THE INITIAL CLINICAL SURVEY AND HOW TO IDENTIFY THE … · So, I put lots of great papers in your notes about central pattern generators, gait, movement disorders, and it’s not

MODULE twO tRANSCRIPt: NEUROLOGY OF AMBULAtION | COPYRIGht © 2016 FUNCtIONAL NEUROLOGY SEMINARS LP | PAGE 1

THE INITIAL CLINICAL SURVEY AND HOW TO IDENTIFY THE LESION BEFORE EXAMINATION (MODULE TWO)

Transcript – Neurology of Ambulation

Presentation by Dr. Datis Kharrazian

Alright guys, we’re going to go over the neurology of ambulation, or the neurology of gait. And for the most part, neurology of gait is really coordination of all your motor systems that are working together in combination with spinal cord, or what are called essential pattern generators. So, within your spinal cord, you have basically a pacemaker of gait. So all the input from the brain, where this motor strip, cortex, cerebellum integrate, they fire down the cord – right? – they all synapse at the anterior horn, and you have essential pattern generators that are basically coordinating movement involuntarily, kind of like a pacemaker of locomotion, just like there’s a pacemaker of the heart. And then these things integrate, and then we have gait, and then we have ambulation. Okay?

So, you can tell a lot about what’s going on with someone’s brain, and their peripheral nervous system, just by the fact that they’re walking, because as they’re walking, they’re using their peripheral nervous system, and they’re engaging in volitional motor activity, and they have volitional motor activities in coordinating with the motor loops, like the cerebellum basal ganglia. And the integration of sensory feedback, visual feedback, vestibular feedback, brain integration centers, then lets you find findings of what areas of the brain could be involved, if it’s right-sided, or if it’s left-sided, or if they have, you know, balance issues, or sensory issues and so forth.

So it’s a very good tool that we like to use.

So, the key concepts that I want to go over with you is: Understanding the neurological pathways involved with ambulation, so we’ll review those, and then really most importantly how they integrate; understanding the role of central pattern generators, which are these spinal cord regions that are involved with making repetitive movements happen with very high levels of efficiency; and then we’ll talk about the integration of cortex, cerebellum, basal ganglia in ambulation.

Okay. So, I put lots of great papers in your notes about central pattern generators, gait, movement disorders, and it’s not a bad idea to get familiar with them. But it’s really… here’s the thing. If you understand how


the motor system integrates, then you understand gait, okay? So as you learn the neurology of movement and ambulation, that really applies to all the other pathways and all the other things related to motor coordination with each other.

So for the most part, when you look at the basic concepts of gait, you have really a few things happening. You have sensory input coming in through the feet, that then goes up to the brain, and you have sensory input coming from the feet, you have sensory input coming from the vestibular system, and you have sensory feedback coming from the visual pathways, right? That’s all there for us to determine where we need to walk.

And then we have cortical initiation of movement. So we have this executive function that we decide to walk down the pathway, walk to move, and then in between sensory inputs coming in from our feet and from our vestibular system and from our eyes, and our executive function of initiating to move, we then fire a response, and all of a sudden we start walking. Well, once we fire that response to start walking, in between sensory input and executive function to move, we have integration of our basal ganglia, motor cortex, the cerebellum, all working together to then cause us to have locomotion. Right?

Now, that locomotion could be changed, because someone could lose their arm swing, or someone could lose both… one arm, one side of arm swing; both sides of arm swing; stride length; if they could sway to one side; they can have a wide-stance gait; they could have a whole list of mechanisms that we’ll go over as people… as we get into gait.

Now, so here’s the thing. There’s characteristic patterns of what happens when the cerebellum fails and what you see with gait. There’s characteristic patterns when the parietal lobe is involved. There’s charac-teristic patterns when the basal ganglia is involved. Right? So you can literally look at someone’s gait, and have an evaluation of what is going on with their brain. So remember, the key focus of really, this module, is to really just, before we get into a detailed exam, just as you observed patients, as you observe things, what’s going on with the patient’s brain, right? Or the patient’s peripheral nervous system.

Now of course, we have to kind of overlap and talk about what the anatomy is, what the exam findings could be, and that becomes part of the big picture altogether. Okay.

Now, the good thing about being… to evaluating gait is, you can literally go anywhere and just start looking at people walking, and you’ll find stuff, right? Just, you can go to the lobby, airport’s a wonderful place for those, the mall… You can just see it, how people are doing when they walk. Okay.

So, here’s the first thing. What I want to try to do as I go over the neurology of gait is, I want to talk about the spinal cord, pathways that fire to the spinal cord, and then talk about the central areas of the brain, and then how they all integrate essential pattern generators, and then I want to show you everything connected, and then I want to go over if one thing breaks down, now does that change gait. Okay?

So, let’s go through the spinal cord first. So, the spinal cord is involved with two main functions with gait. One is, it’s going to have pathways that go up and down. That’s one function. And the second function of the spinal cord is, it has the essential pattern generators. We’re going to hold off on essential pattern generators for now. Let’s just talk about the pathways that are involved with gait.


So, when you look at these, when you look at the spinal cord, and you look at this diagram here, on the right side of the diagram we have sensory inputs that are going up. And when we’re dealing with gait, our sensory inputs are primarily proprioception, position sense, fibers, right? Somatosensory. So, when we look at the posterior columns, we have the gracile and cuneate fasciculus. These go up the posterior horn. These are where we have our two-point discrimination, and vibration sense, and those types of proprioceptive pathways. And as they go up, they cross right at the lower medulla where the arcuate nucleus become the dorsal column pathways, and they go up to the parietal lobe, via the ventral posterior lateral nucleus, and they go to the contralateral side into the homuncular map.

So if someone has a legion… I’m sorry, a lesion of this degeneration in their parietal lobe involving their feet distribution, you could have some changes in their gait, right? But not so much in their hand distribution, or their face distribution. Very much so in their distribution of their feet, right?

So, if you have any type of distribution in the upper parts of the parietal lobe, that people are walking with gait issues, you’ve going to feel like they don’t normally know where their feet is, or they’re going to walk like they’re hurt, or they’re going to walk where things may seem like there’s something wrong with their ankle. You go, “Hey, is there something wrong with your ankle?” “No.” Because they’re not getting that sensory input that’s there, and they might not even know that there’s a change in their gait, right?

So when someone walks that way, and you go, “Hey, is your ankle okay? Is your foot okay?” “Yeah, what do you mean?” Then they could just be, sometimes, cortical based. Right? If they’re kind of careful walking, or walking like something in their shoes, or things like that.

Now, we also have inputs coming from muscle spindles and Golgi tendons. So we have skin somatosensory, muscle somatosensory, but then we have joint and ligament proprioception as well. So within our muscles, we have muscle spindles and Golgi tendons that stretch, than then fires up to spinocerebellar pathways, to the ipsilateral cerebellum, and that lets us know where our limbs are in space. Okay?

So right now, if I take… look at my right foot, right here. Boom, right? My right foot. Stepping down. Right now that sensory perception of all those things are having an impact on my parietal lobe. Right? then my parietal paths are recognize where by foot is in space, and let my brain know where it is, so when I make that initial step, I can feel it. At the same time… but that’s the contralateral parietal lobe. At the same time, as I take steps – right? – I’m having joint position input go into my ipsilateral cerebellum, which then projects to my opposite motor cortex. Right?

So we have spinocerebellar pathways with muscle spindles and Golgi tendons; we have proprioceptive pathways through the dorsal columns up to the contralateral parietal lobe, and they’re just integrating to see what’s going on with the perception of what’s happening with loading and joints and ligaments with their feet. Okay?

At the same time, we have our vestibular apparatus, our utricles and saccules and canals, looking at our head position, feeling where we are. fluids are changing, that’s giving input to our brain, and where we are, our position in space, and then we have visual input. And then they’re all integrating throughout the brain, throughout areas of our parietal, motor, occipital integration areas, and then our brain has the perception of where we are in space. Okay?


Now, at that same time, while all that’s going on, that’s all feedback coming up from the spinal cord, okay? Then there’s feedback coming down from the spinal cord – and this is really critical. So the feedbacks coming down from the spinal cord, ultimately they all synapse. Since we’re talking about motor activity here, gait being a motor response – you’re moving, engaging muscles in sequence – they all have integration that finally these pathways come into the anterior horn. And the anterior horn has different cord levels, and these different cord levels have impacts on whether we’re moving our limbs or moving our feet. Right?

Now, these descending pathways that come down the cord, they’re pyramidal tracts or extrapyramidal tracts. So your pyramidal tracts are your corticospinal tracts. So we’ll go over the corticospinal tracts, what they’re involved with. But the corticospinal tracts just are involved with volitional, explosive types of movements, right? And coordinated types of movements where you actually are coordinating where things go. But it works with other integrative centers to make a difference.

So then you have your rubrospinal pathways. You guys see this over here? Rubrospinal? So rubrospinal pathways are areas of the midbrain where you have the red nucleus, and the cerebellum has major com-munication with the red nucleus, and they have their own pathway where it fires into contralateral flexors, especially of the upper arm and shoulder. So that kind of initial swing of a gait, that’s very much rubrospinal.

And then you have reticulospinal, so throughout the brainstem you have a group of network of neurons called the reticular formation, and the reticular formation is, for the most part an autonomic center that keeps you aroused, right? So the reticular activating system responds to hormones, to sounds, to light, to make you alert and to wake up, right? People go into comas, they don’t have enough activation to their reticular activating system. Okay?

So, when you’re looking at the reticular pathways with motor responses, the reticulospinal pathways, they have a general function of just keeping your back extensor muscles activated. Your general global back muscles are activated, right? So, if you become alert, what do you have to do? You have to fire your exten-sors to some degree, right? So that’s what the reticulospinal pathways do. Rubrospinal is your contralateral flexor; reticulospinal has the bilateral projection just to get your spinal tract pathways up.

You have olivospinal, which is the pathway in the medulla. There’s a nuclei there, or complex there, the inferior… I’m sorry, the olivary, inferior olivary complex, and those pathways I’ll show you in a second. They integrate with the cerebellum and cortex, but they also have influences in tone of muscles, and then you have vestibulospinal.

So, vestibulospinal pathways are there to control your intrinsic spinal muscles. Right? And keep your spine tone there. So your vestibular… your vestibular nuclei are getting input from your vestibular apparatus and your posterior canals, your otoliths and saccules. They fire into the vestibular nuclei. The vestibular nuclei then have descending tracts called vestibulospinal tracts, and those vestibulospinal tracts control the intrinsic spinal muscles. Right?

So, when you look at just, like, overall back, general extension, general overall back extension, you have reticulospinal, gross muscles, the back extension; and then vestibulospinal, intrinsic spinal muscles. Okay?


So for the most part, these are the pathways. Now, when we talk about lateral corticospinal, lateral cortico-spinal, we obviously know that we have our fine motor discrimination of our hands and feet involved with that. It’s on the opposite side, across is the anterior corticospinal fires, usually stays on the same side, and then crosses right at the level it needs to go to. But it crosses as well. The anterior corticospinal controls your trunk. Your trunk muscle. Your volitional trunk activity. Okay?

So, let me recap the spinal cord pathways to make it all make sense, and then I’ll show you from the brain down, and then we’ll go up, and then hopefully you can see all the integration that takes place, okay?

So, lateral corticospinal. Motor strips firing, I’m getting volitional movement of my limbs. Right? Okay.

Anterior corticospinal. Anterior corticospinal, it’s firing, and I’m getting volitional control of my trunk. These are both contralateral. Okay?

Rubrospinal fires from the red nucleus across the sides, and I get a flexor tone, especially in the upper arms of the shoulder girdle.

Reticulospinal fires, and I get a general extensor tone. Gross muscle extensors. Okay?

Olivospinal fires. We don’t know exactly what it does, but it coordinates cerebellar input to the motor centers.

And then we have vestibulospinal fire, and vestibulospinal firing is going to control the intrinsic spinal muscles that are non-volitional. You have no volitional control. You can’t move one vertebra versus the next on your own. It’s just there to keep that spinal tone. Okay?

So if you see someone that’s hunched over, and see someone that’s hunched over and they’re walking like this, what does that tell you what regions are involved? Well, vestibulospinal, reticulospinal, those could be involved, right? So if someone’s in a spastic posture, you know it’s probably corticospinal, because cortico-spinal pathways inhibit anterior horn. So there’s features of each one. Okay? The most common features are this: corticospinal… when the corticospinal tracts get involved, you get spasticity in the contralateral limb, right? You have some increased tone in the anterior cortical trunk areas, but you don’t see that visually. Rubrospinal, you don’t really get to see too much of that, except when people have cerebellar dysfunctions.

Have you guys ever seen someone walk, and they’re, like, walking with extension, when they try to coordinate? So, your cerebellum fires to the red nucleus, through this pathway called the dentatorubral, and that keeps your flexor tone. When people have lack of cerebellar activity, they don’t have that general flexor tone, so when they engage in coordinated activities, you’ll see, like, and extensor compensation when they’re trying to coordinate. “Let me get over here,” and they’re like, the hands are… you guys have seen that, right? Looks totally like they’re… totally discoordinated. That’s lack of cerebellar integration firing into their red nucleus, impacting some activity there.

And then, the vestibulospinal is the seat of changes in trunk. Now, if one vestibulospinal pathway is inef-ficient compared to another, you tend to have a sway to the inefficiency side. Or when you do Romberg’s,


and you have the person close their eyes, and they sway to one side, that’s all vestibulospinal integration. Okay?

So, those are the descending pathways. So the way this works is, you have the sensory pathways going up, and then you have these descending pathways all going to the anterior horn, and they’re all modulating some aspect of tone. So you have corticospinal – right? – lateral corticospinal, anterior corticospinal, vestibulospinal, reticulospinal, rubrospinal, olivospinal. They’re all going out to the anterior horn. And the anterior horn is called the final common pathway for motor activity, and it’s segmental to each region that’s involved. Okay?

So, that’s the spinal cord projection pathway. And then what we need to do is, we need to overlap that with the motor pathways. Okay? But before we do, let me just show you these diagrams.

So once again, review.

Corticospinal. Corticospinal, input comes into the motor strip, you have the homuncular map, crosses at the lower medulla to the opposite side for the lateral corticospinal tract, has major impacts on volitional limb movement.

The anterior spinal, anterior corticospinal tract, stays on the same side, but then once it gets to the cord level, can cross. And that is involved with volitional trunk movement. Everybody good? So if you injure your motor cortex, your motor strip, you’re going to have consequences down this pathway, and these pathways tend to inhibit and excite the anterior horn in modulated pathways, so what you’ll see is weakness and spasticity. So they have weakness at that anterior horn spinal level, because they’re not exciting modal amplitude strength, but they also have input on tone, so you see spastic change. So that’s why you see upper motor neuron patterns causing spastic weakness. Okay?

Now, you guys, unrelated to injury, if the corticospinal tract is getting fatigued or tired and inefficient, you’ll see people just have increased tone in their arm. Right? If you see increased tone in their arm, you know it’s a contralateral motor strip. Something’s going on there. Now, you can compare that to your brain region localization form. If they say when they get tired their arm gets heavy, and then you see their arm swing that’s reduced on that side, you know that the contralateral motor areas could be involved. Okay?

Then you have rubrospinal, and the rubrospinal pathways are right in here. There’s the red nucleus, the red nucleus process, and it impacts flexors, mostly in the upper extremities. That’s why you have the cervical levels there.

Then you have the olivospinal pathways. So there’s the intermediary communication center between the cerebellum and the red nucleus, and back to the cerebellum, called the inferior olivary nucleus. Because what you guys are going to see is the cerebellar pathways, when we get to integration, fires to cortical regions, and those pathways fire back to the cerebellum. So a loop between the cerebellum to the red nucleus down to the inferior olivary complex and back, then forms a tract called the olivospinal tract, which goes down to the spinal cord and lets the anterior horn… gives the anterior horn some feedback of what’s going on with the cerebellar red nucleus kind of integration. Okay?


And then you have the pontomedullary reticulospinal tracts. So the reticulospinal tracts… there’s two components to them. One is, they control general extensor tone, and the other thing with the reticulospinal tracts is that they also have an impact on autonomics. How you shunt blood flow to your muscles when you shunt blood and constrict certain vessels plus other groups to make you have proper movement. Okay?

So, everybody okay with that so far? Spinal cord-related descending in tracts. Okay.

So, what’s happening is this. All these inputs are all coming down through all these different brain regions, integrating together, inputs coming up to the brain. They’re all integrating, it goes down to the spinal cord, and the spinal cord then has what are called central pattern generators. And within the spinal cord, they’ve identified that there’s all these different inner neurons that then coordinate locomotion, kind of like the pacemaker of the heart coordinates its beats, right? So, the pacemaker – if you look at the heart itself, it’s still getting brainstem vagal inputs, right? Areas of the visceral autonomic controls, like the insular cortex – right? – and pathways through the hypothalamic projections, dorsal, longitudinal fasciculus, and medial forebrain bundle… their all integrating, and they’re all having visceral input. They’re going down to heart, but once the input gets to heart, it’s really the pacemaker on its own that’s then firing it, right? So if you activate the pacemaker, you can still get contraction.

So, back in the 60s, they found that if they decerebrated animals, and decreased input to the spinal cord, but if they moved a limb, they would see electrical activity in the contralateral limb. So that they found that there was, in a sense, a locomotion pacemaker in the cord. And this actually changed the entire concept of what the spinal cord was, because they thought the spinal cord was nothing more than pathways coming up and down. But now they’re realizing that the spinal cord actually has this really amazing locomotive pacemaker type of effect, where it just coordinates flexors and extensors on and off in sequence. So you’re not constantly thinking about, “This leg forward, this leg back. This leg forward, this leg back,” when you’re walking, or swimming, or dancing, or doing coordinated movements.

So, once pathways come from the brain and fire there, and that sequence starts to take place, they become more efficient. And the more you do activities, the more plasticity you get with your essential pattern generators to your cord, to continue those activities so they become smoother and easier for you to do, right? So, for example, dancing certain ways may be complex, and then as you learn those movements, it becomes easier. Part of the reason why it’s easier isn’t just motor cortex plasticity, but central pattern generator plasticity as well. Everybody okay with that?

Okay. Now, I put some really good papers in your notes about central pattern generators, and kind of this one I’m showing you, the mammalian central pattern generator for locomotion. It’s like a historical review of how they found, and what they found, what each researcher contributed to, and what they still don’t know about it, and where they’re at. Okay?

So, this is an interesting area of research, because what they’re hoping to do with these essential pattern generators is, if someone has a spinal cord injury, they can activate them to have people walk. Right? I mean, they’re far from that. But that’s what they’re goals are to really understand them.


Now, what they’re unfortunately finding is that the essential pattern generators have a lot of cortical input to make them work. So, even though that you can get some tone and activity, they still need some amplitude and activity from the cortex going down to really make a big enough difference. Okay?

So, when these original models came out, with the essential pattern generators – here you can see flexors and extensors, and then what you see over here are interneurons. And the one that have… the way they illustrated this diagram is, the one that has, like, an opening: Y-shape is excitatory and the one with the circles is inhibitory. So there’s excitatory and inhibitory in the neurons back and forth between these things that then coordinates flexors and extensors for us to have this locomotive-type of activity once we decide to move. At the spinal cord. Right?

And then they went later on with some of the research with how these things involve burst generators, so you have, for example, hip extensors, hip flexors, knee extensor, knee flexor, foot extensor, foot flexor. You have pathways like here, with the dots that are inhibitory pathways with these open Ys that are excitatory. These are all integrating in a sequence in locomotion, to then cause you to be able to swim or to walk, and so forth. Okay?

And then they were able to then continue on and then find antagonists, agonists, motor activity, and these are all excite… These are excitatory inner neurons, these are inhibitory neurons, and they kept mapping out ways that these things integrate. And these things are all interesting. It doesn’t necessarily change your diagnostic evaluation of gait, but you just need to know that that’s what the research is showing, and that’s a big part of what gait is. Right?

So, gait at a point becomes effortless for us, just like walking. We don’t have to really have a lot of thought process involved with it, because once we initiate to move, the essential pattern generators take over. Okay? Now, these essential pattern generators are still completely impacted by what’s happening at cortical levels. So if your cerebellum is impacted, if your basal ganglia is impacted, right? Your motor strip’s impacted, they still have consequences on your gait function, because those other types of pathways control tone and coordination and calibration, and amplitude to the thalamus, which then has an impact. Okay.

Now, with these spinal pattern… the essential pattern generators, they’ve been trying to find ways to trick the brain. So they’re thinking, “Hey, will these essential pattern generators build plasticity? So if someone has a really short stride, why don’t we put him on a treadmill, where one is faster and one’s slower, to make their gait normal? So they took subjects that had normal gaits with lower strides or higher strides; they changed the speed of them to try to make them walk normal, and they had some plastic change, right? Trying to get plasticity there, and then they stopped, and that lasted for a few minutes, and then went back to the normal gait. So they’re finding that yeah, they can try to trick it in; when they had them walk backwards or sideways, had… made no change in changing those responses. So we know there’s a lot of cortical control to the essential pattern generators, okay? Which is what we want to discuss.

So, what is the cortical control? So let’s talk about motor integration.

So, if you guys remember, this is one of these diagrams we used with Module One. But here you have basically the sensory cortex, motor cortex, you have inputs from basal ganglia, and you have the rubrospinal projections that are there. So let’s talk about this area here. The sensory cortex and motor strip.


So, when you look at the brain, as you guys all know, you have the central sulcus. In the posterior portion you have the primary somatosensory cortex, where all your position sense, proprioceptive input from your feet and your homunculus is all mapped down here; and then in the front of the central sulcus you have the primary motor cortex. But the homuncular map, the homuncular distribution for them, are pretty much identical, right? So as you take each step, and feel the ground, those proprioceptive inputs are then coming to the parietal somatosensory cortex, and then that has integration with the motor cortex, and then we have this development of these structures of movement and perception right next to each other in a map that’s close. Right?

So that’s the initial part of the way the central integration works.

Now, when you look at the frontal cortex, the prefrontal area, there are different parts of the frontal cortex involved with gait. So, the prefrontal cortex involved with motor planning, or even deciding to move. “I want to move there.” You make the decision to now take your step, right? That initial process is the prefrontal cortex. You make an executive decision to want to go somewhere.

Then as you go back, you fire up the supplemental motor area, which then coordinates and integrates and thinks about how it can execute that function. And when this area is not working well, people get dyspraxia. They have a hard time coordinating movements. Like, if a patient can’t do this, they’re struggling, they really can’t figure out how to do that, or how to pick up a pen, or that aspect of figuring out how to coordinate that is dyspraxia. That involves the supplemental motor areas. So people could have dyspraxic gaits. They want to take a step; they just can’t really figure out how to do it. You see that with really progressed seniors, or people that have injured their motor cortex. They have strength, they have sensory input, they have motor strength, they just can’ t make the movement happen. Okay?

And then eventually the inputs go back from the supplementary areas to the primary motor cortex. You get excitation, and then you move whatever limb that you’re trying to move, okay?

So when we look at gait, right away we can kind of look at this, and realize one of the lesions that we can see, or one of the imbalances we can see is if the supplemental motor areas get injured, then you have contralateral difficult with coordinating movement despite sensory health and motor health. So the act of initiating the actual doing of something, how you would pick up a pen, or how you would go finger-to-thumb, tell you what’s going on with their contralateral strip. Which means if you do an exam, you can have people do finger-to-thumb as an easy one, go alternating finger-to-thumb, and they can’t… if they can’t really figure out how to do that properly, and they’re staring at it, or they keep missing it, or it’s really… they’re… you see them really focus doing it, so here’s one possibility. They can do it, but it’s very effortful. They’re like, “Huh!” You’re going, “Are you trying?” And this side they’re like, “Yeah, this is easy,” and this side they’re like, “…” Right? That’s letting you know, if they don’t have any weakness, they don’t have any motor issues, that’s a dyspraxic pattern that’s involved with premotor areas of the brain. Contralateral to the limb you check.

So, if you see someone with a weird gate, especially with initiation, you can check things like finger-to-thumb or coordinated movements and see if that’s involved. Does that make sense? Okay. I know I say that all the time, and I read the transcripts. I say “Does that make sense?” like a million times. Cerebellum! I’m


sorry. Everyone’s got their thing. Some people have many. I have many, but that’s one of them. Alright. Cerebellum.

So, let’s go back for a second before I go on to cerebellum. So, you guys understand the cortex role? Executive function, decide to move; motor strip, integrate… I’m sorry, premotor areas, integrate; and then the corticospinal tract and then activate those regions to then cause a response to the anterior horn for contraction. Okay?

Now, let me actually go back for a second. If the motor strip is injured or impaired, then what do you get? If the motor strip is impaired or injured, then what you get is, you get spasticity and weakness in the homuncular distribution of where in the motor strip that was impacted, whether it’s the arm, or their feet, or their face. Okay? Now, that’s going to present as increased tone and posture when they’re moving. And as they get more tired, you, like, you see someone have not have an arm swing. Or you see someone who just is tight on one side. You can passively stretch their arms, flexible on one side and then tighter on the other side. Or their hamstrings. Or their legs. Right? To see what that’s there.

So, those are the key things to pick out with the aspects of the motor cortex and function. Then you have the role of the cerebellum. So, the cerebellum is there to calibrate movements, turn them on and off, and for us to have the ability to turn supinators and pronators off for when you do supination-pronation tests, or when I want to touch my nose, turn my biceps and triceps off in sequence so we can touch it, right? It’s the calibrative effects.

So, do you remember last time we talked about basal ganglia; I gave you an illustration of if I was trying to do a finger-to-nose and I fired different regions of my brain, and I broke it down into frontal cortex, cerebellum, basal ganglia, what would happen? So let me review that. So if I was just trying… if I was going to touch my nose, here’s what’s going to happen. I’m going to have my prefrontal areas decide I’m going to touch my nose. And it’s going to go to my motor coordinator areas, and it’s going to tell me that I have to decide… It’s going to figure out how my muscles are going to turn and fire in coordination with other areas to touch my nose. Right? If my pre-supplemental areas didn’t work, I’m going to be staring here, trying to figure out, “How am I going to touch my nose?” I’ll just be staring at my finger going, “I don’t even know how to do it.” Okay?

Now, once the corticospinal pathways fire, here’s what’s going to happen when I try to touch my nose. Because I don’t have the cerebellum and basal ganglia to fine-tune and gate it. Okay? So just gross move-ment. Now, if I try to touch my nose, right? If I try to touch my nose and my cerebellum is off, I can’t figure out how to turn my biceps and triceps and supinators and pronators off to make it touch my nose efficiently, so I might have uncoordinated movement trying to get to my nose, right? My corticospinal is firing out the input, but my cerebellum can’t turn off my pronators and supinators and biceps and triceps in proper sequence, so I have this kinetic tremor as I touch my nose. In the initial stages of it, it’s a termination tremor only, because that’s when you really fine-tune muscles turning on and off to make that. Because as they get closer and closer here, my move… my coordination, my precision, and my muscles turning on and off have to be more precise to actually get it to target, so that’s when it starts to show. Okay?

Now, if my basal ganglia indirect pathway was not involved, isn’t working, and I was trying to touch my nose, this is what’s going to happen. You guys ready? Trying… It’s getting there… I was able to hit it; able


to contract my muscle. I’m exaggerating, just so you guys know. But the speed was slow, because the basal ganglia indirect pathway increased the amplitude to the thalamic areas, ventrolateral thalamus, where you have increased burst of activity movement. And if my basal ganglia indirect pathway is involved, I’m going to have involuntary movements in my arm before I even touch my nose. Right? So that’s the difference between these different regions.

Now, if I try to touch my nose and I do this, I think my nose is bigger, yeah. Or if I think my nose is smaller, then that’s parietal. So you can watch someone walk, and simply to this finger-to-nose test, and you go, “Oh, these are the areas of your brain that can be somewhat involved,” right? Because you can combine the two. That’s the whole thing with gait. It’s a motor integrative function. It’s dynamic. So it’s easy to see these things just on people without asking them to do an examination finding.

So the cerebellum is trying to coordinate muscles, turning off in sequence, calibrating muscles, turning on and off in sequence, to make the change there, and then the cerebellum fires to the ventrolateral nucleus and then it goes up to the cortex. And then we have a loop, because these cortex pathways then fire down through these projections to the pontine nuclei, and then the pontine nuclei fires back to the cerebellum, so we have a loop. So, this is part of just the motor loop, and this is involved with gait. It’s cerebellum if it’s… Here’s how this works: It’s left cerebellum, right cortex. They cross. Right pontine areas. Okay?

So the way this works is, you have this loop, and people have different names for this that all sound cool, like lots of neuroanatomy, dentatorubrothalamic, corticospinal, pontine cerebellum. You know, you can, like, do all that stuff. It doesn’t matter. Don’t do that. Okay? Cortex to thalamus to pontine to cerebellum and back. Okay? Let’s just make it easy so no one thinks that anyone’s super-cool, alright?

Now, these cerebellar pathways then go up these areas, go down the pontine areas, and come back. You guys ever see the pons? There’s a belly. The belly of the pons is because of the pontine nuclei that inputs from the motor cortex fire down to then fire back to the cerebellum. So that is your cortex. Your frontal areas of your motor cortical areas cause volitional activity through the corticospinal tract to the opposite side. They also fire down to the pontine areas, to let the cerebellum know what’s going on, and those pontine nuclei then project back to the cerebellum. So this is a loop, okay?

So, let’s say we’re talking about my left hand. So, right now my left hand is moving, right? And then maybe it’s my left foot and hand with gait. My propriocept… my position sense fibers, my muscle spindle Golgi tendon stretch, are going to be going through spinocerebellar dorsal column pathways, to my parietal lobe areas and to my cerebellum. That is a sense of what’s going on, right? So then I decide I’m going to move, right? So as I’m deciding to move, my executive function, prefrontal cortex, fires into my supplementary motor areas to then coordinate that, then to my corticospinal tract, and then I’m going to start to fire and move, right? But as I fire and decide my corticospinal tract to move and initiate, and I fire to the corticospinal tract, I immediately fire down to the pontine nuclei. Pontine nuclei fire right back to the cerebellum, and I have a loop, and these things are all communicating together to know what’s going on, okay? So that’s why people say, you know, that’s why left-sided cerebellar pathways fire to the brain, and the brain fires to the left side as well.

So, this is one of the… what we call the big loop of these motor pathways, cerebellar to thalam… to the cortex and back. Now, the cerebellum then fires to a smaller loop. It fires to the red nucleus, and then


the red nucleus fires down to something in the medulla called the inferior olivary complex, and then the inferior olivary complex fires back to the cerebellum, and then you have another loop. So there’s a big loop and a small loop. A big triangle and a small triangle. Right? So the cerebellum is also firing to the red nucleus, and what does the red nucleus do? As the rubrospinal tract, which fires to contralateral flexors in the shoulder girdle, and that fires down to the olivospinal tract, and there’s pathways from the spinal cord called spino-olivary projections, which then let the inferior olivary complex know what’s going on. This inferior olivary complex becomes a neural network between inputs coming in from the red nucleus, inputs from the spinal cord, spino-olivary pathways, and it keeps another loop between the cerebellum and motor movement. Cerebellum, red nucleus, red nucleus down to the inferior olivary complex, and then back to the cerebellum.

This is the picture I was showing you guys in the tract. Here’s a small loop. Cerebellum, red nucleus, inferior olivary complex, and back. Right?

So those two loops are all happening in sequence very time I take a step, contralateral to the arm swing with the motor cortex involved. Everybody good? Okay.

Now, those two loops then… are then also constantly… Well, the big loop is constantly being modulated by the basal ganglia. So the basal ganglia has a direct pathway, indirect pathway. So remember, the structure of the basal ganglia is that it’s just hugging and surrounding the thalamus. So the direct pathway’s going to increase an amplitude to the thalamus; the indirect pathway is going to inhibit pathway. They’re going to gate it or shave off movement, so it’s not too much, not too little. Cerebellum is going to turn muscles off in sequence, motor strip’s going to fire, and then we have movement. Okay? So that’s the summary of how these things… how these things integrate together. Okay?

So, let me review it for you one more time.

Then you have all these loops. All these pathways. Okay. So, let’s make it simple first. The final common pathway for all muscle activity is the anterior horn. The anterior horn is going to get inputs from corticospi-nal, corticospinal from the motor strip, contralateral from the opposite side, right? Volitional movement, contralateral to the limb. Anterior spinothalamic projections, right? Or, I’m sorry, anterior spinothalamic tract projections. They’re going to control volitional tone. Reticulospinal gross distension, vestibulospinal, just intrinsic spinal muscles, rubrospinal, shoulder flexor. Everybody good? Okay. That’s happening.

Then you have cerebellum, turning muscles on and off in sequence, basal ganglia gating, adding increased amplitude or shaving off, so you have smooth movement, corticospinal projecting in relation to homuncular map. Prefrontal executive function deciding to do it, supplementary motor area coordinating how you actually do the movement. That all works in sequence, contralaterally. That.. you fire, decide to move, those are all firing, then your central pattern generators take over, like the pacemaker of locomotion, just like the pacemaker to the heart, and now you’re walking. Okay? That’s basically the neurology of gait. Alright.

Now, let’s put some of these together more clinically for you. Okay.

If you know… if you can just watch it a few times, if you’re new, and learn that, you’ve pretty much learned what the major functions of the motor system are. And then if you then have fun and watch with gait,


you’ll see what’s going on. So if someone has this area involved – so, the cerebellum – how does cerebel-lum contribute to gait? Well, the cerebellum is going to get inputs in from the muscle spindles and Golgi tendons of the feet, kind of let the brain know where joints and things are in position of space. It’s going to coordinate and work with the vestibulospinal system to kind of know where you are in space, right? The vestibular inputs are going to… the vestibular apparatus has these fluids that move hair cells, and as you move your head positions it lets your brain know where you are in space. So you can integrate that vestibular information. It’s going to then fire into the vestibular nuclei, which then fire into the vestibular nucleic tract, which will go down to the intrinsic spinal muscles and keeps that erector spine in control there. Right? And then the cerebellum goes from the cerebellum to the red nucleus, the cortex, the pons, and back, which then coordinates muscles turning on and off in sequence with the motor strip, so when the cerebellum’s involved, you get dysdiadokokinesia, you get kinetic tremors, you get positive Romberg’s, and all those things.

So what will it do to gait? Well, what it will do with gait is, first of all, since muscle spindle Golgi tendon information’s not going to cortex properly, you get hypotonia. So you ever see kids walk, and they’re limbs are all flinging all over the place? That’s hypotonia. You guys may have people, when they lose their balance and integrity because they can’t get their intrinsic spinal muscles working, or their vestibulospinal integra-tion going, not know where they are, or have poor balance, so they have a wide-stance gait. So wide-stance gait, hypotonia during gait, is basically what you’ll see when the cerebellum becomes inefficient. Okay?

If the sensory cortex area, the parietal lobe, gets inefficient, they can’t feel where they are in space. They may have a tendency not even knowing it, walking or swaying to one side, because they just don’t know where these limbs are. It’s not coordinating well. Or, it’s just in their feet. You might feel like they’re walking with, like, something’s wrong with their foot, but there’s nothing wrong with it. So that’s a sensory thing.

Now, if the nerves coming up are involved, then you might get, like, a… they can’t really feel it… a slappage gait. Right? But as far as the parietal cortex is involved, it’s that sensation of what’s going on. Now, sways to one side… So you have someone walking down the room, and they’re going like this more, could be because their vestibulocerebellar issues are off, could be because their parietal areas are… somatosensory’s off. So that’s where you have to then do an exam and find out which one it is. Okay?

Now, what about the prefrontal cortical areas? Well, here’s the thing. The prefrontal supplemental motor areas, if your premotor supplemental areas are involved, then you get dyspraxia gait. You want to move, you want to walk, you just can’t figure out how to do it. You’ll be staring to figure out how to do it. Right? Everything becomes very effortful. So people with dyspraxic gait, you actually see them walking with a lot of effort. You might think they’re weak, but they’re not. They’re not weak. There’s no sensory motor loss. They’re walking with a lot of effort because that motor area isn’t coordinating, executing their motor planning very well.

And if it’s corticospinal, you get increased tone, and weakness. With gait you might see the tone different on one side.

If it’s the basal ganglia that’s involved, if it’s the direct pathway, what would you see happen to gait? You would have slowness of movement. You would see hypokinesia. So very slow gaits, you would think the basal ganglia direct pathway’s involved. Basal ganglia indirect pathway, as far as gait’s involved, is only if


you see any hyperkinetic abnormal movements while they’re walking would you suspect that the basal ganglia indirect pathway’s involved. Okay?

So, let me recap one last time.

Gait is one of your best tools to quickly look at all these systems at once, right? And it’s right in front of you. So during an initial survey, for me, the moment a patient walks in from the front door or is sitting a chair, to where they go next, is a very diagnostic window of time for me. Right? And, you know, when I do an exam, I’ll have people walking down the hallway for me. But before I do that, I just want to get an impression of what’s going on with them, right? So in the initial survey, I’m looking at their facial tone, I’m looking at their facial… you know, their facial tone like their eyelids, do they have any ptosis, do they have any lid lag, do they have any head rotation, head position, head tilt, any angulations, any eye deviations of any kind, right? Any paleness, anything going on with their nails, and then we talk, we communicate. That’s some information. Look at the forms, look at their handwriting, and then we see them walk, and right away you’ve got a whole picture right in front of you. Right?

So when they walk, you’re looking at all these integrated systems together, okay? So, cerebellum turns muscles on and off in sequence and coordination, calibrates movement. Basal ganglia direct pathway adds amplitude to the thalamic pathways to movement. Basal ganglia indirect shaves it off so it’s… the ampli-tude’s efficient. When the basal ganglia direct pathway’s not moving you get hypokinesia, slowness of gait. The frontal cortex is involved, your prefrontal decides, executive function, to move; your supplementary motor area coordinates motor integration, and your corticospinal activates muscles to have an impulse discharge so you can contract. Right?

Now, the way these things work is, muscle spindle Golgi tendons proprioceptors come in from one limb, they go to the contralateral parietal lobe for somatosensory perception, they go to the ipsilateral cerebellum for muscle spindle Golgi tendon tone analysis, right? And then pathways from the cerebellum go through two big loops: cerebellum, ventrolateral nucleus, cortex, motor cortex, down to pontine nuclei, pontine nuclei back to cerebellum. One big loop.

Then you have another small loop: cerebellum to red nucleus, to inferior olivary complex, inferior olivary complex back to cerebellum. Okay?

Then these brainstem… these brainstem cerebellar… these brainstem projections and these cortex projec-tions form corticospinal, volitional movement contralateral side, anterior corticospinal, volitional control of trunk, reticulospinal, general gross extension, vestibulospinal, intrinsic spinal control tone, right? And on to the rubrospinal flexor proximal shoulder flexor tone. Those all integrate, and that’s gait. Okay?

So let’s stop with that, and then Dr. Brock’s going to go over disorders again.

FunctionalNeurologySeminars.com Courses.FunctionalNeurologySeminars.com

https://functionalneurologyseminars.com

http://courses.functionalneurologyseminars.com

Documents

THE INITIAL CLINICAL SURVEY AND HOW TO IDENTIFY THE … · So, I put lots of great papers in your notes about central pattern generators, gait, movement disorders, and it’s not