Dysautonomia Case Review Series - Case 1
– Hello, my name’s Dr. Freddys Garcia. Today we’re gonna be doing a video case review with Dr. Nate Keiser. Dr. Keiser, how are you doing today?
– Doing great and glad to be here.
– Dr. Keiser is spearheading our dysautonomia program, which is taking off in November, but today we are starting off a three-part video case series and this is number one. So you’re ready to jump right into it? You’re ready to do this?
– Yeah. It’s gonna be exciting. Let’s do it.
– All right. So let’s see. What do you got Dr. Keiser?
– Okay, so we’re gonna do a three-part series and the reason we’re doing three parts is we’re gonna… We’re gonna show three different cases that all have a similar mechanism of injury. These are all traumatic brain injury based cases, and they all have a very similar presentation as far as subjective symptoms, right? They all look kind of the same, but what we’re gonna tease out is why we need to make sure that we don’t make those assumptions that of course the treatment is gonna be the same. We rock on our way we go. So we’re gonna really kind of get into the depth of how we think about these cases so that we can dive a little deeper and use that information to be able to modify the treatment so that we get our best outcomes. And that’s really what we wanna solve with these three cases. So, first one, let’s dive in here.
– Dr. Keiser, let me stop you right there. So you’re telling me that all three of these cases, all concussions, that’s how they all started?
– All concussions.
– So I gotta ask, is a dysautonomia common with concussions? I mean, it seems to have three in a row is kinda like, you’re kind of going home one second.
– Yeah, so these cases are all actually from a similar time period. And one of the things that’s probably good for everybody to know is when you start looking at, when we kind of cross over into the chronic range and we get a couple of months in to a concussion, we see that more than 70% of those people, especially in adolescent age groups, report dysautonomia symptoms once we start hitting those chronic phases. So if you’re in the world where you’re seeing cases that are not acute, you’re not seeing them in the first few days, but you’re seeing them weeks or months or years, like you’re gonna see here, when you start seeing them out further, we’re likely going to see dysautonomia as part of the presentation. So it’s super important that we factor that in to not only the diagnostic component, cause it matters, but particularly into the treatment component because now you’ve got a brain injury that also has autonomic limitations to it. And that’s the super important part.
– Wow, fascinating. Okay. Well, sorry I asked that right away. But wow, I’m already learning. All right, let’s do this. Let’s do this.
– All right, let’s see if we can pull it up here. So the case, here we go. So this case was of a 22-year old male as when he presented, had a head trauma in a bicycle crash, and you can read all this right here, it’s pretty simple. But he was a training accident and off his bike, over the handlebars, hits his head on the side of the road and immediately severe head pain, visual disturbance. And then progressive from there, as we’re grabbing it, it’s brain fog and that’s been diagnosed into a POTS. So we actually got this case two years into the accident. So I can remember this first phone call, so the first time I kind of went through this was in a phone call with him and his father and kind of going through these things, you start to see these look very similar to a lot of the things that we look at. With most concussions, you can see head pain, motion intolerance. So this is not just since he’s riding in a car, but also even just trying to get on a bike again, walking around, being in a mall, anything you think of, whether it’s him moving or the world moving, he’s having a hard time with that. And that becomes a big part of what we see. And we actually, to kind of spoil the part we’re gonna look at in a little bit, We see that this motion intolerance actually comes with a pretty drastic spike in heart rate. So that gives us some clues as to what’s going on, but disequilibrium, having balance troubles feeling like he’s moving when he’s walking around, like he’s swaying. And as you can imagine, 20-year old athlete dealing with that, will start to get into some mood components as well, feeling depressed. Can’t go to school, can’t train, it’s like everything you’ve ever wanted to do, you’re just kind of locked out of. So you see concentration, was not able to exercise and he’s an endurance athlete, so you can imagine endurance athlete, not being able to exercise kind of a big deal. Temperature regulation problems is from your Northern country. So dealing with cold became a little bit tricky. Confusion, brain fog, just feeling gross, malaise, fatigue. And again, been dealing with this for two years. So the first conversation that we had was really around is this even possible. He’d been recommended from another physician. That’s how I came across him. And there was a really just a point of dejection where he’s like, we tried, I mean, they’d had tried so many things, are we gonna be able to get anywhere, honestly. And my honest answer at this point is I don’t know. So though all these things are really things that are pretty common in concussion, but the point is like we don’t really know until we see what’s going on, if we’re gonna have any impact. So at this point, even though it’s on the phone, we’re thinking about these questions. Yeah.
– So Dr. Keiser, so you’re telling me, so this person is two years after the injury, but they already arrived, they already have the diagnosis of POTS, which you gotta assume is a little bit better ’cause some patients have POTS and they don’t even know it yet like no doctors even arrived at that, but these patients, they’ve already been trying to treat POTS by this time, I’m assuming and haven’t been able to kind of find their way out of it yet?
– Yeah, that’s a good point. So the trend for a long time was that nobody knew what it was at all. It was very rare to find anybody that had been diagnosed at all. But now you’re seeing bigger institutions are more aware of it. So you’re seeing cardiologists and even some neurologist that will start to diagnose these things, but we diagnose them kind of loosely. And you know, when we think about treatment components, it’s really thought of in more of a symptom management kind of way. So I think we stand poised to really offer the ability to come at it from a mechanistic perspective of like, what is causing this? And being able to start chipping away at that and understanding if we can figure out what’s causing it. Can we then figure out what’s going on, create a solution. And for that we’ve become super popular, which is a really great thing. So kind of thinking about this one, the first part is like, what do we need to rule out? If this guy is going to fly from a long way away, he’s gonna come see me, I wanna make sure that he doesn’t get here and we’re like, oh, we should have checked this first. So ahead of time, we wanna make sure we get all the CT scans sent over. We’re looking at MRIs, we’re looking at everything that’s been done before. Really trying to make sure, I mean, we’re ruling out, there’s no bleeds, obviously we’re two years out. So a lot of those things that we’d see in the acute phases, maybe aren’t as high on the differential as they would have been if this was a week out. But we wanna look at medication lists, make sure we’re not dealing with any kind of protracted pain syndromes based on medications that we’re using, especially in dysautonomia communities. If they have been previously diagnosed, you’re going to find a lot of them will be on either medications that will regulate heart rate or medications that’ll regulate blood pressure. And those are pretty common and also like for the cortisone. So those are really common. So we have to make sure that we understand we’re not gonna take people off of those and put them in a train wreck before they come in. So we wanna make sure we understand when they’re on them, what is this gonna look like? When they’re not on them, what is this gonna look like? How do we treat them within the context of being on these medications? Even if there’s a hope that we can move them away from them, we still have to understand how is this system gonna work under these constraints. So super important with what we were thinking about early on. He doesn’t have any limiting factors as far as that goes, no zebras, no viral things that we’re overly concerned about. All his blood work checks out fine, hormone levels are all okay. So all those things have been looked at at this point. So we really get to cross a lot of things off the list, which is great because then we get to dig in and really kind of see what’s going on. So then we pop forward. So the questions that I’m kinda interested in, maybe for the people to think about at home, just to bird dog on their own would be like, where would you go from here? Obviously this is wide open at this stage. But as I’m looking through that list in my mind, it puts thoughts in my head about what do I think this could be? And what do I wanna prove that it’s not? Freddys, you gotta be weighing in on that. What are your thoughts there?
– Well, you know it’s interesting because I think about it like you’re right. The thing that throws me off about this case already is like, we’re two we’re two years later. Like a moment ago you were saying like, Hey, we think the things a little differently if it was seven days later or three days later, right? So I look at this list, you know, and maybe these things were there for a long time or not, but the fact that he had severe pain and all these things and just the mechanism injury, I’m going all right you know, no subdural bleeds, do they have to do a CAT scan or any of that, or the CAT scan to see, to rule out all the really, really bad stuff that can happen. But the fact that we were two years later and he already has a diagnosis of POTS from the head injury, you know, I actually, I’m not sure exactly which stone to turn over yet to get deeper into this, but this is why you’re here, Dr. Keiser. You’re gonna teach me too.
– Well, yeah. But that’s where it is. So we don’t have anything crazy that we’re looking at here. We’re looking at like, there’s a high probability this is a functional injury. So we wanna understand what’s going on. So if we dive in, he flies out, we fast forward a little bit and we’re in an exam. And we’re just going to hit the high points. We’re not gonna go through the whole thing, but just understanding that this is part of like a pretty comprehensive physical, right? So first thing we’re noticing is we get these pretty pronounced hesitations in a UPDRS scale. So Freddys, I’m gonna throw you on, when you think of UPDRS scale, you’re thinking about what syndromes?
– Well, movement disorders specifically Parkinson’s, since it’s Unified Parkinson’s Disease Rating Scale. I know you’re looking for your hesitations, your freezes, your changes in amplitude and things like that. A grade 3 is kind of like, you know, it’s not perfect, but it’s also not terrible, but it’s definitely not great. So that’s kind of where they ended up being there, And the fact that it was one-sided and not bilateral also gives you some level of triangulating where there could be a functional lesion in this particular patient.
– Yeah, I think it’s beautiful. So grade 3, you know it’s out of four, so grade 4 is pretty severe when we’re thinking about Parkinson’s. This kid’s 22, so we kind of don’t wanna be on the scale at all. And when we think about these, they’re largely built as like a Bradykinesia scale, right? So these are all like subtexts of Bradykinesia. And if we’re thinking about Bradykinesia, we’re thinking about kind of dopamine projections into the basal ganglia, into the cotton* striatum. So if we’re thinking about that, we’re going, man, this kiddo, this guy’s injured enough to where that dopaminergic output is making it Bradykinetic, it’s though he were on a Parkinson’s scale, which is like, to me, that’s pretty significant. I know we talk about these all the time, but to put it in that context really makes you feel like there’s definitely something going on for this poor kiddo. And we see it isolated over that right side. So a lot of people are able to take in their mental model kind of shift with how they’re thinking about that, to that right side. So then in the kind of a similar context, we did some in CAT sub testing, which is simple force plate posturography. And we found that when he turns his head to the right, and when he tips his head back, he tips over backwards and falls, right? So again, coming from a competitive athletic background, like if you’re getting paid to be an athlete, usually your balance is pretty decent.
– In all positions that.
– I was only an athlete for a little while but I remember that part. Yeah, so specifically in those two regions, we see those that come up. So we’re parking that in our brain, we’re thinking about what would have to be true in our nervous system for us to fail in those two instances together. So we think about what’s happening when our eyes are closed, when we steal vision away. What’s happening when we influence neck proprioception in a specific way, what happens when we influence otolithic projections in a specific way. And we start to realize how these things tie together. We had some neurocognitive testing and we did part of the C, excuse me, C-3 logics testing. I don’t have that pulled up here, but we basically had kind of slowing on all those responses. So his latencies were a little high, memory recall, numeric recall, they’re all a little bit slow. And this is for a kid who’s pretty sharp kid. You probably see this a lot too, but I find a lot of people that we have do those tests or that have done them previously coming in, will come in and say, I can pass the impact test or I can pass, you know, pick your test, but I’m not me. Do you know what I mean? Like I hear that. That is like the most common thing is I pass it, but I’m not sharp and I’m not me. So in this case it was, I’m not sharp and I’m not me and I’m not passing this test two years later. So this was a tough one for him. All right, so one of the other big things that we found was just a convergence excess. And so obviously this is with ocular motility, right? So when we think about convergence, we’re thinking about the ability to take our eyes and take them out of this nice yoking pattern and start to deviate them immediately at the same time to maintain visual integrity on a target. That’s when we would see that. We can have convergence spasm, where it gets stuck. And we may see that one eye just fully pegs while the other one deviates. And then we get these kinds of things. What we’re looking at here is a static excess. So we’re not calling out, here’s why this is happening. We’re just observing like when I look at him, his eyes are deviated inward, right? So they’re statically deviated. When he moves around, they kind of stay that way. We haven’t declared why that is yet, we just see that it’s there. And I think that’s kind of important ’cause sometimes we jump to saying something’s a convergence spasm or an accommodative spasm or we don’t know that that is exactly how to diagnose it yet. And that comes with certain line of thinking when we start to classify it that way. So here, we’re just gonna say it’s an excess, if that’s cool. And then we have an optokinetic error. I’m gonna show you guys both of those. The next slide is gonna pull up and it’s gonna play, but we’re gonna be able to see that convergence excess. And we’re gonna also see it overlayed with the nystagmus. We’re gonna be looking at just a simple VOGD readout. So you’ll see the eyes down at the bottom and then you’ll see the graph up above. I won’t go too much depth with the graph. But for those of you that are familiar with looking at them, it’ll be easy, if you’re not familiar with looking at them, no big deal, we’re just looking at eyes like we’re looking at eyes. So the first test is actually, he’s got goggles on and there’s a cover. So you can’t see anything. You’re just looking straight ahead. If your eyes aren’t being seduced to look at anything else, then they usually just sit still and they hang out. If we’ve got interference coming from a different portion of that postural system, whether that’s your inner ear, whether that’s your neck, whether that’s anything in that bias, then we’ll see that those eyes may drift in accordance with that faulty signal. So let’s look at that here if it comes up. Tells me it wants to play. There we go. Okay, so you can see here. Looking straight ahead and then you can see them kind of start to drift toward each other and then out. And then you’re gonna see again right here where they drift toward each other.
– A little bit, yeah?
– You see a little jerk of nystagmus where it’s trying to break it too. That’s a really helpful hint because they’ll drift in and they go, ah, and they try to break apart. So you can see this also looking at the corneal responses there, the corneal light reflex.
– Yeah, so when you look at those little white circles, you see on that left eye, it’s kind of a little bit out toward the lateral part of the eye, whereas on the right one, it’s kind of right in the middle. So those are also a good way for us to see statically where those eyes are positioned in that orbit. So this is really helpful to be able to capture it. Again we talked about this Freddy, we don’t really need this technology to be able to see it. So you can do this with anything, but it is also handy to be able to share it with people so they can see what you see. And that’s really the main purpose of it.
– And I love the charts that a technology like this gives you, but I think you’re 100% right. Showing the patient some of the things that they normally can’t see means the world to them, because then they get an idea as to why maybe another clinician wasn’t able to spot something when you’re not or even just show them something either. You know what I’m saying like that them understanding I think sometimes it’s very calming to patients when they see it themselves. And I think it helps a lot.
– Oh, yeah. I mean, one of the first things you always hear is like, oh, so I’m not nuts, you know? And it’s like, yeah, we can measure it. But I usually make no claims as to whether or not they’re nuts. I haven’t met them that long yet. They might be nuts, but I am too so it’s all good. So let’s also look at the optokinetics. So the optokinetics look a little different. You guys have seen these before. You know that you’re gonna see what looks like a bunch of Christmas trees there lined up next to each other. And with that optokinetic, we’re actually watching it pass by on a screen. But as you know, you can also do this with an optokinetic drum or a tape. The main thing is the speed doesn’t change. And because the speed doesn’t change, the reflex shouldn’t change at all. So it should always just look the same. So whatever those Christmas trees look like, it should just be the same going across the whole screen. If we see that it’s variable, then we can start to kind of understand when we start thinking about why is it changing? Is it changing because we’re perceiving it as going too fast? Are we perceiving it slower than it is? Do we not have the metabolic substrate to maintain it? Meaning we can perceive it for a bit and then we fail and perceive it for a bit and we fail or do we just fail from the get-go? What does that look like? So let’s see if we can pull this one up. This is going to the left, you can see here. And as you watch his eyes, it should just beat like someone beating the basketball against the wall. You can see where he’ll have beats and then it tracks over. And then here we get this really elongated one. So in this sense, you can see him just fatiguing right in front of your eyes and then now flip and do it to the right. And we see this nice little burst of response here, and then it fatigues and then this little burst of response here and then fatigues. And then we start to kick in a few with a square wave jerk. And again. So we see both planes just can’t maintain it. And you can do a little more depth of measurement and you can see that even though he’s getting, when you’re looking at this on a screen, it’s like a screen of green balls. So it’s pretty well illuminated. We see those pupils are still pretty large. And we look at this through pupillography and some different things. This was taken before we had some of that technology, but you can see that they’re dilated more than they should be here. And then if we look at the vertical component, so again, this is like a cascade coming down. You can see there’s very little reflex at all. And then going up, will follow.
– More beats going up, but it’s still not. I wouldn’t say it’s normal.
– And then we get a little elongation here and then a couple of little shallow beats and then a little more fatigue. So I think these are helpful to show people, ’cause there’s not many times where people are gonna be like, Hey, I looked at a waterfall today or I was watching the train today and I noticed that this was going on. My buddy was there and he was looking at my eyes and here’s what we saw. So you don’t get a lot of-
– I think your response, I think your reflex is fatiguing. My buddy just said that.
– I think you’ve got some elongated slow phases and we need to get you somebody.
– Very common conversation there.
– Exactly, so these are super handy for that. And then we kind of think back to that initial presentation, thinking about movement, thinking about migraines, thinking about headaches and you’re like literally watching motion, just tax this poor kid. And I think the thing is if we can spend like five minutes on it, I think it’s helpful to think about. When you have a head injury, we have this normal sequestrations of injured tissue, right? So if I have injured tissue, I don’t have the benefit in my brain of just creating this nice, big, old bruise. Like I would, if I got hit in the face, right? If I get hit in the face, I can have a bruise and it can swell out here and I can get all that nice color, but I can get all that infiltrate there and I can start healing that up. But when it comes to my brain, I don’t have the room for that. I’m locked inside my skull. So you gotta figure out how do you get space somehow? So when you have that injured tissue, you have to decouple cerebral vasculature, meaning we normal have neurovascular coupling. So if I fire a nerve, I also I’m gonna send blood flow along with that activity. And that’s gonna support the firing of the nerve, right? So if I fire that little neuron, I get a little hit of blood flow there with my oxygen and all my substrate. And that’s what keeps that circuit alive and running. But if I’ve gotta send some cytokines and some infiltrate, some inflammation in there, I know that’s a bad word, but we like inflammation in a sense. I gotta send it there to heal, but I gotta be able to cut off some blood supply to make room. So the interesting thing about that is what creates the neurovascular recoupling, right? So if I have an injury in a tissue, I get neurovascular uncoupling, I’m trying to heal it, but then what causes the recoupling again? So there was this school study that was done and they looked at all right, so a cell needs glucose to be able to run, a neuron needs glucose, right? That’s pretty simple, neuron theory. So like, all right, here’s what we’ll do. We’ll take out all the glucose and we’ll see if that cell revascularizes. So if we get that neurovascular coupling to come back together. Doesn’t happen, it doesn’t work. So you can’t beat it with nutrition. Then they thought second, other thing we need, oxygen. Probably should have thought of that first. Oxygen’s a little more important than glucose, but whatever, it’s easier to run an experiment this way. So what do they do? They basically choke the neuron and they think if we choke it enough, the vascularization will come and save the day and we’ll get this coupling. You just end up with choked cells, it doesn’t work. But the one thing that does work, the other thing that you need, is you need some at a sensory activation of the tissue. Right? So you need to actually be able to fire the neuron to the target tissue, to be able to keep that tissue alive. Otherwise through normal neuroplastic responses, if we don’t use it, we lose it. Hebb’s axiom So what we found is that if we can activate it independent of glucose and oxygen, then we can actually recreate neurovascular coupling. Super cool concept, very applicable in the world of dysautonomia, very applicable in the world of anything where you hurt your head. But then we see it here on film ’cause we can actually watch how these are uncoupled. So we can watch him try to create this activity. We can watch him fail to deliver oxygen and we can see the function fall apart kind of rate in the test. So it’s super helpful to be able to see it and to measure it. And I think not just for us, but for the patients. Is that helpful?
– Yeah, that was helpful. Thank you.
– Cool, right on. So we come back here away from the eye movements ad now we’re thinking about, we actually do this earlier in the test, but since we’re talking about dysautonomia and POTS, we’re saving it for last. His resting heart rate is 85 seated. What are your thoughts on that?
– Well, if I remember correctly, you’re looking at what, 70 to 90 or 99 per normal heart rate. So if somebody said my heart rate is 85, because I work with a lot of athletes, I wouldn’t say that’s a great heart rate, but I also wouldn’t say that’s pathological.
– Yeah, so by normal standards, it’s not. But for us at the end of the day, it’s too high. Right, so if you’re thinking about a kiddo, who’s like used to a 50 beat per minute heart rate, and now he’s resting at 85, like something has changed. Probably something beyond conditioning has changed, right? So then we look at what happens when we put them in this normal kind of tilt response. I use an autonomic tilt table. I use an autonomic lab and a tilt table here because it’s a big part of what I do. So it makes a lot of sense. You don’t need a tilt table to be able to do this. You can do a simple test where you’re looking at laying down, you lay down for two minutes, no talking, just relaxing. And then you’re gonna grab heart rate, blood pressure. You need both. You’re gonna look at heart rate and blood pressure. And then you’re gonna have them stand up. In an ideal world, we do the tilt when we stand them up and then they’re not moving and we get no muscular activation and it’s a little bit tighter test. But I’ve had to do it on the field, I’ve had to do this in a hotel room in Switzerland, like there are just times when you’ve gotta do it outside of the lab and it’s available. So in this case we see with no real change in blood pressure, no nominal change in blood pressure, we see the supine heart rate, which is at 85. Again also not perfect, it should have dropped a little bit. And then when we come up to that full standing position within a minute, he’s already at 116. That part’s important. So one of the things we wanna think about in the nature of this tilt test, we wanna know what’s happening with the blood pressure. If we just stop and think about it, your heart rate only really exists to be able to keep your blood pressure stable. So we measure it because it helps us understand what’s going on with mean arterial pressure, but you don’t have a heart rate that’s kind of like on its own, we’d like cut off and we just have essay activity, which is its own diagnosis, right? So when we think about it coming up, but the blood pressure doesn’t change, that means your body is doing the right thing in that context. It is using, it is pulling the lever of increasing heart rate in order to maintain blood pressure. So it’s not like running rogue and your heart’s just doing crazy stuff. It’s very finely tuned heading up to that higher rate to be able to maintain that blood pressure. That’s super, super important. And I don’t think I can say how important that is enough. So in this case, when were looking at that change without a change in blood pressure, we realized like his body is compensating by maintaining a high blood pressure, excuse me, maintaining a high heart rate in order to save that blood pressure, okay? So it’s useful in understanding POTS. He’s also sympathetic, excuse me, he’s also symptomatic at this stage. So when he stands up, he gets a worsening of his headache. He starts to feel like dizzy disequilibrium. So he feels like he’s swaying and all those things kind of tie together. When I think of that swaying and I see that convergence component Freddys, I’m really thinking a lot about that otolithic drive. I’m thinking a lot about I’m having this sense of movement on this kind of linear plane, but then also when I make that orthostatic change, I’m also having this same orientation. I think about that perception and movement here in my postural system is being very akin to that postural system here when I think about my eyes. Okay, so I like this quote. Can you see? Has that come through?
– Yeah, I can see it.
– So this is by one of our colleagues in the dysautonomia world, practices at of University of Toledo. If this is still accurate when you’re watching this, but he wrote in a paper, he said, “The very organ felt to define our humanity, the brain, has been placed in a somewhat precarious position in regards to both vascular perfusion and oxygenation.” Which is pretty slick. What he’s basically saying is it takes a whole lot of machinery to pump blood up and to maintain blood flow above your heart. If you think about everything else on the planet, mostly they’re horizontal. You know what I mean? You think about all cats, dogs, lizards, everything is kinda horizontal. Doesn’t take a whole lot of machinery to make sure that we’re getting perfusion, ’cause it’s just gravity doing the job.
– I mean, it’s literally an uphill battle.
– Exactly, so you gotta have sensors in charge of all of that, right? So if you’re gonna shunt it up, you gotta be able to know how much to shunt up, how fast to do it, how quickly to change it. And how is that gonna change once it enters your skull into cerebral perfusion? Okay, this right here is a normal tool response. So I figured we should probably throw this in here. If you look at this, you can see that the red, if you look at the graph at the top, the red is the heart rate, so red and rate go together. And the blue is the blood pressure. This is what it should look like. Generally speaking, when you go from supine to tilting, to supine in a rockstar person, you’re gonna see very little change at all. You will see some data that says it’s gonna change. You’re gonna get a little slight drop in blood pressure when you come up and a little slight elevation of heart rate as you come up, but it’s not particularly big. And the more and more cases I see of this, people that are relatively normal, it looks pretty flat and straight. What we’re looking for is any of these big accelerations of heart rate when we go up. We wanna see, does it happen quickly, or does it happen over a protracted period of time? Does it come with symptoms when it happens? Do we have to stop the test because they just can’t hang. And then we look at when they come back down, does it resolve back to normal? Does it stay up for a period of time and maintain that elevation? Does it drop lower? Do we see blood pressure changes also? So those are kinds of things we’re looking at. The second graph here, I leave that on ’cause we’re also looking at respiration rates. As you know, Freddy, when we think about tachycardia, we also tend to have a little bit of hypercapnia. We tend to hyperventilate, right? So if I’m hyperventilating, I’m gonna be blowing off more carbon, which can also put me in a position to have an increase in my heart rate. So we see a lot of POTS can come from these hyperventilation syndromes, where they come up, they hyperventilate, and we actually see the POTS induced there. When we see that happen in this graph, or when you’re looking at it in real life, if you’re just watching somebody stand up, you’re looking at the respiration rate when they’re laying down, does it change when they come up? If they start breathing faster. And we notice that their heart rate’s coming up, or we noticed that blood pressure’s pretty much the same, maybe dipping a little bit, could be rising a little bit too, but it’s generally pretty much the same. Then we put a rebreather on and we have them rebreathe that oxygen slow their rate and then we watch to see if that impacts our graph. So that’s an ad-on test that we do in the midst of that test. So when we set out to do it, we’re just kind of watching, watching, watching, and then as the test goes, we may choose to augment the test as we’re working on it. So in this case, you can see that respiration rate, if you kind of watch, stays pretty similar throughout the whole thing. So we didn’t really read on this one, but even with the kiddo that we shared, this isn’t his, by the way, this is a normal one. I figured we should talk about normal before we get into pathology, but this is what we expect it to look like. Okay. How do you feel about doing just a little bit of this?
– Well, yeah, let’s dive into it.
– Okay, so with our patient here, we’re really thinking about a couple of components. This is just a high level schematic thinking about brainstem pathways of the autonomic system. A lot of times we break these down into sympathetic and parasympathetic types of activities. It’s easy to think about that way. I would like to advance that thought a little bit in thinking about when we’re in the central system, we’re still kind of in an integrative set, meaning we’ve got some reciprocity between these areas where we get pre-synaptic inputs into some sympathetic fibers. We get pre-synaptic inputs into parasympathetic nuclei, but we’ve got some crossover still. So this really simply, we were looking at the nucleus tractus solitarius, which is a sensory receptor for the parasympathetic system, but largely through the bagel apparatus. And then we’ve got the RVLM, the rostral ventrolateral medulla, which largely gives its projections down as to sympathetic outpouchings, right? So if you look along the left hand side of that screen, we see several things that all have monosynaptic inputs back into this system. But the ones that are really interesting to us in this case are where we see some of those exam findings show up. These visual and vestibular systems. We know that he’s got an otolithic crisis. And we also think about these skeletal muscle receptors. He’s also got a bit of a neck injury here, right? So when we think about these fibers coming in, we didn’t share that when we put him in those positions also, he has an influx in his heart rate. So his heart rate also goes up when he’s exposed to the optokinetics, we tested that a second time. But these tend to fire into that rostral ventrolateral medulla. If you’d look at the trigeminal nucleus, you can see that we also get some of the firing into both the RVLM and the NTS as well. So we think about it through this mechanism. Using neuromodulation or electro modulation, is very popular and I think people in the world of functional neurology have a specific talent for it, which is really great. And we used it in this case. In this case I used specifically to initiate, what we would think of as the trigeminal cardiac reflex or kind of part of what would be considered diver response. Just really quickly, this is a good paper, the DOI numbers at the bottom. But what it’s talking about is we have some differentiation from this trigeminal nerve afferent pathway, where sometimes we get activation of both the sympathetic and the parasympathetic system together, right? We kind of get this phase lock sort of an activation. But in other instances, we actually change that bias specifically when we’re looking at the component of the trigeminal pathway related to the hypoglossal system or the skin on the face, we actually see, we get suppression of sympathetic activity and acceleration of parasympathetic activity in that order. So we see withdrawal of the sympathetic activity and then a slight increase in parasympathetic activity, which is pretty cool. So we use this specifically for him because he’s got a resting heart rate at 85. Because it’s resting there, he doesn’t have to do anything special and it’s already clipping away. So when he’s sitting his, body’s basically treating it like he’s exercising, which is not ideal, if you’re not. So we use that as a way to augment that system before doing rehab ’cause we can use that reflex to artificially drop that heart rate. And as we’re artificially dropping it and increasing that parasympathetic drive, we’re breaking that sort of reflexogenic loop. Remember at the same time, when we activate a peripheral stimulus, we’re activating that portion in the brain. So we are making sure that that vascular system is coupled, that neurovascular system is coupled, so that when we use it, we can fire in and we can get a sustained activity. So we’re not using this kind of a tongue square wave stimulus as necessarily a treatment, but we’re using it as a bridge to be able to break the heart rate down, to be able to initiate the rehab so that we’re not firing it into constricted vasculature. We’re not firing it into an already hypoxic system. And that component, after having the opportunity to work with Dr. Carrick and really trying to focus on learning the things not to do, that was high on the list, right? So you have this whole world of things open at your fingertips that you can do, but what you gotta be good at is figuring out how to get rid of 90% of them and just focus the thing that’s gonna work. And this is one of those instances where understanding what is going to help us get to a vascular stability that we’re gonna be able to initiate that movement. That’s really what we’re after, so that’s why we did this. I’m talking a lot. Freddys, you got anything to add?
– No, I’m actually getting little jumps from everything you’re saying by the way. I’m enjoying this very much. Thank you, please continue.
– Awesome. I put this in there as well. This is a very similar graph, but it more closely ties in those otolithic inputs. And because this is kind of an otolithic syndrome, this is what we’re looking at. So I really wanna talk more about this one, but we should probably save this for another one. So this is on the order of the type of stimulation we did. This is what we have available in our current clinic. At the time that we saw this young man, I didn’t use this tool. I think that’s important. You can use a desk chair. I specifically like a drafting stool because they’re taller, are great tools to be able to do this. So you don’t need big old burly equipment, although it is kind of nice to be able to have, and we wanna make sure we teach you how to use it, but you can see in the lower right-hand corner, there’s a VOG tied to this as well. So you can see the eyes moving. This one’s in the dark because we’re using that as a stimulus. But basically for him, for the patient that we’re talking about, we use a right sided rotation with a fixation target after doing the steam on his tongue. Specific for him, we augmented his seat in the chair a little bit. If you think about like where that otolith is located, right, you’re about four centimeters off the mid axis. So if I’m four centimeters off the mid axis in either direction, that puts me right on top. If I’m thinking about the otolith, it’s always active under any gravicepted load. So as long as you’re on this planet and you’re not in like free gravity, you’re not like cruising around Mars, they got some gravity too, but not the same. You’re gonna have otolithic activation. So we’re trying to skew activity toward that right-hand side because of the projections we wanna use to fire into the somatosensory cortex. So we’re using a rightward rotation, but on top of that, we’re trying to make sure that we bias that right-sided otolith. So what we did was we centered the left otolith over top of the axis of the chair. So we had him scoot to the right, so to speak. So if he’s scooting to the right, what that does, is it takes the left one and the left one is spinning on axis. So if you imagine like a little top or dreidel, it’s just spinning in place. So it doesn’t get a huge deflection. If you think about what’s happening with the otoconia, with the kind of psyllium, they’re not gonna get a huge deflection. Have you ever been on one of those fare rides where it spins you so fast, you like push against the wall?
– Stick to the walls. Yeah, those are always fun.
– I can’t do them, but I know what they are. So if you imagine, like the further you are out, the more force that was gonna be developed. So as we move that right ear out off the axis, we’re gonna create a bias in the force generation. Right? So when I do that, I’m gonna have a centrifugal force of my right ear, so then I’m gonna get a greater activation of that right ear. And if I get a greater activation that right ear, I’m going to get a little better drive over into that side of the somatosensory cortex I’m interested in because I really wanna stabilize those receptor pathways for what I’m gonna later think about in terms of the UPDRS scale. So can I get a better feed forward into my basal ganglia? It helps stabilize that nigral system so that I can have a better output from a frontal perspective. Remember we’ve got cognitive issues, we’ve got emotionality issues so that’s what we’re thinking about.
– I gotta tell you Dr. Keiser, that’s very clever. What you are doing there. I mean, it’s such a simple thing that you’re doing there, but the way it’s allowing you to bias a system, because you’re familiar with the anatomy and physiology and how you’re leveraging it, that is very clever. And I’m gonna think about that and see if I can put that into my toolbox. That’s very clever, like I feel like I could stop right here and I’m like, all right, I got my good treat for the day. This is awesome.
– Well, I’m glad that helps. Yeah, it’s nice. Actually, I can’t take all the credit for that. That actually is a thought that exists in other places. I can send you guys some resources on that, the way it was studied. But this chair that you see in this picture actually has the ability to offset specifically to that four centimeter mark, which is kind of slick. But yeah, super helpful though. And you don’t need anything fancy to do it. You just line up over top of the axis of the chair.
– Well look, that’s what I was gonna ask you here, ’cause we’re looking at this technology and I know you have very, very sophisticated lab, which is why people literally fly in from all around the world to have you help them as the expert on dysautonomias. And it makes a lot of sense that you have this technology, but for a clinician who attends a dysautonomia program with you in the Carrick Institute, do they need stuff like this? I mean, you mentioned you like the stool, right?
– Yeah, I spend a lot of time not practicing like this. I had the opportunity to work. I had some very fortunate, lucky incidences after working with Dr. Carrick to be able to kind of go all over and treat and you just don’t have this stuff all over the world, that’s the reality. You kinda are limited to what you can fit in a doctor’s bag. So I spent a lot of my time in my career doing things, not using high levels of technology. And in some ways it makes you better because you gotta use your own resources. And I appreciate that a lot. I think the biggest thing, my interpretation, and nobody else has to think this way either. But I think the thing that we have to offer our patient populations is our ability to think, to be able to troubleshoot and troubleshoot in a meaningful way towards a solution. You can make anything a tool if you understand what you’re trying to do with it.
– All right, so I guess you’re saying you could have all the nice technology, but the best tool is still going to be this one, right? And make sure this is make sure this is the sharpest tool.
– I think so. I don’t know unless e-learn gets the singularity, I think we have an edge there. So that’s what I would focus on for sure. Okay, so that was the main thing we did, it was very simple treatment. It doesn’t have to be complex. Sometimes the more tools you have, the more you wanna use. This isn’t one of those cases. You can see here after three days, we don’t have that convergence spasm. Those eyes are pretty still, which is pretty cool. You can look at these optokinetic reflexes again, this is third day. You know, they’re compelling, obviously we’re showing our home runs here but this is the optokinetic response that you just kind of wanna print in your head. So when you’re doing with that tape coming by, whether you’re doing using a iPad or you’re doing it on a big screen, that’s what it should look like. And the same thing going on.
– Can you hear Dr. Carrick saying that the chart should look like a bread knife, like a saw blade? Boom, boom, boom, boom, boom. I could hear him saying.
– Yeah. I always say Christmas trees, ’cause I got red and green there. It makes me feel very festive. But yeah, bread knife, but that beat, like someone’s dribbling a ball to a beat. So when you’re thinking about it, when you’re watching it, it’s skipping beats. If it’s not rhythm, if you couldn’t play music to it, then we wanna investigate. And the same thing going in the vertical plane here.
– Those are very significant. That’s a very big difference from the first one.
– Yeah and this happens. So as you guys know, I’m not telling you anything you don’t know, but we’re really focused on the objective findings. And we really hope that we track subjective changes with that. Sometimes we can get chasing our own tail if we’re chasing subjective findings. So the objective set’s really handy, but we also wanna seem to work together. So it also, by this time headache’s clearing, we’re not getting dizzy. And we actually got him back on a bike this day, the afternoon of this day, which was a big win for him, just like in soul, like on a personal level. So that was a really big deal. And he was able to keep doing that. That finger tapping cleaned up very quickly. I mean, you know the deal sometimes if you didn’t know better, you’d think it was magic, which is pretty fun to be a part of. Again, balance comes back really well when you start normalizing that otolithic system. We looked at convergence through the lens of that, of the VOG, but more traditionally we would use a Maddox rod. I like using a 20-foot distance in the Maddox rod, but he went to normal Maddox rod testing. We see that resting heart rate start to slide down just a couple of days. And then going from that supine to standing, we’re able to get him from a 68 to a 78, no symptoms. At that point is when we start initiating active rehab. I have a really hard bias. So a lot of dysautonomia and a lot of POTS treatment is centered around cardiovascular activity, which if you’re in a de-conditioned state makes sense. But if you’re in a state where your body is just like working its tail off, trying to do normal, to me stressing that system further, I have a hard time wrapping my head around why we would do that because all we’re doing is basically taking the things already overcompensating and just pour and more onto their desk. So I don’t like doing that. So I don’t usually use active cardiovascular strategies until we hit a point where we see we can trend away from that pegged heart rate. We have to get like normal ability in the heart rate and blood pressure before I usually feel comfortable moving people into the next phase, which would be more active rehab. I think that’s the thing that’s probably useful to think about it that way. What do you think?
– No, you are 100%, it makes perfect sense. It’s like it doesn’t make sense to tax a system that isn’t doing it so well. The problem is that most people don’t realize it’s not doing so well and automatically try to go, well, here’s my protocol for somebody who has issues kind of like yours, but I’m not really sure what they are, ’cause nobody’s really labeled it yet. I mean, I get it, I get it.
– I think it’s really important ’cause if you were to do like a Google search and be like, POTS treatment, the thing that’s gonna come up most likely is a form of cardiovascular exercise.
– Yeah, actually try to increase exercise tolerance.
– To increase tolerance, which I think is a great thing in the right context. So I think the thing that really sets us apart is being able to say, people to take it apart, put it in the right context, get ourselves to where the brain can actually do the thing it’s supposed to do and then we get stronger, then we work on-
– This reminds me, ’cause I mean, you know me well enough. I come from an athletic development background. This is like when coaches are working with somebody that wants to get faster and they’re like, work harder, get faster. Like that’s the extent of the coaching. And it’s like, okay, well, I’d like to, but can you deconstruct me, figure out what’s holding me back and then rebuild me better, right? I mean, that’s what you’re doing as opposed to not realizing that a system is not working so well and saying, well, let’s increase your exercise tolerance by having you do more exercise. That’ll happen at the right time. First let’s deconstruct you, find out what we need to do, and in this scenario it a little bit, you said it was a little bit, right? Three days later, things are better, a little electro modulation in specific places ad you showed the diagrams for that along with some very cleverly biased whole body rotation. Right? And that was-
– It’s not for this case.
– What’s complex is knowing what to do, right? This reminds me of a story about the engineer who invoiced the company when he only turned to one screw and he goes, Hey, you didn’t pay me for the 10 minutes of work, you paid me ’cause I knew what screw to turn. You know like that’s the beauty of what you’re doing, you know exactly what to do, but you know, if somebody is not trained appropriately, they’re gonna, well I have 400 knobs, well, how do I approach this? And I think that’s what happens to a lot of clinicians. Right, there are actually are a lot of things you could do depending on where you’re coming from. And I think that’s one of the things that’s about the functional neurology people. They’re not just manual therapists. ‘Cause we have some clinicians that aren’t doing lots of manual therapy. We have some that are doing tons. We have some that are doing osseous adjusting. We have some that are doing only soft tissue. We have some that are doing just, I work with neurovisual therapy, right? So they have this receptor based model, but it’s all again for the purpose of creating positive plasticity to affect the brain, which then just like you showed in that other diagram, as it’s cascading effects all the way down to our autonomic nervous system, we’ve had sympathetic and parasympathetic tones that are happening together. That’s all right but we got a little bit of a rant. This is what I talk about all day with doctors, as we find out how to take them to the next level, you know?
– Yeah and I think this is an area that we have the ability to make a significant impact for people. And I say for people, because it’s in the people we treat, but also in the people that we affect, because we can advance where we’re going with it, we can do it a little better. And I think because we can do a little better, it brings the standard up. And that’s what I hope we can achieve through this process.
– This is your last slide, right Dr. Keiser.
– I believe so. Well, I have one more here. Yeah, go ahead.
– Well, I was gonna say, I think now well we can say that slide for the next one ’cause this is a case series, right?
– Yeah, so now’s a good time to tell everybody again, if this is an area of study in clinical practices, is fascinating to you that Dr. Keiser and the Carrick Institute are kicking off the dysautonomia program starts in November. The program title is Dysautonomia, a modern clinical approach to diagnosis and rehabilitation. You’re gonna be learning appropriate physical neurological exam. Again, everything evidence-based, you’re gonna learn the diagnostic criteria for all the different types of dysautonomias, you’re gonna start learning the anatomy physiology. They need to know for them to understand that pathophysiology of the various conditions. You know what to do with your patients, because if you don’t understand the conditions and the structures involved, you don’t know the ways into them. So if you looked at some of these charts and you’re going, or these diagrams that Dr. Keiser put up and you say, all right, I know a little bit of them, but I don’t really know them, we wanna get to the point where you know them. So you know where you want to, you know, what knob do you want to turn in your patient? Right, that’s a good way to say, all right, you see all those different times you go, yeah? You need to know what not to turn in the patient. Dr. Keiser is gonna teach you that. The course is gonna be done in the way that the Carrick Institute likes to deliver it, which is really done well. We’re gonna have a flip classroom, we’re gonna have lecture. This one’s gonna be five modules of three days each. And then we’re doing a very special two-day module of grand rounds up in Michigan in probably the room that you’re in right now. So we’re gonna bring in live patients. You’re gonna see Dr. Keiser put into practice and wrap it all up together for you in regards to the science and the art and the protocols you’ve learned, what it looks like in real life. So we’re gonna kind of tie it up with a ball, make it really nice, so you feel confident in your skill set because the Carrick Institute is committed to making the best clinicians in the world. So we’re gonna keep working with the best faculty in the world. And that’s why Dr. Keiser’s here spearheading that program. It kicks off in November. If you wanna learn more about it, go to carrickinstitute.com. Dr. Keiser, thank you very much for taking your time out of your busy day to teach us this. And I know we have two more, which I guess, looks similar, but are all going to be different. And I think at the end, when people look at the series, I think a couple of things are gonna happen. One, they’re gonna realize that they probably missed a lot of dysautonomias. You know, they’re going to realize that. And two, they’re gonna realize that if you understand the anatomy, physiology, and diagnostic criteria, you can make small changes that don’t have very profound effect on your patients because this alone, this was already impressive. You know, like I looked at this and I go, well, there are these clinicians out there who are going, I can’t get past this hurdle with my patient. And they just missed a little bit of what you shared here to get them passed to the next level. You know, like it’s happening right now. It’s happening right now. And we need to help those doctors so they can help those patients. That’s what I get passionate about because I get to hear both sides. I get to hear patients calling us. I do, I get to your patients calling us every day and I get to hear doctors calling us. And they’re both saying, help. At the end of the day, that’s a bold thing. But doctors are saying, Hey, what do I do for this patient? Can you talk to me about it? Who do I refer them to? We’ve got patients calling us saying, Hey, I’ve gone to eight doctors. We’ve heard about you guys, what doctor can I go to? And that’s why if it’s a dysautonomia, I’m sending them to you, I know you’re the man. And I guess in the day, everybody doesn’t know it yet, but they’re gonna be very grateful that you’re sharing your expertise when it comes to this. ‘Cause you continue to impress me and the rest of the Carrick Institute faculty and more importantly though, your patients with the results you’re getting them. So hopefully we are gonna share that and elevate everybody just like you said.
– I can’t wait, I’m excited for it.
– So to learn more about it, carrickinstitute.com. Dr. Keiser, thank you very much for your time today. To everybody else, keep an eye on your email and your social media for case study number two and three that we’ll do via video. Everybody have a great day, so long Dr. Keiser. Thank you.
Dysautonomia - A Modern Clinical Approach to Diagnosis & Rehabilitation
Presented by: Dr. Nathan Keiser
Dysautonomia is often present in patients and is missed by clinicians. This program aims to never let that happen to you by teaching what you need to know to become an expert in the diagnosis and rehabilitation of dysautonomia.
Carrick Institute is proud to bring you it’s newest specialty program titled Dysautonomia – A Modern Clinical Approach to Diagnosis & Rehabilitation, presented by Dr. Nate Keiser.
The Carrick Institute’s mission is to offer the highest quality training in an effort to help produce the world’s best clinicians. Dysautonomia is a set of conditions that are often either the direct cause of our patient’s disease or as a concomitant of what they are suffering from. Clinicians must be trained to recognize and rehabilitate dysautonomia to serve their patients at the highest levels possible.
Scholars who attend this program will learn to assess their patient’s neurophysiology through an evidence-based physical and neurological exam, learn the pathophysiology of the spectrum of dysautonomia conditions, know how to arrive at the appropriate diagnosis, and with precision learn how to create customized rehabilitation programs for that specific patient.
This is not teaching a cookie-cutter approach to dysautonomia rehab but rather teaches you how to think about each patient on a case-by-case basis so you can deliver a customized and effective solution for them.
- Autonomic Syndromes
- Central ANS physiology and pathopysiology
- Peripheral ANS physiology and pathopysiology
- Myelopathic lesions
- POTS and subtypes
- Syncope and its variants
- Neurodegeneration and Dysautonomia
- CSF Disorders
- Autoimmune Syndromes
- and more
Scholars Will Learn
- Physical and Neurological Exam Skills
- Pertinent Anatomy, Pathophysiology & differential diagnosis criteria
- How to create individualized rehabilitative strategies for your patients
Prepayment Tuition for all 6 modules: $6500
Early-Bird Tuition: $1250 (must register 30 days before class)
General Tuition: $1450 (if registering within 30 days of class)
Grand-Round Module (module 6): $799
All tuition is priced in USD.
Included in Your Tuition
- 140 hours of training with Dr. Nate Keiser (consists of five 3-day modules and one 2-day grand rounds module)
- All-access to the digital recording of the class
- Any future updates to the course videos or other materials
- 140 Neurology Hours towards the ACFN (American College of Functional Neurology) & ACNB (American Chiropractic Neurology Board) with each module
- Access to the flipped classroom with lifetime updates
- 3 months of unlimited access to Medline upon completion of the module
*Scholars will receive CEU & neurology hours upon their first completion of the module. Any re-attendance is considered an audit. Scholars must maintain an active account to receive benefits.
Re-attendance policy: Scholars who have registered and completed a course after December 2019 have the ability to re-attend the course with no additional fee. When re-attending a course, the scholar will not receive continuing education credits and will receive an audit. Carrick Institute is not responsible for providing new materials for class audits, including but not limited to manuals, shirts, equipment, etc. If manuals have been updated since the original attendance date, the updated materials will be available via PDF on the scholar’s online portal. If the scholar would like to purchase a new paper manual, they may do so before the course start date.
To view full Terms & Conditions, click here.
October 8-9, 2022 | Grand Rounds in Michigan – Limited seating – First available for those who sign up with the prepayment bundle
Grand Rounds Information
PreOrder: Clinical Skill Acquisition for the Health Care Practitioner (971)$799.00 Add to cart
Updated Clinical Neuroscience Program
Embryology & Physiology of the Nervous System (CNS01)$599.00 Add to cart