, we’re going to have you… Mathias, I’m going to have you stand back a little bit farther. Close – okay – go ahead and close your eyes.

You see his head rotation to the left when he closes his eyes?

Okay.

It’s just increased tone there.


And then go ahead and put one foot in front of the other, and then… Open your eyes first. Go ahead and put one foot in front of the other, and stay in that position with your eyes open. Then eyes closed.

Is that stable? No. He didn’t have any posterior column issues.

Okay, and then switch feet the other way with your eyes open first.

No neuropathy.

Eyes open first. Try to stay in that position. Okay close your eyes.

See his titubations? He’s not stable. Which way is he going?

Okay.

He’s kind of all over the place.

Okay. And then we’ll have you try to walk in a straight line heel-to-toe all the way across the room. “Eyes open or closed?” Eyes open first.

He’s adapting a little bit here but he’s…

Okay, I’ll have you go back. And this time we’ll do it knees… Eyes closed.

There he goes.

Okay. So you guys see some of the things that we look at. So, what did you see with the exam findings? So you saw the left head rotation. We know he’s got left lateral rectus weakness. We know he’s got left dysdiadochokinesia, okay? And we know he’s got a little bit of left facial paresis, so the left cerebellum fires to the cortex, the cortex fires to the contralateral facial nuclei, which impacts the lower face.

[30.05]

And we know he’s got some significant ataxia, which is associated with vestibulocerebellum, spinocerebellum.

So then what I wanted to do is, I really wanted to check his vestibulo-ocular reflexes, because I’m really thinking his vestibulocerebellum may be involved. Okay? Now, I didn’t have it on video, because I was there with him alone, so I couldn’t do BPPV testing on video, but no problems with positional testing. Okay? And look at his vestibulo-ocular reflex.

I want you to see something. This movement here is the vestibulo-ocular reflex, and after five seconds, it flattens out. You guys see that? So that’s endurance issues. His vestibulocerebellum doesn’t have any endurance. It’s just completely fatiguing. So we do it for five seconds and it’s gone. So when I play the video, what you’re going to see is, his eyes are going to move with the proper vestibular reflex, and then it stops, and his eye dilates, and he gets ptosis on the left. Okay? So watch.


He’s watching a screen with a red-and-white strip going through. He’s actually optokinetic. And then after… There, he’s done. He’s cooked. He can’t do this. Look at his ptosis developing. Look at his fatigue. Okay, so which way… Should we put him in a chair and start spinning him? Well, it’s the left side. I mean, I think we can spin him in a chair and do it, right? It’s not fantastic? No. We didn’t do that. Okay.

Now, I want you to see him before his injury, so you have an idea the degree of deficit he got. Okay? Now, I want you to watch him as a professional skateboarder before the injury, okay? And then ask the question: How do you think his vestibular system is? Is it an efficient vestibular system or not? And then, actually, when you spend some time looking at that, ask a second question: Is there any athlete you know that might have a better vestibular system than him? Just think… Ask those questions. Okay. So, there’s some music on this, so it’s from a video. Okay. So, let’s play this.

[music playing “what is wrong with me”]

He’s flipping those with his toes. These halfpipes are about fifteen feet. How’s his parietal lobe? How’s his vestibular system? How’s his cerebellum? How’s his otolith? How’s his canals? Okay. Which athlete has a better vestibular system? A gymnast? I don’t think so. Because he’s going fast. He’s flipping this with his intrinsic toe muscles and landing on it and spinning, and sliding. See that? So when you see where he was, you guys see how significant his injury was? So if someone just had bad balance, and never did vestibular integration, and they had that, you’re, “Okay, not so bad. I get that dysdiadochokinesia. But with him, it is pretty, pretty significant, okay?

So, lets go through the first question. How significant is his history? It’s significant. You guys have to compare patients to themselves before and after if you have trauma or brain injury. You can’t compare them to other people. Don’t be the person that does, “Well, I have ataxia too, so that’s okay. That’s normal.” Because it’s not. It just means you have a bad cerebellum and vestibular system, okay? Think of how he was, and where he is now. Okay.

Now, when you look at this, we want to go through and we want to rule out some things. At this point, we know it’s not BPPV from the testing we’ve done, and now we’re trying to ask the question: Are there any neurochemical issues that are involved? And before I do that, did his exam findings get better or worse with repeat testing? Got worse. Which means if you go in there and try to do aggressive therapy, you’re going to fry this guy, which he’s already had done. Okay? When he went to see the otoneurologist, and they put him an Epley device, and kept spinning him and spinning him, and doing things hoping that it would be BPPV, he got really, really dizzy and had problems with that, okay?

Now, here’s the first question: Did you identify any neurochemical pathways of this region? Did you identify any metabolic factors? Because here’s where I’m going clinically: I’m not going to rehab this guy right away. I’m going to go in there and I’m going to try to help Mathias, and try to go in there and see if I can improve his metabolic endurance. Because if he can’t do an optokinetic for five seconds, and completely shut down, and then need a break, there’s no stimulation I’m going to do to his vestibular system, okay? Now, the vestibular system that was involved with him was his left side. His left vestibular cerebellum was involved, as you can tell from the exam findings.


So, here’s some things from his history that are metabolic factors. He had symptoms worse with caffeine, and what does caffeine do? Well, caffeine has the ability to discharge calcium receptors in the cerebellum. And, he was on acetaminophen, which is an ototoxic compound, for many years, at a prescription dose for very high levels, which actually deplete glutathione. And once you deplete glutathione, what do you get? You get ototoxicity. But he’s not really having bilateral symptoms, which you might expect if it gets – you know – if it gets into the blood supply and vasculature. He just has unilateral symptoms. But I still don’t like it. So I’m not convinced if that’s the only thing, but you’ve got to have the discussion, and go, “Hey, you need to cut down on the acetaminophen,” and you have to do what? Increase his glutathione levels.

So, biotransformation pathways: caffeine, acetaminophen, they get metabolized in the liver and become water-soluble and non-reactive if they go through oxygen reduction involving glutathione and phase II conjugation involving glutathione. So he’s all… His whole system is all glutathione.

I was a little bit more thorough. He had a history of lung puncture, so I do spirometric testing in my office. His numbers were good. We ran some blood work. And on blood work, we did chem-20 screens. The general screen panel and homocysteine, he had functional low glucose, so he’s kind of… a little bit hypoglycemic. He had some elevations of transaminase, his markers that some people call liver enzymes, but they’re not liver enzymes. They’re found in muscle tissue, they’re found in kidneys, they’re found in pretty much most tissues of the body. Some slight elevations there. But no pattern that was specific to liver disease or kidney disease, just a slight elevation, which sometimes happen when people deplete their glutathione from medication, especially GGT. So literature shows, when people deplete their glutathione, GGT can become elevated. So you get a slight elevation in GGT. Okay? And he had a slight elevation of homocysteine.

So we went through, and go, “Okay, here’s what we’re going to do. Here’s what we think may be going on with him.” He had glutathione depletion. He had a little bit of iron deficiency. Now, why do you think he had iron deficiency? Because someone chelated him right before. And what do chelators bind to? Metals and iron. The chelation probably made him iron-deficient. Okay? And then a little blood sugar issues, homocysteine just a little bit elevated, and those are the things that we did.

So what kind of nutritional strategies would you consider doing? And this is – again – this is where it’s going to be personal. You guys, you can do it a whole bunch of different ways. There’s no right answer. Just want to show a mechanism, try an application, see how he does. You know, there’s a saying that when you’re working with people that are chronic, and have conditions that are difficult to figure out and manage and treat, you have to work through the case. You have to work through the case. Now listen: We can… We were able to, like, put him and just move him, give him some little left rotations in a chair without exceeding his metabolic fatigue levels, and his dysdiadochokinesia would improve; he’d get a little more stable. That’s what we call a party trick. So if I just did that, and go, “Yeah! You’ve… That’s it! You’re going to get better!” that’s crazy. He’s not. You have to do a thorough workup.

And like I’ve said before, guys, it’s not about doing functional medicine and functional neurology. It’s about you either do a competent, full workup, or you don’t. That’s it. You’re either a competent practitioner and look at blood, and look at inflammation, and look at exams, and do all the things, or you don’t. Okay? That’s why I never call myself a functional neurologist, I don’t call myself a functional medicine practitioner, I just call myself Datis. And I don’t want any labels, and I don’t care, because I don’t want to be – you know – labeled that way. Okay? Now, if you ever look at my office stuff, it’s nothing there. Alright.


Glutathione, IV is what we put him on. We put him on some glutathione precursors. We stabilized blood sugar. We gave him some methyl donors. We gave him some anti-inflammatory flavonoids. Okay? This was the first thing. Like, “Hey, you are too compromised. We can’t do any therapy yet; we need to load you up.” So his response was, “God, more supplements?” I go, “Yes, because these actually are specific, not just random to your lab markers and the things that are going on.” Okay.

So then what we did is, we went through… We wanted to go through the next step, identify any exercises to activate the involved region. So I want to see his endurance improve before we go into any kind of therapy. You guys understand? Once his vestibular reflexes get normal, then we’ll do some… We’ll go over and do some therapy.

[39.59]

But we found it was left vestibular cerebellum. We gave him some left vestibular cerebellum exercises once he started to recover. You know what I gave him? “I want you to stand on your skateboard and keep turning to the left. I want you to picture only moving to the left.” And we did some – you know – various things like that. But if he had any symptoms, he would stop, and we’d figure out his fatigue levels, but only after we got his OPKs improved.

We want to look at what are presynaptic projections to his vestibulocerebellum, or to his brain, or to the areas that are involved? Well, we know it’s the left vestibular apparatus. We know it probably has impact on right vestibular cortex. His brain is probably inflamed. Cerebellum is probably inflamed. And then, let’s go back. If we think his vestibular cerebellum is inflamed, which blood vessels are involved? What’s the vasculature to the cerebellum? Posterior inferior cerebellar artery, Anterior inferior cerebellar artery, and superior cerebellar artery. So just doing… So I can back off and not do vestibular therapy, because it’s going to crash him, and then do some lateral supination-pronation, and then see if that gets blood flow to his cerebellum without really pushing the area of the injury. Because if I do this, and he coordinates now with his left hand, he shunts blood there, and it has an effect – you know – more on the lateral, but it shunts blood to the entire cerebellum, and it’s just going to – as I give him nutrients and supplements – it’s going to support him. So I want to give him supplements, but I want him to get to the area. So we went off some of those – you know – specific areas, and we did some vestibulocerebellar exercises.

But the arteries are left PICA, and AICA, SCA, and right… MCA for the right vestibulo-insular cortex. So we decided to do some left vestibulocerebellar exercises, and if you look at your applications, it’s right out of your… And you can theoretically use any one of these on your complication chart, and just play around with it, and see what changes your exam findings. Please don’t think you have to know exactly what specific exercise to do, and if you don’t you can’t figure it out. That’s what people do when they want to make neurology complicated. It is not complicated. Okay? So if someone tells you this is the way to do it and any other way would make them worse, they’re probably wrong, especially if they didn’t test it, and they come up with that conclusion. That’s one of the things that’s just terrible that happens out there. So everyone becomes insecure. Try various things, do what you need to do, and see what makes a difference.

Now, let me show you his pretreatment response again, so you can see.


See him fatigue after five seconds. See the ptosis there. See his dilated pupil gets worse as he does it. And he’s cooked. That was the initial exam.

So we engaged in, initially, some nutritional strategies to make the change there, and then we gave him some exercise to do. Now, one of the things I also want to show you is, we have two clinical thought process flow charts. One of them is… So we supported the metabolic factors for two weeks prior to brain rehab, and then one of the things we wanted to do is go in there, and I want to show you this. We went down the flow chart this way. Abnormal exam findings, repeat testing kept getting worse, so we needed to address his metabolic concerns first. So that’s what we did first. We addressed his metabolic concerns first, and that allowed us to support his metabolic factors, and here he is post-treatment.

Now we’re ready to do rehab. You guys see the lines are all the way through? Did you see any ptosis? No. Stable. And the test, you know. runs for – the way I have it set up – ten seconds. No problem. Pretty good movements all the way through.

So this is an example where – you know – you go through a differential diagnosis with all the things you learned. You then look at an application. You see if it got worse or better. We made the clinical call? Do we treat nutritional things first? Do we do brain rehab first? And then that’s where we went with that case. And if you get a chance, you know, kind of go through this and as you work up some patients… Like, you should work up some patients that are friends, or that could be patient with you. And I strongly encourage you to make your own exam form for each part of the exam you do, in order, instead of memorizing it, and then take the two flow charts we use – the clinical decision-making tree, and the flowchart where we look at identifying neurofatigue – go through that, and then put it in there, and then the clinical thought process becomes very effective.

If you learn it from the beginning, it just saves you so much time, okay? If you go around it and take time and just want to jump into what you do, and start doing random stuff, you just never get that efficient clinical though process. It actually doesn’t take long to do it. I mean, you could do an exam really quickly, going through all these things really quick, as you get used to it, and go faster and faster. Okay?

So, I hope this case kind of showed you how we can apply some of the principles. It’s pretty straightforward. We went through all the… You guys all went through all the diff-dis. It was really good; you guys all pretty much got it, and then you guys see how we did the vestibular applications. Okay?

So, I’m done with my case, and Dr. Brock is going to go through his case. Just give us a minute for the transition, and he’ll go through his case, then we’ll do a review, and then we’ll do questions.

[45.20]

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