THE INITIAL CLINICAL SURVEY AND HOW TO IDENTIFY THE LESION BEFORE EXAMINATION (MODULE TWO)
Transcript – Gait Analysis
Presentation by Dr. Brandon Brock
So, we’re going to break this down nice and simple for you, I think. In other words, try to make it to where you can just do simple observation. So Dr. Kharrazian just did a very good job of giving you some physiology on what makes you move, what causes locomotion, what causes you to, you know, perceive where your limb is, how you coordinate the limb, what’s the feedback from the limb, how does it get integrated. So you know a little bit of the physiology behind it.
We have a lot of modules over gait, where I will give you… See, there’s different levels of understanding gait. There’s “This person obviously is hemiplegic,” versus “This person’s center of pressure is not quite what it should be, and as a result of their center of pressure, it’s changing their muscle tone, and changing their muscle tone is changing their ambulation, and changing their ambulation is hurting them.” Do you guys understand the difference?
So there’s really multiple layers of gait here. But what we’ve found is, if we jump straight to all these perceived center of pressures versus actual center of pressures, and correlating it with eyes, and correlating it with pursuits, and all these different things, everybody’s like, “I don’t know… what do you… what are you talking about?” So right now, I just want you to understand, like, what a slappage gait is. And I want you to understand what a hemiplegic gait is. And a scissor gait, and an ataxic gait. And I’m going to go through why each of them exists, so that when you see them, you can say, “Alright, look. At least I’m not missing the major gait.” And you’re going to be at the airport, and you’re going to see all of these if you hang out in a major airport for more than a couple of hours. You get laid over, and you’re sitting there watching, and all of you guys that have been teachers and instructors traveling all over the place doing stuff, you’ve seen them all. You’re like, “Wow, look at that ataxia. Woo, look at that slappage gait.” And I’ll always hit my wife; I’m like, “Where’s the lesion?” She’s like, “I don’t know where the lesion is.” I’m like, “Alright.”
So, when we go through this, we have to say to ourselves, “Can we identify it? And not only ‘can we identify it?’ can we say why it is there?”
So, some key concepts real quick is, your intake forms. And your intake forms are going to tell you a lot about this. You should again be able to look at this and say, “Wow, man. This person’s got peripheral nerve disease, they’ve got cortical disease, and they’ve got gait issues,” and then wait until we give you the vestibular intake form. That will take it to the next level. And then we’re going to give you intake forms for multiple… We’ve got a whole movement disorder intake form we’re going to give you. So there’s lots of these intake forms that we will be going through.
Some of the physiology of gait, why you see different components in different places as it pertains to, like, why is it slapping? Why is it stepping? Why is it dragging? Why is it shuffling? What is it called? Where is this at in the brain? Can I see it? Can I do it myself? Can I reproduce it? Hopefully none of you have any of these. Alright?
Look at the components of ambulation a little bit, stationary, and I’m going to show you a little bit, just introduce you somewhat to limits of stability and center of pressure. Again, me standing here, and what I do with my sway, and where I’m at with the eyes open and the eyes closed, head turned, head up, head back; all these things, we’ll get to them, and what they mean. But again, baby steps. I need you to understand an ataxic gait before we start talking about the minutiae of center of pressure. Does everybody understand that? And by the way, I’ll give you notes just as good on all the center of pressure stuff.
If you look inside your patient handout… or your student handout thing, there are a lot of papers on gait. We just had a bunch of them. So you can go read through this, and it’s really priming you for the next sections, where we actually start talking about “Wow, this person’s got a head tilt, and a skew deviation, and a dynamic otolithic problem, and as a result their center of pressure’s doing this, and they perceive themselves turning this way.” There’s a lot to gait that’s not just watching them walk across the floor. Make sense? Okay.
And then, we’re going to go through some of these basic gait pathologies, and make sure that you understand what it is that you’re seeing. This is just like everything else. Hey, do you understand weakness-weakness patterns? Do you understand sensory-sensory patterns? Do you understand all the different longitudinal levels of the lesions we’ve talked about, and the different parts of the brain, being the frontal, the posterior part of the brain, the parietal, the inside, the outside, the limbic system? The gaits are the same thing. I need to make sure that you understand them.
But, can you link them to the other systems? See, this is sort of the final frontier of linkage, on some of the observation fronts. Now, there’s always going to be observation, but this is one of the final things that we’ll start to observe, and then we have to come back, link all these forms together, then we have to come back and make sure you understand all the case studies, and then we have to finish the day and then we can say this: You should be able to observe just about anything. Now we have to come back and start the whole process over again with a physical examination, and start looking at how these systems deteriorate.
So do you see how we’re layering in it? I’m kind of taking a second to make sure that you understand the direction that we’re going in, because that’s important to me.
So, as we go through this, this is my questionnaire, and it’s like, “Hey, are you…” And I’ve already shown you this, but I want to go through it again in context of what Dr. Kharrazian just said. Well, “Are you falling?” I
mean, some people are so hemiplegic they fall. Some people are so diplegic they fall. Some people have so much vertigo, they fall. Now, that’s not necessarily a gait pathology, that’s a vestibular pathology making them fall. So, it’s an indirect gait pathology.
“Are you always falling to one side?” That’s a huge indicator. If they say, “Yep, I’m falling a whole lot…” So if you go on here, and it’s like, “Yeah, I’m falling a ton,” and it’s, “How often,” and they say, like, “Daily,” and, “I can’t stand on my…” That’s different. We’ll come back to that in a second. But they’re always falling to one side, that tells you a whole lot about the site of the vestibular problem.
Now, when we take this intake form, and then we teach you how to correlate it with our vestibular intake form that we’ve made, you’ll be able to say, “This looks like it’s peripheral vestibular problems. They’re falling towards that side. It’s a fistula, because they just went up into an airplane, got off the airplane, went scuba diving, got out of the scuba diving thing, and then got a fistula. And then had a cough and a sneeze attack.” So, we’ll be able to put it together very well for you. And not all of it’s ablative; some of it just… it doesn’t integrate well. So I’ll teach you how to integrate the horizontal component to the vertical component, and then show you what it means will all of the ocular findings. And we’ll try to do it bedside, so you don’t have to spend a lot of money on equipment.
“Do you have a hard time standing on your toes or heels?” Do you think that would have anything to do with the lecture that I just gave you earlier? Right here. Standing on my toes. If I had a tibial nerve lesion, could that create a problem? If I had an S1 nerve lesion, could it create that problem? If I had a sciatic nerve lesion, could it create that problem? If I was spastic, could it create that problem? Yeah. So when somebody says, “You know what? Like, I can’t stand on my toes or my heels,” you have to ask the question, “Why?” Is it because they have no muscle tone, and they’re atonic, and they’re flaccid? Or is it because they’re spastic and they can’t move? Or is it because they have diabetes and they don’t know where their feet are in space?
So, when you look at these, you have take… again, you have to take the text and put it in context. Let’s kind of keep going here.
“Do you walk with your legs wide or far apart?” That is explaining an ataxic gait. So you really should walk with your feet just one right in front of the other, or no more than the width of your shoulders. If somebody starts to widen their gait, so – I hope that won’t fall off the back of the stage here – as I’m walking, and it starts to get a little bit wider, and you’ll see my body shift side to side, that starts to become an ataxic gait. So you start to see that translation. So if I’m just walking straight ahead, my hips will be like this, and my shoulders will be like this. But as soon as my feet come outside of that, you’ll start to see, a lot of times I’m translating like this, and if they become very unstable, then they’ll have their arms out like this, and you won’t see them shift side to side; they’re just like this. And they’ll almost slide along the floor. And you see that in a lot of people that aren’t necessarily ataxic because of cerebellar disease, but what they’re having is a vestibular component, and they feel like they need to grab onto the planet. Have you ever seen anybody like this? So there’s no wall to grab onto, so they’re just like, they’re real wide-based, and their sliding, and they’re doing this kind of thing. Almost like watching somebody walk in the dark.
A waddle gait. A waddle gait basically means this: You’re having to use your body to sling your leg up, because your bigger proximal muscles are starting to go away. Now, where do we see this? You see this in muscle disease, where you’re losing the bigger hip muscles. Now, that’s different than diplegic, where you
have the leg turned in this way, and a leg turned in this way, and it’s like CP, and you kind of have this kind of walk. That’s not necessarily a waddle gait. A waddle gait is where you really… you see them having to pull their leg up like this to get it around, because they can’t use their bigger proximal muscles to do what they need to do.
And then of course if somebody has a gait issue, they may not be able to go up or down stairs. That may help you; it may not.
And ask about a spastic gait. Now, here’s what I… We kind of discussed this. Like, somebody’s going to come in and say yeah, they’re spastic. Do they even know what spastic means? Most people do? So when they know they have a hemiplegia, they know they have a spastic limb. If they don’t know it, they don’t check it, watch them, and as they’re walking, if you see spasticity, check it on there.
So, with these intake forms, when you see things, here’s what you have to do. You look at these assessment forms, and one of the things you’re going to do is, you’re going to go through it, and anything that’s really outrageous or high, you’re going to start asking them questions about it, and then write notes. And when you do that, you’re going to figure out the meaning of each thing that has a really high score. Is that fair enough? Okay.
So, if they’re spastic in their arm, or spastic in their leg… for instance, you may have somebody that has a certain type of stroke, like an anterior cerebral artery stroke, where their leg is much more affected than anything else, so it’s really tight. Whereas a capsular stroke works the arm and the leg. Or maybe they had, like, that dystonic type of posturing that I showed you earlier, where you just saw the tightness in that arm, and it was there because of the focalization or the segmentalization of it.
So, the next thing is, “Are both your legs spastic?” Well, that can be, of course, CP. And sometimes you see it… usually see it in the legs more than arms, but sometimes you’ll see it in both.
Now, “Do your feet slap when you walk?” Why in the world would the feet slap when they walk? So, as I’m walking, and I step, what’s the first thing that strikes? My heel. So if my anterior musculature doesn’t have the tone to keep my foot up, and then roll into it and then push off, it’ll just do this. And we see this a lot with peripheral nerve damage, and we see it a lot with L5 root lesions, and we see it a lot with polyneuropathic disease. “I don’t know where my feet are at.” So they’re just ckh ckh, slapping around.
Now, one thing I want you to understand is if somebody’s slapping, that means they have a problem with what? Dorsi- or plantar flexion? They can’t dorsiflex well, okay? So when they lift their foot up, in order to keep their foot from dragging, what do they do? They high-step. So it ends up making the steppage, the slap, louder the higher they step. So people will get very insecure. They may have… if you go back to the last module, the very first case I showed you, she had a gait where one leg didn’t work.
Remember the girl that couldn’t walk, and then she got to the point where she could walk better? When she first started walking, she couldn’t lift her proximal… She couldn’t flex her hip. But she also couldn’t control her foot, so she was having to drag this along, and her foot would get stuck, and if her center of gravity got over her foot, and she couldn’t react fast enough, she would just fall. So we had to teach her how to use her proximal limb set first, get it up high enough, and if this was weak, she could then propel it forward and then
step on it and let it slap down. So, people that have slappage, and they can’t do steppage, end up getting trippage. They just do. They drag… and you’ll see a lot of them. The ends of their shoes will be, like, flat or worn out. Because they’re doing this a lot. You’re like, “Wow!” And then a lot of them adapt by doing this.
Now, if somebody’s lost complete proprioception, they may not have the slappage, but they have the steppage, because they’re like this. They don’t really know where their limb is at. So they’re actually trying to go up and they can’t feel the floor, they don’t know where it’s at. So just imagine walking on air.
So, then we go to the – again – the high step. I just talked about that, and I’m going to break each one of them down again, show you examples. This is sort of like one of those easy sections before lunch, okay? A lot of people are like, “No.”
The next thing is shuffling. So now you have this kind of stuff. I can already see the pictures being put on Facebook now. So look: I’m camptocormic, I’m [arching] forward, I have lid retraction, I have a masked face, I have a resting tremor. I’m not even going to do it. I have a resting tremor. And so what happens is, you get paralysis agitans. The basal ganglia doesn’t want to work, so it’s a shuffle gait. Okay? Now, it’s hard for people with Parkinson’s to do several things. They can’t get going. But once they get going, they’ll go, and they can’t step over lines a lot of times.
But the other thing that occurs is, they can’t turn. So when they go to walk, and they’re walking, and you say, “Okay turn,” they go … and then they’ll walk back this way. You should be able to just walk, step, and turn. Unless you’re Derek Zoolander, then you’re an ambiturner. No? Okay.
So you’re going to watch this: Do they shuffle? Do they do more than two to three steps when they turn? When they turn do they fall off to one side? And then with cortical failure or damage, you may see a reduction in arm swing. So you want to see arm swing, and you want the arms to swing symmetric with the legs, and you don’t want the hands turned in and the shoulders rotated. You want the ears lined up in their plumb line, you want their feet to be within their shoulders, you don’t want to see a lot of hip movement laterally, you want to see the body propelling forward, and you want their gait to be nice and quiet unless they’re wearing shoes that make it louder. So you want it to hit, roll, push off; hit, roll, push off. And you want to see their arms propelling their body, and have the ability to turn their head and do different things as they’re moving.
Just trust me. Start looking at gait. I will take you through some very advanced gait situations. But just looking at these basic things, you will be mind-blown about how many people just walk strange. Not only that, but everybody has a unique walk. Have you ever noticed, like if somebody… Have you ever just seen somebody kind of move by you, didn’t see their face; you’re like, “I know exactly who that is, because that’s exactly how they walk.” And it’s not that they have a pathology. I’m at this place one night, it’s a speakeasy. You guys have heard of speakeasies, right? There used to be this really cool one in Dallas, and… I had this one girl, she came in and she had SCA – she had spinal cerebellar ataxia. And the biggest thing was, I didn’t know if it was from alcoholism or from the actual genetic component, and of course the genetic test is seventeen thousand dollars. So… yeah. Going to have to have a fundraiser for that one, right.
So I just said, quit drinking, and then we’ll do some other stuff and see how it goes. So I’m at this place, and all of a sudden out of the corner of my eye I see just this weird ataxic sort of, like, two steps go by.
I didn’t see the person, and I go, “I think that’s such-and-such.” So I went around, this lady walks to the bathroom, she walks out, and I see her, and I’m like, “You’re drinking.” She’s, “What did you do, follow me to the club?” I’m like, “No, I’m here too, but you have cerebellar atrophy, and you’re drinking.” She goes, “I cannot believe you just saw me at the club and, like, eh…” “This is not a club, this is a speakeasy, okay? So, relax.” But every time she drank, she went further downhill. So come to find out she had massive, massive, massive thiamine deficiency, she had B vitamin deficiency, she had Purkinje antibodies, and she had genetic propensity towards spinocerebellar atrophy. You combine that all together, she became so ataxic she couldn’t walk. So, not cool.
“Is it hard to turn if you stop walking?” That’s more the Parkinson thing, and we’ll go through that.
So if you take this – and just kind of follow me for a second – and if you take this, and you snap it together with the peripheral nerve intake form, you can say, “Okay, there’s a gait change, but is the gait change because of the peripheral nerve lesion? Cool. Is it a nerve root lesion? Cool. Is it a polyneuropathy? Cool.” Or, you can take this and say, “Is it because of cortical damage? Like, look at the basal ganglia section, and look at the frontal lobe section. Look at the cerebellar section. The cerebellum, it will be lit up on that intake form with an ataxia probably. With a shuffling gait, it will be lit up on the basal ganglia section. With kind of a magnetic gait, where they can’t really get off the floor and get going, and they have no tremor but they’re frozen, the frontal section will probably not be so good.
So you start looking at this, and you’re like, “Gait is one more notch that I can use and say this: This is where I think the problem is; now I need to go back and examine it and figure it out.” So we’re doing this. We’re giving you another tool to look at a person and say, “This isn’t right, this isn’t right, this isn’t right, this isn’t right, because I’ve learned to see all of it, and once I’ve learned to see all of it, I can now go back and examine it and say I’ve got to do something.”
You can possibly get good enough – and we do some very interesting things, like I help fighters do this: I watch their opponent. And every single time, their gait, facial features, and posture will change when they’re fixing to punch you. That’s a pretty cool thing to know if you’re fighting somebody, don’t you think? Gait is the same way. You can get to the point where you can say, “This muscle’s not firing in sync with this muscle, and their center of pressure is off here, so they’re loading this muscle group compared to that, so every time they move this way it’s going to exceed the elastic element, and they’re going to tear their hamstring over and over and over.” Why? Because when their center of pressure is off, and they’re perceiv-ing themselves in one way, and they’re activating another group of muscles to pull them back up to their reality, it activates one muscle group and turns off another, so they continuously damage a muscle or a joint.
And this is one of the ways we treat chronic hamstring injuries, with vestibular therapy. “Uh-oh, now it’s getting crazy,” when it really isn’t. You go in there, you do all the soft-tissue work you want, but in reality, the brain is still saying, “I’ve got to make more tone in one group than the other,” because they think that you’re at an eighty-degree angle almost flat, because your frontal lobe is damaged. Had a lot of football players with chronic, chronic hamstring injuries, and it’s just because their body has been… they’ve been hit so hard they literally think they’re at an angle that is way off. And that has changed the entire biomechanical cascade from the chin down. And you’re like, “Wow, every time they activate this one group, they defacilitate the muscles that they need to stabilize and to spurt and to shunt.
So now I want to tell you something. Gait, right now, is easy. Gait later on is going to get complicated. When I put a runner up on the screen, and you see him running, and there’s just this much difference in the way he should be moving, that is when you’ll know it. So there’s different levels of this. This is a good place to start. But I also want you to know where we’re going. Okay?
How many of you do gait assessments on athletes? Okay, quite a few of you. So this is really nothing new, right? This is the basic cycle, the stance phase. So right here you’re in between on the toe, and you’re fixing to have a heel. So you have a heel strike, and you have all the weight on this leg. Now, here’s the thing. If this leg right here – and I’ll use a little pen, that way I can mark on it – if this leg right here is weak because of a nerve lesion, or you don’t know where it is because of somatosensory damage, or because of peripheral nerve damage, or because the contralateral cortex doesn’t know where it is, when it lands, bad things are going to happen. It will either go too far out, or too far in, so you’ll start to sway off of a midline.
So, not only are we going to watch people walk, and see if they have good arm swing, we’re going to have them walk and see if they stay in a normal line. I’m going to say, “Just walk straight. Turn around and walk straight back.” And they start doing stuff like this. And you’re like, “Wow, that looks good.” That looks like some people I saw last night. Now, right here, that leg. If this leg, right here, does not have the ability to push off with the toes, curl down, push off, and have the capacity to plantar flex, then you’re going to have a very bad component of propelling yourself forward, okay? And then this right here pushes even further back. Now the other leg is going to step. You land on it, now you have to have the ability to stabilize here, bend the knee here, lift the leg up far enough for the toes to clear, so that you can come back through. If you don’t, and you don’t have good foot clearance, you’re going to trip over your own foot. And that’s why people go steppage and slappage.
And then right here, you’re vertical again, and then you’re going to take this out and you’re going to have a foot strike. So this is where your foot’s sliding through, and then it’s going to strike down.
So, I’m just kind of going through some simple mechanics. I mean, most people understand this already, but if you have a problem with heel strike, or you have a problem with a, you know, a push off, and if you have a problem with putting the limb down and knowing where it is in space, and maintaining weight on it, there’s going to be a change in your gait, okay? And you have to have range of motion.
So, these are the things we look at. And I don’t want to reiterate what Dr. Kharrazian just did so perfectly, but I just want to say this: Your somatosensory component, right here, has to work. You have to know where your limbs are. Well, what are some conditions that can screw with somatosensory input? Diabetes. Peripheral neuropathy. Traumatic nerve damage. Nerve root damage like from radiculopathy. Plexopathy. Anything that damages peripheral nerve function or feedback from muscles. Feedback can damage your somatosensory input.
Now also, the somatosensory integrators, like the parietal lobe, can do the same thing. So, here’s the test. How do I know which one of these it is? So I go down to the legs, and I go, “Hey, do you feel this?” And they’re like, “Yeah, I feel it.” And then you go on there, and you start drawing complex numbers and letters and their legs. “Tell me what these are.” They’re like, “I don’t know.” That’s highly parietal. But you go down there and it’s a clear stocking distribution, or stocking loss. They can still feel it, but not a lot, but they can tell you that if you draw a number or letter on there, they’re like, “That’s a six. That’s a nine.” And always do
Bs compared to Ds, sixes compared to nines and Ps. Do things that people can invert and flip over, because that will tell you if it’s somatosensory, if it’s loss, especially on the left side, if it’s inferior. Pretty cool, right?
So, when you start doing this, you can say, “This looks like it’s somatosensory because it’s peripheral nerve damage. This looks like it’s somatosensory because it’s parietal lobe damage.” And by the way, it can be damaged anywhere along between the end organ and the cortex, including the spinal cord. But you have to be able to say to yourself, “Is it there?” And then the cool thing is this: When somebody has, like, a little bit of diabetes, and their parietal lobe… What do you think the parietal lobe’s going to do secondarily, because they don’t have good feedback from their actual feet? It will start to shut down a little bit. So then you vibrate their foot, and you some, like, just put a tuning fork on there, and you just do some infinite move-ment, and do some large-diameter activation, and then you go back and you do graphesthesia again, and they’re like “That’s a six. That’s a nine. That’s a P. That’s a B.” And they start getting it again, and you’re like, “Whoa. Their parietal lobe can actually wake up. We just have to figure out a way to increase the amount of somatosensory input into this system, because they don’t have much of it, because they’re diabetic.”
This becomes very fun. So, the somatosensory can be messed up, or the vestibular system can be messed up, which makes your gait abnormal, or the visual system can be messed up, because you can’t process the field that you’re walking in. So if you can’t understand translation or up or down with your otoliths, that’s bad. If you can’t understand angular rotation because of your canal integration, that’s bad. If you perceive the world as skewed and tilted, and you’re doing something like this, that’s not good. If what you see visu-ally, your eyes are so off you have depth contamination and you can’t focus, and you can’t accommodate, that’s bad. So, when you’re looking at gait, one of the things you’re going to have to do is say, “What kind of gait is this? Why is it there?” and “Which system isn’t integrating appropriately? Is it somatosensory? Is it vestibular? Is it motor output? Is it visual? Is it joint? Is it constrictures? What is it?” And when you can do that, gait becomes very easy.
Now, the patterns… there’s one other thing that I’m going to tell you. You can take it to another nth degree. The pattern of muscle firing… Do you remember when I showed you that EMG earlier? How I showed you how a motor unit will activate? Here’s the cool thing: A motor unit will activate, and after it fires at about five to ten hertz, another motor unit will recruit in, and it will go a little bit faster, and then when that goes, you’ve got those two firing, and another five hertz, another one jumps in. So it goes dit dit dit dit dit, and then it goes dit dididit dididit dididit dididit, and then you can hear two, three, four, and it goes all the way up to about forty-five hertz. When the brain changes down to the ventral horn cell system, and you have a changing gamma and alpha motor output, they recruit differently, and at different speeds, so the limb will move different. And when the flexor moves, it has to work in conjunction with the extensor, so that you don’t injure a joint or move [in]appropriately.
I am going to take it down to that level for you. Not today, but we are going to get there. Because many of us are dealing with high-performance athletes, and many of us are doing muscle testing. And so we have to talk about weakness just outside of the realm of a lower motor neuron lesion. Okay? I’m fully aware of that.
Now, some people don’t know where their ankles are, or they actually just move with their ankles. So they have ankle strategies, trunk and neck, eye and head strategies. So, we have to be able to do this: Which one of these is screwed up? Eye-head? We can test it. Trunk and neck? We can test it. Ankle and thigh? We can test it. Is it somatosensory, vestibular, or visual? And all of this stuff gives us general body movements,
and environmental interaction, and when we look at all these together, we get balance control in gait. I will take this exact same slide later on, break it all down for you, and we will go through gaits very detailed.
Here’s a great test. I will tell you right now, this is from a NeuroCom machine. I could care less if you get one. You shouldn’t. Well, unless you’ve got a lot of money. But look at this, right here. It puts you through different types of scenarios where you’re just standing there statically. And this person doesn’t do good in session five and session six. So there’ll be different things where the… It’s in an encased area. It will move, the floor will move, different types of environments will move, the plate will become unsteady. And so it does this, that it measures everything together, and it spits this out, and it says, “Look, homeboy. You’re somatosensory’s good, but your vestibular system’s terrible.”
So you start going through this, and you find out the person’s got a major, major vestibulopathy. And then when they do their strategy analysis, you find out they’re massively ankle-dominant, and they’re hip-deficient. And then you go over here and you find out their center of gravity, which tells you everything about their actual and perceived center of pressure – which I’ll go over later – this person’s leaning back. So now they’re leaning back to compensate, and this activates – I’m going to exaggerate – this changes everything, biomechanically, all the way through their body. They way they stand here, the way they utilize this leg, the way they build muscle mass here, the way these muscles activate to try to pull them up… They’re probably compensating here because their brain perceives them way up forward. So now they’re being pulled up this way. So now every time they go this way, these muscles can engage, and it doesn’t work right, so you can damage a compartment.
So I look at this, and I’m like, “You’re a baseball player, and you’re actually back and leaning away in your stance. So if anybody throws a pitch on the outside, you’re probably going to have to reach for it, and as soon as you do that, you miss.” So you go through this, and you’re like, “Hey, I think I can do vestibular augmentation, give you some hip strategies, reduce the capacity for you to use your ankles for all your bal-ance, get you to where you’re more centered, and you can reach out and swing, and have eye tracking,” and lo and behold, their batting average goes up. Now, is that gait? Kind of. It’s just neurological enhancement. Okay? But it starts by knowing how the body moves in accordance with brain function.
Now, this is static. This is them not moving. They’re just standing there. Now, here is them trying to lean to different areas. This has so much meaning to it, and I’ll get into it later, but as they go forward, they become a little bit unsteady. Notice as they go to the left, they start to spokewheel. Everything’s going this way. So when you see this, you’re like, “Wow, man.” And this is so crazy. They’re spoking in this direction, and this quadrant. I wonder what part of the brain this quadrant deals with, and why they would spoke that way?
So you can start to outlay their cortical representation, and their cerebellar perception of where they’re at, and you can correlate this with simple things, like, “Hey, stand and walk in place.” And they’ll do things like this. You’re like, “Whoa. That Fukuda’s a little bizarre.” We’ll go through limits of stability on top of basic gait.
So, Dr. Kharrazian talked about this. Planning a movement, the initiation of movement, and the execution of movement. And of course the execution has a lot to do with cerebellum. The cerebellum is the guy that says this: “You moved. Do it better next time.” The brain is the guy that said, “Hey, thanks for the instruc-tions from the cerebellum. Let me just coordinate these and execute it.” And then in between, you have
the basal ganglia, and it’s the finger that pushes the start or stop button, like, “Hey, can you just go?” Or, “Hey, can you just stop?”
All the pathways in the spinal cord are going to come down and say, “Muscles do this,” or information from the muscles and joints that says, “Hey, do that.” Okay.
So, I’m going to jump right into this. Here’s a nice chart. These aren’t hard. So you just go through, and you can see them, and you can say this: “Cortical or subcortical.” So maybe it’s Parkinsonian. Maybe you have some sort of frontal lobe syndrome. Maybe you have some sort of white matter disease. But the feet will barely leave the floor. And sometimes that’s what I’m saying: it’s so bad it’s magnetic. Like they’re stuck to the floor. But whenever you start seeing basal ganglia, and cortical and subcortical stuff, don’t expect them to be like this [whistles]. I mean, they’re not going to do that. Okay? They’re going to be like this: “I’m slow. I’m apraxic. I don’t lift well. And if I’m Parkinsonian, I’m like this and I’m just going to shuffle.” And when you see those things, you have to say, “I wonder what their brain region index is going to say? I wonder what their basal ganglia is going to look like?”
And then when we start doing physical exam, we can say things like this: “What are our primitive reflexes going to look like? What are our segmental reflexes going to look like? What are our optokinetic and eye and pursuit and everything else that we’re going to go through… How does it correlate with what you see on your initial observations?” You see, here’s the cool thing: If you get good on these observations, the physical exam is just as easy, and even easier when you can observe. Because you already know what you’re looking for. I’ve never seen a class of students learn to observe as quickly as y’all. So it’s actually pretty cool.
Cerebellum and brainstem: They can give us ataxias.
Thalamus: Man, that can give us positive Romberg’s, and it can give us an ataxia as well. When I say spinal cord, you’re going to say this: They’re going to be stiff, and they’re going to have kicking steps. So they may be stiff, and they may kind of do this kind of stuff. Because they’re so stiff, they’re having to kick through to get to the next point, to exceed the spasticity of the resisting muscle that’s keeping them from stepping through. So now if their posterior compartment is really, really stiff, and they’ve got to get their foot to here, they’ll have to kind of push it through and kick through to do that.
Visual. I love this. Subjectively off. These are the people that think that this is straight. They have one eye here, one eye here, and they’re like, “I’m confused because this eye is still over here and this eye is here,” or they’re not quite off enough to get a massive suppressive amblyopia, so they may have some depth contamination that you have to fix. There’s all kinds of visual processing disorders, where people just have bad gaits, and they bump into things, and they don’t do well.
You guys know orthopedic. Orthopedic is this: “Do you have a bad knee? You’re going to limp.”
Vestibular input. They almost always get wide based. So you’ve got to be careful. Just because somebody has a wide-based gait does not mean they’re ataxic. Wide-based may just mean, “I feel like I’m going to fly off the planet, and I don’t know where I’m at.”
So when you look at this, you’re like, “Cerebellum.” They’re stooped, leaning forward, wide-based, their posture, reflexes might be variable. You go through this, they have staggering, they’re lurching, they may veer. All these types of things.
Sensory. They’re stooped, but they’re upright. Wide-based, again, like cerebellum. Posture’s intact, everything. They’re high steppers. So you’re like, “Is it a cerebellar gait? Or is it a sensory ataxia? Sensory ataxias step higher than cerebellar. So cerebellar gaits, they stagger. They’re just kind of like this. Whereas, if I have a wide-based gait because I have a sensory problem, they lift it up, because they don’t know where they’re at. So that’s more of a sensory-based wide-based gait.
And then of course the frontal lobe person, they’re totally upright. They’re wide-based, but they’re impaired and they’re absent. Because they have all the cortical stuff. So they’re like, their mouth is parted, they’re open, they may be slower, they may be apraxic. So this person may have a wide-based gait, and they’re like this. They look absent. Okay?
Parkinsonian patients are usually not wide. They’re just as narrow. They just shuffle. And they’re usually fairly stable; they don’t fall a lot. Okay?
So this just shows gait ataxias. Is your gait ataxia because of the cerebellum, the sensory system, or the frontal lobe? I need you to understand. Not every ataxia is because you have a cerebellar lesion. So you have to say this: Is it wide-based? And is it staggering? Or is it wide-based and is it high-stepping? Or is it wide-based and short shuffling with flatness? Because they all matter.
So here’s sort of a breakdown approach for ataxias for you. And I just kind of threw this up here for you to kind of read a little bit later. There’s a nice… There’s a bunch of really good papers on gait ataxia in your folder.
This is really the main thing that I needed you to get, and say, “Hey look, everybody that has an ataxia has cerebellar disease, right?” Wrong. Now, if you have a sensory problem, you may end up with a secondary cerebellar issue, and if you have a frontal issue, you may end up with a secondary cerebellar issue as well. In other words, one will probably perpetuate the other and perpetuate the other, so eventually down the road you end up just not doing well at all. If your sensory system’s off, you’ll get secondary changes in your cerebellum. If your cerebellum’s off, you’ll get secondary or tertiary changes in your frontal lobe. If your frontal lobe is damaged, then you’ll have the inability to initiate motor sequencing inappropriately.
So this kind of gait loops on itself. If you have one, it will cascade into another, and then cascade into another, and you’ll have a progressive ataxia that now may have a little bit of steppage, with some shuffling, with some flatness. And you look at it, and you’re like, “This person’s going downhill. Quick.”
If you want to see abnormal gaits, go to psychiatric units. You’ll be amazed at what you see. People who have very… have lost cognitive function, now there’s a decrease in mental capacity… Very seldom do you see an awesome arm swing like this [whistles]. “Hey…” Unless you go to the manic section, where everybody thinks… and I love going to the manic section. You go there and you’re like, “Okay, you all think you’re God,” and there’s, like, eight of them sitting there and you’re like, “Who’s not God? Because you all can’t be God.
Which one is God?” And they’re all looking at each other. They’re like, “I’m God. No, you’re God. No, I’m God.” Becomes very unusual.
Here’s Parkinson’s. So, you can see them head forward, shuffling. You can see this is the spastic circumduc-tion gait that we talked about, and they may lean off to one side, and it’s very hard. And sometimes they may lean off to the side that’s spastic, but sometimes they may fall into the area where the neglect is, because they just don’t know what’s over here.
This is your ataxic gait that we just went through. This is your frontal apraxic ataxic gait. And I’m not sure why this guy doesn’t have any clothes on right here, but this is your lumbar spine gait. I don’t know, it’s just for your entertainment only, alright?
And then of course we’ve got somebody using a cane, and stuff like that. This is a nice little image from Netter.
So, spastic gait. There he is. See how the leg is turned in? See the cortical fist? Here’s a scissor gait. You see these scissor gaits with bilateral types of diplegias. Look at this propulsive gait. This guy is what? Stooped forward, looking upward, probably has some frontal lobe changes. I don’t know if this is frontal lobe pathol-ogy. He’s probably not shuffling due to the distance in the feet. With a shuffling gait, your heels don’t come off the floor. That’s the difference. So when you see this right here, this is one gait versus this. You see the difference? On one, your heel doesn’t really leave the floor.
So when you look at this, you’re like, “Dude, that guy looks Parkinsonian, but his heel’s leaving the floor, so I wonder if he has just a frontal lobe syndrome, or maybe he’s just not quite bad Parkinson enough to where he’s completely shuffling. Maybe he has a supranuclear palsy where he’s not shuffling and he’s just getting frontal lobe demise.
Next module is all about neurodegeneration. It’s going to be very, very, very cool. Probably maybe my favorite module.
Steppage gait. Loot at that. Foot’s down, having to step up. Doesn’t know where she’s at.
And then this little kid right here, he’s waddling because of why? What’s the most common type of muscle disease in children? Muscular dystrophy. What is muscular dystrophy in older folks? Becker’s dystrophy. I was one of those unfortunate people that did a bunch of fellowship work in muscle disease, and I’ve had two in ten years. Okay.
So here’s your hemiplegia. See the fist around there? Guy’s got to use a cane. Why is he not using the cane in this arm? Because he can’t hold it there. So here’s Parkinson’s disease; he’s going to shuffle. Here’s an ataxic gait, where it’s wide-based. Here’s a foot drop, maybe because of nerve root damage. And here’s a sensory ataxia. Why is the foot up higher? So right here he’s kind of staggering; right here he’s doing what? He’s stepping up higher because he doesn’t know where he’s at. And here they are, all summarized into one nice little chart for you.
And in the very end, here’s a flow chart. Inability to initiate gait, waddling, exaggerated foot raise, sensory abnormalities, all the way down to Parkinson’s, spastic, peripheral neuropathy, cerebellar disease. This is your nice little flow chart, just like I had for speech and language.
So, your homework is to be able to go and name five areas that control gait in relation to the nervous system. Cerebellum, cortex, peripheral nerves, joints. Be able to determine if it’s cerebellar versus cortical versus nerve root versus peripheral nerve. All the different types of ataxias, steppage, slappage that you can get, and why. And then please, when you do this – this is the last point – when you’re doing your fifteen to thirty minutes a day and you’re going through all those peripheral nerves and you’re drawing them out, please write off to the side what it would do to the gait, if it indeed influences gait.
Now do you see how we’re layering things out? And then, by the way, if you do have that polyneuropathy, please start to describe what part of the brain would have secondary breakdown. Like the parietal lobe. And then, if you have poor motor output, please write down the area, left or right, that’s not functioning well, and then if that person has bad executive function, or if they have bad motor planning, or if they have impulsiveness, start to write that down. So start to make your own dot connections. And you’ll start to realize this: Your patients that walk into your office, you’re like, “I’ve been treating this person for three years. I’ve missed everything. Now what do I do? Dr. Brock, what do I do? Tell me what to do.”
We’re going to get there. We’ll get into body sway and center of pressure a lot later on. Right now I need to know this: Do you know basic gait? And now we are at lunch. We will be back at 1:30. Is that correct? Okay. 1:30. Everybody enjoy.
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