Week 3 Neuroscience of Movement Coordination Flashcards

1
Q

So we’ve seen this picture before, the decerebrate cat. So the cat has had the cerebral cortex separated from its central nervous system. We put the cat on the treadmill and the cat is able to produce rhythmic ambulatory motion. For what it is, it’s a fairly complex rhythmic motion because it’s not just two limbs – it has the forelimb and the hind limb. The hind limb that has to be controlled in order for ambulation to occur. So we get to this idea of where do these patterns sit? And we’re not very creative with our name. And we call this a _____ pattern generator. Ben Lindemman started to talk a little bit about synergistic patterns that are produced with a cortical injury. The synergy patterns are ingredients that go into this central pattern generator. At some point, we learn and put together patterns and we store them away somewhere. And they are basic, but they let us function In somewhat of a primitive way, but it still allows us to function. So in week 3 or week 4, we discussed the idea of something coming at your head. What do you do? Most of us are going to put out our hands and try to protect ourselves, right? We talked about all the muscles that are involved. When we think about all the muscles that were involved, they all sat along a very similar C7 distribution. That’s an example of something that we call ______ and we’re going to be talking more about synergistic patterns and representations because that’s how we start to put together movement patterns and skilled movement.

A

central; synergy

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2
Q

But at the end of the day, we know that there’s a central pattern generator somewhere within our brains. Somewhere between the (midbrain/hindbrain) and the (basal ganglia/brainstem), maybe with some cortical input that when the cortex is under duress or we’re just starting to learn motion. So if you’re an infant, infants tend to present in synergistic patterns. Or if you’re an adult and we have a cortical injury, we go back to these base root synergies. But everything that we do, a lot of what we do from a movement perspective is synergistic and we talked about this, but we’ll bring it back into view in this particular picture. That decerebration line where we separated the cortex from the spinal cord was right (below/above) the midbrain. If it goes lower and we get the midbrain out of the picture and we cut the pattern right off of the spinal cord, the central pattern generator (is/is not) able to impact movement and decerebrate cat (is/is not) able to continue walking on a treadmill. So there’s definitely something about the mid-brain that is important.

A

midbrain; brainstem; above; is not; is not;

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3
Q

When we take a look at human beings, depending on the level of injury of the spinal cord, whether it’s a complete spinal cord injury or an incomplete spinal cord injury. There are different levels of body weight supported gait that the individual is able to produce. But also when we look at individuals with critical injuries, when we take a look at strokes in brain injuries, just simply putting the human being onto a treadmill and allowing for movement, we don’t get the same type of reciprocal gait pattern that we do from a decerebrate cat, which brings into the idea that humans have a little bit (less/more) cortical input into the central pattern generator than quadrupedal animals. So there’s a little bit (less/more) thinking and there’s a little bit (less/more) skill involved, perhaps in terms of how humans have to move. And we don’t know why that is because if you look at some animals and look at how they produce movement, just the agility and nimbleness, It’s hard to think that we require more cortical inputs for what we do. But somehow the wiring seems to come out that way.

A

more; more; more;

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4
Q

When we take a look at central pattern generators a little bit more and look at that reflexive walking, what’s interesting is, if we cut in the middle - So if we follow that blue line and cut the cord and the connections from the brain right in the middle of the midbrain, the animal (is/is not) able to produce reciprocal walking, but it (can/can’t) hold itself upright. So you have to put the cat on a truss to be able to control posture and then allow for the stimulation in the sensory input that’s coming from the treadmill touching the foot and impacting gait to happen. If you go just a few millimeters up and you cut where the midbrain meets the cerebral cortex, the animal (is/is not) able to walk in this reflexive pattern with postural control. So there’s something that happens within humans (we’re talking maybe 3-4 millimeters, in smaller animals, you’re talking about a millimeter) within that millimeter of processing that is the difference between being able to hold postural control and impact your environment and not have postural control as you impact the environment. But there is a singular problem with that - It doesn’t result in the ability to adapt to the environment, you’re just responding. So how do we start to put together motion that integrates environmental impact on what it is that we do? That comes down to the control of movement.

A

is; can’t; is

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5
Q

The control of movement reintroduces anatomical regions, which is the primary motor cortex - (M1/M2). It reintroduces the premotor cortex and it reintroduces the supplemental motor cortex into the picture. We went over gross functions of these, but want to start putting things together a little bit more in terms of what it is they do and how they do it. I’m going to add a new word into your vocabulary, which is the pre-motor area, which is confusing because we have a premotor cortex. So in some motor development and motor learning models, they clump together M2, which is the ______ motor cortex and the PMC, which is the ______ cortex and they refer to those two areas as the premotor area. I just always remember that P with premotor cortex and what it does, which is (postural/sequencing) adjustments and then supplemental area, I think of the S in supplemental and start thinking about the (sequencing/postural) of movement.

A

M1; supplemental; premotor; postural; sequencing

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6
Q

M1 is proportional to the (body mass/complexity) of the individual. So what is happening at M1? M1 primary motor cortex is the region that is connecting with our spinal cord, with our (upper/lower) motor neurons. And it’s the one that’s responsible for executing (motion/sensation). So the larger you are, the (more/less) motor units you have. So M1 is not necessarily dictated by how skilled you are in movement, but how big you are. So we want to consider that. The premotor area grows with the level of (body mass/skill) that’s responsible for movement. What’s interesting is that the premotor area is anywhere from three to six times (smaller/larger) in humans than other primates. The only real difference that we have between us and other primates is an opposable thumb, as well as the ability to produce (vision/speech). So we are able to take our mouths and our tongues and orient them and organize them in ways to produce words that make sense, whereas other primates don’t. And we have fine motor control of opposable thumbs and finger control that other primates have. So the thought is, the larger representation is really just based on the complexity of producing speech and the function of producing (gross/fine) motor coordination.

A

body mass; lower; motion; more; skill; larger; speech; fine

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7
Q

We now have technology that is relating to transcranial magnetic stimulation and transcranial direct current stimulation. With these techniques we’re able to study what’s happening by either exciting or in other cases, changing the excitability of the motor pathways and the sensory pathways to get a sense of if we stimulate this area, what happens? So now we’re able to take individuals that are neurologically intact and get a sense of what they’re doing and what their brain is responsible for. So what happens when we look at motor region stimulation? When we go and excite just the primary motor cortex, we only see movement at a (single/multi) joint. So you have one muscle contracting, maybe two muscles contracting, but it is not a coordinated control movement, it is just movement through a particular joint. We used to think the primary motor cortex is a big one, it must do everything. That’s not necessarily the case. It goes back to reinforce that M1, or the primary motor cortex, is really just responsible for producing the force of movement at a (single/multiple) joint. When we stimulate the premotor area (M2 – supplemental motor cortex and premotor cortex) we start to get these (small/large) complex movement patterns involving (single/multi joints), which reinforces the idea that it’s those regions in the brain that are the most important to us from a movement production perspective. If we go back and think, where do these regions sit in the brain? They sit in the (frontal/occipital) lobe. What else happens at the frontal lobe? Judgment, decision-making, cognitive processing. So we think that there is a relationship in terms of the complexity of movement sitting at the frontal lobe because everything that we do is planned and we have to have judgment in terms of what we’re doing.

A

single; single; large; multi; frontal;

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8
Q

Motor Cortex Muscle Mapping

Individual neurons from motor cortex (do/do not) innervate individual muscles. They innervate (individual muscle/small GROUPS) of muscles.

(Primary Motor Cortex/Pre motor area) codes the FORCE of movement of muscle groups - Limb Force and limb velocity is modulated by the (anterolateral/rubrospinal) tract.

Individual neurons from the motor cortex (do/do not) innervate individual muscles. So we have upper motor neuron A - that doesn’t go to the biceps lower motor neuron A, it goes to limb flexors. So at that level it’s not controlling individual muscles, but groups of similar muscles that need to work together. Where is that information turfed out? That information probably is turfed out through the spinal cord levels. But again, if you go back to having to protect your face from a moving object, it’s not an individual muscle that M1 is controlling. Its controlling the group of neurons. Especially if it’s something that’s simple, or if you’re about to fall off the edge of a cliff and you have to step back. You don’t want 15 different pieces having to come together, you want one to control a wide network. So when we take a look at cortical mapping, it’s not a one-to-one relationship of one motor neuron from the cortex goes down to one motor neuron down at the spinal cord level, down to one motor unit.

A

do not; small GROUPS; Primary Motor Cortex; rubrospinal; do not;

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9
Q

Motor Cortex Muscle Mapping

The (primary motor cortex/premotor area) codes the force of movement of muscle groups. It looks like limb force and limb velocity is modulated once that directive is created by the motor cortex, the directive, in terms of modulating it to meet the environmental circumstances, is modulated by the (lateral corticospinal/rubrospinal) tract. Besides the primitive responses that we saw in the very beginning of the term last year, now that we know a little bit more, what else is the red nucleus hooking onto? The (basal ganglia/cerebellum)! There’s a big component of the cerebellum into the red nucleus and out of the red nucleus. So as we start to look at what’s happening, that modulation by the red nucleus is highly likely cerebellar inputs that are being considered in terms of choosing the appropriate response. In everything that we consider from a coordination and control of movement is the appropriateness of the response. You’re able to produce an appropriate response where somebody that has cortical injury, cortical damage or injury might not be able to produce the appropriate response. And then as Ben starts to go into cerebellum and basal ganglia disorders in neuro E&I II, you’ll start to see that most of the diagnostic features are in relation to inappropriate movements - So moving faster than you really want to, producing ballistic motions when they’re not necessary, etc.

A

primary motor cortex; rubrospinal; cerebellum;

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10
Q

So M1, as the primary motor cortex it’s bottom of the barrel in terms of all the processes that actually have to happen, it just (plans/executes) the movement, so that’s all M1 does, that’s all the primary motor cortex does.

A

executes

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11
Q

The supplemental motor area/cortex is involved in the planning of movement and the idea of initiating movements versus externally triggered movements. What’s an externally triggered movement? It’s a reflex. If we think about the flexor withdrawal, you step on something, it hurts, that external stimulus results in you stepping away with the involved limb and thrusting down with the uninvolved limb to give you limb support. So those we consider externally triggered, whereas throwing a ball (is/is not) the supplemental motor cortex. You want to actually take the ball, throw it at a target. You want that ball to get there at a very specific time. All of those things that you are initiating is being carried through to the supplemental motor area. There’s also the difference of catching a ball. While the act of catching a ball is not necessarily reflex because there’s visual input that has to be processed. There’s the speed of the ball that has to be processed. There’s the where do I put my arm? That appears (to be/to not be) controlled by supplemental motor area because it’s an externally triggered response. The thing that we want to consider about the supplemental motor areas are that it does things that we want to do and have to do. So it’s not as simple as one particular cortical region. And is probably more a relay. A feedforward and feedback. The supplemental motor area is also responsible for action selection. So how do we produce the motion that we want? And in general, we see supplemental motor cortex activating at about _ milliseconds (prior/after) to the initiation of movement.

A

is; to not be; 60; prior

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12
Q

The premotor cortex is the (sequencing/preparation) to move – the postural control. We’ll see that at about _ milliseconds (prior/after) to the movement. So the premotor cortex starts to activate (before/after) any other planning has to happen because we have to control for posture first. We have to be able to control our center of mass before we start to expand upon limb use. So the postural control is critical to be able to produce controlled movement at the limbs.

A

preparation; 100; prior; before

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13
Q

Got it

A

Gotit

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14
Q

Medial Pathway

Phylogenetically, (youngest/oldest) part of movement system

The main components of the medial pathway consist of:
(Cerebrocerebellar/Vestibulospinal) - Where am I in space? Am i upside down? Am i heading straight? Where is my head in space?
(Spinalcerebellar/Reticulospinal) - Alertness. There has to be some level of alertness to what you want to do.
(Tegmental/Tectospinal) tracts - The tectum is comprised of the superior and inferior colliculus. So those are response to auditory stimuli and visual stimuli.

(Advanced/Basic) Postural control - all of those tracks if you go back, sit (lateral/medial). And their response is at the trunk musculature. So the medial pathway really responsible for the most basic of postural control.

(Doesn’t have/Has) cortical input: may have (LESS/MORE) pre motor cortex input

A

oldest; Vestibulospinal; Reticulospinal; Tectospinal; Basic; medial; Has; more;

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15
Q

So when we take a look at postural control, it is run by a very specific pathway called the (lateral/medial) pathway. If we take the central nervous system and we break it down into two components, we have a cerebral cortical and then we have a brainstem and spinal cord structure. And so really what we’re dealing with in terms of the medial pathway.. think about what sits in the brainstem – rubraspinal, reticulospinal, tectospinal, spinal cerebellar. It doesn’t need a whole lot of cortical input just yet. But those are the things that are sitting along the brainstem pathways that we’ve gone over at this point. Those pathways along with the spinal cord are what’s working together with input from the (premotor/M2) cortex. So it takes information from the premotor cortex, likely (less/more) information from the premotor cortex than other regions of the cerebrum and it uses that to influence what’s happening along this medial pathway. The medial pathway is also where we start taking subcortical structures like the basal ganglia, the subthalamic nucleus, the ventral tegmental area, and the substantia nigra - all of those structures that sit deep within because if you look at it from a lateral to medial perspective, all those structures are medial with respects to the cortical structures. So those are the inputs that are responsible for postural control. So it’s not necessarily one particular part of the brain, but a connection that puts together the idea of feedforward and feedback controllers.

A

medial; premotor; more;

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16
Q

So what we want to consider about postural control is that is is a (regulatory/non regulatory) process. So what is regulation? It’s keeping a certain level of order. It is something that’s there to keep things just the right temperature. And that right temperature is keeping your center of mass over the base of support, so that’s its sole job - figure out ways to maintain your center of mass over the base of support. It requires three very particular inputs: 1) It requires (ligament/muscle) proprioception - So the spindles, because the Golgi tendon organs are there as a safety valve - there’s too much load happening across the muscle so you need to shut it down because the loads too heavy. But our main proprioceptors are our muscle spindles. So the stretch that happens across the spindles is where we get the majority of our (motor/sensory) input, not so much the ligaments, not so much the thing sitting within the joint. 2) (Auditory/Vestibular) receptors, and 3) Changes that are happening within the (hypoglossal/visual) field are all inputs that we are using as an organism to be able to regulate or maintain the base of support over the center of mass.

A

regulatory; muscle; sensory; Vestibular; visual;

17
Q

So what we call balance is this postural control and it follows a (proximal to distal/distal to proximal) order. To balance there is an ankle strategy and a hip strategy. If the level of force is not that huge, what do you do? You try to balance yourself using your ankles (first/second). If that doesn’t work, then what do you do? You start to use the hips to sway a little bit more to reorganize, you might use the knees a little bit more to reorganize. And if the balance disturbance is greater than those systems can compensate for. What do you do? You take a step. One of the things that we start to see in aging is that we start to move more towards (proximal to distal/distal to proximal) order. What we start to see in people with chronic back pain, hip pain, they also have a change in this order of postural control where they’re no longer going from distal, they automatically go to a hip strategy. So different pathological situations can impact postural control and different degenerative processes can impact postural control. Big thing that we want to keep in mind is that it’s (a singular effort/a combination) of feedback and feedforward loops that keep the system working together.

A

distal to proximal; first; proximal to distal; a combination

18
Q

Feedback and feedforward is happening within the medial pathway with processing that’s happening at the (supplemental/premotor) cortex all to be able to produce a correct postural control.

A

premotor

19
Q

APAs are a little bit (less/more) complex than just postural control. So we think APA’s are kind of a step up from postural control. It’s anticipatory, so there isn’t a response that’s occurring, the human has to produce a movement. So in this particular diagram, the bell goes off. When the bell goes off, he has to pull the lever or the band backwards. The center of mass displacement that’s being produced by the biceps goes in one direction. Because it’s a planned motion, before any of that motion execution happens.. Remember we’re thinking distal to proximal, let’s start by using the gastrocs (first/last), let’s turn the gastrocs on to be able to fight the center of mass disturbance that the body is going to be going through. And this is a very simple picture of the APA, but the APA is much more complicated than just postural control alone.

A

more; first;

20
Q

So the big picture to take away is these are the things that are happening just from a trunk-wall perspective. And these, if you think about these, whether it’s erector spinae or rectus abdominis, they’re sagittal plane muscles – flexors and extensors. We are just getting to transverse plane control with external oblique and internal oblique. There’s a whole nother set of transverse plane controllers that are happening about the lumbar multifidus. There’s a whole nother level of transverse plane and frontal plane control that’s happening between gluteus medius, maximus, and then all your internal hip rotators. So there’s a lot that has to be put together from a central nervous processing picture to produce the APA. So that anticipatory postural adjustment is a little bit different than the medial pathway that posture control is coming from.

REST IS “FLUFF”

On an exam, I’m not going to be expecting you guys to figure out which muscles are turning on to what type of disturbance. But let’s just take a look to see what’s happening here. Here we’re just looking at the trunk musculature, abdominals, internal oblique, rectus abdominis, and internal oblique. We haven’t even gone into the posterior chain muscles of the hamstrings, lumbar multifidus, erector spinae, we’re just looking at what’s happening on the anterior wall. So look at what’s happening milliseconds before the person starts to extend their arm back. There’s a sequence of movements that has to happen before movement. So rectus abdominis, internal oblique. And what’s the other one here? External oblique have to turn on, but they’re doing it asymmetrically. Why is it happening asymmetrically? He’s only using one limb. So based on the laterality of the movement, is there going to be a center of mass disturbance that makes us lean one way versus the second picture down at the bottom, which also looks a little bit different because both limbs are going backwards versus the other limb where it is now the right limb that is moving versus the left limb. All of those produce unique responses at the rectus abdominis, internal oblique and external oblique. That’s not including what’s happening between our transversospinalis muscles, erector spinae muscles, that’s not including what is happening at the gluteus medius level, the quadriceps, tib anterior, and gastroc levels to control for all of this. So when the individual plans for movement, the picture and the EMG recordings are completely different. So it’s that level of complexity that seems to make the APA different from postural control and the pieces of the brain and the central nervous system that are involved.

A

Got it

21
Q

APA

Reticulospinal tract - (Small/Large) roll in APA
RF Pons: (on/off) cells - Excites axial muscles and (back/limb) extensors.
RF Medulla (on/off) cells: neck/ (limb/back) extensors
On: (flexors/extensors)

Coordinates input from (visual/vestibular) system

Ultimate APA response is dependent on excitability of the (cerebellum/spinal cord)

(M1/SMC (MII)) may oversee the APA response

A

Large; on; limb; off; back; flexors; vestibular; spinal cord; SMC (MII)

22
Q

That APA seems to come from the (rubrospinal/reticulospinal) tract. We talked about these a little bit, but the idea of on cells and off cells sitting within the reticular formation, within the medulla and the pons. We talked about it when we were discussing the nociceptive pathways. These on and off cells also play a role in the anticipatory postural adjustments. It coordinates input from the (visual/vestibular) system because you have to have a sense of where am I, where am I in space. And the ultimate goal of the APA is to try to stabilize the system. And the overall response that you see from the APA is largely dictated by (cerebellum/spinal cord) excitability. So when we talk about spinal cord excitability, it, it’s an idea of a spinal cord that has been primed for motion. So if you have a cold spinal cord that hasn’t done anything and it’s not excited… But let’s say you prepped the system and you’re warmed up and you produce motion, there’s a level of excitability that’s happening at the spinal cord. So it enhances the response of the APA. So the role of warming up and getting the spinal cord primed seems to be an important aspect. But the other issue is there are injuries that can result in excitability of the spinal cord. So different neurologic injuries can result in just a general resting elevation because the spinal cord is more excited than it really needs to be. Ex: SCIs and strokes. And what we see about the APA is that (M1/M2), or the supplemental motor cortex is overseeing this APA response. This makes sense because the premotor cortex is just posture, just trunk. The supplemental motor cortex starts to pull in more of the limbs. So we need that system working together to be able to produce distal to proximal border.

A

reticulospinal; vestibular; spinal cord; M2;

23
Q

So the overall big picture take-home message is the APA and the (medial/lateral) system is necessary to form the base that you are going to build more complex movements off of. If you do not have that base, if you do not have that preparatory postural control that is sequenced and you do not have that preparatory adjustment that’s happening, the likelihood of creating refined movements is (likely/slim to none).

A

medial; slim to none

24
Q

Got it

A

Got it

25
Q

So voluntary movement is different from adjustments and different from reflexes. And the two columns really highlight what’s different about voluntary movement. So the first one is something that we call the presence of motor equivalences. And really what a motor equivalent is, is I have a task and it’s to reach for this water bottle. The goal is reach the water bottle, I can do this 5,6,10 different ways. There’s variability in how I can do this. A reflex, stretch, reflex of the quadriceps - There’s one outcome, quadriceps, contraction and extension of the knee. So there is a flexibility in movement strategy that reflexes (have/do not have). You push somebody, they take a step, they’re probably gonna take that same step every single time, depending on where the external stimulus came from. Was it coming straight on and I just had to take a step back? Was it coming off an oblique and I have to take a step back and into abduction? The stimulus is going to drive the response, but that response is going to be very similar. It does not have to be very sophisticated because I’m just trying to stay upright which is very different from something that I want to do. So voluntary movement is synonymous with (flexibility/rigidness) of a movement strategy. Voluntary movement also (improves/declines) with practice and learning. Motor and voluntary movement becomes more efficient the more we practice it. External stimulus precursor (is/is not) necessary to result in voluntary movement. I don’t need a pin coming in poking the bottom of my foot for me to want to move my foot away. I want to get that bottle. I am going to take that bottle. So it doesn’t need this external sensory input to produce motion. We can initiate it whenever we want to. And with the abundance of motor strategy or the motor equivalence, we could do it whichever way that we want to do it.

A

do not have; flexibility; improves; is not;

26
Q

There are components of voluntary movement, which are target or goal identification - What do I want to do?, planning of the activation, then executing that motor response. Those are the three things that have to occur. And as I talked about the beginning, these are all decision-making processes. And that is highly likely why the motor processes sit within that (frontal/occipital) lobe because that’s where a lot of our judgment or cognitive processes are happening. So location matters.

A

frontal

27
Q

The pathway that the voluntary movement system uses, we refer to as the (medial/lateral) pathway. Think about the structures that are being used in terms of creating voluntary movement. Cortical drive from the cortical inputs down through the corticospinal tract. They travel a little bit medially to get the signal, but then where do they go? They travel on the outermost aspects of the brainstem, right? The two lateral pathways that we are concerned about is the (anterior/lateral) corticospinal tract and the (reticulospinal/rubrospinal) tract. The lateral pathway probably has a little bit (less/more) supplemental motor area/ than the premotor cortex just because of the skill and variability that’s involved.

A

lateral; lateral; rubrospinal; more

28
Q

A module is something that is prefabricated. It’s a building structure that has all the necessary components and you just drop it in there. So here is an example of a modular building that is being put up. In terms of human movement. These modules are what we call synergy patterns. So when we start to put together human movement, we move in synergies that are put together as we experience life. So the more you do things, there’s a learning that has to happen. And based on your body type, your muscle mass, your necessary strength, and range of motion and overall available strength and range of motion, we start to prefabricate different patterns and different movements at a very young age. And we practice them over and over and over again. And they are learned. And then they’re stored away so that every time we want to do something, we’re not thinking, we’re not thinking of turning on specific muscles like the glute med on the contralateral side when walking. As we go through movement, everything that we practice together starts to get laid out into these prefabricated motor chunks that are created in the brain and then stored in motor cortices. And when we’re asked to do something, it’s simply just representation of these motor synergies in order to produce the movement. When you start to learn something new, what do you have to do? You have to practice it over and over and over again until you get that skill down right. Taking range of motion, mobilizing a joint. These are new things to you. So what do you do? You practice it over and over again. You find the most comfortable way for you to do it. What are you doing there? You are creating more modules. You’re creating more synergies to be able to be stored, put away so that when you need them, they get called to the forefront again. And that’s how we keep movement efficient. We don’t think about every single thing that happens. When we think about what we have to do, say on a practical exam and you haven’t practiced your shoulder range of motion or whatever it is and now you have to do it in front of the individual and it takes a little bit longer. Why? Because you are thinking through the process. You are not recalling a motor synergy that has been produced.

A

got it

29
Q

The other thing that the author talks about is that there’s an optimal muscle pattern for the necessary task space. So, yeah, we’re not thinking about this particular picture when we’re very young - walking down a hallway is a very different task space. The environment that we have to produce that motion is going to be very different than if we have to run around an obstacle course. So how do you get good at it? You practice over and over again. And you expose the child to (singular/multiple) environments and we develop a certain pathway for it. And then if we have an injury and we lose the synergies, we lose where those synergies are stored because there’s damage to the area. Well, what do we have to do? You have to re-learn the task again? What do you have to do from a physical therapist perspective? You really have to introduce them to (singular/multiple) environments again because they have to start building a good motor plan, a good motor modules so that they can start packing away these prefabricated, pre-packaged motions again.

A

multiple; multiple

30
Q

So as we go through now there’s a specific neuroanatomy and physiology of synergy creation and development. Right now we’re going to keep it simple. And the overall neuroanatomy and physiology is practice, motor learning and practice in different environments. And then the synergy has to be coded so it can be put away. We call that motor learn. And then synergy recall - when you’re asked to do something, you have to be able to pull that pre-fabricated system out again. Where this all happens is likely from the (pre/supplemental) motor cortex impacting the execution at M1. But it’s very important to keep in mind that we need variability of movement, we need to practice it, and we need to give the individual time to make these prefabricated movement patterns again.

A

supplemental

31
Q

Human movement follows a theory called the Uncontrolled Manifold Hypothesis. It’s a very important theory. There’s a lot of physical therapists that buy into this. And really what we’re looking at is here we have manifold where air goes in. And then there are four different chambers, 10 different chambers, you pick. And if we have an uncontrolled manifold, air can come out of any one of these portals. And that’s what we call motor abundance. I want to move, I want to pick up this water bottle. I should be able to produce it in any particular way that I want to. If you think from a simplistic perspective, if every time I move to pick up this bottle, I use biceps and deltoids and that’s all I do. What do you think happens after 1000 repetitions? Overuse syndrome. If you keep using one manifold, if you keep using one expression of your motor abilities to do something over and over again, eventually, that’s going to break down. So now all of these different pathways are what we call different synergies. We’ve practiced different ways to produce movement because that variability is important in keeping the musculoskeletal system healthy. You don’t want one way of doing something. And most of the time we’re treating somebody because they do something just one way. So the idea is to have this uncontrolled manifold where the human being can express movement in any way he or she desires because if you start blocking off portals and you only use one portal, the likelihood for breakdown is very (low/high).

A

high

32
Q

If we break down the manifold in a car, your car’s not running. We would also think that a broken manifold and a person can result in injuries. And in fact, in some repetitive strain injuries, repetitive stress injuries that is what we see. The variability in how they do things is very limited. Certain times, you don’t have a choice in order to get optimal athletic performance. You have to do it the same way over and over and over again. But What’s the downside of that? The risk for injuries (decrease/increase) because you keep using that same motor pattern over and over and over again.

A

increase

33
Q

This was a study that we published five or six years ago looking at motor recruitment and looking at motor variability. And if we take healthy individuals, the key thing to focus on is this table here (pic to the right). Don’t worry about these numbers for now. This is a movement pattern used in a special test to diagnose individuals with low back pain called a prone instability test. When we take a look at the synergy patterns just used in lifting up the leg, individuals without low back pain have (two/three) different synergies that they use to be able to provide that movement. Individuals with a history of low back pain express only (two/three). So we consider that a pretty big difference because in healthy individuals there are different ways to move. The reduction in overall synergies that are available for human movement could potentially be what’s producing this type of overuse response. So variability is key to maintaining healthy human movement.

A

three; two;

34
Q

When comparing the torques acting at four arm joints during fast reaching movements in different directions, muscle pattern dimensionalities are higher than torque dimensionalities. Basically, what they’re saying is the joint only moves in four ways. But when we measure how people do it, the motor variance is (small/huge) across healthy individuals. The dimensions in muscle patterns far outweigh the different torques that are necessary to produce one particular movement.

A

huge

35
Q

Then we have to add force to the picture. If we consider multifidus, if we consider quadriceps, you think about the muscle orientation, the fascicle orientation of those guys. They run across multiple orientations. There are multiple planes of origin and insertion about those muscles. In order for us to produce smooth movement, we have to have (synchronous/asynchronous) activation at the motor unit. And it’s no different than what we had here. We need something to initiate the movement. We need something to complete the movement. The blue line (top pic) is the smoothness of motion. The orange and red lines are motor unit activations. We have to have motor units turning on at (the same time/different times) in order for the motion to stay smooth. But if demand increases and you have to turn all the motor units on because you’re lifting something heavy.. You’ve probably seen this at the gym when somebody’s lifting something heavy, how smooth does it look? Not very smooth because you have to turn all the motor units on to try to lift that thing. And then it has to pause for a little bit to reorganize and lift through the remaining excursion again. If the muscle runs out and gets into active insufficiency, what do you have to do? You have to turn that muscle off, reorganize it, and turn it back on again. So there’s a juttery type of a movement that occurs if somebody’s lifting something that’s too heavy. So all we’re really looking at is as you start movement and continue movement, how do you keep it smooth? The only way that you keep it smooth is by bringing in the right motor units at the right time. If you turn on brachioradialis and biceps at the same time, you’re going to run out of room. We have to turn on the brachioradialis and biceps brachii at separate intervals to continue through controlled, smooth motion. The more that you start to coordinate movement and the more you start to get co-contraction, the more (smooth/unsmooth) motion that we see.

A

asynchronous; different times; unsmooth

36
Q

So these are correlations. This is a paper that we’re working on looking at individuals with unsmooth motion with respects to low back pain. They have a juttery kind of shaking type of motion as they go through forward bend. If you look at healthy individuals and you run correlations between internal oblique, external oblique, rectus abdominis, lumbar multifidus, lumbar erector spinae, thoracic erector spinae. Look at the correlation between those muscles. They’re fairly (low/high). As you start to get into people with low back pain who do have unsmooth motions, the correlation starts to become (low/high) because they’re turning on at the same time. Higher numbers – more motor units are firing (asynchronously/synchronously).

A

low; high; synchronously

37
Q

The authors talk about this neural substrate that has to be produced. And that substrate is the key, the backbone that we build all of our movements off. And those substrates need to be recalled every single time we want to move. If we want to keep that movement efficient. And those substrates are what we referred to as synergies. So those substrates are the basic building blocks of movement. The substrates have to be created, coded, and recalled.

A

Got it

38
Q

Variability and motor abundance (are/aren’t) important for healthy movement

A

are