Good morning, everyone. Welcome, and thank you for helping us launch the Spotlight Series. I am John Cianca, as Ryan had said. I am the chair of the Medical Education Committee, and I want to just give you a little bit of an introduction to what the Spotlight Series and the Kinetic Chain sessions are going to be about. We are embarking on more and more virtual education or digital education. The Spotlight Series will be a varied amount of presentations throughout the year, generally a half to a full day of education spotlighting or singularly focused on a topic of interest that we hope will catch on with everyone. We're going to aim for one and maybe two a quarter. Currently, we're developing the Spotlight Series in two veins. There's a general series of topics, and then there's the Kinetic Chain Revisited, which is what we're starting with today. The idea for this, the Kinetic Chain, came to me, was handed to me actually by our Academy President, Stuart Weinstein. As we talked, I really liked the idea. It resonated with me from my education. I began developing this series of sessions that will be devoted to different aspects of the Kinetic Chain. This first one will be on gait. As you know, the Kinetic Chain is an integrated linkage of movements that the body employs to get a specific task done. That's been part of physiatric repertoire for many years. It was first introduced by Franz Rouleau in 1875. He's a mechanical engineer who postulated that any mechanical system has overlapping joints acting sequentially with each other, forming and creating a kinetic linkage. This was subsequently adapted to medicine by Arthur Steinbler, who was an orthopedic surgeon in Iowa. As far as physical medicine and rehabilitation is concerned, it really came to the fore in the early 1990s with the formation of Passor. As a result of that interest, AAPMNR has built courses over the years around this concept, with it becoming central to the thinking of physical medicine and rehabilitation specialists, particularly in MSK, but not exclusively. We study movement, we study function, and the Kinetic Chain model fits this quite nicely. That's what spurred me to continue to move with the idea that Dr. Weinstein gave me. Hopefully, over the course of the next two years, we'll see more and more of these come out. I'd also like to reference Sam Chu, who's a colleague of ours in Chicago at Shirley Ryan. He recently, in 2016, authored the Kinetic Chain Revisited New Concepts on Throwing Mechanics in Injury, which was published in PMNR in March 2016. His co-authors were Joel Press and Ben Kibler, who have long been champions of the Kinetic Chain in musculoskeletal medicine. With that, I'd like to introduce this series. I hope you all find it useful and helpful in your practices. I think it's going to be very interesting. This session in particular was developed over the last couple of months with the experts that I'll introduce shortly. As I said, I'd like to be able, with the help of the National Grand Rounds Committee, to present at least another one this year, if not two. Stay tuned for that. Right now, I'd like to introduce our first speaker, Casey Kerrigan. I can't think of a better person to launch this series. She's been a physiatrist for many years. She's written 100 peer-reviewed studies on the biomechanics of gait. She's well-known for discovering the link between women's shoes and osteoarthritis. Her research led her to co-found a shoe company called Osh in 2011. She's been manufacturing healthy footwear for women based on science. She has her MD from Harvard Medical School and also has an MS in kinesiology from UCLA. She's the former chair of the PM&R Department at the University of Virginia. She also has her own tractor, which I'm particularly jealous of, for her garden in Virginia. Casey, good morning and welcome, and please take the stage. Okay. Yeah, awesome. Okay, so normal gait. Gosh, 15 minutes. Where do I start? I thought I would show this picture of my oldest daughter when she was just learning how to take her first steps. Only a gait expert would throw all these markers on her and put her in a gait lab to try to actually study that. But you look on her face, it's like she has no idea what to do. Walking is really pretty complex. How do we break it down when we're trying to study normal gait, understanding gait in general? I try to think about it. There's three fundamentals that you want to think about. One is forward progression. You're putting one foot in front of the other. That's it. That's actually pretty easy. You put one foot in front of the other over and over again. That's the easy part. The second part is probably the hardest. It's the stance stability. You got to do it in a way that you don't fall down each time you take a step. So we're going to talk a lot about stance stability. And then energy conservation. It would be really good if you could do this energy efficiently. So as we're talking about the kinetic change, the first thing we have to do is talk about the difference between kinematics and kinetics. Kinematics is what you see. Kinematics is what you're used to. It's what you see in the clinic. It's observational. You can actually measure it too, but it's essentially the position of the joints and the limb segments throughout each phase of the gait cycle. They can be observed or measured with motion analysis. Now, kinetics is what you don't see. Well, you don't see very easily. I'm going to show you some really cool pictures where you can see it, but that's with good tech. Essentially what we're doing is we're measuring the joint torques or moments, torque and moments basically synonymous, that's calculated from a combination of 3D motion analysis and force plate analysis. And from that, we can tell what the stresses and strains are through all the soft tissues, even the structures of the joints. Basically, kinetics is where it's all at. And I'm just going to give you like a sneak peek into what we can measure in a gait lab. We can measure that green line, the ground reaction force. We can measure the muscles, what the stresses are through them, how far that is from the joints. Okay, but first I need to describe what 3D gait analysis people talk about. What's gait analysis? What's gait analysis in a modern gait laboratory? Well, there's 3D motion analysis, then there's 3D force plate analysis, and then you may have heard of there's dynamic EMG. Now, dynamic EMG, people always say, why don't we just measure muscle activity to understand what's going on? Well, muscle activity is really only good for assessing the muscle activity, timing, not really to try to quantitate it. But you're going to hear later about how EMG can be very useful, probably for spasticity when muscles are inappropriately firing. But for the most part, muscles are active because the kinetics say they should be active. So 3D motion analysis is, you just basically have these cameras all around a room, and these cameras capture these markers that you put on the body. And the markers go in such a way that you can measure the limb segments. You can measure the joint rotations in all three planes. So not just like in sagittal plane, there's a lot of motion going on, rotation, coronal plane. So we can actually measure in 3D what this motion is, but we can also measure the joint position. Now, the joint position is important when we start to measure the joint force. So the ground reaction force, or it's really, you can think about it as like the body weight, all right? It's like the body weight dropped down to the plate. And it follows this butterfly pattern, at least during walking. And these force plates, you embed in the walkway or in a treadmill. And the key is combining that 3D motion analysis. So knowing where the joint centers are with respect to where that ground reaction force line is, that's what gives you sort of that true kinetic assessment. And then you have dynamic EMG. So dynamic EMG, you can have surface electrodes. You can actually put fine wire electrodes into the muscles. And then you can get a sense of what the muscle timing is. And it's nice. It's descriptive. Again, I think this is really important when you're evaluating upper motor neuron disorders and trying to get a sense, is the muscle overly active during a particular part of the gait cycle? But as far as for normal gait, it really, the muscle activities are really predicted by the kinetics. Okay. So I'm talking about normal gait. And the first thing is, well, what about these six determinants of gait and what the energy? Isn't gait, and I got to include this as in my normal gait lecture, six determinants of gait. And I think the thing is back in, this was actually back in 1953. So they didn't have kinetic analysis back then. They were trying to just describe things happening based on the kinematics. And what they observed, and then trying to again, simplify this, is that the actual vertical displacement of the center of mass, when you walk up, when you walk, the center of mass oscillates up and down, that the actual vertical displacement of that center of mass, because that takes energy, of course, to raise your center of mass, is only a half of what would be predicted if you just walk with a straight compass. Okay. So in the hypothetical compass gait, so it just, the path is just kind of this circular pattern. But in fact, the center of mass really only displaces about half. And we showed this, and it's actually pretty simple. This looks complicated. It's just the compass gait model. And just showing with Pythagorean's theorem that X, the amount of displacement in mid stance, with the straight up line is in mid stance, and when the legs are in double limb support, what that distance is. And we evaluated all the different parts of the center of mass displacement described by Saunders, and there's pelvic rotation, there's pelvic tilt, knee flexion and stance, and all that good stuff. And found that actually none of the six determinants described by them really substantially reduce center of mass vertical displacement. In fact, knee flexion and stance increases center of mass vertical displacement. So the only thing that occurs at the end of stance, so the only thing that actually reduces center of mass displacement is heel rise. And by that, I mean, so if you're trying to memorize what the six determinants of gait are, you can say it simplifies it. There's only one. There's heel rise. So if you get asked that on a board question or something, that's the answer, heel rise. So what is heel rise? It's really just at the end of stance, the fact that you have a foot connected to the leg. And so at the end of stance, that foot raises, and that's just a function of one. It's not just plantar flexor activity, but it's also just control, being able to control that ankle and have the tibia rotate over and then into push off. So that's great. Minimizing center of mass is useful in reducing center of mass a little bit, but it's not the whole story. Because if it were, we'd all be walking like Groucho Marx. Groucho Marx is like keeping the center of mass perfectly still. Or we would be race walking. So this is kind of neat that during race walking, there's really no center of mass displacement. The reason is during walking, center of mass is highest in mid stance, and during running, center of mass is lowest in mid stance. So race walking is kind of when those cross, and so there's no center of mass displacement. So what else is going on reducing or conserving our energy? So what we do is we depend on anything that's not our muscles to maintain stability. So we can start with just quiet standing, and you've probably seen this type of slide in one form or another. But if you look at the ground reaction force, and that's the line with the arrow that goes straight up and down, that's your body weight force, which we can measure. And if you look at that line with respect to where it is next to the joint, so you can see it's a little bit behind the hip, it's a little bit in front of the knee, and then it's in front of the ankle. And what that means is because we understand anatomy, that we know we can basically hang on our Y ligaments at the hip, so we don't need any muscle activity there. We can hang on our posterior knee ligaments, maybe the anterior knee joint structures, so we don't need any muscle about the knee. But then it's in front of the ankle, and we really don't have anything to stabilize the ankle, so we need to have our soleus on to maintain stability. So if you look at that, and we can verify that by putting EMG on and show, yep, in quite standing, except for if we move around and shift weight and all that, that you can see that the only muscle activity we would see is what's occurring in the soleus. Now all we got to do is apply that same principle throughout the whole gait cycle, and then we understand gait. We can understand where all the muscles are on, we can understand where the pressures are in the joints, where the stresses and strains are, but we're really just doing that throughout the whole gait cycle. So from initial contact into loading response, mid-stance, terminal stance, in pre-swing, we can see what muscles need to be on, and then we can also get a sense of the stresses and strains through the associated soft tissues and bone and joints. Then we can quantify all this, so we can know, we quantify that ground reaction force line, then we know basically from the motion analysis how far that ground reaction force line is from the joint center. That gives us a lever arm, and then just remember physics, ground reaction force line times the lever arm is going to give you joint torque or the joint moment. So joint torques tell us, of course, more than what muscles are active. The higher the joint torque, the higher the stresses and strains. Exactly where those stresses and strains occur depends on the anatomy of the joint and surrounding structures. It could be in muscles, tendons, ligaments, or structures of the joint itself. Then I just showed you pictures of the sagittal plane. We do the exact same thing in the chronoplane and in the transverse plane. This is the sagittal plane, so this is the cool tech part. We can see all this from measure. This isn't actually a simulation. This picture was taken from a composite of data collected in the gait lab, so this is all true data, but represented. You can see that green line, and you can see just where when it's going through the joints that not much activity is needed, but the further away it gets from the joints, the more muscle activity, the more stresses and strains. Now we're going to switch over to the chronoplane, and this is where I think especially where we understand how important things are in stability in the chronoplane. The transverse plane is a little bit harder to see visually, so I can't really show it. We can see it graphically, but the same kind of thing is going on. I'm going to end with that. Then we can quantify these joints and torques, so we can see, we can graph it, we can measure it, and we can understand this in all sorts of different conditions. I think I'm going to end there. Thank you, Casey. Now I'm going to introduce James Richardson. He's a physiatrist professor at the University of Michigan in Ann Arbor. He does medical training at the University of Cincinnati and his residency at the University of Michigan. He's board certified in physical medicine and rehabilitation, as well as electrodiagnostic medicine and internal medicine. His practice combines research and teaching, and his clinical interests are in neuropathic gait, focal peripheral neuropathies, and clinical measurement of reaction time. His research is centered on gait balance and the risk of falls. Dr. Richardson, the floor is yours. Good morning, everyone. I wish I could see you. If it is, I would be looking forward to this. I have to be open and tell you that an audience absent their bored looks or on rare occasions entertaining looks or changes in body posture is a difficult audience. I wish I could see you. I'll just say with that. The presentation would be less bad if I could, because I would respond to your bored looks and I'd move along. Apologies in advance if you're zoning out and I can't pick it up, but I just can't. It's a limitation of the damndemic. We'll talk about some gait disorders, this is very clinical in nature. These are all people I actually saw and I'll present their problems as they came along. And we'll start out with some CNS disorders later. We'll talk about some peripheral neurologic things. Let's see, walking is very good for us, but only in moderation. As you can see, Ellen DeGeneres weighed in on the topic. So, and the reality is you might say, gee, how important is walking to your health? It's huge. And I remember a paper, there are so many on just a little bit of walking matters. And I'll give you one example where people with hemiparetic stroke who could walk greater than 50 feet, their risk for DVT, for deep vein thrombosis was one fifth, 20% of those people who could not walk 50 feet. So sometimes, you know, it's not easy in physical medicine rehabilitation. At times think, man, am I making a difference? Are we making a difference here? And surprisingly, a little amount of walking can do a lot. So I just want to offer that. Obviously Ellen DeGeneres is a great aunt, did much. So watching patients walk, here's a statement I have to make at the start. I want to thank these people. Each of these people, when I mentioned that I want to video you, video them for educational purposes, boom, they did not hesitate. And I respect that. And I admire each of them for their willingness to do this. And the battle they do daily with their neuromuscular difficulties. They dual task for a living. The rest of us walk automatically. And we'll hit this theme off and on again. But I want to mention it now that really walking can occur, as you know, without your frontal cortex. You don't need to think about it much. If your basal ganglia, cerebellum, brainstem nuclei, and the spinal cord are hanging in there, they're all intact, then you can walk pretty much automatically, subcortically. And your cortex is free to do other things. You can argue with your spouse, think about where you want to go eat. You can text with cars hurtling toward you. But not people who have neuromuscular difficulties. They must moment to moment consciously moderate, modulate, care for their gait in order to stay upright. Because they're walking different from the pattern they've used since age two. And so I want you to keep that in the back of your mind as we go through these people. First patient was a patient who came to me and she wanted, well, her situation was that her daughter was pregnant and her daughter wished for this patient to be a caregiver. But the problem is the patient, my patient, the baby's grandparent was falling and she wanted to quit falling so she could take care of her unborn grandson. So here's a picture of her walking and see if we can figure out why the heck she's falling, or video, I should say. And when I watch people walk, I try and think of swing phase errors and stance phase errors. Well, watch her and her stance isn't too bad. I mean, maybe the hips are a little weak. Maybe there's a bit of what we call Trendelenburg and we'll look at force diagrams later to talk about that. But I also want to look at swing phase and see what her foot placement's doing. And all of these videos we'll do twice. Here we go again. Let's watch that foot placement. Swing, stance phase isn't bad. She's not glad to be walking. Stance phase isn't bad. She's not glad, boy, my goodness gracious. She is crossing over. Look at this one. Whoa. I mean, seriously, the question is not why she's falling. The question is why she isn't falling with every step. Why isn't she, why is she just falling, you know, once a week? Why isn't she falling daily, minutely, hourly? And she was stunned, by the way, when she saw this video of herself. She couldn't believe she was walking this way. So clearly she could have foot collisions. And if you look at her swing phase, it's a little stiff. It's just a little rigid and there's a little scissoring going on. Maybe there's a lot of scissoring going on. So you think about that and you say, okay, that seems to be an upper motor neuron problem. And in general, upper motor neuron problems lead to more swing phase errors and lower motor neuron disease tends to lead to more stance phase errors. So this is a clearly swing phase error, upper motor neuron. And I can tell you that she's sharp as a tack. So there's no way I think there's anything in her brain going on. So, and cerebellar testing was good. And by the way, basal ganglia, people with Parkinson's, they take a turn with many steps. And so basal ganglia dysfunction, many turns, let's look at how many steps it takes her to go 180. Here she's facing this way and she's gonna face us, watch this. Head turn, boom, wow. Just turns fluidly. No way her basal ganglia are the problem with that kind of a turn. So great stuff. So we say, okay, the brain's intact, her brainstem's intact. I can tell you that her face looks good. So we'll just tap a reflex or two, see what's going on. You'll see there's her face looking good. I can tell you that. She's got a big fuzzy sweater on and even through the fuzzy sweater, I'm getting a pretty jazzy reflex. Obviously, I don't know what the hell I'm doing so it's hard for me to get reflexes. So if I get one any, I always think it's hyperreflexic. So there we go. Pretty jazzy through the fuzzy sweater, not necessarily pathologic, but on the high end of active. Boom, notice I stand out of the way. I've often been kicked, so no fool me. Look at her Achilles reflex. It's interesting. Shows up pretty easily, pretty brisk, right on time. So we have this hint of hyperreflexia. I try and look for clonus. I don't find it, but it's interesting. Her toe sort of extends, doesn't it? Makes you wonder if she's got a Wienski, but I wasn't smart enough to check. So at that point we say, wow, the brainstem's okay. Because her cranial nerves are good. Her cortex is okay, basal ganglia are good, but she's hyperreflexic and it must be above C5 because those biceps seem a little jazzy. So we got an MRI and lo and behold, bang. Here's the big nerve, spinal cord coming down, cerebellum's up here. So we're looking for a little bit of a precursor. White is fluid, spinal cord coming down, coming down, coming down. And there's a little white within the spinal cord. That was bad. And if you look next door, look at this horrible looking segment of the spine. I went back and took her history some more and two things were notable. One was for the absolute absence of neck pain, by the way. Why doesn't that hurt? I will ask that. Why doesn't that hurt? That should hurt. It hurts me just to look at it, but it did not. And so I find that interesting. In case you have a patient with cervical myofascial pain and they say they want an MRI, don't get one. MRIs are really sensitive. But the other thing is I took her history and she had fallen a few times, but one time really hard and fell forward and had a powerful neck flexion maneuver. And after that, she fell even more. So I think she had that neck flexion maneuver likely led to this edema here within the cord and that made her fall even more than she came to me. So I sent her to neurosurgery. They said they could make her worse, but they could not make her better. At least they were honest. So I sent her to PT. She's highly motivated with an intact frontal cortex and she wanted to walk with a lower risk of falling. She came back to us and there she goes. No crossovers, turns like a, oh boy, she turned beautifully. Turns like a cat. Now this is a tribute to her. It feels like she just got off a horse. She's hugely AB ducting at the hips is her sensation. And the reason that she's able to do this, I want to mention, is that her frontal cortex is totally intact. She is able to cortically walk. Her brain can take over for the automatic subcortical processes that normally make people walk since age two. And this is a burden. So she dual tasks everywhere she goes. You and I would go walk to pick up the milk on the other side of the kitchen. And that's all we do. We think about getting the milk. She has to think about getting the milk, what she wants to do. And she has to think about walking correctly. That's a conscious effort. It doesn't become subcortical, it's a conscious effort. Similarly, she's out to watch, just watch a beautiful sunset in the park as she's walking. She admires the sunset, has to think about while she's walking. She's dual tasking throughout her life. And you can see the challenge that this is. You give her some dementia or mild cognitive impairment, she's not gonna have this great outcome. But it's highly motivated, intact, cognitive resources, and she can modify her gait and do this. All right. So that's case one. Case two is a gentleman who has the following disease. I will take a quick look. Let's watch him walk. Notice sort of slow initiating movements. Takes a slow turn. Not much arm swing. Let's watch this turn, how many steps it takes. One, two, three, four, five, six. Wow. Six steps to turn, certainly different from a myelopathy patient. And at the end, you'll notice he took some big steps. That was to show that he can do this. He can take big steps if he wants to. It's just really hard. Let's count the number of steps it takes to go down there. One, two, three, four, five, six. Seven, eight, nine, 10, 11, 12, 13, 14, 15, 16. And he finally starts turning at 16, and he doesn't quite make it to our restroom door over here. And the other thing about him, let's watch that turn again. And it almost looks like his, it almost looks like guide wires are attached from his acromion to his interspiratory spine or his greater trochanter. Like guide wires keep his shoulders and his hips together. And a guide wire keeps his chin stuck on his sternum. Notice when he turns, he doesn't turn his head. The whole thing's turned and block. All turning, turning, turning. And notice the lack of arm swing. All the fluid proximal movements are gone. He can do some distal movements okay, but the fluid proximal movements are gone. So this is Parkinson's disease, also has sort of a unexpressed facies, but he has no dementia. He's a very, very intelligent man. He was kind enough to do something for us, which was to take his medicines and come back. So we'll now see him with medicines on board. And we'll count some steps again. Here he comes, he gets up, boom. Notice the lack of Brady can eat, jaunty little wave, you know, jaunty little point. And notice how quickly he gets up and initiates his gait. Very different from before. Let's watch his steps. One, two, three, four, five, six, seven, eight, nine, 10, 11, 12, 13. And he's really already there with 12 or 13 steps. And he's beyond where he was before with 16 steps. Notice there's always an idiot that passes in the hall. I don't know what that is, but we always have one. Drives me crazy every time we video. And then let's look at the number of steps needed to turn 180. One, two, three, four, that's less than six. And sorry about that. That happens when I click too many times, the program gets upset. So getting one more time, let's look at that neck position when he turns. Remember before the neck was just, the chin was just glued to the sternum. Let's watch him turn. We know it takes fewer steps to turn. And now maybe he's turning his head to watch the idiot that's going by in the hall, but boom, head turns and he follows right along. Much more like the patient with cervical myelopathy who had intact basal ganglia. And this is a lot like divers do. And gymnasts, they want to do a dive, they turn their head and they do a half twist. They want to flip forward, they put their head down, they flip forward. It's like cats do when you drop them, they turn over, the head turns first, the body follows. And that's what he's now got is some degree of that. So I think that's him. Much more fluid gait. And that's back to the other one. Interestingly, even though you'd like that the medications would improve function, they do improve function, but they don't necessarily improve fall risk, which is a bummer. And possibly it's because people move faster and do more. And they still have, so it makes them more functional, but they still have sufficient bradykinesia that the ability to respond to a perturbation, which is a loss in about 300 to 500 milliseconds, or about a third of a second to initiate a response or all is lost. The meds don't allow that much quickness, but they allow them to do, the patient to do more. So fall risk does not improve in this situation. This gentleman came to me from neurology and neurology said that he had lumbar stenosis and they wanted me to manage it. That was the purpose of the referral. They said it was at L3, L4, because his predominant problem was getting out of a chair and he had trouble straightening up. So they assumed his quads were weak and that was why he was sent to me. So I took his history and he didn't have any history consistent with spinal stenosis. I then did a bold move and tapped his reflexes at his patella and they were easily there, not pathologic, just present, very similar to his biceps. And so that made me question if L3, L4 compression from spinal stenosis would be enough to reduce the strength in his quads to keep from getting up. So then I'm not sure about this. Then I felt his quads, they're huge, not Lance Armstrong, but still big quads. And it's like, I just don't, I'm not buying this for his difficulty to get up. So I watched him walk, which is what I do a lot of the time. And so now you get to watch him walk. And he's gonna walk a set distance pre and post a procedure. And so we'll count the number of steps it takes for him to get down and back. And then we'll count the number of steps it takes for him to turn 180 degrees. So here we go. Proceed at any time. Let's watch him reach for his cane also. His feet are almost glued to the ground. It'd be easier to step to get the cane, but watch, he won't step. He doesn't, ah, just keeps that foot stuck to the ground. One, two, three, four, five, six, seven, eight. Nine, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20. One, 22, 23, 24, 25, 26, 27, 28. So that's it, 28 steps forward. You notice there's a white thrombus in the hallway as all the med students are watching what's going on. So it's 28 steps on the way back. 29, 30, 31, 32, 33, 34, 35, 36, 37, 38. 49, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, all right, 54, 55. Now let's look at the number of steps needed to turn 180 degrees. One, two, three, four, five, six, seven, eight, nine, 10 steps to 180 degrees, which may be an indoor record. I mean, that's a lot of steps. And I think there were 59 steps going down and back. So that's him. And notice those steps are just, he's just glued to the ground when he's walking. Let's take a look on the way back. The foot clearance is trivial and the step length is trivial. That's something you sort of look for if we're right about this. Just shuffling along. Just like the floor is sucking his feet into him. Sorry, sucking his feet into the floor. Like it's hyper-gravitational during swing phase there. All right, so let's see. We did a diagnostic procedure and let's check him out after the diagnostic procedure. First of all, he does reach, he takes a step to reach for the cane. That is cool right there. One, two, three, four, five, six, seven, eight, nine, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, stop, 25, turns around. 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48. You turn around at eight or nine or so. So there are a lot fewer steps to go the same distance. And if any of you bothered to time it, it's like one minute and 14 seconds the first time, about 58, 59 seconds the second time. So step length tends to translate into speed. Tends to translate into speed. And it did in this case. Let's see. I want to see the number of steps it takes him to turn around now. It took 10 before. One, two, three, four, five, six. From 10 steps to six, huge change, huge change. Now what he has, we did an MRI, is normal pressure hydrocephalus. And you can see the characteristic white matter changes around the ventricles. The ventricles are considered generous in size. That's the neuroradiologist reading. I don't have a clue. Similarly, there's these flow that radiologists, neuroradiologists were loving this. This is a flow, the CSF, that apparently has sort of a pulsatile flow. It used to be think there was obstruction. Now the thinking is it's more, there's sort of a bit of a pulsatile flow rather than a nice smooth laminar flow. And this pulsatile flow eventually, which is depicted by this cord signal or this CSF signal here, causes the white matter changes here. And it's thought that the corpus callosum, particularly the fibers that cross and are serving the lower limbs, that those are predominantly affected. And this leads to the lower limb difficulties, difficulty initiating movements and difficulty standing up, difficulty initiating walking and that sort of thing, and really inhibits gait. So we did, actually Dr. Little did a high volume tap and took out a whole bunch of cerebrospinal fluid. And what you don't know is as you know, he has a lot of degenerative change in L3, L4, and L2. So when they did the tap, it was very difficult. It took an hour or two. The guy was miserable. He came away from the tap saying, I can't see out of one eye, I'm in agony. I mean, I thought there's no way he's gonna walk better because it was not a therapeutic tap in terms of the event itself. He was feeling awful and he had a headache and it was just miserable for him. And yet, he walked so much better. And I think what really interests me also here is that those fibers that were messed up, those lower limb fibers that are being disturbed by the sclerosis and the excessive pulsatile pressure, they must in the brain, the axons, it must have been conduction block. Because if the axons were destroyed, the tap wouldn't help. But the tap lower the pressure temporarily, and those, those, those neurons came to life and allowed him to walk better. And I really find it's almost miraculous. But normal pressure hydrocephalus is what this gentleman had, presumably, we don't look for it often enough. But it is a treatable form of gait disorder. You know, they also there's also concerns about incontinence. And for this gentleman, he had prostate disease. So that was sort of confounded, we really couldn't tell. That was already sort of a difficulty. And as far as dementia, this gentleman was a judge and his vocabulary was extraordinary. And so if he had dementia, it was like, well, so that was hidden. I mean, he had so much reserve that we had no, no sense of that. So when I was another CNS disorder that I want to mention. The last one is this gentleman. And he doesn't have too surprising of a gait pattern, nothing that you don't see too often. Let's take a look at it. You know, stance phase is not bad, the left hip pops out a little bit so consistent with maybe a little hip abductor weakness. But it's really swing phase, it's messed up. No, during swing phase, the limb should shorten for you. It should shorten by hip flexion, knee flexion, dorsiflexion, and maybe a little contralateral hip abduction, contralateral stabilization on the stance limb. And that allows this thing to be shorter, but his is not shortening. So that's, that's a problem. The other thing about it, if you look at during stance phase on the parietic limb, when it comes towards us, I think during mid to late stance, there's a bit of extension at the knee. We'll take a look at that. This gentleman had vasculitis. So it was a pure MCA stroke with nothing else going on. And it's amazing what the let's let's take a look at this this knee during right there, boom, boom, see it snapping back a little bit there, get that sense of hyperextension. Yeah. So that's, that's the main stance phase there. And then swing phases is a mess. He has to circumduct, he has to hip hike. He's working really hard to shorten that limb during swing phase. So, again, I want to mention though, the healthy brain, this is otherwise healthy brain in that relatively young man, athletic guy played football. And just, you know, just a single MCA hit. He was still working full time. He was leasing oil fields and other things around the entire state of Michigan. He was umpiring and refereeing. And it was father and husband and active, active family man. So there was no aspect of his life, it wasn't highly functional. So it's amazing what can happen in someone with a brain that hasn't had 10 TIAs. So that was him walking. Let's take a look at his neck scape. This one, there's a difference. He's wearing his AFO. So we'll see how this goes. And it looks a little easier for him during swing phase, just a touch, not much because, you know, we're not doing anything with the AFO to change hip flexion or knee flexion, which are still a little stiff. But we do, you know, improve dorsiflexion a little bit. Now let's look during stance phase and see what his knee is doing. Because this guy's on his feet all the time. He's a big man. So we can't have his knee snapping back all the time. And as he approaches, I hope you can approach that that knee is now flexing during mid stance and not extending. Get a sense of that? So that's a, that's an improvement for him that I think probably is important to his knee in the long term. So I thought we'd take a little look at that. So we have a, just a depiction of if the plantar flexors are activated and presumably, quote, a spasticity pattern can powerfully activate the plantar flexors. This is a powerful man. And so when you're weight bearing and the plantar flexors activate, you know, the ground is going to keep, the floor surface is going to keep the foot from actually plantar flexing. You just can't, most floor surface, I mean, if it was sponge or foam, you could plantar flex and keep the tibia vertical. But when you have a firm surface and you plantar flex, then there's a tendency, the only way you can do that is to drive the knee joint posteriorly. And then this achieves the plantar flexion angle that the muscles are making happen. So that was where he was without his AFO. Move along to give him the AFO. Conversely, if we can keep his ankle and dorsiflexion, and I've probably exaggerated this with the diagram, but keep the ankle and dorsiflexion so that his forefoot is dorsiflexed. The only way to achieve with a flat, with a firm ground to achieve that is to have his knee move anteriorly. And that allows a dorsiflexion, that allows quote, dorsiflexion to occur. And so this is the way that, you know, use ankle foot orthosis to sort of control, control the knee a little bit. And he was a good demonstration of that. So remarkable man, doesn't fall much and is a highly functional gentleman. So that is the end of my presentation, I believe. Yeah, that's the end of what I have. And I will, I guess stop share and see if there's any questions and we're moving on. So thank you, Dr. Richardson. We're going to save questions till the end. Although I have a question for you and that'll ask later. And Dr. Richardson will join us again after Dr. Morganroth. So Dr. Morganroth is an Associate Professor and Vice Chair for Research in the Department of Rehabilitation Medicine at the University of Washington in Seattle. He is the Associate Director of the Amputation Rehabilitation Fellowship at the VA Puget Sound Healthcare System. He's a core investigator in VA Rehabilitation Research and Development Center for Limb Loss and Mobility, otherwise known as CLIMB. Dr. Morganroth's clinical care and research focuses on improving mobility and the quality of life in people with limb loss through rehabilitation, prosthetics, and gait biomechanics. So David, please take the stage and happy to have you with us. All right. Thanks, John. All right, let me share my screen. And I'll, I'll echo what Dr. Richardson said that it's, I wish we could all be in person to do this, especially when talking about gait. I really like to stand up and walk around in front of the class and demonstrate things and have you all walk around and try things to get a real feeling for this. So it's, it's more challenging in the virtual environment, but we will do our best to do our best. So we're going to change gears a little. You now have a really nice background in normal gait from Dr. Kerrigan and in CNS impaired gait from Dr. Richardson. And now we're going to move on to talking about gait in people with limb loss. And the first slide, you know, I think probably some of you have quite a bit of experience in the audience and working with people with limb loss and others maybe don't. But I think the first slide is a little bit more challenging. So I'm going to people with limb loss and others maybe don't. And I think a number of you are residents. So I just want to mention that this is really a cornerstone of the field of PM&R. And as a matter of fact, back when the field was a young field early on, this was a huge part of the field. And it's not as large a part of the field anymore, as far as what people tend to focus on is the field has expanded quite a bit, but it's still a vital part of the field. And I find to be an incredibly satisfying part of the field for a whole number of reasons that are that are listed here. The one we're going to obviously hone in on here is gait analysis and gait rehabilitation to maximize mobility. And one of the cool things about working with people with limb loss is you can make incredibly significant changes sometimes, not necessarily instantaneously, but very quickly. And that's, that can be a bit rare within PM&R. I think we all chose this field because we're not impatient people. And we recognize that sometimes things take a long time to make improvements, whether it's the person with CNS impairment that has to go through eight weeks of PT to really notice the improvements or a whole host of other disorders. So this is a circumstance where by changing an alignment of a prosthesis within a clinic in a multidisciplinary amputee clinic, we can, it can be the difference between someone who's limping and barely walking at all, because it hurts so much to walk with their prosthesis to someone who walks out and whistles off into the sunset almost, almost literally from the clinical setting. So quite satisfying. The outline of what I'm going to cover is just a few more normal gait concepts, just to build on what Dr. Kerrigan talked about in her first talk. And then we're going to break things down into coronal plane gait and alignment, and then sagittal plane. And this really mimics, at least the way I do things in clinic, where as we're observing gait, we're doing it from both the sagittal as well as the coronal plane, because there's different abnormalities we're going to see in both of those settings. So a few of these basic concepts to build on. And I think this is hopefully going to be a review for most of you, but just so we're on the same page, because these concepts are important when you think about the gait of people with limb loss and how we're going to modify alignment to try and improve upon things. The center of mass, pictured here in the coronal plane, and if we were sitting around the table in person, I'd have you all stand up and try this, but feel free to do so if you'd like. But if you stand there on both of your feet, and if you imagine dropping a plumb line down from your center of mass, it would fall right between your feet for most people. And that's a very stable situation. Most people are very stable and don't fall down when they're standing like this. And the reason for that is your center of mass is projected over your base of support. What happens if you lift up one foot? Well, your center of mass shifts over. And this is where it's fun to do the demonstration, because you can actually witness this in real time. If you kind of point your finger towards your umbilicus and lift up one foot, you see your center of mass shift, or where you're pointing to, imagining your center of mass. And the reason for that, I think you all know, is we want to stay stable, and we want to keep our center of mass projected over our base of support, which now becomes narrowed to the points of contact under that single foot. The center of mass as we walk moves, and I'm going to focus on the side-to-side motion. Dr. Kerrigan talked a bunch about the determinants of gait and the vertical motion a little bit more. But there is this side-to-side motion. What you see here, this two centimeter and four centimeter, that doesn't cover everybody. That's sort of an average across people. But when you think about the side-to-side motion, I want you to think about that last slide I showed, where just standing or marching in place through that side-to-side shift. And now imagine a bird's eye view of moving back and forth between stance feet on the left and the right, and then the left and the right as you're walking and progressing in that direction. And hopefully you can all see my, can you all see my cursor as I move it around here? David, yes. Great, great. So this line is the projection of the center of mass. And so you can see when you're just in single limb stance on the left side, typically that center of mass is projected right over that left foot. So you have that stable situation of the center of mass being projected over the base of support. But then as you step towards the contralateral foot, your center of mass has to shift to get over that base of support to get over that foot. And as a matter of fact, there's, there is a, for most people, part of the gait cycle, where before this foot has stepped down, the center of mass line is outside of the base of support, leading to actually an unstable situation. And I had a medical student in the biomechanics course I teach years ago who said, so wait, so walking is really controlled falling. And I loved that. I thought, you know, a lot of people, walking is controlled falling. And the idea is you're falling until you put this other foot down, which most of us do quite well. And then of course, if you have a CMS impairment, like Dr. Richardson described, that may not be the case. Or if your foot placement for some other reason is not where you intend it to be, then you create an unstable situation. Okay, so let's keep that in mind as we move forward and talk about coronoplane alignment. And I want to start with normal bench alignment. And so this is the first thing a prosthetist does typically, when they put the pieces of a prosthesis together. So you've got the socket, the pylon and the foot, you have to line them up somehow. And so the normal bench alignment, which you can see this is not connected to a person here, is just, if you have this plumb line drop down from the posterior brim of the socket, right in the midline here, it falls right through that heel. And so this is a really nice neutral bench alignment. Now, is this what we end up with? Usually not. And so this is a starting place. And then when we have an individual with limb loss walk, then we have to make adjustments because dynamically, that's not going to be the best alignment. So it's a starting place only. And in remember that we're in the coronoplane here. So we can make alignment shifts where we either have shifts to the outset or to the inset of the foot. And we can do this in a couple ways, we can do a linear translation. And this is exaggerated here, this would probably fall apart if someone tried to walk on it. You can see it's translated laterally, the pylon is relative to the socket, or we can do an angulation as you see here, but the net effect is the same. We look at our plumb line. Now our heel is lateral in the posterior view here to where the plumb line is in either of these circumstances. So we may do this dynamically, but sometimes we have someone come into clinic and actually quite often, where it's not optimized, so we have to adjust it. So if we have a laterally displaced foot, let's look back at that diagram, that bird's eye view. And let's think about what happens if the foot is, let's say, displaced too far laterally, which is a common scenario we might see in the clinical setting. So now what's in red is the new situation where we have the laterally outset foot. So now, we have to have a mechanism for getting our center of mass to travel a little further laterally, such that we stay stable again, because we want to get it over that projection of our base of support once we're stepping down on that right foot, which is the prosthetic side in this case. So we have to have some mechanism to do that. So what most people do is they, excuse me, they have a lateral trunk shift. So what you know, what you think of as a Trendelenburg gait is what you tend to see here. So is that a problem? Well, it can be. So it can be a problem in terms, potentially in terms of gait efficiency. It can be a problem if you imagine many cycles of a trunk shift, perhaps putting strain on the structures in the spine, and amputees tend to get low back pain at a significantly higher prevalence than the general population. So we want to do anything we can to prevent that situation. And then it can be an issue for gait aesthetics. I actually remember an article that Dr. Kerrigan wrote more than 20 years ago on the aesthetics of gait, and I really enjoyed it. And the idea, if I'm remembering correctly, was thinking that we have to be conscious not just of gait efficiencies and falling, but also how it feels to someone who's walking in a way that might look different than other people, and whether that's a problem or not for them as we think about how to treat the gait impairments. Okay, so that's what we see in terms of observing their gait. What about issues with the residual limb? And this is a huge or a common scenario where you have someone come into your clinic and say, you know, it just really hurts when I'm walking, and you take off their prosthesis, and on their residual limb, you see either an area of redness, or even sometimes ulceration. And this can really challenge someone, even the highest functioning of individuals with limb loss, who are maybe doing all sorts of different sports, but they come in, they say, you know, I've had to stay out of my limb for the most part for the last couple weeks because of this. So really hampers their functional quality of life. So remember, we're talking about this case where that the foot is too far outset, and I've exaggerated it here in this drawing. But what I want you to think about here, and now we're going to bring back this concept that Dr. Kerrigan talked about of the ground reaction force and joint torques, but we're going to apply it to what we call a pseudoarthrosis. So instead of looking at the knee joint itself in the coronal plane, we're going to look at the relationship between the prosthetic socket and the residual limb. And even in the best fitting socket, we have a scenario where there is a little bit of relative motion, because there's soft tissues to compress and such. So if we have a ground reaction force that is lateral to that center of rotation between the prosthetic socket and the residual limb, then that's going to tend to cause a rotation in this direction of the socket on the residual limb. And what that's going to cause is increased pressure, proximal lateral, and decreased pressure, or what we call a medial thrust of the proximal socket brim, or rather proximal medial. We'll have the inverse of those effects distally, but we tend to notice them most proximally. So I want you to focus more on the proximate side. So what will you actually see? Well, you will literally see what looks like a knee thrust medially, but it's actually the medial proximal brim of the socket thrusting away from the medial femoral condyle of the residual limb. And then you'll tend to see wounds or redness, or patients will point to discomfort in the proximal lateral portion of the residual limb. So that's the kind of things you'll hear about on history and see on physical exam. Okay, let's review. We have increased, this is the excessively laterally placed foot, we have increased width of basal support, we have a medial thrust of the proximal socket brim during the prosthetic stance phase, and we also tend to see this increased lateral trunk motion to the prosthetic side. And now we're going to try and watch that in real time. And I want you to try and notice those three things as best you can. Again, we're seeing that lateral trunk shift on the prosthetic side. You're seeing a little bit of that shift of the socket thrusting medially. Okay, so let's move on to the opposite scenario. This is going to get easier now, because take everything you just learned and flip it around to the other side, the medially displaced foot. So now if we have a foot that is displaced too far medially, and again, there's different ways of adjusting alignment here with the translation or the rotation. Now we have this scenario where on the prosthetic side, what you see in red is the more medially displaced foot. So do we have a good mechanism, is the question, for moving the center of mass less far laterally as we step down with a more of a medially displaced foot? And this is trickier, because it's one thing to shift your trunk laterally, and this is again where I wish we were in person to have you all stand up and walk around the room and try this. Feel free to do so if you want to do it wherever you are right now, but it's a lot trickier to do this. And this tends to cause more of a loss of balance situation towards the prosthetic side, because what ends up happening is the center of mass tends to move outside of our base of support, leading us to fall towards the prosthetic side for the individual with this alignment abnormality to fall. What about at the residual limb? Just the opposite of what we said before. So remember that pseudoarthrosis. Again, I've drawn it really exaggerated here so you can see easily. We have our ground reaction force which is acting medially now to that pseudoarthrosis, that center of rotation, causing this rotation of the socket on the residual limb. Thus, now we're going to have our increased pressure and maybe our redness or wound or discomfort, at least, on the proximal medial aspect of the residual limb. And now we're going to see a thrust of the lateral proximal socket brim away, or what might look like a lateral knee thrust to you, as the individuals in prosthetic stance phase. Here's our review slide before we watch the video of this scenario. It's a narrowed base of support, lateral thrust at the proximal socket brim during prosthetic stance phase, which again, remember, you might not be able to tell it's the socket itself. It almost just looks like the whole knee is thrusting, but it is actually the socket sort of moving in that direction, as well as pulling the knee sort of in that direction to some extent. And a possible loss of balance to the prosthetic side during prosthetic stance phase. So let's watch that connection. Oh, there's that loss of balance, so that's an obvious one. And I recognize that the thrusting medially and laterally of the socket brim can be a little more challenging to see. I think it's easier to see in this circumstance. I'll show that one more time, of the medially displaced foot with the lateral thrust in the proximal socket brim. That's a little easier to see than the laterally displaced foot. And you can see that narrowed base of support as well. And I'll tell you, these videos, so this was an individual patient of ours some years ago, and you can tell it's quite a few years ago because of the quality of the video, but this is someone who is a pretty high-functioning individual, and so we just adjusted his alignment and asked him to walk, and so all you're seeing is what you would see in real life with a patient with those alignments adjusted in that manner. Okay, let's move along to the sagittal plane, and we're going to talk a little about the kinetics and kinematics here. But really what I want to hone in on, since you got a good review of normal gait in the beginning, is just this one concept of reiterating the when you think about the grand reaction force and the effect on joints, so in terms of the external moments. So during heel contact or foot contact, depending on how someone walks, you see that ground reaction force line in red, and it's coming from under the center pressure of the foot, which at this point is that main point of contact under the heel, moving up towards the center of mass of the body. And in this case, it is posterior to the ankle center rotation, which is identified here by this little white box, and it is also posterior to the knee joint center of rotation. So this is going to, and this is where, again, I prefer to teach interactively and have you guys tell me the answers to these, but because we can't do it so easily here, I'll just tell you what I think you already know, which is this is going to tend to cause, this external moment is going to tend to cause plantar flexion at the ankle and flexion or knee flexion here at the knee just because of this relationship. Now, we have internal moments with our muscles and other body structures that are acting on the joints, which are counteracting these, and it's actually an eccentric loading scenario at both of these joints here. So that's the normal gait review, and this is just as you move to mid stance, you can see that ground reaction force vector now swings anteriorly to both the ankle and the knee, so you're going to have the opposite external joint torques. So now let's talk about in your patient with limb loss how we can think about alignment in the sagittal plane with that in mind and really keeping an eye on the ground reaction force. So again, we have this normal bench alignment situation here, and then we can either posteriorly translate the pylon or anteriorly translate the pylon relative to the socket, and I like to talk in terms of relative because prosthetists tend to see things from the prosthesis up, and we as PM&R physicians tend to see things as the patient down, so if we talk about one part of the prosthesis relative together, we don't get confused when we talk between ourselves, and of course you can also do that with angulations, and it's beyond the scope of this talk to really explain why you might do more of an angulation and more of a translation, but just so you know that that's a possibility. There's another scenario that's really important to consider, though. It's not just the alignment that matters, but in the sagittal plane, if an individual changes shoes, so I'm guessing that all of you have more than one pair of shoes, and maybe some of you have shoes that are very low heel height shoes and shoes that are very high heel height shoes, and I know that if any of you have read Dr. Kerrigan's work, you wouldn't be wearing any high-heeled shoes anymore because you know of the deleterious effects on the medial tibial femoral joint, but the point being here that this changes the alignment if you change shoes with any heel height differences, so this has to be kept in mind, and for some individuals, it might mean we actually need to give them more than one prosthesis if insurance will afford that, and so I'll give you an example. I have a firefighter who has to, who's a patient of mine, who has to wear these big firefighting boots with a big heel on them, but he doesn't like to wear shoes like that when he's walking around town, and as a matter of fact, it's also challenging to get these firefighting boots off the prosthesis because they're so, they lace up so high, so we avoid this whole issue of effect on alignment by having just two separate prostheses, each aligned differently, so let's talk about the net effect when we have an increased heel lever or, and a decreased toe lever. The heel lever just means the distance behind this plumb line here, so the more the plumb line is moved posteriorly, the smaller your heel lever is, and the larger your toe lever is, and then vice versa the other way, so in this scenario where we have an excessively increased heel lever, an excessively decreased toe lever, which means that we have essentially the foot translated posteriorly, what's going to happen? And it actually gets slightly more complicated than we see in the coronal plane, so now we still follow that ground reaction force line and think about the effect on not just the joint, but now again that pseudoarthrosis, so now if we move that whole foot more posteriorly, our ground reaction force line is going to be more posterior, thus we're going to have a larger perpendicular moment arm from that center of rotation or lever, and thus we're going to increase that external knee flexion moment, and so what do we do in an intact limb if we have an increased knee flexion moment? Well, we fire our quads more so that we counteract that with more of an internal knee extension moment. The challenge here for someone with limb loss is when they fire their quads, the first thing that happens before they're able to stabilize at the knee is that tibia has to compress all the soft tissue pushing up against the socket, and so it's sort of like getting hit in the shins every time, so if you could imagine if you've ever played soccer or something and got struck in the shins, it's like every step you take you're slamming that discal anterior tibia up against the anterior socket. It's not comfortable, and this is a really common problem you see. You also get this drop off at the end of stance phase for the same reason if you follow that ground reaction force line, so in summary, if we have this excessively increased heel lever and decreased toe lever, we're going to see rapid excessive knee flexion with heel contact with early and mid stance. We're going to see drop off or continued excessive knee flexion in late stance, and then we're going to see a rapid swing of the contralateral limb because we have this drop off and you have to get that other limb down for stability, so let's watch that. And this, if you're having trouble seeing this, it takes a lot of practice, gait observation, and because this is a real-life scenario with a real patient of ours, it's a bit subtle, so again, I'm just going to remind you, look for that rapid excessive knee flexion and heel contact through early and mid stance, that drop off at the end of stance, and the rapid swing of the contralateral limb. Excessive knee flexion and heel contact through early and mid stance, that drop off at the end of stance, and the rapid swing of the contralateral limb. a little bit of that early knee flexion, and knee flexion during early stance phase is normal, but it just happens a little more quickly and more excessively in a case like this, and then that terminal drop. What about the opposite scenario? If now we have an excessively small heel lever and large toe lever, so this is like the whole, think of the whole foot being translated anteriorly. Well, now we have insufficient knee flexion because we have our ground reaction forces moved anteriorly, and thus we're decreasing our knee flexion moment, even to the point that it may become a knee extension moment. So the other problem with this is during later on in stance, as we're trying to progress through the stance phase, if the ground reaction force stays anterior to the knee joint, we don't have that external knee flexion moment that enables us to go into pre-swing and then swing phase. So you end up with this delayed heel rise because it's sort of like the whole ground reaction force is pushing the limb to try and maintain knee extension. So what are we going to see when we watch this video? We're going to see reduced knee flexion in early stance, we're going to see difficulty progressing the center of mass over the stance phase foot, and we're going to see a shortened intact limb step length. So now instead of that rapid swing through, because we have the delayed heel rise, now the other side, the intact limb swinging through, is going to have a harder time progressing far enough. So let's watch that video. And there's a little hitch in the video there, that's just the poor quality of the video, so sorry about that. So you see there's a little bit of difficulty progressing and you get that shortened step length. I'll show it one more time because these are harder in this actual plane. So a little shortened step length from the intact side. And look for that limited knee flexion during early stance. So typically we go through about 10 to 15 degrees of knee flexion during early stance. He doesn't seem to go through any at all. Okay, we've reached our summary slide here. Thanks for bearing with me through all that. I know that can be, for some of you, there's a little bit of PTSD from your 10th grade physics class for those who didn't love physics, but hopefully we kept it kept it basic enough that you could apply those concepts. So the summary is observe from the side and observe from behind or behind and in front. Look at both planes. Don't assume that you can watch from one plane and know what's going on. When you're observing gait with people with limb loss, this knee tells all in quotes is really, this doesn't cover everything, but I just want you to recognize that the knee tells a lot of the information, at least in people with trans-tibial amputation. Of course, you're going to look at the trunk as well to look for those lateral trunk shifts. You're going to look at, we didn't even talk about the transverse plane. You're going to look down at the foot to see what the transverse plane alignment looks like. And you're going to look at what's happening at the level of the hip as well. But the knee really gives you a lot of the information. I didn't have time to talk to you guys today about transfemoral amputee gait, but there's a whole host of other considerations when it comes to that. And obviously, as you think about things like hip disarticulation or other levels, there's other considerations. But this is sort of bread and butter stuff that is hopefully helpful for the boards for those of you who have to deal with that and for your everyday clinical practice for those of you working with patients with limb loss. So thanks again for listening. And unfortunately, I can't stay on too much longer, so I'm not going to be around later when you have the question and answer session, but thanks all for your attention. David, thank you very much. I have a question, and there's one question in the chat or in the question and answer. So can I ask, with the advance of prosthetics, now we have amputees and double amputees able to keep pace with world-class able-bodied athletes, which is amazing, given 30 years ago that wouldn't have happened, how much fine-tuning plays into that for them? Obviously, the prosthetics are tremendous, but I imagine subtle abnormalities or subtle adjustments can have a big effect on their ability to perform. Can you comment on that? Yeah, absolutely. So what I'll first mention is that when it comes to technology, for instance, for a sprinter with, let's say, a bilateral trans-tibial sprinter to be competing against the top intact runners in the world with fully intact limbs, the technology is actually fairly straightforward. It is a carbon fiber leaf spring design that's been around for about 20 to 30 years now, and it's the same technology that most of the walking feet employ, except it's a much larger leaf spring design. So these are not powered limbs, and it's a bit of a misnomer when there's these concerns that these are individuals who are taking advantage of technology and running much faster because they've got these limbs that just have this incredible technology. It's really just a carbon fiber leaf spring, which is actually mimicking the way intact limbs work when we run. The entire limb acts as a linear spring, and then the joints themselves, especially the ankle joint, acts as a torsional spring when we run. The difference is, as intact individuals, we can put that energy back in with every step if we need to, whereas someone with an amputation can't. But you're absolutely right that alignment adjustments, as you increase the force through the ground reaction force, are going to have much larger effects. So optimizing that alignment in runners is a huge deal. And if you watch, for instance, when there was a lot of media coverage of Oscar Pistorius, and you watched him after a sprint trying to walk on those prosthetic limbs, he walked terribly. And this is the fastest person in the world, or one of the bestest people in the world. And it's because, in prosthetics, there's no prosthetic limb that can achieve the huge variety of functionality of our intact biological foot and ankle system. It's a system that has trade-offs. And so a carbon fiber leaf spring has to be designed with just the right stiffness properties for running, but it's not good for walking. Really poor balance. So I hope that answered your question, John. Yes, it did. I mean, it is true. I mean, I've watched him walk afterwards, and he's pretty stilted, as if he can't control the leaf spring anymore. Yeah, exactly. Okay, should I jump to this question in the Q&A here? Yes, go right ahead. Okay, so with artificial intelligence, machine learning, etc., on the rise, do you envision the day when an ordinary PM&R physician or prosthetist can prescribe precise adjustments using a handheld device and sensors placed on the patient's limb and pulse? Yeah, good question. So the way I might answer this is, I'll tell you about a research project that we're working on that's sort of in this direction, that could hopefully, in the future, transform the way we prescribe prosthetic limbs. So the current prosthetic prescription practice, as most of you probably know, is you have a patient in the clinic. They come in, and either they have experience walking on different prosthetic limbs, or they don't. But we ask them a bunch of questions, we examine them, we watch them walk a bit, and then we say, you get this prosthetic limb. So when it comes to, for instance, prosthetic feet, there's 200 plus feet on the market, quite a variety. And we somehow have to say, based on those questions and looking at them, as clinicians, we say, okay, here's the prosthetic foot you get. And this is the foot that they have to walk around on every day of their life. Imagine if you went to a car dealership, and you went to one car dealership, and that car dealer said to you, let me ask you a few questions, let me sort of look you up and down, see what you look like. And here you go, you get a Hyundai, and you say, but I wanted the Ferrari, or the, you know, the Porsche, or this other car. Nope, that's what you get, that's what you have to drive. It's not a situation that is optimal for the patient, because there's no experiential input. And so we're studying a test drive strategy for prosthetic prescription using a robotic prosthetic foot emulator, where we can program it to act like a lot of different kinds of feet. So they put the patient in the driver's seat, and you let them provide experiential input by walking, by just changing the software in real time. And so it's a ways away from the clinical setting at this point. It's, you know, within the first five years of research right now. But we're moving things somewhat in that direction for choice of prosthetic foot. When it comes to the technologies of the feet themselves, there is a lot of advanced technology. But thus far, what most people use is technology that's 20, 30 years old, because for most people, it works better than the powered limbs, which tend to be exceedingly expensive, quite heavy, and can have other issues as well. So there's a lot of potential there, but a lot more work needs to be done. So hopefully that answered your question to an anonymous attendee who wrote that. Dr. Morganroth, thank you very much. I hope you have a great rest of the weekend, and thank you for contributing to this. Yeah, thanks for having me. Take care, everyone. Next, I'd like to bring back Dr. Richardson, who's going to speak to us now more about neuropathic gait. All right, hopefully we're set. Good to talk with everyone again. Same concerns before, apply in a continuous fashion. We'll now focus on some peripheral neurologic disorders, and let's see what we got here. Oh, so, and by the way, when I mention a peripheral neuropathy, I'll mean a, what we really, a distal symmetric polyneuropathy, where the longer the nerve is, the more it's affected, and so the feet tend to be affected first, the sensory fibers often, more often than the motor fibers, foot intrinsic muscles may be next, and then things progress, and maybe by the time it gets to the knee or the shin, you might have some distal upper limb sensation. So that's what I'll mean by a peripheral neuropathy, just so we're all on the same page. The blue segments there obviously indicate a disease nerve, and the pink one's healthy. Okay, so I thought we'd just watch an ostensibly an ostensibly normal subject walk. Let's look at step width variability in particular, and the feet stay pretty evenly apart in this, in theory, intact specimen. So I want you to keep that foot placement in mind, and, and, and because we'll see some, some different, different gaits. All right, so this patient came to me, young woman, and she was with her family walking on hikes, and they like to go through the woods, over hill, over dale, and she was routinely twisting her ankle, and at times almost falling, and she was uncertain why, and she came to me for this purpose. And so with, let's, let's look at that step width variability, and, and, and we'll go back here again. I want to look at this. So what we refer to is, you know, in the frontal plane, how, if you were to put your right foot on a railway rail and your left foot on a railway rail about 12 inches apart, and you stayed on those rails, that'd be a step with variability of zero. So let's look at that again, because we're going to look at this patient, and so there you go. That's, like I said, an ostensibly normal person. So let's move the next one. Let's look at this patient, look at her step width variability, because she's concerned about postural instability on uneven surfaces. Little subtle wavering, isn't there? Little chaos. Let's watch her again from the moment she takes off. Wide, a little narrow, a little crossover step, then broad afterwards, another one going the other way. Not much, but enough, where you wonder, you know, what's going on? And so I said, okay, well, let's And so I said, okay, well, let's do a brief neurologic examination. Tap some reflexes, and I can get a little one in the biceps. Got a little one there, not much. Brachioradialis, yeah, a little one going on. So there they are, and those are pretty short nerves, right? Biceps is a muscutaneous going down from the neck, pretty short. Patella is not too long of a nerve either, because it's coming from L3, and just that distance, so that's okay. I'm whacking her tibial tuberosity there, rather than her patella tendon. Then we look at the, these Achilles reflex, those are not jumping right in, are they? Those are a little, those are a little muted. I mean, I think they're sort of there, but certainly not what the rest of them were. So the Achilles reflex, not so good. You look at the foot morphology, awfully aggressive arch there. Check out her strength, and my thumb is beating her extensor allis longus pretty easily, and that's not normal for me. My thumbs are pretty lame, actually. I use two fingers for dorsiflexion, can't make any headway on the right, on the left, but on the right, I can break it with no problem. And by the way, manual muscle testing, I have to just parenthetically mention, this really falls down with grade four strength, you know, anti-gravity plus resistance, or whatever that is, especially in the lower limb. Sometimes I'll use the number of fingers to break, like a biceps, number of fingers to break it, one, two, three, or four, which at least breaks down anti-gravity plus resistance in a way that's meaningful for me. So there you go. She's got high arched feet. Achilles reflexes are blunted. Her extensor allus is longus weak, or intertibialis is weak. Got to do an EMG, and this is a mess of an EMG, but take a quick look. The serral responses are gone. The peroneal motor recording at the extensor digitorum brevis is gone. The peroneal motor, when recording at the intertibialis, moving proximally is present. And we go over here to look at conduction velocities, normal, greater than 41 meters a second. And typically people are 50 meters a second. If you're ever at a football game and you look at the end zone and look at the 50 yard line and think, whoa, in a single second, a nerve conducts that quick, quickly, not bad. This patient, however, is 19 meters a second. And in the upper limb, she's like 30 and 28 meters a second. So she definitely meets the demyelinating criteria. And she has a Charcot-Marie-Tooth is her difficulty. And that's her disorder. And so it easily explains why she's falling. And this step with variability that you see in the frontal plane when walking is one of your early clues to mild neuropathy. Even mild distal symmetric polyneuropathy due to diabetes or anything else causes this, what I call irregularly irregular frontal plane step variability. It's almost like atrial fibrillation. It just sort of is a bit chaotic in the frontal plane. And if you look for that, you say right away, their fall risk is increased. Peripheral neuropathy always increases fall risk. And that's what's happening. So for this patient in terms of treating her, when she's on her, we talked about how weak her ankle inverters were, endorsed flexors, and simply she doesn't have the strength to negotiate an uneven surface, should she unfortunately land on one, a rock or something else. So she uses some ankle orthoses that athletes use, active ankle, but you can use whatever you want that support things in the frontal plane. And that's done well for her. But she also had questions about long-term. You know, am I going to, is this going to put me in a wheelchair? What's going to happen? It's like, no, this is not going to put you in a wheelchair, but the broken hip or the subdural hematoma you get from falling back could put you in a wheelchair at some point. So one of the, a couple of things I've always mentioned to her, the things you need to compensate for neuropathy and you can compensate is excellent strength in your hips. Hip strength can actually compensate for poor ankle proprioceptive thresholds for coarse ankle proprioception, hip strength can compensate for that. I'm not going to drag you through the statistics on that, but that I'm not saying that out of, I just think it, we have some research that really showed that. And then the other thing you need is a quick brain. It's this type of patient that you do not want her loaded up with anticholinergics. You don't want her on a bunch of antidepressants or mood stabilizers or sleepers or anything else or stimulants or maybe stimulants, but you do not want her on any anticholinergic medicine over time. And you don't want her to acquire mild cognitive impairment or dementia. So, you know, she started taking up painting and also her aerobic exercise. She stayed up with it. And this, if she has a quick brain and strong hips, she can compensate for this neuropathy. And so can other people and they can have pretty good likelihood of staying upright and not injured. So, the other thing this does is put her in control of the disease rather than disease in control of her. So, that was that case of Charcot-Marie-Tooth that showed up out of nowhere. This patient, what happened was Dr. Little, a neurologist, just took a video of this patient. I didn't see the patient, said, why is she doing this? Why is she walking like this? Let's take a look at her walking. And it's a little not easy to see on the way there, but on the way back, it's really obvious what she's doing. Well, the strategy for what she's doing. We'll watch again. She is really on the way back. She does not want to load her toes, does she? She keeps her center of mass, which lives somewhere behind her belly button in front of her sacrum. She keeps that backwards. She does not want to get that center of mass forward and load her forefoot. She doesn't want to rise up on her toes. It doesn't look like she can rise up on her toes. She's keeping her weight back. That's safe for her. So, she's walking tilted backwards, which is safe. So, you think about that and say, why would she do that? So, here's my horrific depiction of the center of mass. It's just, and she's static, dropping straight down here. And what happens? So, that's an okay place for this patient to be, right? But what happens if her center of mass or anyone's center of mass, while you're standing, drifts forward? Let's have it drift anteriorly. What do you do? Well, if you were standing and you drift, and this is where all together, we'd stand and drift. And let that happen. You'd feel yourself activate your plantar flexors, okay? You'd activate, and the other thing, well, we'll go activate plantar flexors, and I'll get back to the other picture, which, okay. So, what I think about with balance, let's back up for a second, is because I'm not too physically oriented. So, I think of standing balance like sheep and a sheep dog. And so, I imagine out in the great Southwest, there's a plateau, and it's a round plateau. And it's maybe half, you know, quarter mile across. And the sheep, there's a flock of sheep up there. And they're migrating around stupidly. They're sheep after all. They'll just fall right off if you let them. You know, they just have no brains whatsoever. But, so the thing that keeps them from falling off is the sheep dog. And the sheep dog, it has to keep track of the sheep. And when the sheep start to drift too far to the West, sheep dog runs quickly to the West, gets between the sheep and the abyss, and barks at them, and pushes them back the other way, and does the same thing North, South, East, West. And the sheep then stay on the plateau. That's my, what I think about when I think of standing balance with, and the sheep are your center of mass, which, like I said, lives behind your belly button. And it drifts around stupidly when you're standing. And you can watch patients sway during a rhombar. And then the ground reaction force is the sheep dog. And so the patient has to activate their muscles to get the ground reaction force anteriorly to the center of mass, just like the sheepdog had to get further west than the sheep and push them back to the east. In this situation, the ground reaction force, when the center mass tips forward, has to get further forward than the center mass and push it back, and so she must not be able to do that because she does not want to, she's tilting back like this, she does not want to go forward, so I'm assuming your plantar flexors are no good. Similarly, the other thing you can do when you're drifting forward is you can at least become a rigid body rather than jackknifing on your face, and then you activate your glutes, and she's not doing that either, she's leaning back, her glutes are not useful. So I think, well, what does, what do the plantar flexors and the glutes have in common? If we think about it for a while, they have the S1 nerve root in common, and so we do the, we want to do an MRI, but she had too much hardware, and so I did a myelogram, as you can see, there's flow coming down, and then all of a sudden, there is no flow down here at L5-S1, and so her S1 nerve roots are just kiboshed, they're squished, and for that reason, she has minimal hip extensor strength, minimal plantar flexor strength, and so her gait is necessarily performed with the center mass posterior, because if it gets anteriorly, she's falling on her face. That's why she did that, and that solved the problem. Didn't help her so much, in my opinion, she'd be great with a walker, because then you got, as long as you have good triceps and good grip, good shoulder depressors, got a walker, it's in front of you, then if you pitch forward, you can save yourself, but I wasn't taking care of her. Hopefully, she did that. Next patient was mine. She had an old L5 radiculopathy, and I'd seen her two years before, and she had a couple epidural steroid injections, let time go by, she did really well, so her pain went away, and she's very happy with the outcome, and then she came back and said, my, it's back, my pain is back. It's like, oh, bummer, man, but that happens, and so I said, let's watch you walk, so we'll watch your walk. She'll do a couple laps. All right, you can come back. Good job. We'll have you do another lap as soon as you get back here. You're doing great. Yes, thank you. Let's take a look here. During stance phase on the right, that sweater ring stays horizontal, and I didn't ask her to do this sweater thing, but if I, I wish I had, because it was a brilliant idea on her part. Stance phase on the left, that contralateral hemipelvis drops, suggesting that the hip abductors and the lateral hip stabilizers on the left are weak, and they are. Boom, and her old radic was on the left. She had an L5 radiculopathy on that side. L5, again, you can see this, boom, boom, there it is, oh, sorry. L5 tends to affect gluteus medius to a large extent, gluteus max to some extent, so long-term L5, you've got some lateral hip weakness, and so then that's what was going on. I took her history, and it was much more consistent with lateral hip pain, not so consistent with radiculopathy, and when you watch her walk, it's like, yeah, of course you have lateral hip pain. The, you know, the greater trochanter is Grand Central Station for a bunch of, a bunch of tendons, and the bone tendon junction on the tendons tend to get, tend to get, have some degeneration there, and you have lateral hip pain. Some people get bursitis, probably not many, but again, what we had here is that lateral pain likely is a consequence of L5 radic, and if you keep these things in mind, what tends to happen is the neuromuscular flows in the musculoskeletal, and this is a good example of that, where L5 weakness led to some musculoskeletal pain in the, in just by chance in the same distribution. I've seen similar things for people with upper limb problems. I had a patient with rotator cuff impingement on the left from kayaking. It was very clear she had rotator cuff impingement, and then I evaluated her strength, and her external rotator strength, her infraspinatus strength was horrible, and then I asked her about her history, and in college, after she received her injections to go to school, she'd had severe pain in the shoulder, followed by weakness, sounding very much like break, Parsonage-Turner, whatever term you want to use for that, brachial neuritis or brachial neuralgia, which actually is changing nomenclature quickly, but we'll call it Parsonage-Turner syndrome, but again, the idea was that her infraspinatus was weak long term. It never got stronger, and that predisposed when she started kayaking to impingement as the humor head moved without good control, so in that similar situation as here, the neuromuscular problem flowed into the musculoskeletal problem later on downstream, and that's one thing. Whoever had a musculoskeletal problem, always like, well, why on that side? Why not on the other, and so this is sometimes the answer is a past neurologic event. All right, let's see. I want to, I think I talked a little bit about the frontal plane, about that Trondelmer Gate we just saw, and I love the frontal plane. It's much more important, and we ignore it a lot, and yet for balance and falls, which is my primary interest, it's important, so watch. Oh, come on. Show me this. I love this video. All right, here we go. So here we go. Watch these people. Boom. Gone. Down. Isn't that great? They'll do it again in slow motion. It shows the challenge of keeping your balance in the frontal plane, so these people, what happened was the car skidded to a stop and took this mat along with it, and all these people were displaced laterally, and they went down uniformly without fight, yet I think if this happened anterior-posterior, if they had to step back or forward, briefly forward, they could probably take that big step and recover, but laterally, no way, so I'm very interested in frontal plane, and so real quick, we have a depiction, and I apologize in advance. These are my graphics. Center mass is in the middle. The patient's taking a step walking toward you, so their left foot's in the air, and so 5'6 body weight, which is the head, arms, trunk, and one lower limb, but not the stance limb, is loaded, is the center mass here, is loaded upon the left hip, which is here, and it does so in a ratio that is one to three. The center mass is further away from the axis of rotation of the hip than the muscles are that are controlling that action, so the muscles are at a disadvantage, and so without good lateral hip strength, you have a dip, which you saw in the patient that we just had, and that led to, you know, stressing of these tendons, the gluteal tendons, and the iliotibial band, and the lateral hip pain that she had. Also leads to foot collisions if you're not careful, which is, of course, another concern. If the patient's strong, these medius minus are working, then there's just a gentle eccentric drop, eccentric contraction of those muscles, and a very controlled drop of the swing limb hemipelvis. All right, so we'll watch her one more time with that in mind, and you can see why the left hip would develop lateral hip pain, gluteus medius minimus tendinopathy, and the right one's doing okay. All right, now there's another strategy that you can use for combating hip weakness, and let's look at it right here. Who's this dude? That is FDR, and what he's doing, would it surprise you there's another strategy you can use if you're really weak, and that is to make the gluteus medius minimus, the abductors, do very little. You take your center mass and throw it over the hip joint, and if you can get it all the way over the hip joint, this lateral hip doesn't have to do anything, as we can get it all the way over there, and so FDR had an incredibly weak right hip joint, and so he was able to get it all the way over the right hip stabilizers, and so he threw his center mass over the side, even use a cane to help him keep from going too far, and so that's why that terrific lateral center mass dislocation during stance phase on the right, and by the way, I want you to look at the guy with him. I just want you to point out that when the leader of the free world, most powerful man in the world tilts to the right, hell, we all tilt to the right. Look at him walking along there. See, we're all tilting. The big man does it. We all do it. I do it too. Love it. He apparently had people that he liked to walk with more than others, and I can see why that would be a guy he'd like there, so that was the other strategy. All right, so moving on from hip abductor weakness and L5 stuff, we'll move on to this patient with type 1 diabetes for like 40 years. Amazing woman, and she walked, and here we go. Let's, here we go. I'll just tell you. It causes me pain just to watch this. Scares me each time. She wanted to do it. Very courageous woman, so let's watch the step with variability again, which in neuropathy is increased. Her steps will be somewhat chaotic in the frontal plane. Wide base, she keeps it. She's very smart to keep it wide base, so avoid foot collision and crossovers, but even as smart as she is, and she's exceptional, there is a crossover coming up right there. The orthopedic crossover of death happens right there, and obviously, she's got the swing phase difficulty with the foot drop on one side and shoulder flexion weakness on the other, so amazing woman. That's her severe neuropathic gait. Give her some AFOs, and she's already got a quick brain, and she's already got strong hips. Given those two things, let's see if she can compensate for neuropathy. Yes, she does. Beautifully compensates. Strong hips, quick brain, intact executive function, good basal ganglia, all that. She compensates quite well. Really remarkable difference that the AFOs offer her. Give her some dementia, not so good. Make her 300 pounds with weak hips, not so good, but given these attributes, even severe neuropathy can be compensated for with excellent hip and core strength, which she'll demonstrate, I think, right here. Check this out. She does a lot of yoga, and that lateral trunk stabilization is incredible. She can do a long plank for double figure seconds, and that, along with her good brain, is what allows her to stay upright and not fall, despite the severity of her neuropathy. I think I already mentioned to balance the sheep and the sheepdog. There's a sheepdog that is in a patient with healthy, good peripheral nerves, and this is a sheepdog in someone with neuropathy. The sheep move, and the sheepdog has no idea because their ankle core perception is disturbed, and then when they finally do figure it out, the ankle muscles are relatively weak. They generate torque slowly, and so the sheepdog's late getting there, and the patient falls. Let's see. I'm going to go back. I'm going to come back to sheer force, and here we go. I'll go back. I want to show a couple people doing one-legged balance. First is me, and you'll see what an idiot I am. I put my foot. I'm going to stand on my left foot. I put my right foot on the ground briefly, and then I pick it up. At first, my eyes are open, and then I close them, and when I close them, I'll pick my foot up, and you'll see how hard I work to keep my balance, but it's going to be an ankle strategy. You're going to see a video of an ankle strategy of rapid ankle inversion and eversion, and remember the ankle eversion allows the sheepdog to move quickly laterally. Ankle inversion allows the sheepdog to move medially and keep my center mass in place, and there I am. I can't feel this, but it's actually happening, and I can feel it, so I lift my foot up, close my eyes, and now you'll start to see a lot of motion as my ankle inverts-everts to keep that center mass in control, and I finally fail. Now, I thought that's the only way you could stand on one leg reliably, and then I met this guy who had bad diabetic neuropathy. I mean, his feet are sort of a stone from here on down. He really didn't feel a thing, and yet he could stand on one foot using a hip strategy better than anyone I've ever seen, and so check this guy out. He had incredibly powerful hip musculature. He's a farmer, and he said he didn't fall very often. Now, his knee, by the way, is not touching the table. I wish I'd videoed it better, but it's not, and I think you'll get that sense, so let's watch this. Stand on one foot. Here we go. Ten seconds, if you can. Look at that. His ankle can't do the job, so he changes torques at his hip and creates a sheer force on the floor, and by this means, since his ankle inverts-everts, can't do it due to neuropathy, he's able to keep his balance. Just incredible. I mean, totally different from me, but probably more effective. Watch it one more time, and then we'll talk about sheer force with some diagrams I had behind there. Quick brain, strong hips, compensating for neuropathy. All right, so we'll go back. We'll take a quick look, and you say this sheer force, does this really matter? Sheer force, yeah. Well, consider a ball. This is something we all know. Let's have the ball fall straight down onto the pavement. There's a ground reaction force created, and the ground reaction force is the opposite of the force of the ball striking the ground, and so the ball goes straight up. Bing. There you go. That we're used to. Now, let's spin the ball, and we drop it. Now, there is a ground reaction force. It's vertical, but there's a sheer ground reaction force as well, a sheer force this way, and so the reaction to the sheer is in the opposite direction. There's an upward ground reaction force in the sheer going in the opposite direction, so now the ball is going to go sideways. To prove that will be my son Connor, who's now 6'2 and 16, but at that point was a little guy, and there we go. Spin it away. Same way. There we go. Clearly, sheer force works. It deflects the basketball, so let's consider the situation when the center mass goes laterally, which is a bad thing. When it goes medially, it's okay on one foot because you got your swing limb to rescue you, but when it goes laterally, you got nothing out there except for your hip and maybe your wrist to break, so let's take a look and see what the patient can do, so here's the center mass has migrated laterally beyond the center of the axis of the foot beyond the range with ankle inversion injury. Ankle inversion strategy can provide rescue, so they got to think of something else, so the hip adductors will really fire, and again, if we were together, we could do this. You could drift laterally on one foot, and you could feel your ankle invert, and then you'd feel the hip adductors fire. There's also going to be contraction of the core muscles because obviously the pelvis can't be wiggling around once these things fire. The core muscles firing also makes your lever angle longer, so you're not collapsing a little, but you're a longer level, and then you sway and fall more slowly, which is an advantage, so those things happen, and down here, you got that shear force generated this way. The ground reaction to the shear goes the other way, so the adductors fire. The shear force is medial, but the ground reaction to the shear is lateral. It inclines the frontal plane ground reaction force, gets it outside the center mass, and pushes the sheep back to the midline, and this is what this gentleman was doing, which I find just remarkable. Let's see here, so once again, again, this is the mechanism. Strong hips can control, compensate, I should say, for poor ankle function. All right, let's see, how much time do I have? Another case here, yeah, I can do this real fast. I mentioned briefly that the core staying strong helps you fall slower, and so you resist perturbation, as opposed to if the core collapses, you fall quickly, and you're done, so lengthening the lever is a good thing. So, watch this football player. He's going to get hit from the side. He's running back here. He's going to get hammered from the side. Boom! Right there, but the linebacker hits him high. He doesn't hit him low enough, where I think the hips would have collapsed. Hits him high, and the guy is, you know, displaced laterally big time, but he's going to do a crossover step, and notice his body doesn't collapse. It's trying, but it doesn't quite, and so now he's still in business because he stayed vertically. He fell slowly because that core was so strong and withstood the hit, and now his center mass, he gets a little torn by this guy. Also gives him a deflection at the end, and so now his center mass is rotating a little bit, but, and here's his biggest chance of going down is after the after these perturbations. You'll see his hips give way, and right there, you're really worried about him. Okay, you weren't when he got hit, interestingly, but now we're worried he may go down, or you're hopeful if you're cheering for the defense, but he has the power and strength to take a recovery step way out wide, and that step is probably as far lateral as it is forward, probably farther lateral than it is forward. He has the strength to do that. Did that really happen? Oh, yeah, that did happen. So, here he goes. There's the big hit, and boom, there's the sideways, and then the recovery step right there. Strength through that, stays upright, quad strength, hip abductor strength, and then he goes to celebrate. So, again, the idea that both having a strong hip and a strong core improves your stability. Rapidly available strength dip allows elongation of the inverted pendulum, so you fall slower, generation of shear forces, and rapid placement of the swing limb for rescue. Finally, I show you one last case. This patient had severe afferent loss. Her sensory loss in her lower limb was almost complete from radiation plexopathy. She had a cancer, so she had radiation, and so both lower limbs are very, very reduced sensory function. Couldn't feel a tuning fork really until early at crest. Markedly diminished large fiber function, and so her proprioception was horrible. So, watch her step with variability on the way down. Crossover step, just chaotically, just really bad. Watch that one more time just to get a sense of it on the way down. Then, on the way back, I tell her to touch the wall. I say, go ahead and touch the wall. Just touch it lightly, and look what just light touch does for her. She's just trailing along, and yet those steps, that step with is so much better than the usual idiot and all to distract us um so much better and there's really very little biomechanical relevance to that touch it's just light touch the other rule light touch improves proprioception i think in people with we're able to substitute um certainly and there's a guy called jake a jk that made tenure 10 times over writing papers on light touch and one-legged balance um okay closing quote uh newly discovered knowledge even if trivial is rarely true with the one who discovers it uh and from bill murray ghostbusters back off man i'm a scientist um it's been a pleasure to address you today even though i didn't see you um let's see there's my email if you have any questions or thoughts that you want to get to me on and have a great weekend um i hope you found this to be of some use let's see there it is all right have a good weekend thank you dr richardson we'll come back to you in a bit for some questions um next i want to bring on again dr casey kerrigan who's going to talk to us about running gate awesome awesome okay so um running gate um i oh i'm sorry there's some geese in the background here you might hear some honking um uh we have with us um bob wilder i hear is um is listening in here so he's so bob please text me if i say something stupid he is now the present uh chair of the department of physical medicine and rehabilitation and we did a lot of this work together um that i'm going to show so um um running is actually a lot easier than walking um this is our youngest when um she was first trying to walk but you know we were we've been looking at walking and it's complicated because we've got a double limb support um we have actually two different phases in a grant in the ground reaction force that's occurring during during walking and in running it's so much easier um and that's because the peak stresses occur really only once so instead of having this ground reaction force where you have this double like a butterfly pattern you really only have one major um hump so this is in the sagittal plane of course the ground reaction forces are much bigger um than in walking but you know you only have one limb um and foot contact at a time so it's just it's just a lot easier this is in the coronal plane and um we're going to get back to this but i want you to appreciate how the coronal plane sorry about the geese um that the the coronal plane the uh ground reaction force is further away from the joints and um so we actually have more um loads in the coronal plane than we do in the sagittal plane even though it's the sagittal plane that's making us go go forward all righty so um just to get an idea you know in in walking we always have no matter what graph we're showing the torques um or the ground reaction force you get this sort of this double hump pattern and that's you know in in all planes but in you just have sort of this one this one uh mountain and that's across all the joints um this graph shows the typical measurements that we would get in a study where you have the ankle the knee the hip you have the sagittal plane motion or sagittal plane motion or moments then you have um the coronal plane and then you have the transverse plane so i wish i could point out on the slide but basically the top is sagittal the the middle is the uh coronal and the um bottom is the transverse plane this is actually taken from um we did a study of um treadmill running on a decline i believe it was a four degree uh incline four degree decline and then level and then look at the differences in all of the moments it's interesting we didn't see much difference in in moments but we saw more uh ankle power in the incline and more knee power absorption and decline and i we haven't really talked about power we can measure power power is really just the torques now knowing which direction um that ankle or that joint is moving okay so it gives you um a power a joint power that's positive is means that there's some sort of concentric activity and a power that's negative means there's eccentric um activity so this kind of makes sense so you there's more you need more power at the ankle in incline um but in decline if you you know you're running downhill and your knees get sore there's a lot of absorption going on in at the knee and decline compared to incline okay so i just want to get you familiar with these sort of graphs um uh but so this was this was a paper we published that looking at the moderately sloped running and our conclusions from all that is that the the joint torques um are really about the same so when we worry about um people who have joint pain um we say you know at least at this point with the with the moderate um incline decline there's not much difference and so it's probably safe all right now another thing um that we did was look at overground versus treadmill running and we have this instrumented um treadmill with a force plate in there and put the markers on so we can basically look at compare treadmill running to overground running where we basically did the same thing but just on um force plates that were embedded in the ground and then we saw a whole bunch of differences not a lot of differences um it's funny when we publish this people are asking well you know oh you know treadmill running is so different than overground because the treadmill is pulling your your the limb back and all this stuff and really there really wasn't that much difference um there's some some kinematic changes some slight differences you can see the arrows um and this is just the kinematics the only difference we really saw was in knee flexion um and then in the kinetics we actually saw some interesting things we saw a reduction in the moments in the um uh with with being on a treadmill so um i'm sorry at at the uh at the knee and then increased moments at um in treadmill running but you know these are these are slight and um but again i just kind of want to point out that you know things are you you really just have these this sort of this one hump that's occurring and um that's all you really have to worry about is just that what's happening at that one peak okay and then this this paper we looked at um the effect of running shoes on lower extremity joint torques um and this study actually this was just right before i left uva to to uh start my shoe company but this this paper kind of really hit the fan um and what we showed is again we just looked at joint torques um and showed that well we looked at everything of course but the the key thing here is in if you look in the very middle graph you see that the knee varus torque was um a lot higher um when wearing a running shoe compared to being barefoot and it's at you know how much load you have on the medial compartment of the knee compared to the lateral compartment of the knee this was basically the same finding that we found with with high heel shoes and so we were showing this with um with your basic running shoe and it didn't matter whether it was a motion control shoe and even nike free all in any sort of traditional shoe was showing these increase in um uh joint torques so um we published this you know on uh not that um you know this kind of came out about the same time that uh christopher dougall wrote the um his book on um that um born to run and it was kind of like the perfect storm and a lot of people used our paper to then promote the um barefoot running movement which i don't condone um and i'll explain why um but basically you know we had this this increased knee varus torque um but there was more to it than just what we published oh before i get into that it's like you know why why do um how does footwear affect these torques it's a number of things it's it's the cushioning it's the heel elevation it was just all these side-to-side contours in a shoe that disrupt that um where that basically where the ground reaction force is in under the foot and um we showed even arch supports increase this um uh the knee varus torque within in this study we showed that even just a little arch cushion from spanco and uh here's fun fact i think it's william spencer he's a the founder of spanco is actually uh was a uh was a physiatrist um so anyway so just even even just a tiny little arch cushion increases this uh this torque and why well there's this sort of like this natural springiness of the foot during gait um and uh again the top the top curve is in walking um and the bottom curve is in in running and you can see this is the singular hump but if you look at the those colored lines um that go through the not the dotted lines that's what's happening that's your your foot the navicular arch dropping and so it it's dropping and then it's coming back in sort of perfect tune with when the ground reaction force is at its highest um during the second phase when during push-off and walking but then just during the main peak in running so it's just it's a springiness effect of the foot you're you're taking that away when you're putting a an arch support under it that's one reason the other thing is just how it's shifting that's the center of mass okay but that's just the torques now i want you to look at this time looking at these same graphs um where the arrow is now where that arrow is is the moment of impact and it's that the top of the mountain that's that's the active peak of running so there's this initial um little peak it's called the moment of of impact and this is where everybody has assumed um that injuries occur and when you look at this graph and kind of really understand the kinetics you just it's kind of like a no-brainer it's like how the heck does that explain any injury it really it has to occur at the tops of the peaks and really i think until we actually studied this i don't think anyone really appreciated the difference between what's happening at this little at the little blip of impact versus at the top of the mountain so we break it down look at that you know that very first um peak um that first peak that impact has nothing to do with injury the second peak the active peak has everything to do with injury and i want to convince you of that um with just some pictures um so this is just a picture i just pulled this from somewhere a picture of some runners and you look at the one that the picture of the person just making initial impact on the lateral part of their of their of their uh heel at impact and then versus planted so there's very little there's nothing really going on at impact and implanted you can almost see look at look at you know how look at the muscle activity on his on his leg and his thigh and his his tibia even the his facial expression that's that that's where it's all happening that's where everything is maximally stressed and um uh that's the most challenging probably part of running um so if we look at and this is just just a screenshot of uh how the data looks when we when we analyze it right at impact you see this little lip of a yellow line underneath the foot that is the ground reaction force and this is what it is in the chronoplane so um just this tiny little yellow blip right at initial contact and now here it is in mid stance so correspond that with that the guy who was in mid stance so look at that yellow line and look how far it is from the joints you just look how huge it is okay and that's in the coronal plane it's also in the sagittal plane and then if we look at you know that that impact peak force maybe it's even important um and by the way you don't even have that in peak peak force i i believe where it's coming from is the fact that you have this foot attached to your to your leg and so you're it's contacting that it's contacting the foot the heel first before sort of the whole the whole rest of the body um and there's some simple experiments you can do like with a bowling ball um uh attached like the like the idea of um if you drop it you get sort of this one peak but now if you attach something to it you get this what looks like this little blip anyways there could be you know that this impacting forces is beneficial but let's just concentrate on what's happening in mid stance and this is where you know another um uh computer generated model of what's happening the red being the ground reaction force and how far away that is from the the joints are from that that ground reaction force and how so much is occurring in the coronal plane in the sagittal plane things line up really well with the joints um and the coronal they don't and so i just if you look at this you look at where the ground reaction force is i could make a a case that we could explain a lot of what you see um a lot of the injuries that you see in running um because this is all just basically stresses and strains where they're the max um at this particular point in the gait cycle and all with respect to the coronal plane okay and again this is um another picture i i uh took a picture of this i actually took a whole bunch of pictures of this of this race and it's amazing how it just you know in that that mid stance you can see the you know you can you can see all the stresses and strains that are occurring that initial contact there's just there's just nothing going on okay so um what can we do to um to sort of you know we understand that it's basically that this the top of the curve it's not impact or what happens right at impact if it is like if we you know the idea that we could protect against injury by cushioning that impact is um is wrong i think um you know what makes more sense is to worry about that the the peak active force and um going along with this i think the best evidence we have for focusing on that that active peak is the harvard indoor track which is a compliant surface so um back in 1977 this guy named tom mcmahon who's a biomechanist he had this idea that if you had a springy track that you could reduce injuries you would you're basically providing the spring and um replacing the concrete surface and indeed injuries reduced by 50 percent in the first year it was installed so um all the harvard runners their um their times um went down by two to three percent when they ran on it uh if they had people coming in so the other ivy league schools running on it when they ran on it similar um that they had less injuries and uh improved race times so kind of went hand in hand with improved energy efficiency and reduced energy and i'm sorry reduced injury so so basically it was just plywood draped across these like you know two by fours or two by somethings and so you've got this this springy um effect and that springy effect provides compliance um this sort of this compression in the release by about one centimeter that's occurring at the exact same time as that is the rise in the ground reaction force that active peak so it's tuned perfectly and so this is sort of the spring mass model representing a runner's leg uh when it's contacting this compliant surface it's just a spring there's another example of a compliant ground surface well ground surface of a prosthesis but it's a spring so i'm gonna just you know think about the um you know um the spring effect that the most important thing that's occurring during running it's that top of the peak it's not um at this this blip of an impact and everything we do i think it explains and in everything we think about it uh what's occurring in the coronal plane, we can understand a lot with respect to injury. And, and as far as, you know, training surfaces go, I didn't, when I showed you the study of the overground versus the treadmill training, or treadmill paper, what's interesting is that, you know, that treadmill, even though we have a pretty stiff treadmill, there, there was still some compliance. And that little bit of compliance, we did see reductions in our, in the joint torques, especially at the knee. So then this, of course, then led to my developing a shoe company and making shoes that are flat, heel to toe direction, because that increases joint torques, flatten the side to side direction, because that's affecting in the coronal plane, no arch support, no cushioning or dampening, which in a way causes this unwanted contouring. And again, you know, you're, you're really all you can do is cushion that little blip of an impact. And then to have a true responsiveness or springiness, and a perfectly flat sole that works in unison with the foot, this natural foot compliance. And if you look at, I mean, it's amazing what the foot, you know, sort of that, that natural compliance that's occurring, how that affects those, those joint torques. And, you know, we'll talk about, you know, you know, pronation, you know, just that, that, that natural pronation, pronation is really just the foot giving that spring. And then that spring is what helps reduce the torques all the way up. And that is it, I think, end with. Casey, thanks very much. I have several questions I'm going to ask you later, but let's move ahead. I'm going to introduce Dr. Alter, Catherine Alter. She's a senior research clinician in pediatric and adult physical medicine rehabilitation at the National Institutes of Health in Bethesda, Maryland. She trained at the Medical College of Toledo for medical school as well as residency. And she did a residency in pediatrics and in physical medicine and rehabilitation. She has been a clinical faculty at Mount Washington Pediatric Hospital and formerly was a clinical chief there. Her interests are in the assessment and treatment of neurologic and musculoskeletal impairments in children and adults. And she's an expert in movement disorders, cerebral palsy, stroke, muscle hypertonia, brachial plexus palsy, and several other topics. And she is doing active research in noninvasive functional brain injury, botulinum toxin denervation, and the utilization of ultrasound imaging for musculoskeletal and neurologic disorders. I've had the pleasure of working with Dr. Alter for years. She's a giant presence in AAPM and ours educational programs and the STEP program in particular. So Catherine, please go ahead and tell us what you know. Thanks for that nice introduction, John. And Dr. Richardson already talked about the intersection between neurological and musculoskeletal problems. And I'm going to continue that theme today. And these are my disclosures, none of which are really relevant to this talk. And I'm going to cover today a topic that may be less familiar to the audience, which is task-specific sports dystonias, specifically runner's dystonia, and the use of motion analysis as part of the assessment. And to start this off, because people may be less familiar with dystonia, I'm going to cover that topic as well, just a brief review, and talk about the reports from the literature and present some case studies. So the first thing I'm going to start off with is actually a case study that's going to recur throughout my presentation. And this is a person that self-referred to us with complaints of an altered gait during running. And so she's a 38-year-old long-distance runner who presented to us that she was landing on the outside of her left foot and felt that she was having difficulty controlling her initial contact of her foot. And this problem occurred only when running. So if you see her walking gait, it looks completely normal. What happened was that it's worse on a decline, and it's also worse at the end of running, particularly long runs. She reports no provoking injuries. And this began after she was training for a marathon, and she'd increased her distances. And her running history varied, but whether she was training for marathons or triathlons or not, and her injury history was relatively unremarkable other than some ankle sprains. And the one history point that was important was that 18 months prior to her symptoms, she had changed from a heel strike gait in running to a toe-toe gait in running. So she's had lots of prior assessments, and she'd been to a trainer, several physical therapists, an orthopedic surgeon, and at least one or two sports medicine physicians. And she'd also had multiple interventions, including physical therapy, three shoe changes, orthotics. And it had been suggested that this problem might be related to instability at her ATFL. And so there was a question of whether she should have PRP injections to help with this. So our first step when she was referred to us was to observe her walking during running gait. And hang on one sec here. And when we watched her walking and when we watched her running, we really couldn't see any gait deviations, either running or walking. And one of the, you know, the issues is we have her running on a treadmill as well, which I'll cover a little bit later in the talk, but Casey's already mentioned. So the question for us was, could her symptoms be related to dystonia? And to answer that question, I have to cover at this point the question about what is dystonia and what is dystonia in runners. And I'm not going to, this talk can't really go into detail on the etiology and management of dystonia, but I want to cover the basics. So dystonia is a condition that has many different causes, and there are many different types of dystonia. It's also important to recognize that dystonia can either be a clinical sign or symptoms, but it's also a syndrome or a disease, or it can be. So we have patients present with genetic etiologies of dystonia. And then we have patients who present with symptoms of dystonia that are in and of its own without an other etiology. So what are the clinical features here of dystonia? First of all, it's the third most common movement disorder, and it has a number of different features. Features include postures or movements which are sustained or intermittent. They often have a twisting appearance. In many patients, the movements appear patterned or stereotyped. And for an individual patient, the movements tend to stay within the same muscle group, so they repeatedly involve the same groups. And if you see the movements in the patient on the top, she has hyperkinetic movements where her toes are continuously moving, whereas the patient on the bottom has a fixed dystonic posture of her fingers in extension at the interphalangeal joint and flexion at the MCP joints. So dystonia can have also…patients may have tremors or associated jerks can be present with this, so the movements may appear inconsistent. Typically, dystonia is activated by voluntary movement. You don't see it at rest, but in some patients, you will also see the dystonia at rest, like this patient with the moving toes in the top video. There are a number of types of dystonias that can be task-specific, including sports dystonias like runner's dystonia, but also in patients that have writer's cramp or musician's cramp, where the dystonia only occurs with a specific task. So with a writer, they only develop dystonia when they are holding a pen, but they can type or brush their teeth or do other tasks without having dystonia. Many patients with dystonia will have an associated sensory trick or geste antagoniste that decreases their symptoms, and a key to this is that many patients with dystonia, you will not see rigidity or hypertonia. Now, in some patients, you will in patients that have other syndromes that are associated with both these conditions. So what about classification of dystonia? Dystonia can be classified by age for the pediatric patient on the top or the adult patient on the bottom. It could also be generalized, again, like the pediatric patient on the top. It can involve the entire body where she has her upper limbs are going into extension, or you can have a focal problem, the patient on the bottom who has writer's cramp with involuntary extension of his wrist during writing, and his left hand is the symptomatic hand. We're looking for mirror dystonia when he writes with the right hand. Today, we're going to be talking about mostly focal dystonias that affect one body part or a segmental dystonia that affects two continuous limb regions, and remember that the causes of dystonia can range significantly from genetic or secondary causes, and secondary, I mean injury to the central nervous system, from other conditions, or they can be idiopathic, and in other words, we haven't discovered the cause of the dystonia yet, so we call it idiopathic. The most common, if we focus now just on idiopathic focal dystonia, which is what we're going to talk about mostly today, the most common idiopathic focal dystonia is cervical dystonia, followed by blepharospasm, upper limb dystonias, and craniofacial dystonias. Much more, much less common are lower limb or trunk dystonias, so the lower limb task-specific trunk dystonias or lower limb dystonias, again, are less common. So this is a video of one of my musicians who has a focal dystonia involving the D4 inflection of the MCP joint, I'm sorry, inflection of the PIP joint that's affecting his playing, and he can't extend his finger to the keyboard, and focal dystonia in the upper limb is very common. It's most often task-specific and is typically idiopathic, and that includes some of the conditions that I have listed. In contrast, idiopathic task-specific lower limb dystonia, so a patient presenting with just dystonia in the lower limb as a presenting sign is, as an idiopathic condition, is very uncommon. Most often, dystonia presenting in the lower limb is actually a symptom or sign of another condition, metabolic, central nervous system, genetic or inherited conditions, or even psychogenic, or what we term functional disorders at this point. So it's very uncommon, and focal dystonia is presenting in the lower limb compared to all focal dystonias. It's only 0.7% of adults with idiopathic focal dystonia percent with lower limb involvement, and there's only 100-150 cases reported in the literature at this point, and because it's so rare and because it's so commonly associated with other conditions, it's really important that an extensive workup is performed because this is really a diagnosis of exclusion. You need to exclude all of the other potential causes that could be masquerading as a focal dystonia, like in this patient who is a runner who presented to our lab for evaluation of a task-specific focal dystonia only involving her right foot. It initially occurred only during running, and it generalized to affect walking at this point, and the extensive workup in her led to a diagnosis of multiple sclerosis, and this has stayed stable over many years, and she really hasn't progressed, but she doesn't really have idiopathic dystonia, and that is in contrast to some of the other patients that we see. So if we look at patients with true idiopathic adult onset focal dystonia in the lower limb, that it typically occurs in middle-aged patients in the fourth to sixth decade. Runners tend to be a little bit younger than the general population with idiopathic dystonia. There's a female predominance in both patients that are runners or those without runner's dystonia, and exercise or sports-specific lower limb focal dystonia is associated with a many-year running history. Again, repetitive skilled tasks, just like a musician. Runners are performing a skilled task, and it's exercise-induced dystonia doesn't just involve running. It also includes cycling, golf, dance, and we see this in upper limb as well in table tennis and golf as well, and pool playing as well, so billiards. So I want you to listen to this video. This is one of my patients. Top is one of his photos from a long time ago, but I want you to just listen to him in the gait lab. I always describe this to the fellows that we're training is that I hear his dystonia as much as I see it, and typically with focal dystonia, it affects distal more than proximal muscles. Now the patient in this video actually has a knee flexion dystonia, which is resulting in that gait, but you can see either distal or proximal muscles involved, and for most of the patients, runners with idiopathic dystonia, the duration of their symptoms prior to a diagnosis in our setting is somewhere between one to five years, and it's very often associated with a change in training like that first case that I talked about at the beginning of my talk, and the patients will report that the first thing that happens is a peer that they run with tells them that their gait has somehow changed, and clinically, they report a lot loss of automaticity. They feel like it requires a conscious effort to continue running if their speed is decreased, and they have particular problems with change in direction or speed, and sometimes they'll describe a pulling position or other problems with pain. So again, we'll see this guy is landing flat on his foot. He can't extend his left knee completely. So what about additional features? We've talked about some of the features of dystonia and the demographics. Another feature of patients with runner's dystonia or exercise dystonia is task specificity. It only occurs when they're performing a specific task like running, so this is a patient with runner's dystonia where her symptoms have generalized, and by the time patients are referred to us, more often than not, their task specificity is lost, so that this patient is walking with a stiff knee gait, and it occurs whenever she's walking. However, it doesn't occur when she walks backwards, so task specificity, if you cause the patient to or ask the patient to do a task that's unfamiliar, they may be able to do that task without presence of dystonia, so we'll ask them to perform a variety of different tasks, including marching and backwards walking. So what's the true incidence of sports dystonia, including runner's dystonia? Well, it's likely underreported or underrecognized because most of the time, it's thought to be a musculoskeletal problem initially and misdiagnosed, and the causes of idiopathic focal dystonias, including lower limb dystonias, are not well characterized and are likely multifactorial. There's a sort of an intersection between environmental factors associated with genetic factors and the task repetition that leads to this. There is an association with trauma or a change in training in many of our patients, and the same thing in musicians, a sudden change in their playing or their training for a performance. If, again, beyond the scope of this talk, to really talk about all the different potential causes of dystonia, but one of the leading thoughts is that this is a defective local inhibition at multiple layers in the central nervous system that leads to reduced zone inhibition and over-recruitment in many muscles instead of just the muscles required for a task. So what about, what are the, when we're evaluating runner's dystonia, what are the pitfalls of evaluating dystonia, idiopathic dystonia? Well, part of it is that it's, because it's so rare, we have runners that will present with what appears to be runner's dystonia, but maybe something else. So you've sort of seen this gait before from Dr. Richardson's presentation, this is a patient who presented to us with runner's dystonia, who, if you look at her gait, when she's running, looks asymmetric, when she's walking, her lower limbs look symmetric, but she has decreased arm swing on the left, and watch that left arm when running and watch her left leg when running, she's not advancing the left leg, and that also affects her gait on the right side as well. So for gait evaluation, at minimum, when you're, when you're evaluating the patient, it at least requires observational gait, and we've, we film all of our patients on either a camera, a digital camera or cell phone, even if we're not doing motion analysis, we, we do this both in frontal and sagittal plane, we do this in and out of shoes, and we have patients doing we do this in and out of shoes, and we have patients doing forward and backward walking, marching, and for runners in the motion analysis laboratory, we try to do some overground running as well as running on the, on the treadmill, and we try to get videos, like in the patient above, in the real world, to get, get another analysis. So if we look at this patient here versus this patient on the bottom, their gaits look pretty similar, they have that, both of them have a decreased knee extension and movement, but the patient on the top has a reduction in arm swing that the patient on the bottom does not have. Now, the patient on the bottom has a true runner's dystonia, where the patient on the top had a presentation of focal dystonia in her left lower limb as the initial symptom of Parkinson's disease. It's important to rule that condition out and not establish incorrectly a diagnosis of focal dystonia. All right. So we use motion analysis in situations where observational assessment is insufficient to establish a diagnosis, or when we need more information to inform treatment planning in our patients. And not every patient receives motion analysis assessment, but vast majority of our runners do have this. Dr. Kerrigan has already talked about the, you know, the data that we collect, including temporal-spatial data, which is the velocity of gait, step, and stride length. We look at kinematics, which are joint angles and timing of movement, and electromyography, or EMG, focusing on the timing, duration, and amplitude of movements. And in our world, we're really looking for co-contractions and synergies where multiple muscles are contracting at the same time and they're out of phase. And in runners or other focal dystonias, we're comparing side-to-side data, and we're comparing control data, and we'll look at different tasks. So if you look in this patient, we're looking at, this is a fine wire EMG electrode versus surface electrodes here, but you can see this continual activation in the tibialis posterior muscle in a patient with inversion deformity, or an inversion gait. Red is right. Unfortunately, I couldn't find the kinematics for this specific patient, but the kinematic pattern would be in-toeing with an abnormal activation in the tibialis posterior as a cause of an equinus or inversion during running or walking. So what do we measure? As I said, we measure, and we look for asymmetries in gait comparing different muscles and co-contraction, but we also look for this task specificity. So this is that same patient in forward walking where you see this continuous activation of the tibialis posterior, but when the patient reverts to backwards walking, you'll see that that continuous activation in tib posterior is extinguished or certainly reduced. The reason why there's no left data on this is the patient didn't want me to place another fine wire. After I did the first fine wire, they didn't want me to insert the second fine wire, so we didn't have that second data. So instrumented motion analysis, what are the benefits? So, well, the benefits, it does provide detailed quantitative data. We get information about kinetics, kinematics, EMG, particularly EMG for dystonia is important, and this data really does help us with treatment planning, but what are the limitations? Well, it's important to recognize that dystonia in the affected limb, it's not like the upper limb where your limbs are functioning independent of one another. When you have dystonia and dystonic movements in an affected limb, it's going to change your movements in the unaffected limb as well, so we frequently see bilateral abnormalities in gait, EMG activation, and kinematics, and we get all this information, but you have to sort of sort out which is caused by the dystonia and which is a compensation from the normal limb, and discriminating the dystonic movements from compensatory movements or activation can be really challenging, particularly in patients who actually present with bilateral lower limb dystonia. It can be very difficult to sort this all out, so there are limitations to motion analysis, and some of this is just our ability to interpret the data, and it's critical, however, to discriminate these compensations from the actual dystonic movements, particularly if you're thinking about treating the patient with botulinum toxin because if you treat the compensatory movement, you may actually make their dystonic gait or their gait abnormalities worse rather than better, so let's go back to our 38-year-old, this person at the very beginning who came to us. She had minimal symptoms during motion analysis, and remember, she told us that her symptoms were worse on decline and worse at the end of a long run, and trust me, she ran for a very long time in the motion analysis laboratory, but unfortunately was on a treadmill, and she told us that her symptoms were always less on a treadmill than they were over ground, and we couldn't really run her in the motion analysis laboratory because of the short runway in the gait lab, and we were unable to decline or incline the treadmill, so we really couldn't provoke her symptoms that way either, so there is another alternative to a traditional motion analysis laboratory, which is the Karen gait laboratory that involves use of a dual split-belt treadmill with force plates that's embedded in a six-degree-of-freedom movable platform, and that platform can be inclined in any different direction, and it also involves an immersive environment, which really replicates real-world running, so that would be the ideal environment for the patient in this situation where we really had trouble provoking her dystonia, so we covered sort of what dystonia is and what we measure, and what's the current state of the published literature? Well, it hasn't been reported not that long ago. It was the first case report was in 2006 by Dr. Jankovic, who is a movement disorder neurologist in Texas, in Houston, where Dr. Cianca is, and he reported a case of a single patient or a few patients, and then they expanded this in 2008 to a larger case series, and they reported that most of their patients were females, more than 60%, and the mean age was in the 40s, as I described earlier. Their initial case series or case report was that proximal symptoms were more common, but later up, their later larger case series was more consistent with the current literature, which is that dystonia involvement is more predominant, and this was a 2008 review by the Mayo Clinic, and they reviewed 10 years, or I'm sorry, 20 years of cases, no, 10 years of cases here, and they were looking at patients presenting with adult-onset idiopathic or adult-onset lower-limb dystonias, and so adult-onset lower-limb dystonias, 86% were female. The mean age was, again, in the late 40s, and their symptom durations ranged from 1 to 96 months before they were referred, with a mean of 28 months, and left side was more predominant. When they looked at this further, you know, the initial diagnosis in these patients, 100% of them were diagnosed with idiopathic focal lower-limb dystonia. However, when they then looked at their final diagnosis of these patients, idiopathic focal lower-limb dystonia was present in only 39% of the patients, so 61% of the patients that they initially thought had idiopathic lower-limb dystonia actually had some other case, like this patient who initially presented with idiopathic lower-limb dystonia in her right leg, who clearly has another more complicated cause for this, and this patient actually has a genetic dystonia that's also associated with ataxia, so the other potential causes in patients referred to with potential dystonia and this involving lower limbs, it could be post-traumatic, and the biggest association that we see is an association with complex regional pain syndrome, but the post-traumatic dystonias almost always occur very quickly after an injury rather than a prolonged onset of symptoms. Parkinson's disease, so just like in our case series, Parkinson's disease was one of the most common non-idiopathic causes of runner's dystonia, and again, stiff person syndrome, functional disorders, a stroke, and in our series, we also saw patients with MS, so for those patients who were eventually that 39% who were eventually diagnosed correctly with idiopathic focal dystonia, none of them progressed to another diagnosis, and oral meds were largely ineffective, and botulinum toxin had the highest success rate, and there are conclusions that was in contrast to other forms of focal dystonia. Lower limb dystonia, alternate diagnosis are common and need to be considered. This was another case review that looked at another group in 2016 that looked at dystonias in the lower, presenting in the lower limb, and they were looking at exercise-induced dystonias, including running, and they separated them out, and they identified 413 patients with focal lower limb dystonia, and of those 413, only 20 actually met inclusion criteria for an exercise-induced idiopathic lower limb dystonia, and of those, 65% were runners and 35% were non-runners, and you can see the other causes of focal dystonia in athletes in the lower limb. Their demographics were similar. You can see with the duration that most of the patients had many-year histories. As I said, 15 to 20 years, typical distal female time delays in duration, and also this presence of a sensory trick was much higher in runners than it was in non-runners, and this is a key piece here, is if you look at the patients and what they've had done prior to getting the correct diagnosis, of the runners, eight of eight had surgical interventions prior to having an established correct diagnosis, so surgeries that were not necessary but were thought necessary because of the misdiagnosis, so their conclusions, again, from this study was that on EMG, that co-contraction between agonist-antagonist, just the highlighted part I'm going to go through here, was most consistent with dystonia, and that in 78% of their patients, as I mentioned earlier, they had bilateral abnormalities, and of the listed treatments, botulinum toxin was the most effective, and that at least 45% of the patients had partial return to their preferred exercise with botulinum toxin therapy, 30% were forced to change activities, and 25% were unable to exercise. Their conclusions, I've already sort of talked about this, is that it's unusual, potential triggers are running in other activities, and that treatment is largely toxin or botulinum toxin is the most effective. This was our case series of patients with runner's dystonia looking at kinematics or gait analysis, and it's consistent with the literature in demographics, and also the issue of co-activation or co-contraction is the primary sign that we felt was consistent with dystonia, and that the instrumented gait analysis helped us develop a treatment plan for many of our patients. In our case series, we had a fair number of patients that had distal involvement, but we also saw quite a few patients, a third of them that had proximal involvement, and our case series, as far as the return, we had at least 78% of the patients that we treated had some benefit from toxin, with 22% having no response, but a larger percentage of patients having some response and an ability to return back to an exercise, including their preferred exercise of long-distance running. So our conclusions were that motion analysis was an assistance. This is a patient pre- and post-injection of hamstrings. With a knee flexion, involuntary dystonia, and that where the dystonic movements were obvious, the motion analysis really confirmed this, but where it was more helpful was in cases where it was difficult to determine which muscles were involved, and it really did help us with this. So I'm going to go back to our cases in the final few minutes here. So I'm going back to our 38-year-old, this lady that ran on the treadmill for, I don't know, it was like an hour, almost an hour and a half, that she ran on the treadmill, and again, walking kinematics and EMG were normal, and she only had these brief periods at the very end of the motion analysis where she had symptoms. We were able to analyze the time-linked EMG and kinematics during these brief periods, and so the question was, did she have dystonia? And when we carefully analyzed both the video and her kinematics and her EMG, she lands on the outside of her lateral foot on the left side only. This is her left side, almost initial contact here, and that she has a plantarflexion and inversion moment or movement of the left foot, both initial contact, more so actually in stride, which you can see in mid-stride here, but there's also this subtle asymmetry in her EMG on the left of more continuous activation of her left tibialis anterior, but these findings were relatively subtle, so we recommended a repeat motion analysis using the CAREN system where we could put her in a decline and run her in a different environment to see if this would help make the diagnosis. So this is a maybe motion analysis was helpful to point us in the direction of a patient who may have early-onset dystonia that's relatively mild and still task-specific. This is our case two of the runner with a stiff right knee where she has been running for many years, a long-term marathoner. By the time we saw her, she couldn't run. She'd had multiple steroid injections, arthroscopy, a bunch of different stuff done with her knee without much benefit, and the motion analysis, we didn't really need motion analysis to show that her kinematics, I'm just focusing on her knee here, that on the right side, she has reduced right knee flexion, right is red, blue is left, and decreased toe-off or push-off of the right foot, and in EMG, you can see that she's, we're looking at this asymmetry in her quadriceps and hamstrings activation. She has this continuous, somewhat phasic, but over-activation on her quads and her hamstrings on the right as well as her TA, and we felt that she likely had dystonia in her quadricep muscles. You can see that her kinematics and as well as her EMG, I don't have that on here, were completely normal on the right when she's doing backwards walking, so we decided to do botulinum toxin in her rectus femoris, and these are her post-injection frontal plane and sagittal plane videos, and you can see this is four weeks post-botulinum toxin. She had significant improvement, and she was actually able to return to running. Her kinematics, this is pre- and post-kinematics. You can see the improvement in both her right knee flexion. It's not the same as her left, but her toe-off and her knee flexion have significantly improved, so this is one of our kind of slam-dunk improvement cases post-injection, and this is a change in her EMG pre and post, which shows that the overactivation in her quadriceps has reduced post-injection, and that overactivity co-contraction in her hamstrings has also reduced. This is just in one more minute, and this is a case of what isn't runner's dystonia, so this is a patient that was referred to us, again, with runner's dystonia, and her symptoms were not only present when running, but also with biking and swimming, anything that required high speed, and on exam, she also had dystonia in her right hand with writing, and on exam, she had no weakness, rigidity, spasticity, reflexes were normal, but she had this subtle change in arm swing on the right side and decreased right hip flexion, so we recommended motion analysis, and when we watched her run, this is what you see. She really can't advance her right leg during swing, and she has decreased hip flexion, decreased on the right side, particularly in stance here, so EMG was really telling as well. I did fine wires into her iliopsoas bilaterally, and this is when she was asymptomatic jogging, and the right side is symptomatic jogging. You see a dropout of EMG activity in her right hip flexors during speed activities, and so our conclusion in this patient that she didn't have dystonia, she actually had bradykinesia and decreased movements, and after an extensive workup, she was eventually diagnosed with Parkinson's disease, so my conclusions here that task-specific focal dystonias are uncommon, and because of this, they require really detailed assessment to establish this diagnosis, and that they are likely, even though they're rare, they're likely misdiagnosed or underdiagnosed, and many of these patients receive unnecessary treatments or evaluations, including invasive interventions, so it's important for both the MSK and neurospecialists that see patients with movement problems that they recognize this as a potential diagnosis to reduce the delays in referring the patients to appropriate intervention. And the most appropriate intervention for most of these patients are going to be botulinum toxins. And that motion analysis does provide an assistance with some limitations, but may help you with establishing the diagnosis of runner's dystonia. And I think I'll conclude there. Katherine, thank you very much. All right, we have I think just about 10 minutes. Is that correct, Brian? Can we go over a little for some questions? Yes, we can go over just a little bit. Okay, so I see there's several questions in the question and answer. Brian, why don't you go ahead and let those go, and then I'll throw in my own at the end if we have time. I think Dr. Richardson may have, or is in the process of answering this, but in a private musculoskeletal solo practice without a gait lab or the related amenities, how would you recommend a practical application of some of these gait and related kinetic chain concepts? I believe that's to anyone. Is that correct? Correct. Okay, whoever wants to chime in. I wrote my answers, so I won't add anything further. You can easily replicate a lot of what we do. And I think Dr. Richardson already said this, is you film patients. Use your cell phone, use another camera, but it's really important that you do coronal plane and sagittal plane, because if you don't do both, you may miss some of the sagittal plane abnormalities that at least we see in patients with dystonia. But we review these pre and post injection on a fairly regular basis. And I've been filming patients in clinical practice when I wasn't at National Institutes of Health. And I've done single patient pre and post toxin injection, whether it's for CP or any other problems. So it's not expensive to do this. It takes a couple of minutes in your practice and that's it. The main problem is frontal plane is easy to do. It's sometimes hard to get a big enough window in sagittal plane to do this. I'm sure Casey has something to say about this as well. Yeah, you know, I just, yeah, going back to the, even though I said, you can't see those kinetics, I think you can appreciate them. You always appreciate them. And you just look at a patient differently or you look at anybody differently and just understand that that's what's going on underneath. I don't think, I don't think that clinically gait analysis is gonna be that contributory. Honestly. Was that the question? It was mainly how, if you don't have a motion lab, how do you look at some of this stuff? Yeah, I think it's okay. I think it's, you know, you look at it observationally, you know, a video camera is great, just, you know, just your phone and videoing just because a lot's going on observationally. But if you can take a video and slow it down, you'll get the essential components. But, you know, like I said, it's just, you know, getting the kinetics, the EMG is fantastic for spastic paresis and understanding. And I would say with testonia, it's gonna be equally as important because you'll see the muscle activity, you know, that's inappropriate. And I don't know, just in my experience clinically, what I saw with hemiparetic gait, we had some stiff-legged gait. I studied stiff-legged gait for a long time and found that when you study in individual patients, the reasons were different. Somebody would have overactivity in their quadriceps or actually just even one head of the quadriceps where we could give a Botox just to that one head. So that's a great clinical use, I suppose. But I think for the most part, we kind of understood some sort of global things that apply to all patients that might be, I think, more important, like the fact that knee flexion occurs passively and that it's not an active event. And that if we can improve hip flexor strength in all of these patients, then we can improve gait. So anyways, I don't know, it's varied. I guess, you know, depending on patient presentations. Brian, do we have another question you want to throw out? Yeah, so thank you so much for a great morning. Dr. Alter, which doses of BTX do you use in Renner's dystonia? That's like a two-hour lecture. Remember that each one of the toxins, these are biological agents, not drugs. There are currently four available botulinum products in the US and the dosing between at least three of them is completely different. What I will say is the general response is that the doses for dystonia and particularly focal dystonia are much lower than doses for spasticity, starting in the range of about 20% of what you might use in the same muscle for spasticity. For spasticity or spastic dystonia, secondary dystonia, I would say secondary dystonia is more like spasticity. You may use higher doses. Even when I'm dosing for spasticity, I dose based on the severity of the movement or spasticity, the size of the muscle and what the functional goal is. And the same thing is true with dystonia. So if I'm treating a musician with a focal dystonia involving one fascicle of FDS, I may start with a dose range of anabotulinum toxin A or INCO of 2.5 units, where with abobotulinum toxin A, I might use five to seven units in the lower limb. The same thing if I'm treating somebody with spasticity in the tib posterior. And for spasticity, I might start with ANA or INCO at 50 to 75 units if it's severe, and then I'm using 20 or 25 units of that same, or let's say 50 units of ABO in that same muscle. So I'm using a much lower dose is the main things. And sort of the general principle is lower starts slower because these patients don't have involuntary muscle activity at rest, they don't have increased tone. So it's easier to overshoot the mark. And I have made several patients worse by over-weakening the muscle. So I usually will start lower and tell patients that you may have no benefit on the first injection. Catherine, as a corollary to that, have you found, or at least with the case that you presented, during the period where the botulinum toxin was active, do they effectively unlearn the dystonia or do you have to continue to treat them? Most people don't unlearn the dystonia, you have to continue to treat them. What does happen is over time is you get a longer, you may see a longer duration between injections. And that may be in part, although the biological effect of the toxin, we know the blocking effect is somewhere around 12 to 14 weeks. Over time, remember you're inducing denervation atrophy in the muscle. So that denervation atrophy, if you don't let it recover between injections, the denervation atrophy lasts longer than the effect of the toxin. So whereas initially for our runners or other patients, we may be injecting them every 12 weeks. Many patients, like that one runner, the runner with a knee flexion dystonia, this is a patient of mine that's run 53 consecutive Boston marathons and currently holds the streak. We time all of his injections based on what runs his runs and races that he's running. And he tends to be injected at four to five month intervals. Now, where initially he was injected at three months. So I don't think he doesn't, and we let them tell us when it's time to re-inject and also when it's time to inject based on a race, because you may not really want to inject them and have them do a race four weeks later, because if they're gonna have weakness, it's gonna be at about four to six weeks. So we time the injections based on peak effect and duration. More discouraging than I would have liked. So can you equate the YIPS in golf to dystonia? Absolutely. It's in not everybody. It's not choking, it's dystonia. So YIPS in golf is in many people is a form of dystonia as is table tennis dystonia. I was at a meeting in Hanover, Germany about a year ago. Well, I guess it's been a year and a half ago now because of COVID. And it was just a sports and exercise induced dystonia meeting with like a thousand people there from all over the world. And there's people with billiards dystonia. Every sport that requires a skilled task has a dystonia. It just hasn't been reported yet. All right. Thank you. Brian, any other questions that we haven't gotten to yet on the air? Yeah, this was not directed towards anybody, but have you seen any correlation between lower extremity dystonia and idiopathic orthopedic deformity such as a femoral antiversion with no underlying neurological genetic or neuropathic diagnosis? Guess that's sort of to either Dr. Richardson or to me, maybe. Do you have a comment, Dr. Richardson? I don't want to dominate. I didn't even understand the question. I'd have to reread it several times. So go ahead. I'll look at it and think about it. The answer is a femoral antiversion is obviously a chain and I assume this is a medial antiversion or lateral antiversion. Usually occurs with repetitive forces changing the femur alignment. It happens more in children with cerebral palsy where the chronic force changes the femur shape essentially. We don't see that as often in adults. So if somebody, and remember, there are lots of folks that have femoral antiversion that don't have dystonia or neurological problems. And so it just may be coincidence that the patient has both of these things. If they have dystonia from early childhood, then yes, it's likely related. For adults with idiopathic antiversion and idiopathic dystonia, I don't know that anyone's ever reported an association with this. I don't see it commonly in our adults with focal dystonia. Dr. Richardson, I had a question from your first presentation where you alluded to differences in swing phase pathologies versus stance phase pathologies and how different portions of the nervous system affect that. Could you go into that a bit more? So maybe I'll try. Let's see. So I think of an upper motor neuron process as a tensiline dysplasticity. So often there's some useful strength when the lower limb is doing its stance phase job, which is to just be strong enough to keep the center mass from collapsing, which is a pretty coarse need. And so although there's altered control, the muscles fire often in unison and inappropriately, but they're all sort of co-contracting at the same time. And so the stance phase job for an upper motor neuron process tends to be done. I think of the swing phase job, and that's to shorten. And I think of shortening via hip flexion, knee flexion, dorsiflexion, and contralateral hip abduction. That job requires some relaxation of some muscles. And if there's co-contractions due to spasticity, then upper motor neuron processes lead to swing phase errors. So often things look funkier during swing phase with an upper motor neuron process than they do during stance. Conversely, lower motor neuron problems, atrophy and weakness, then it has trouble supporting the body's center of mass, the body's mass during stance phase. And so there's often some adjustment made, and we showed an adjustment where they could let the hip collapse and quickly move forward. We had another one where Roosevelt tilted to the side, and then we had the lady with plantar flexion and glute weakness tilting back during stance phase. So that's, hopefully that clarifies why I think lower motor neuron processes tend to show up more during stance, and upper motor neuron processes tend to show up more during swing. Thank you. Yeah, it does help. I appreciate that. Brian, anything we've got left to cover? If we're good, we can, I think we have just time for one more question. What goes, this was not addressed to anybody specific, what goes into your thought process for determining dosing of botulinum toxin for lower limb dystonia in order to maintain athlete's ability to perform? I think that I sort of covered that, is that the dose with dystonia is lower. Starting dose is much lower than what you would for a patient with spasticity, in part because of the performance level for athletes. And my initial goal is to not make them so weak that they can't walk or run. So I will actually ask the patient, I said, look, usually I start off low and it may take a couple of two to three injection cycles before we get to the right dose and right pattern of injection. Typically it's mostly dose because it's one or two muscles we're injecting. And I'll give the patient an option. I said, I can go higher on the dose, but I may make you weak. If you're weak, you're gonna be weak for two to three weeks at the peak, from four to eight weeks. And which do you prefer? And it's also based on, do they have an upcoming race that they're going to be running? So the main thing is a generic based on muscle size, the severity of their dystonia and where you are in their performance cycle. But I would recommend starting low and going slow if you're treating focal dystonia, especially in smaller muscles. I actually have a question for John. And this is a question that came out of actually a recent group of patients that we've seen. So we've seen kind of a rash of adults, idiopathic dystonias with runners dystonia who all have knee extensor dystonia. And in three out of three recent patients, they all have Baker's cysts and or super patellar knee joint infusions. This is like back to the intersection between MSK and neurological problems. These are patients actually referred to me because they had neurological problems, but we suspected that based on their sort of an antalgic gait pattern that there was something else going on. And we did ultrasound of their knee joint and all three of these people had these knee joint infusions. Now, I don't think the infusion was the cause of their dystonia, but it was, it served as a block. We theorized that the patient had a mechanical block to knee flexion because of this infusion. Do you think that that's possible? Yeah, I do. I think based on what the musculoskeletal implications is that joint doesn't work well. So its ability to handle forces is probably off and or painful. So they might preferentially not do something to avoid irritation of the joint or pain that result. It's a bit of conjecture, but I think that probably would fit. Yep. And so far I've sent all three of these people to colleagues, to my sports medicine colleagues. One person had the knee joint aspirated or that Baker's cyst aspirated and got better. They had improved knee flexion. The other person actually got, their hyperextension got worse. And I think that it might be because I removed that mechanical block. Right. It may be too far down the field or down the road with the disease. Right. And then of course we can't really cure OIA. We can just sort of make it less bothersome. But I'm gonna take the privilege of asking the last question. And I wanted to ask Casey, with regard to your peak forces, and I got the implication that surface could matter with that. Have you found, or do you believe that trail running would be then less injurious than running on paved surfaces, roads, sidewalks, that sort of thing? Yeah. I mean, yeah, it's more of a compliant surface. Trails, it definitely is a compliant surface. Grass, yeah, compared to, you know, it's better than concrete. Absolutely. Well, we are at a little past one. So I think we should close. I wanna thank all of our speakers. This was fabulous. I'm really happy that this came off so well. I hope everybody in the audience enjoyed it. I think certainly it was intellectually stimulating. I hope it brought to you some clinical clarity as well. This was hopefully the first of many. Thank you again for attending to my speakers. Thank you very, very much. I hope everybody has a good weekend. Brian, anything that you need to say in closing, or are we good to go? We are good. Just as a friendly reminder, this has been recorded and will be posted in your Academy's online portal starting on Tuesday. And at that time, you'll be able to go back into your account and claim your CME. So thank you. Thank you to the faculty and everybody who joined us. All right. Thanks everyone. Have a good weekend. Bye-bye.

running gait

walking

running

joint torques

running shoes

hip strength

core stability

falls

neuropathy

compliant surfaces

injury rates

energy efficiency

runner's dystonia

motion analysis

botulinum toxin injections