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Hi, everyone. Good evening. Uh My name is Anushka and I'm the preclinical lead for be a this year. So today we have an amazing neurology lecture on motor control and movement disorders um by Trisha who is indicating at the moment in cardiovascular sciences in Imperial, but is originally from B UNI. So I will hand over in a minute but just quickly a few announcements for the people who are watching. Uh So firstly, guys, if you have any questions, make sure you put them in the chart and Trisha or myself can answer them throughout the uh lecture. Um as well as that, make sure that you um fill in the feedback form at the end as that will ensure that you get your certificate at the end of your attendance. And just a reminder, guys, we have these preclinical lectures every Tuesday and every Thursday at 7 p.m. Ok. So I'll pass on to Tricia now. Uh Hi, everyone. Um So yeah, my name is Trisha and welcome to I believe the third um neurology talk in the Preclinical Series. Uh So today I'm gonna be talking to you guys about motor control and movement disorders Um So just a bit about myself first, like as uh I introduced, I'm a medical student from Brighton Sussex Medical School and I'm in intercalating between my 3rd and 4th year. Um And currently I'm doing a BSC in Cardiovascular Sciences at Imperial, I've sort of split the lecture into three sections. Um So the first section we'll be covering is motor control and just going through a basic overview, I'm gonna be talking about the mo motor cortex and the descending pathways. And then we'll look at the basal ganglia and the cerebellum as kind of additional structures that help in motor control. And then we'll go through some key um movement disorders and then we'll end with some S PA S. Uh I've also um and included within the talk and sds as well that hopefully you'll be able to join uh through miter. OK. So covering how to control the basics. So if you guys can actually join Miter right now um with the QR code um and oh with that code there, and I'll just start presenting the, the first question and just let me know if um there's a problem joining it with the chat. OK. Can anyone can, can anyone join the beer? OK. If not, then can you guys just type in the chat? OK. OK. I can see some responses now. OK. OK. Wait a couple more seconds. OK. Yeah. So the multi cortex is actually located within the frontal lobe Um So I think uh some you answered correctly. OK. So moving on um talking about the motor cortex. Um so the motor cortex is an area within the frontal lobe that controls voluntary movement and it can be further split up anatomically and functionally into three areas. So there's a primary motor cortex which is known, also known as a precentral gyrus uh which you can see with this um on the image uh towards the uh towards the left hand side, you can see that blue strip and that's a motor cortex. And then I've also labeled on this diagram, the black line which is a central sulcus. Um And then the motor cortex is further split up into three functional areas. So you've got the primary motor cortex which is kind of a red strip. And then you've got the premotor cortex and you've got the supplementary motor area. So the primary motor cortex um is involved in movement execution and is the origin of the upper motor neurons, which I'll talk about more when talking about the descending pathways. And then you have the premotor cortex. Uh so that light blue strip in the diagram and that assists the primary motor cortex to plan and carry out voluntary movement. It also stores information about past activity and integrates sensory information to help plan future voluntary movements. Um So when executing um motor movements, you also get uh signals from the uh somatosensory cortex which is located in the parietal wall. Um, and then you've got a supplementary motor cortex, uh which is, uh which carries out. Um. Ok. Um Can you? Ok. I don't know. How can you hear me clearly now? Yeah. Um, hopefully you can hear me through now. I'll just, I'll try and speak up a bit uh, if that helps. Um, but yeah, if it, if it gets too bad, just let me know again. Uh ok. I don't know if I can change my brows in now. Um OK. Um OK. So carrying on, so the supplementary motor cortex um carries out complex sequence of movements and it actually can carry out bilateral movements. So it coordinates uh two sides of the body. OK. So then in terms of the primary motor cortex again, OK. Uh Yeah. So carry on about the primary motor cortex. So it's arranged in a way that activating different parts of it correlates to movement in muscles of different areas of the body. So that map is known as a bonus and you can see an image of it here. OK. Um So the map presents also the degree of control that the primary motor cortex has on muscles in different parts of the body. So for example, from this image here, we can see that the hands uh occupy more space um or, or a bigger area of the motor cortex. And for example, the lower limbs. So that just shows that the primary motor cortex has more control over movement in hands and fingers than uh your lower limbs. OK. And yeah, I would say that this is, this uh becomes clinically important. For example, if you have a stroke, um and if you have a more like medial lesion or a more lateral lesion, then you can kind of tell uh which body parts gonna be affected more. Uh But we'll come on to that when I start talking about movement disorders. OK. So now um uh the arrangement of descending motor pathways. So um the motor signals are transmitted from the motor cortex to the appropriate muscles uh directly or indirectly in descending pathways. And what I mean by indirectly is that they go through accessory pathways such as the basal ganglia. Um OK. And I'm going to look at um uh direct pathways now. OK. So there's two types, there's pyramidal and extrapyramidal. We're gonna come on to the main pyramidal one on the next slide, but I'm just gonna briefly talk you through extrapyramidal pathways. So, the difference between the two is that extrapyramidal pathways do not pass through the med uh the pyramids of the medulla and they control groups of muscles. So, for example, flexor or extensor, as opposed to the pyramidal pathways that will um control um a single muscle. Um And another key difference between pyramidal and extrapyramidal pathways is that they do not directly innervate the lower motor neurons like the pyramidal tract, but instead they target interneurons within the spinal cord that then can either excite or inhibit lower motor neurons. Um So, pathology within these extrapyramidal uh pathways actually leads to movement disorders. And you've got three main ones which you can see in the um in the images that I put below. Uh So the first one that I'll talk about is the rubral spinal tract. So in terms of the anatomy, you don't really need to know the like everything about it. But I would say as long as you know the function of it and where the tract originates, which you can understand if you um learn the name. Uh So talking about the rubrospinal tract first. So rubra refers to red. Um So it just means that it starts in the red nucleus which is a nucleus within the midbrain. OK. And then um the motor neuron will project down to uh interneurons within the spinal cord. And the function of the rubrospinal tract is um execution of voluntary movements. And then you've got the lateral vestibular spinal. OK. Sorry. Do you have a question? Um OK. Let me OK. I'll carry on and if you have a question, just type it in fully. Uh OK. So the lateral vestibulospinal tract. So this originates from the vestibular nucleus. So that's located within OK. Is this sound really interfering for other people as well or is it just um is it just you? OK. OK. Is that better or is that still as bad. OK. Um Let me just see if I can actually change to a different browser. I'll give you one. OK. Can people see my slides now? Ok. Hopefully that works better now. Uh Sorry, I'm just gonna go back to where I was. OK. So yeah, the extrapyramidal pathways. Um OK. So yeah, talking about the rubrospinal tract again. Um So rubber is red. Um like it means red. So you can guess that the rubrospinal tract starts in the red nucleus which is just a nucleus uh within the midbrain. Um And its function is to control um voluntary movements. And then you've got the lateral vestibular spinal tract. So the lateral vestibular spinal tract starts within the uh vestibular nucleus, which is located within the inner ear, uh uh the vestibular apparatus um which projects neurons onto the lateral vestibular nucleus within the medulla. And then uh those uh neurons will project down to interneurons within the spinal cord and that um controls ba balance and posture. So you can kind of um guess that anything to do with the vestibular apparatus is to do with balance. So you can kind of with the name, you can kind of guess the function. Um and then you've got the reticulospinal tract. So the reticulospinal tract can be uh split up into two again. So you've got the medial and the lateral er the medial reticular um formation is located within the pons and then the lateral reticular formation is located within the medulla. And these tracks work uh to control posture, movement and uh automatic movements. For example, um the movement of the intercostal muscles for breathing. Um OK. Uh So then moving on, I'm gonna talk about now, the main pyramidal tract. So the main pyramidal tract you need to remember is the corticospinal tract. So this is the only one that I would kind of remember the neuroanatomy for. Um So the function of the corticospinal tract is it sends signals to carry out voluntary movements. And the key concept that you need to get is that pathway consists of two neurons. So, in the diagram below, um the one that shows like the brain, uh you can see that there's a, there's two neurons, one is an upper motor neuron that originates within the motor cortex and then that synapses onto a lower motor neuron which then will innervate your muscle. And just as a question, um if you guys can uh answer where the lower motor neurons exit the spinal cord, just type it in the chat. Sure. So where the lower motor neurons leave the spinal cord? I'll just give people a minute to answer. Yeah, exactly. So they exit the spinal cord via the anterior horn and then following on from that, where do you think that the sensory neurons then exit the spinal cord? Ok. Um OK, I'll answer the question then. Um so the sensory neurons uh exit via the dorsal horn. Um So in terms of your spine, this, this is just a brief overview. So just in terms of your uh spinal cord arrangement, you have your um you have your motor neurons located anteriorly and then you have your sensory um kind of pathways located uh posteriorly. And the way that I used to remember it is uh with an acronym, same Dave. So if you think that same, so s is for sensory and A is for afferent. So sensory information goes towards the C NS and then you've your motor information which is efferent. So it goes away from the C NS and then um dorsal is afferent. So your sensory information is uh dorsally located and then you've got your er efferent information, which is your motor information, which is ventrally located and if that would help anyone, but that's a way that I used to remember it. Um Yeah. OK. So now talking about the pathway of the neuron. So you can see in the image here. So you've got your upper motor neuron which is locate, which is originating within your motor cortex and that's gonna travel down the internal capsule to reach the brainstem. And here the neurons uh form the pyramids of the medulla. So if I go back a slide just so um you know what I'm exactly talking about. So you can see er in the image here, the, the red circular bit is the pyramid, OK. Of the medulla. And that's where your uh upper motor neurons originating, originating from your motor cortex will pass through. OK. Um So at this level, 90% of your motor neurons cross over. Um and they form the lateral cortical spinal tract, but 10% of the upper motor neurons don't cross over and carry on as it is. And they form the anterior cortical spinal tract within the spinal cord. So I've just included an image of that here. So um you can see the spinal cord and I've just labeled uh the anterior columns and then the lateral columns, er the anterior columns actually control trunk muscle, er and the lateral columns control your limb muscles. Um OK. And so then as we mentioned earlier, the lower motor neurons then just exit the spinal cord through the anterior horn and go innovate the muscles. Um It's also important to note that the um so the fibers that um the the anterior corticospinal tract fibers, they do cross over but they just cross over in the spinal cord as oppo as opposed to uh crossing over in the medullar, like the lateral corticospinal tract fibers do. OK. Um OK. So now I'm gonna talk about the basal ganglia. Um So just as definition, the basal ganglia is a group of subcortical nuclei. So just basically means that they are located underneath the cortex and they work in association with the cerebral cortex to filter out action plans and um help choose uh the right action to be performed and they also help with the execution of smooth muscle movements. Um So this um flow chart here is a very um simple diagram of how this happens. So you get signals from the uh cerebral cortex going to the basal ganglia via two pathways which I'm gonna talk about um regarding the physiology in the next slide. Um So then the information goes from the cerebral cortex to the basal ganglia and then that projects onto the thalamus and then the thalamus will then either inhibit or excite the cerebral cortex for the action to take place. And we look at the pathways uh in the next slide. OK. So I've just included this um picture here to show you the neuroanatomy. So in terms of structures that actually make up the basal ganglia, uh these include the cordate nucleus, er the putamen and then you've got the Globus Pallidus, Internus, internal and external. And then you've got your subthalamic nuclei and then you've got your substantia nigra, which can be split up into two parts. You've got your pars compactor and then your pars reticulata. Um You really need to remember the pars compactor because that plays an important role in Parkinson's disease, which we'll come on to in a second. Uh But yeah, so that's just a coronal slice of the brain. And then the top image um shows like a sagittal image. So you can see that the cordate nucleus actually forms a, a kind of ac shape um thing. So that's, that helps with remembering um the name. OK. Uh Sometimes the terminology for the basal ganglia can get a little bit confusing because like different textbooks start using different things. Um But basically, uh when anything refers to the striatum, it just basically means a cordate and the putamen. Um and just as a question for you guys, can anyone um tell me what, what's the name given for? Uh the structures? Puterine, uh Globus Pallidus, Internus and Externus. Like, what are they collectively known as if anyone can type it in the chat and I'll give you guys a minute. Mhm OK. Uh I'll rephrase the question. Um So what's the name given for the structures like collectively Putamen Globus Pallidus, Internus and Globus Pallidus externus? OK. Um OK. So it's not the striatum, it's actually the lentiform nucleus. So the striatum is just the chordate and the puterine together and then the Puterine, the Globus Pallidus, Internus and Globus Pallidus externus um are known as the lentiform nucleus. So, um yeah, if that's clear, OK, I'm going to move on now. Um OK. So this is another menter question. So hopefully you guys have already joined and if you can answer uh that question. OK. So what's the main uh excitatory neurotransmitter in the C NS? OK. Yeah. So it's glutamate. That's fine. OK. Um OK. So now I'm gonna talk about the physiology of the basal ganglia. Um OK. So there's two pathways that you need to remember uh really the indirect and direct pathway. So the direct pathway can also be known as a go pathway and that facilitates movements. And then you've got your indirect pathway which is your no go pathway which uh stops movements from happening. Um So talking through the uh direct pathway first. So I just want you to ignore. Yeah. OK. Uh So I just want you to ignore the um like the, the part on the diagram that says the substantia Niagra pars compactor as of yet as of now. And then I'll come to it in a second. Um So just uh going over like some key things, um the main excitatory neurotransmitter is glutamate, which I guys asked, which I asked you guys in the last question. And then Gabaa is your main inhibitory uh neurotransmitter. And then you have dopamine which is released from substantia Niagra pars compactor. But I'll come on to how that affects the actual pathways in a second. So in terms of your direct pathway, um the motor cortex, uh so the cerebral cortex sends excitatory signals to the striatum. OK. And just so I know that you guys are like listening. Uh Can anyone type in the chat again of what uh what structures the striatum consists of? So what two structures make up the striatum? Yeah. So it's um yeah, that's correct. So it's a cordate and the putamen. OK. Um So the cerebral cortex sends excitatory signals to the striatum and then the striatum sends inhibitory signals to the globus pallidus internus and uh the substantia nigra and both of er those structures then send um uh send inhibitory signals to the thalamus and, and what that happened and what uh that causes is di dis inhibition of the thalamus. So then excitatory signals are eventually sent to the cerebral cortex. Ok. So I think that's a key thing that uh people struggle to get their head around. But what you need to remember is that um the direct pathway eventually just causes disinhibition of the thalamus. So overall, you're going to get excitatory signals sent to the cerebral cortex. OK. Um So hopefully, when we go through the indirect pathway, um it'll become a bit more clear. Um So, in terms of your indirect pathway, again, your cerebral cortex is going to send excitatory signals to the striatum which is formed of your cordate and your Putamen and then your striatum is gonna send inhibitory signals to the Globus Pallidus externus this time because it's the indirect pathway. So it's um it's a longer pathway. Um And then you are going to get um the Globus Pallidus externus sending inhibitory signals to the subthalamic nuclei. So, in this diagram, I just want you to ignore the black crosses. Um Now, because I'll go over that th those become more relevant when I talk about dopamine. Uh But yeah, so you just basically get um inhibitory signals sent from the Globus Pallidus externus, the subthalamic nuclei and then the subthalamic um nuclei is are going to send um excitatory signals to the Globus Pallidus Internus and the substantia nigra, which is gonna inhibit your thalamus. And then um you're gonna get inhibitory signals sent uh from the thalamus to the motor cortex which is gonna result in inhibition of um uh movement. OK. Uh Does anyone have any questions about that? Because I understand that they like the pathways can get quite confusing to understand. Uh So, before I move on, uh if you guys wanna ask anything or you guys want me to repeat anything, then I can try my best to do that. OK. Um So OK. Um Yeah, the feedback form will come towards the end. I think. So when you, yeah, when the lectures finished, then you'll get the feedback form. OK. Um So coming to how dopamine plays a role. So I think the key thing that you need to remember is that dopamine causes an activation of the direct pathway and it'll inhibit the indirect pathway. So in the presence of dopamine, there's going to be more movement. OK? And lack of it in diseases such as Parkinson's disease um will cause less movement because you'll get more activation of the indirect pathway. OK. Uh So moving on. OK. So now I'm gonna talk about the cerebellum. So the cerebellum is an additional brain structure that helps with your motor control. Uh So the main functions are coordination of movement, control of posture and balance and fine motor movement as well. It also plays a role in motor learning, uh which I won't be covering in this lecture because um that's, that's a different concept. Er But hopefully you guys will cover it in your lectures uh in uni. So anatomically, the cerebellum can be split up into two hemispheres which is separated by a vermis, the central structure of the vermis, which you can see um in the green and purple diagrams on the slides. Um and then just like the normal brain, the cerebellum also has lobes. So you've got the posterior lobe in green, you've got an anterior lobe in purple and then you've got your floccular nodular lobe in um orange. OK. And then you've got um like more like flattened version of your cerebellum here, which is showing your vermis as well and then your two hemispheres. Um So the cerebellum is split up into different functional zones as well because it receives uh different areas of the cerebellum, receive inputs uh from different uh areas of the body. Um So, basically, in this bluish diagram down here, you can see that the vermis um forms um receives signals from signals from the spinal cord and it forms a tract knows known as a spinal cerebellar tract and that controls movement of the trunk muscles. And then you've got your two he uh two hemispheres uh which form uh this the cerebral cerebellar tract. So they receive information or inputs from the cerebral cortex and um they control planning and movement especially um of the of the limbs. Ok. Um So that was just a quick overview of the cerebellum. And then we're gonna move on now to the second part of the lecture, which is movement disorders. Uh So I thought uh it's really important especially in preclinical years to understand the differentiation between upper motor and uh lower motor neuron lesions. So I'm just gonna cover that quickly. And then I'm also going to talk about um some examples of what causes upper motor neuron and low motor neuron lesions. So upper motor neuron lesion occurs when you have pathology um anywhere within the cerebral hemisphere or any pathology affecting the motor neuron um traveling from the cerebral hemisphere to the anterior horn of the spinal cord because that's the upper motor neuron. OK. So, in terms of then uh clinical signs, you get hypertonia with uh upper motor neuron lesions and you get um spasticity. Um So spasticity is velocity dependent uh hypertonia in uh meaning that the faster you move a limb, uh the worse the tone gets. Ok. Uh Then in terms of your power, you're going to have um reduced power overall, but it affects the upper limb extensors more than the lower limb flexor. OK. So that's just a pattern of uh upper motor neuron weakness. OK? That you guys uh need to learn. And then in terms of your reflexes, you get hyperreflexia. So you get more brisk reflexes. So when you do your neuro exam um and doing your patella tap, for example, um you get more, yeah, like you just get faster reflexes. Um And then in terms of your babinski reflex, um there's an upward going or what we call an extensor babinski response. And I've included an image here just to sh uh just to show uh what that would look like. You don't get muscle wasting predominantly in upper motor neuron lesion as compared to lower motor neuron lesion. And you also don't get fasciculations. Uh then in terms of your lower motor neurons. So this occurs when the lesion is uh anywhere between your anterior horn cell to the relevant muscle that that nerve is innervating. And in terms of tone, you're gonna get hypotonia and you're gonna get a flaccid tone. OK. In terms of power, your power again is gonna be reduced. Um And in this time, instead of it affecting your upper limb extensors and lower limb flexor more, it's gonna be in the distribution of the affected motor root or nerve. In terms of reflexes. Um Y you're gonna get uh low like hyporeflexia as opposed to hyporeflexia. Your babinski reflex is gonna be normal in low motor neuron lesions. You will have um more muscle wasting uh with low motor neuron lesions. And this time you also get fasciculations. So, fasciculations are visible involuntary twitching of individual muscles and that you might come across um when you're doing, for example, a neuro exam, uh when you go to the wards, OK. So in terms of some pathologies that can cause uh upper motor neuron lesions, you've got a stroke and then you've got motor neuron disease, which I'm going to touch on briefly. Um So, before I move on and talk about strokes, does anyone know uh what the two major classifications of strokes are? So, if you guys can just type in the chat again, uh what the two major um classifications of them are. Yeah, that's correct. Um So you have an ischemic, you have ischemic strokes and you have hemorrhagic strokes. So that helps explain your pathology. Um So, in terms, so just uh summarizing strokes. So, ischemic strokes is uh an ischemic stroke is basically when you have an occlusion of the blood vessel and that accounts for 85% of your strokes. Um and that can be due to an emboli uh thrombus or dissection um of the vessel. And then you get hemorrhagic strokes which account for 15% of uh the strokes. And that just means that there's some sort of bleeding occurring from the vessel uh into your tissues. So, I've also included in a diagram here that shows the uh territories of the uh circulation. Um So you've got your posterior cerebral artery and if there's an infarct, then which part of the brain um that's gonna affect and then your middle cerebral artery is gonna affect more the lateral hemispheres of your uh brain. And then you've got your anterior cerebral artery which is gonna affect the more uh medial and frontal parts of the brain. And then um in terms of like, especially when you're in clinical years, that's important because uh it, it varies on how like the, the clinical manifestation of the stroke. Uh But yeah. Ok. So in terms of epidemiology, there are around 100 and 10,000 cases each year and it can cause um 11% mortality. And in terms of the investigations that you need to do when you have a stroke. So you would need to do a noncontrast ct head or a CT angiogram, you would do an ECG just to check for um other pathology and causes. So, for example, if the patient has underlying af um et cetera and then you would do uh bloods to check for risk factors as well. So you would check for things like high cholesterol, uh diabetes, diabe diabetes control with H B1 AC. Um uh Yeah. Ok. And also you would uh check for some stroke mimics, but that's more clinical. So I won't touch on that. Ok. So then in terms of your management, you've got uh different options for whether your stroke is ischemic or hemorrhagic. So, um ischemic stroke, you need to uh stabilize the patient using conservative measures. So you kind of your at e assessment and then you would use um antiplatelets, you would only offer the patient thrombolysis if uh the patient presents within less than 4.5 hours of symptom onset and you would exclude hemorrhagic stroke. Um And then for hemorrhagic, you would kind of stop your anticoagulation. Um And you would um escalate the case to a neurosurgeon. Um ok. So in terms of complications that you can get from strokes, you can get a DVT um in your recovery phase because of the immobility, you can get aspiration pneumonia because um because you can get dysphasia because uh because of the lack of uh blood supply to the neurons that control um your swa the muscles of when you swallow, uh you can get weakness and impaired mobility and seizures. You can get depression because obviously, you can imagine living after a stroke can be quite stressful for a patient as well. Um You, they need nutritional support, especially uh if their swallowing is gonna be weak and the prognosis generally depends on the type of stroke. Ok. So I'm just gonna touch briefly on motor neuron disease as well. Uh So, motor neurone disease uh is a neurodegenerative disorder and it can affect both your upper motor and lower motor neurons. Um It's a selective loss of the neurons in the motor cortex. Uh and it can affect cranial nerve nuclei and anterior horn cells as well. But motor neuron disease never affects eye movements, senses or your spinsters. So there are different types of motor neuron disease. And the most common one is amyotrophic lateral sclerosis. So I'll just uh talk through this briefly. Um And then yeah, I'll just put the rest on there for own revision purposes. Sorry, I forgot to change the card. Yeah. Ok. Um Yeah. So amnio TriC lateral sclerosis uh accounts for 50% of your motor neuron disease and it affects your upper motor neurons and your lower motor neuron. So it affects uh so it presents with both uh upper motor neuron, low motor, lower motor neuron signs, which we went through uh in the slides before. So in terms of epidemiology, it uh affects people above 40 it can affect 4 to 5 people in 100,000. So in terms of your investigation, it's majorly a clinical diagnosis, but you can uh do other things such as nerve conduction studies or MRI of spines to uh an MRI of the spine to rule out other pathology. Uh Because if you could imagine that if you have anything impinging your nerve um coming out your spine, then you also get lower motor neuron syndrome. So you need to rule out that as a differential diagnosis. Um and in terms of your prognosis and complications, you have a short lifespan. Most people die actually due to respiratory failure and uh then generally depends on the subtype for your prognosis. So I think uh that progressive bulbar palsy actually has a much worse prognosis than the other uh types of uh motor neuron disease. Um Yeah, you have a poor respiratory function. Um then you, you, you have worse uh prognostic factors and you can get uh complications such as aspiration pneumonia, bronchial pneumonia and respiratory failure. Ok. So then coming on to uh lower motor neuron lesions. So some causes can include things like trauma or um A LS. So you are amyotrophic lateral sclerosis. So, in this slide, I've just included um two different types of syndromes that can occur with low motor neuron lesion. So you can get anterior cord syndrome. Um um OK. Uh Sorry. Can, can anyone see my slides? Ok. OK. That's fine then. Um OK. So I'll carry on then. Um Yeah. So you can get uh so with low motor neuron lesions, it can present as different um syndromes. So you can get anterior cord syndrome, uh which which would result in loss of motor function below that level. Um And then you get a Brown Sicard syndrome which causes uh which is basically a hem of the spinal cord and you'll get unilateral spastic paralysis. You'll get spastic paralysis because your upper motor neuron uh will be affected because you're still within the spinal cord. Um Yeah. Ok. And then they also uh those two syndromes also present as um different uh sensory symptoms, but I won't touch on that because of time and because we're talking about motor control. OK. Um So this is another question you can, yeah, you can either join on ment meter or you can just like type the answer in the chat to be honest. Um So which of the following clinical findings are typically associated with upper motor neuron lesions as opposed to low motor neuron lesions. And then you've got those options there. OK. Yeah. OK. Yeah, that's correct. Uh So you get hyperreflexia and spasticity with um upper motor neuron lesions. The rest of the signs are associated with uh low motor neuron lesions. Ok. Cool. Uh So then coming on to basal ganglia movement disorders. Uh So I've split back up into hypokinetic and hyperkinetic. So your main uh hypokinetic um movement disorders are Parkinson's disease and Parkinsonism. So, Parkinsonism is basically you get the um you get the triad, which I'll talk about in a second, but it's not because of like Parkinson's disease. Uh There's different causes that can cause those uh symptoms like low body dementia. Um There's vascular causes, there's also some drugs uh like uh neuroleptics or met uh metoclopramide, which is an antiemetic and then you have your hyperkinetic movement disorders, um like hemiballismus, kaya and then ticks, which I'll talk about. Um So I would say in terms of like diseases you kind of need to know Parkinson's disease. I would say the most, uh especially in preclinical, you don't focus on diseases much, but in uh especially with the pathophysiology. Um So it's again, a neurodegenerative disorder and you get a loss of dopaminergic neurons in the substantia agra pars compactor. So you might be asked that question um in your end of your knowledge tests. Um and it's etiology is idiopathic. They think that we think there might be a genetic involvement, but we're not um e exactly sure. Uh in terms of your histology, what you see is, oh Sorry for you. Yeah. Uh So in terms of your histology, what you see um is uh inclusion bodies. So what inclusion bodies are, are basically misfolded um alpha sle uh proteins um within the substantia nigra pa compactor. So basically, yeah, you get a lot of dopaminergic neurons because of that misfolded protein and that image there uh just basic, basically shows um the histology of the disease. Um So Parkinsonism refers to um uh this like this set of um symptoms. So you get bradykinesia, you get tremors. Um Can anyone tell me what type of tremor that you get with Parkinson's disease if you can just type it in the chat? Yeah. So you get a resting tremor. Do you know what specific type of like what the resting tremor is called specifically? So there's like there's a specific name for it or what? Yeah. Yeah. So it's a pill rolling tremor. Um And what you get with Parkinson's. Um and you can also get a postural instability. So that image there is just like in terms of your own revision, you can go through it and it will just, it helps you with the symptoms that you get. Um, ok, so in terms of your epidemiology, it mainly affects uh elderly patients and investigations wise you, it's a Parkinson's disease is mostly a clinical diagnosis. You can do um MRI brain scans, but that doesn't diagnose Parkinson's disease. And you can also do something that's uh more like recent technology, which is a dopamine uh uptake scan. So it will show uh how much uh dopamine is like dopamine uptake, there is in the basal ganglia and obviously, with someone with Parkinson's disease that will be reduced. So, in terms of management, the key thing that you need to remember is that you give uh levodopa. Um does anyone know why we give levodopa in do in Parkinson's disease instead of giving um dopamine um by itself? So why you give Levodopa instead of giving, just dopamine? And does anyone know what levodopa is? Um ok. Uh So I'll OK, I'll answer the question. So leave it. Yeah. Yeah. So, exactly. So uh levodopa is given. So, Levodopa is uh dopamines precursor. Um and we give levodopa because it can cross the blood brain barrier, um which dopamine wouldn't. Uh we also give it with a decarboxylase inhibitor. Um, so that um, it's not broken down in, outside the C NS. Ok. Um, and there are other classes of medications that you can give. So you can give dopamine agonists, uh like uh ropinirole and you can give monoamine oxidase inhibitors. Um Does anyone know um, why we can give monoamine oxidase inhibitors? Does anyone know like why we would use that class of drugs uh to treat Parkinson's disease? Ok. Um So you, you can use monoamine um oxidase inhibitors because um that's the enzyme that breaks down dopamine within the synaptic cleft. So, if you inhibit monoamine monoamine oxidase, then you won't get dopamine broken down. Ok. Uh OK. Hopefully. Um I explain that now. Um OK. So in terms of non pharmacological treatment, um you can also do something known as uh deep brain stimulation and that would and targeting subthalamic nuclei. Uh that's also a way to treat Parkinson's disease as well. Um So in terms of the prognosis and complications, it's a chronic and progressive disease. So, the key thing is that there's no cure to Parkinson's. Um you just kind of, it's, it's all supportive treatment, the life expectancy of the patient is definitely reduced and you also have an increased risk of dementia. Um Yeah, which you will probably see again when you go into the wards. Um So now in terms of uh uh hyperkinetic movement disorders, I'm just gonna touch on these briefly because it is like nearing eight o'clock. Um But we only have a little bit left. Um So, um you get, there's something called hemiballismus. So I've included youtube links as well. So when you guys fill out the feedback forms and get slides, um you can have a look uh at how, what, what these um movement disorders actually look like. So the definition of hemiballismus is sudden flailing movements of an entire limb and the most common cause of this is a lesion in the subthalamus and mo and it's most commonly caused by a stroke. Um, that you can also, you pro all of you have probably heard of uh ticks and it's basically a brief uh stereotype, repeated movements. And patients with Tourette's syndrome have both motor and vocal tics and uh ticks are also associated with co mor morbid conditions. And then you have uh ka movements. So these are defined as jerky brief, irregular contractions and they're not repetitive or rhythmic, but they um flow rhythmically. So it's, it's meant to be dance like, but you know, you can watch the video and see like, see, um, in terms of the pathophysiology, um multiple small lesions in the putamen is the most common cause. Um, another cause is Huntington's disease, which you probably need to remember the uh the genetics of because that can be a question that comes up in your end of year exams. So, Huntington's disease is an autosomal dominant condition and it's caused by a trinucleotide repeat. It's the, the trinucleotide is CG and that results in degeneration of cholinergic and uh, gabaergic er neurons. And that's er, because of an a defect in the Huntington gene on chromosome number four. Ok. Uh, so now moving on to cerebellar lesions. So I'm just gonna go through this again quite briefly. Um, so, so again, yeah, this, uh, we went through the cerebellum. So the main um, symptoms that you need to remember which occur with cerebellar lesions. So, the cerebellar syndrome um can be remembered via the Pneumonic Danish. So, dyskinesia which refers to the inability to perform rapid alternative movements. You get ataxia. So you can see uh the image in the middle which is showing uh somebody who has broad based gait. Um Yeah. And then you get nystagmus which is problems with your eyes. Uh you can get an intention tremor. So an intention tremor uh occurs when um so, for example, uh if you ask uh in a neuro neuro exam, uh somebody to touch uh their nose and then touch your index finger. If the pa if the patient's finger starts shaking uh towards uh whilst touching your finger, that's known as an intention tremor. And then you can also get slurred and stick out a speech and you can also get hypotonia and some causes can include um stroke. So that will be in the posterior circulation. You can get space occupying lesions, um infections and metabolic causes can all cause cerebellar lesions? Um OK. So just answer the question, what's the difference between resting and intention tremors? So, intention tremors occur when like I explained. So for example, you're, you're doing some things. So you're reaching for a cup and then the patient's hands start shaking whilst like just as reaching for the cup, that will be the intention tremor. Uh A resting tremor would be um in Parkinson's, for example, a pill rolling tremor. So they're doing nothing. They're just sat there and the tremor happens. And I also think that when they then do an action, the tremor goes away. So does that make it clear, do not understand the difference between them? Um OK. So essential tremors, um Essential tremors are kind of like a genetic uh I think they have genetic diseases. Um And basically, um it can cause involuntary arrhythmic shaking. Um And it can occur when doing um simple tasks like drinking from your glass or tying your shoe. They say. So I think the key difference is the timing that the Yeah. Yeah, of course, I also get confused. Um So don't worry. Um Yeah, so I think it's just the timing that they occur. So resting doesn't occur when, but when, when you're just sat there, it occurs, an intention tremor is towards like uh when you're reaching for something and towards the end of the movement. Um and then essential tremor would kind of occur when you're doing an action if that kind of makes sense. Hopefully, that was clear. Um OK, so now we're on to the third part of the lecture. Uh So I just included some more um SBA S for you guys to practice your exam technique and hopefully, um you guys have learned something. Um So you can answer these again on mental me, just feel free to kind of like answer them in your head or put like the answer in the chat. And then, um, I will go over the answer and see if you guys have any questions about, um, the answers. So the first one is which of the following is not a characteristic of Parkinson's disease. So, bradykinesia resting tremor, excessive production of acetylcholine uh rigidity or postural instability. Yeah. Yeah, that's correct. So, um, there is no excessive production of acetylcholine in Parkinson's disease. Uh The rest are all uh symptoms that can occur in Parkinson's disease. Ok. So the next question is, um, so a 52 year old woman is referred to a neurology clinic as she's been experiencing jerky movements of her arms and legs that she finds difficult to control and the most likely diagnosis in Huntington's disease. Um So one neurotransmitters will predominantly be affected to cause this woman's symptoms. Yeah. Ok. Yeah. So the answer is, uh, a so it will be Gabaa and acetylcholine. Um, as we went over when we were going through the hyperkinetic um, movement disorders Yeah, you get degeneration of cholinergic and gabaergic neurons. Ok. So that's good. Um And then finally, what structure is a common target for deep brain stimulation? Parkinson's disease? Ok. Yeah, that's correct. Yeah. So uh it's a subthalamic nucleus that's targeted. Yeah. So like we went over in the disease summary, the subthalamic nucleus can be targeted with deep brain stimulation as um a treatment of Parkinson's disease as well. Ok, guys, so that brings me to the end of the talk. Uh I hope you guys um found it useful and I hope you guys learned something. I also included some resources that I found quite useful uh when I was in 1st and 2nd year to help me with um with the neuro block. Uh Because yeah, I also found uh neuroscience quite confusing. Um So there's some youtube channels. Um and also some um examples of websites you can use for question banks and uh textbooks. Um I would also recommend you guys to actually use your lectures um in terms of learning your facts because most of your questions come from uh the lecturers themselves and they usually like include the informations within them, but you use other resources to kind of like understand uh what they tell you and build your foundations. Um So yeah, uh that's the end of that. Um If you guys have any questions, then just put them in the chart and I'll try my best to answer them. Um if not, then uh we're, we're done now. Um Thank you guys. I hope. Um OK, thank you. Thank you for attending. Uh Yeah. So, uh there is a feedback form. I think that um I believe that the metal sends you the feedback form themselves. Um That's what I've been told. So I think that's what happens. OK.