Transcribed by Jacqueline Heath

February 28, 2014

Basal Ganglia and Cerebellum Lecture – by Dr. Schiff Note: this lecture did not have slides, so I separated the lecture as best as I could by themes.  …For regulating voluntary movement and the reflexes that intervene there. And the corticospinal tract is sometimes known as the pyramidal tract. There is sort of a reason for that. And if you. It used to be thought that these large cells in the cortex, which are also present in the primary motor cortex, the pyramidal cells of Betz. The big cell bodies. And they are sort of pyramid shaped and a single axon comes out. They contribute to the CST. In the early days it was thought that they were the CST and after naming them for the pyramidal cells, it was referred to as the pyramidal tract. It turns out that if you have an area of ground with a few boulders on it and pebbles sprinkled around, you’re likely to name it for some configuration of the boulders. But even though they are a hundred times more pebbles in the gravel in between than there are large rocks. Here, turns out that the pyramidal cells of betz make up at most 3 percent of the CST and about 97% of the CST are much smaller neurons. So to call it the pyramidal tract is a bit of a misnomer. But it’s one of those old names that stuck. Basically what you have is, if this is M1, the primary motor cortex, on this side of the body, say this is the right. And you have a cell with a cell body here, it heads down into the brainstem, crosses at the medulla, so here’s the midline. And you have the axon travelling down to whatever appropriate level of the spinal cord there is and eventually it synapses either directly or indirectly through an interneuron onto an alpha motor neuron and go to the muscle. Or onto a gamma motor neuron, things like that. And based on the fact that this is wrongly called the pyramidal tract very often, there are two systems of sort of side branches that provide feedback back onto the pyramidal tract, or the cortical cells of the pyramidal tract that are referred to collectively as extrapyramidal pathways because they are not part of the pyramidal tract but they interact with it. And the extrapyramidal pathways include those that refer to as the basal ganglia, or sometimes called basal nuclei, and those that deal with the cerebellum. Now I’m not going to go into a whole description of the anatomy or structure basal ganglia, Dr. Jeung (sp) did that, or of the cerebellum (she also covered that). I’m going to just, as my usual practice, draw schematic type diagrams. Basically what happens, this first hour I’ll stick to basal ganglia and what happens there. Then we will look at the cerebellum in the second hour. Then I’ll tell you about the busy frantic time I had in between this morning’s section from 8-10 and you guys which involved me running around all over the place. That’s for later. The axon that comes down from the cortex and essentially becomes part of the upper motor neuron for the most part, sends off a little branch and it goes to the basal ganglia, BG, and then basically what happens is the output from the BG feeds back across the midline to the thalamus and then you have an output from the thalamus back to the motor cortex. So what happens here is when your cortex gives a command, do something, contract that muscle, or whatever, it sends a copy, it CCs the basal ganglia. And the basal ganglia then do some sort of processing and tell the motor cortex by way of

this pathway back through the thalamus, to modify that, do it a little faster/slower, whatever. And so what we are trying to do is figure out, actually what it is the basal ganglia do collectively and how they do it. Now, the BG together are the collection of deep nuclei within the brain and they basically consist of two nuclei here, the caudate nucleus and the putamen. And the input from the M1 essentially enters the system about there. Then there is a pathway from the caudate and putamen to the globus pallidus. And the output goes by way of the globus pallidus back to the thalamus and then to M1 again. Plus, there is a pathway back and forth from the caudate and putamen to the substantia niagra. And there is a pathway to and from, or from and to the globus pallidus to something called the subthalamic nucleus. And this is the overall scheme of the connections here. There are additional pathways. There are inputs directly to the globus pallidus. There are outputs from other than the globus pallidus. But for the majority of input/output relationships through the BG, the globus pallidus is the main output pathway going to the thalamus. Now the question is, we’ve got these things, what exactly do they do? Now as we have seen, in the course of this whole course, one of the ways in which we learn what happens or what function a particular part of the brain has, is we find someone who has lost that particular function, or is malfunctioning, can’t do something that he used to be able to do, after something traumatic happened, well it doesn’t have to be acute traumatic like he got shot in the head, or maybe he developed a tumor somewhere that is pressing on the brain, and he lost some ability to do something. And then, what you do is you wait til he dies, you’ve got to be patient for this sort of research, and you autopsy the brain and see where the damage is. If the damage done here caused him the inability to do such and such, you might be able to conclude that this is somewhere along the pathway or somewhere in the control center that regulates. That question was dropped from the quiz. Because you can’t safely assume, you can’t safely conclude that just because interfering with a particular area interferes with the ability to do something, that that’s the control center, or one of several control centers, or that’s just on the route and some axons go through that area and incidentally get damaged. So you can’t come through any of the above. Enough about the quiz. Because I was convinced by your curriculum reps, basically as it was worded it was a question more about logic than knowledge, so I figured okay, it’s gone. Anyway. If there are lesions somewhere in this area, what do they prevent you from doing? Ok so you look at people who have lesions somewhere in the basal ganglia, and what do you find? Well there is a whole collection of these and I listed them on the handout on NYUclasses, I don’t expect you to remember them all, it’s a whole zoo and some textbooks have slightly different versions of the list and different terms are defined in different ways in different books and I don’t want you to get bogged down trying to memorize different stuff. But, basically what happens is people with lesions in various parts of the subthalamic nucleus in the globus pallidus develop spontaneous movements of all strange things. In other words, a person with a lesion in the subthalamic nucleus might develop what are called ballistic movements or ballisms in which sitting quietly not doing much of anything, and suddenly throw an arm out. And often they are

unilateral, they are contralateral to the site of the image. And then sitting quietly, and then suddenly, that. There are lesions that can cause what are choreas, as in, not the country, chorea as in choreography, dance like movements, twisting, writhing, all sort of spontaneous movements they develop with lesions in parts of the basal ganglia. So from our usual way of analyzing this sort of data, we might conclude that the basal ganglia are involved in not doing these things. One of the basic principles we have seen over and over again in evolution is that there is a tendency towards simplification. Unwanted complications only make trouble. When the human genome was finally analyzed how many years ago it was found there are far fewer genes in humans than they expected to find. There is really a tendency toward simplicity and economy because if you don’t have so many details to take care of, you can keep doing things right and not make mistakes. The more things you do, the more things that can go wrong. That’s why men have nipples. Because it would be very complicated bit of coding to have half the population with them and half without them. So men have nipples even though they are totally useless because it’s cheaper to encode DNA and so on for everyone to develop these things. Okay. So it doesn’t really make sense that we would evolve a whole complicated bunch of deep brain nuclei, these basal ganglia, just to avoid certain twitches. Why not just, you know, get along without them? And indeed, there are people who have these various spontaneous movements that they can’t control, in which, now this is a call only the patient can make, and has to analyze the risk-benefit ratio. There is a risk for any surgery, especially when poking things into the brain. Now the benefit might be to eliminate these spontaneous movements. But who knows what else it might do. Is it worth it/ that’s up to the patient. But one thing that has been done experimentally is you cut this pathway from the globus pallidus output, bringing the output from the globus pallidus to the thalamus. And that eliminates the symptoms. But one thing it always does as well is it induces certain of what we might call negative symptoms. Because once that pathway is cut, one of the symptoms a patient develops is a mask0like face- loss of facial expression. Emotions, excitation, nervousness, whatever you normally express on your face, doesn’t happen anymore. The other thing that occurs as a negative symptom of all of this is a sort of bradykinesia. Brady means slow. People move, these people after the surgery move more slowly. No major problem, but they move more slowly than they used to. Their professional tennis career is down the tube. And these are generally referred to as negative symptoms, which are created by eliminating the basal ganglia effectively because if this path is cut and it’s the only output of all of these centers, then all of these centers of the basal ganglia might as well not be there because nothing gets out. Doesn’t matter what’s in a black box if nothing gets out of it. So it’s become generally accepted that somewhere in the basal ganglia when they are working right, play a role in facial expression. And they seem to allow us to move, change direction, act a little more quickly. Mechanism are not fully understood. Now, of all of these various syndromes, there is one that has been very thoroughly analyzed in conjunction with damage and lesions with the substantia niagra. And that is Parkinson’s

disease. Because people with lesions of various types in the substantia niagra can develop this constellation, this fixed mixture, of symptoms that we refer to as Parkinson’s disease. And Parkinson’s disease includes, among other things, mask-like face, no facial expression, and slowness of movement, bradykinesia. They also include certain spontaneous movements. And other modifications of standard movement. The patient with Parkinson’s will generally walk slowly because of bradykinesia, but he doesn’t lift his feet, he kind of shuffles. And he’s stooped over a little. And he carries his arms sort of flexed, not hanging down. So you have shuffling gate, shuffling… uh stooped posture, flexed arms, and this spontaneous tremor. This spontaneous movement of the fingers. And this is known as a pill-rolling tremor. Because what it looks like, someone who is watching it, as though he has a small ball/big pill, and he is rolling over it over and over again in his fingers, and this goes on constantly. Subject to two conditions. When he is not doing anything else with his hands. If he wants to make a purposeful movement with his hands and do something,… mike went out… Ok. What you’ve got is the pill rolling tremor occurs when you’re not doing anything. When you decide to do something with your hands, it disappears. And the second characteristic of Parkinson’s disease pill rolling tremor is that it only occurs when the person is awake, it disappears when they are asleep. There are different systems that are a part of this constellation. In addition to the pill rolling tremor of the hands, you have a mandibular tremor. Opens closes, wiggles a big. And possibly linked to that there is also dysphagia- difficulty swallowing. And as a result of the dysphagia, you are constantly secreting saliva and swallowing it without even thinking about it or being aware of it. The person with dysphagia is secreting saliva and not swallowing it, so they drool a little. Especially when the mandibular tremor is keeping them from keeping their mouth closed. Their speech is rather soft and slurred and they mumble. If they start to write something, it’ll start out normal but the script will get smaller and smaller into something called micrographia. And one other thing is that normal person, if put my hand on the chest of someone normal and push. What is he going to do? He’s going to start falling back and catch up. Take one step back, maybe two steps and then he’s vertical again. The person with Parkinson’s, because of bradykinesia, can’t step back fast enough. So he keeps falling back and falling back and trying to catch up and stepping backwards. Don’t do this to a person standing in front of a window. Haha. Eventually he’ll hit a wall and stop. So that’s your basic thing with Parkinson’s disease. And it was linked a long time ago from autopsies results to a defect in the substantia niagra. One thing that was learned was that the substantia niagra compared to the caudate and putamen, is part of a feedback loop. They send axons that release ach which stimulates the substantia niagra. The substantia niagra has its axons going back to the caudate and putamen, and they release dopamine. Now, dopamine as a transmitter, inhibits the caudate and putamen, but something happens in Parkinson’s attacks and destroys or disables the neurons in the substantia niagra so they don’t secrete or synthesize enough dopamine. How that defect here leads to all of these symptoms is not fully understood. However… these people also occasionally hallucinate. But they are very rational about it. One woman with long term Parkinson’s said… if there is someone in the room, I reach out and touch them, if he’s not there, then I don’t talk to him. Haha. Gotta cope somehow.

One other interesting symptom related to Parkinson’s is what’s known as freezing. And freezing has to do with the way in which we initiate movements. Your M1, your primary motor cortex, when you’re about to say move fingers of your right hand, your life primary motor cortex starts to discharge action potentials, sends little messages that there is some stuff that can be picked up by an EEG, before you send down the motor commands to the hand to contract the muscles, these are anticipatory commands. Basically they are saying, this is what we’re gonna do feelas, get ready. And then the command comes along. It slows stuff down a bit but keeps things orderly. Things get mixed up with those anticipatory messages that are being sent from the motor cortex. So what happens is a person will start to do something, getting up out of the chair, there is a series of movements with getting up out of a chair, you shift your center of gravity forward, you start using your leg extensors, as you shift gravity forwards so your legs extend under your body. If there is an arm on the chair you might get a little extra support. The person with Parkinson’s starts getting out of the chair and then kind of freezes in that position. Possibly for a minute or two. And then might start again and actually be able to get up. So this freezing is something to do, it seems, with the cortical activity involved in initiating movements. Now, when the initiation of movements, when the Parkinson’s gets extreme, when you’re really depleted of dopamine production in the substantia niagra, these people remain frozen. They can’t move. At all. And this is a very extreme advanced case of this. And hardly ever seen clinically until the 1960’s. Now what happened in the 1960’s with the drug culture that developed, more in San Francisco than anywhere else in the world. A bit of background… there’s the way the drug laws are written in the US, there is a list of drugs you can’t sell. You can’t go out on the street and sell heroin, or cocaine. And you can’t go out and sell certain hallucinogens. Well, there are also laws about possessing but that’s another story. But if you can synthesize in your basement lab something that isn’t on the list, you might start out with something on the list and modify the molecule a bit, then it’s legal until they make a law to make it illegal. You’re still selling drugs without a license, so you’re still in trouble, but not the big felony stuff. And a lot of basement chemists, you know in the hippie culture and all that, were coming up with custom drugs as hallucinogens or opiates that were not on the list of forbidden drugs, cuz there is a lot of profit there. And somebody came up with a thing called MPTP. It’s related to ecstasy but not quite. And they are selling it. And suddenly there were these young people who apparently were healthy in most other ways, were found totally paralyzed, unable to move. Apparently conscious, but trapped in their bodies unable to initiate any movement. And it turns out what happens is MPTP can cross the blood-brain barrier, so you take it orally or inject it directly into the blood stream, and it can cross the blood brain barrier. No electric charge on the molecule so it can get through. Once it crosses into the brain, it’s enzymatically converted into a slightly different molecule MPP+. I’m not going into the chemistry, even if I could remember the spelled out names of all of these. And this behaves like an amine. Now think of these dopamine neurons in the substantia niagra. They release dopamine under normal conditions. How is the activity of dopamine terminated? By reuptake, exactly. And the reuptake transporter that takes dopamine back into these cells, also takes MPP+ into the

cells. And once inside the cells, they kill the cell. It’s a suicide molecule. So people that take MPTP, it converts to MPP+ inside the brain and destroys dopamine neurons. So these people were going from healthy, and after one dose, going to very advanced Parkinson’s disease. Until it was finally figured out what was going on, there was nothing that could be done for them. Then, it was figured out what was going on, and that confirmed of course, our understanding the mechanisms of Parkinson’s, because, after all, these people had advanced Parkinson’s because they were unable to make dopamine in the substantia niagra. So that led to a treatment, it was the first time drug treatment based on the physiology of a disease was actually successful. What you want to do is replace the dopamine that these cells are not making. And what the initial thought would be, give them dopamine. NO, because dopamine has a charge so it won’t get across the blood-brain barrier so it stays in your peripheral system. It’s a vaso constrictor, it can raise your blood pressure through the roof. So what you do again is well, the precursor to dopamine is something called DOPA. Dihydroxy phenylalanine. Phenylalanine the amino acid- you know all your amino acids, right. You inject DOPA, which itself it electrically neural, so it gets across the blood- brain barrier into the brain where the normal synthetic enzyme, a decarboxylase, removes the carboxy group. Remember the amino acid has a carboxy acid part and the amino. One has a negative and the other has a positive charge so it cancels the charge so the DOPA can get across the blood-brain barrier. But then the decarboxy enzyme removes the carboxy group, leaving a charge on the amine, dopamine. And that sort of replaces the missing dopamine that would normally be coming to the caudate and putamen from the sub niagra. So it relieves the symptoms of Parkinson’s disease. The only problem is, if you just give DOPA in the periphery, there are peripheral decarboxylases that will change it into dopamine in the outside and raise the blood pressure, dangerously so. And only a fraction of the DOPA will actually cross the blood brain barrier, because a lot of it gets converted in the periphery. So you give a combination of DOPA and an inhibitor of the decarboxylase enzyme. And that way the DOPA stays DOPA in the periphery and more gets into the brain, the decarboxylase inhibitor doesn’t get into the brain, so it gets converted in the brain to dopamine and you have a fairly successful treatment of Parkinson’s. But over the long term, it develops side effects of its own. So, you administer this DOPA plus the decarboxylase inhibitor in the periphery to these young people that are paralyzed, and they are able to move. Wonderful. And of course they were then able to testify where they got this stuff, and what it was they took, and so on and so forth. And yes, a lot of these drugs, especially MPTP have been added to the illegal list, but there are always chemists out there that will try for another variant. We have, therefore, a treatment of Parkinson’s disease based on our understanding of the mechanism that produced it. There are occasionally people who develop this total immobility from a natural Parkinson’s disease that just happened and advanced very far. And of course the other problem with the treatment is it doesn’t stop the destruction of the dopamine neurons. So the disease is progressing despite your relieving the symptoms. And there is a point beyond which it doesn’t work that well because remember what you started out in the ideal case is a series of neurons with cell

bodies here sending axons here and releasing dopamine at the right time and right place. And now what you’re doing is taking a bucket of dopamine on the caudate and putamen. That’s not the ideal situation. So it’s not going to last forever and these people eventually become very treatment resistant. There was a book which was then made into a movie with… who was it… Robin Williams, called Awakenings, that dealt with discovering that these people could be woken up. Also if you digs a little bit, there was an episode of House where John was in that situation and House managed to wake him up with dopamine treatment. Anyway, so much for Parkinson’s’ disease. The other things that go wrong with the basal ganglia, we still don’t’ have a full understanding of what it is these nuclei are doing, and we don’t have a full understanding either of what the mechanisms are that are involved. We stumbled across this situation with Parkinson’s and we are very fortunate, but there are still, as Michael J fox will tell you, a lot of research even to be done in Parkinson’s. So progress is slow. Okay. That is, this is, with those basal ganglia, one of the extrapyramial pathways that modify the action of the motor cortex. Another extrapyramidal pathway involves the cerebellum. You know what it looks like, where it is. Dr. Jung went over the structure, the functions, the pedicles and all of that. And I’ll take care of that after a five minute break. Okay why don’t we get back to work. The other extrapyramidal set of pathways is the cerebellum. And the cerebellum, as you know, is sort of on the back of the brainstem behind brainstem and pons, and you have the various connections to the brainstem, and uh, inputs and outputs and whatnot. And if you were to look at the cerebellum, it sort of looks like this and there is a little fissure here that separates the anterior from posterior lobes. And tucked down in here is a third lobe called the flocculonodulus. But the separation into lobes of the anterior from the posterior, which make most of the cerebellum, is not a functional separation. Actually the functional separation is seen when you’re looking down onto the cerebellum. Here is your cerebellum as you’re looking at it, and here is the separation from anterior and posterior lobes, and the folcculonodulus is down here, it has little side wings going out. And but, functionally, the way it is divided is this way- medial versus lateral. The lateral portion, is referred to as the neocerebellum. The medial portion, with the exception of the center strip, so the medial portion here is referred to as the spinalcerebellum. And the flocculonodulus is referred to as the archicerebellum. And the point though is that the entire cortex of the cerebellum has essentially the same architecture that involves about seven different kinds of cells. And anywhere in the cerebellum you see the same sort of things. There is the surface, there is a cell body, which puts out enormous tree of dendrites. And sends an axon heading deep inward to the interior of the cerebellum. And these are known as purkinje cells. And the purkinje cells’ axons are the sole output pathway for the cortex of the cerebellum, so inputs come in by way of two other forms of cells, what are called climbing fibers and mossy fibers. And they synapse onto the purkinje cell. The only output from the cortex is by way of the axon of the Purkinje cell but it doesn’t leave the cerebellum entirely. What you instead

have is a set of deep nuclei that the Purkinje cell axon synapses onto. And their cells exit from the cerebellum going into the brainstem. And so what you’ve got here is a two stage pathway from the cerebellar cortex back into the brainstem. Now about this input of climbing fibers, mossy fibers, where are they coming from ultimately? Well they’re coming from the pons, but what you’ve got is, here is your motor cortex. Here is a cell, it’s sending its descending pathway, decussates at the medulla, so here’s the midline, right. And it goes on down to the muscle, the alpha motor neuron. It’s your upper motor neuron. But one of the things the upper motor neuron does is it sends a collateral fiber, a branch of the alpha motor neuron, into the pons where it synapses onto a neuron within the pons. And the pons sends this neuron out to the cerebellum. So just like the basal ganglia, the cerebellum is basically being CCed on all of the instructions going out from the cortex. But there is another factor involved with the cerebellum and that gets an additional input. And that is it gets an input from the periphery of the body from proprioceptive transducers. What’s a proprioceptive transducer? It tells you what’s going on in your body. It could be Golgi tendon organ or muscle spindles, other receptors in joints that indicate how much the joint is bent or straight. The proprioceptors enter the spinal cord. The proprioceptive sensory axons enter the spinal cord and ascend, same side of the midline because these are dorsal side senses, you know, touch and proprioception travel in the dorsal column pathways up to the gracilis and cuneate nuclei. Then they synapse here, and as you know, the postsynaptic cell, the second order neuron in any sensory pathway is always the one that cross the midline. So you have the sensory input going to the thalamus, and the thalamus sends information back to the cortex. That’s like any sensory pathway. But what happens here is from the thalamus, or from just before the thalamus another branch comes off, crosses over the pons and heads to the cerebellar cortex. So what have you got here now? Stuff originating in the right, assuming this person is facing you, this is right, and this is left. Material originating in the right cortex, which is controlling the left side of the body, the motor pathways decussate at the medulla and go down the left side of the spinal cord. That’s your anterolateral pathway. Now they send carbon copies by way of the pons into the right, into the left cerebellum. So the left cerebellum is getting information from the right cortex about what the right cortex is telling the muscles on the left side of the body to do. So left cerebellum is getting information about messages being sent to the left side muscles. On the sensory pathway, left side muscles send the sensory pathways from the proprioceptors up the dorsal columns, they crossover heading for the thalamus but then recross the midline to go to back to the left side cerebellum. So essentially the cerebellum is getting proprioceptive information from the left side of the body as well. So unlike any of the other circuits we have dealt with about, the cerebellum processes ipsilateral data with respect to the body. If you have problem controlling the left side of your body, the problem is with the left cerebellar lobes. Okay. Now what sort of processing does it do? Well, the neocerebelum, neo means new, it’s recent in evolution, we’ve got more of it than anyone else in town. Other primates have a lot but not as much as we do. And because it’s new. It’s neocerebellum.

And it’s involved in two categories of things. Precise movements, skilled movements. And also language. Because he neocerebellum, this is new stuff that older animals don’t necessarily have. So you have skilled movements and language. The medial portion here, except for the central portion which is called the vermis. Is referred to as the spinalcerebelum cuz it deals with the spinal cord, it deals with more proximal things, and it’s older. It’s sometimes called the paleocerebellum, as opposed to this the new one, paleo means old, like paleontology, and archi means first, or oldest. And basically what it does is it takes data that commands that you are sending down from your cortex telling this muscle to move, and it also gets data from the proprioceptors about where this particular joint, finger or hand is at the moment. And it makes corrections. Well you know your cortex may have though the hand is here, but it’s really here, so you want to modify the motion command exactly what you want to do under the circumstances. So the neocerebellum is needed for skilled movements because it enables your body to compare where you are now versus where you want to go, and calculate the best route to get there. Damage to the neocerebellum can cause a certain number of deficits. Lesion in the neocerebellum, and remember these are generally ipsilateral, same side of the body, effects. One, is probably best known, and also a good spelling bee word is Dysdiadochokinesia. Basically what it has to do is a defect in alternating movements. If you want to move your hand from here to here, and then back again, a normal person can do that. It doesn’t even require much attention once you get started. A problem a person with a lesion in the neocerebellum will have a difficulty doing that on that side. The other hand might be perfectly good. But if there is a lesion let’s say on the right cerebellum, he might actually have to think about moving his hand there and think about moving it back, and can’t do it therefore very fast because he has to think about it very fast. Another version of Dysdiadochokinesia is putting your hand palm down, palm up. Same thing. You could also test it with the feet with moving your feet between two spots. Oh, one thing I forgot to mention. I said output from the cortex is by way of purkinje fiber axons. But where do those purkinje axons go? They don’t leave the cerebellum, they go to deep nuclei embedded into the cerebellum. And these deep nuclei are specialized. That’s what I never quite got to. Deep nuclei. The largest of them are the dentate nuclei. And then there are two slightly smaller nuclei, the emboliform and the globosus. And then there is the fastigial. The neocerebellar cortex projects to the dentate. Those purkinje cells project to the dentate nucleus. The spinocerebellum purkinje cell axons project to the emboliform and the globosus. They kind of operate together. And the archicerebellum, that cortex projects to the fastigial nuclei. And cells arising, neuron arising with their cell bodies in these nuclei then exit the cerebellar structure, reenter the brainstem, and then of course they project back to M1 by way of the thalamus. To the thalamus and then M1 the way the basal ganglia did. Second problem with neocerebellar defect is what’s known as an intention tremor. Remember the Parkinson’s tremor is a different sort of tremor. It’s a tremor at rest, it disappears when you’re doing something and disappears in sleep. The intention tremor is, I’m planning to move my hand from here to here. Just as I’m anticipating moving my hand from here to there, I develop a tremor perpendicular to the path I’m going to take.

That‘s initiation tremor. An initial tremor. And then after I’ve moved my hand to here, when I stop, there might be another tremor at right angles to the path, called a terminal tremor. So you’ve got your intention tremor and terminal tremor. But they don’t exist at rest. Only when you’re anticipating or have just completed a voluntary movement. Third sign of a neocerebellar lesion is what’s called dysmetria. Sometimes called past-pointing. And in dysmetria what happens is this. I’m standing here, I can point up to the clock on the wall. I’m normal, I close my eyes and I can point to it again. Now here is the key. I turn slightly, my eyes are still closed, and I can point to the clock again. I got it right. That’s assuming my cerebellum is normal. There might not be anything else normal with me. But m cerebellum is okay. The person with a cerebellar lesion can point to the clock, close his eyes, point to the clock, no problem. But then he turns his body slightly and overcorrects for the turn of the body. If he turned this way, he’d be pointing off there. Overcorrecting. He’s pointing past the clock. Which is why it’s sometimes called past pointing. The ability to point to a clock isn’t going to get you far in this world. But where this type of skill is really useful is this. You’re taking a shower, you drop your soap. You’ve got soap in your eyes so you shower with your eyes closed. You’re looking for the soap where it dropped so you open your eyes for a fraction of a second and you get a glance of the floor and see the soap over there. So then you have to turn slightly, take a step, reach down and pick up the soap with your eyes still closed. And you’re able to do it. That’s because your cerebellum is working correctly. Just as I could turn partway and do all sorts of things and still point to the clock I can still point to the soap. Believe me, finding the soap when you’ve dropped it is more useful day to day than being able to point to a clock. It’s also useful, the cerebellum helps you in learning processes. Such, just as the Dysdiadochokinesia when your cerebellum is normal you can set up a program it keeps going and you don’t’ pay attention to it and you talk about something else and your hand keeps doing what it was doing. You also have over the course of your lives learned certain relatively simple procedures, like tying your shoe. Everybody has learned to tie his shoe once, and then that’s about it. You know how to tie your shoe, you don’t’ have to look at it, you don’t have to think about it. The person with a cerebellar lesion will have difficulty learning to tie the shoe. He’ll have to count off step by step the way a little kid does when he’s learning. Actually most people learn to tie their shoes twice in a lifetime. The first time you learned to tie your shoe, think back, you did left over right and left over right again and you ended up with a bow with loops going up and down. And then someone taught you that if you did left over right then right over left, you’d end up with a bow with the loops horizontal. So you learned to tie your shoes a second time. Something you have to learn twice in a lifetime. Alright. Those of you whose shoe bow loops are vertical have a way to go. Okay, the other thing is, as I said, the neocerebellum is involved in, besides skilled hand movements, with speech. And lesion in the neocerebellar cortex, or the deep nuclei, the dentate nuclei, can also lead to speech problems. Now speech is a bilateral thing. So essentially a lesion on either side can lead to a speech problem. And there are certain specific speech problems that occur. The main one with cerebellar lesions is what’s called scanning speech, also called telegraphic speech. The person with the

cerebellar lesion loses the normal rhythms of speaking when he says something each syllable has equal stress as each other syllable. A lesion in the spinocerebellum or in the emboliform or globosus nuclei, leads to problems with stance or gait. A person with a lesion in the medial or spinocerebellum will tend to stand with what’s called a broad based stance. His feet are further apart. And that’s accompanied by a broad based gate. Think john wayne. Now, which side, which spinocerebellum causes a lesion if your legs are further apart and your feet are further apart. You can’t tell which leg is apart just based on that. But a person walking with a broad based stance turns and walks in a different direction, he could either do this, or, he could do this, swinging the leg wide. And that indicates a right cerebellar lesion and the problem is with the right side of the body and right cerebellum. The other way to distinguish if a person has a spinocerebellar lesion is with the old myotatic reflex. In the normal leg, you hit the patellar tendon with a little hammer with a rubber triangular head and the foot kicks. And it just kicks and that’s it. If the person has a that-side cerebellar lesion, what you end up with is a pendullar myotatic reflex, as in a pendulum. It swings and continues to swing for a while. So you have your broad based stance, broad based gait, and pendullar myotatic reflex. What about the flocculonodulus? Well the flocculonodulus and the vermis which sort of work together, operate in conjunction with the vestibular system. What you’ve basically got here is sensory input here is coming from proprioceptors to the anterior and posterior lobes of the cerebellum. The sensory input from here is coming from here, and here. Cranial nerve eight. The vestibular portion. And somehow this sends feedback to the cranial nerve XII nuclei which have descending pathways to maintain extensor tone if you’re tilted or something and also go upward through CN nuclei VI, IV and III to regulate eye movements. And what happens is if you have a lesion in your flocculonodulus or vermis or vestibular nuclei, what happens is, if you try to stand on one foot with your eyes closed, you’ll fall over. Now, to be sure, a person who has a vestibular system lesion or an XIII nerve lesion in the vestibular portion, if he tries to stand on his right leg with his eyes closed, he will feel dizzy and will likely fall. Even if he is standing up straight he will feel like he’s falling. The person with a lesion in the f or vermis, doesn’t feel like he’s falling. He feels fine. That’s how you distinguish them. You ask after he falls, you ask if he felt dizzy. If he says no, it’s the cerebellum, if he says no, it’s the vestibular system. Now, to be sure, you would think that while he was falling, his vestibular system would tell him that he was falling. But he doesn’t get that dizziness sensation, this vertigo, with the flocculonodular or festigial nucleus lesion, so what happens is the first real information that he gets is when his shoulder hits the floor. And his reaction is, I must have fallen. So you’ve got a sort of question-answer way of distinguishing where the lesion is in terms of the vestibular system versus the cerebellum when a person just falls over. Okay. Now actually I’m done a bit early, but it was fun. And the fun is really beginning now, Monday, Organ systems starts! Haha. I mean this course is not over at this point right now, you still have a quiz, midterm and final. But organ systems starts Monday

unless there is 8 or 9 or 12 inches of snow on the ground on Monday AND the university decides to close. Because last time that happened the university didn’t decide to close but later in the day they decided to close early when the weather was fine. Remember that? Didn’t make any sense at all. It required all the shuffling around and rescheduling of lectures because I wasn’t able to get in on that day and I actually had six hours of lecture on that day. And so you gain a little you lose a little and they were all made up. But the first lectures for Organ systems start on Monday if the university is open. I have contingency plans incase Monday is a snow day and the university is closed. Which we won’t likely know about until 6 am the earliest. I have complained to the dean about this, he complained to the people at the square but nothing happens. At least they tell us at 6 instead of 8 or 10. So bottom line- if Monday is closed, the Monday lecture will be on Tuesday. We have make up sessions scheduled for septodont on Wednesday to make up the thing, so WATCH YOUR EMAIL.

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