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Well, welcome everyone. Thank you so much for the invitation today. I'd like to talk to you about, about an approach to weakness now because we're a small group. I invite you to interrupt me with any questions. Um You can type it into the chat, but if in case I don't see it, please just shut out. Um And also if you are able no pressure, but if you're able to turn on your cameras, that would be great. So let's just dive right in. Um and I wanted to um make sure that people have uh the opportunity to pose some questions. So, um well, let's hope to get through now. You can all see my screen now. Is that right? Okay. A part of it? Okay. Well, let's go on. Do you now see it? There's just a gray block on the top of it, there's a gray block. Okay. I think that's where the zoom, uh where the zoom is. That's probably why. Okay. Hopefully that will come down a little bit afterward says I'm screen sharing. Okay. But you can see. So I'd like to make some sorry just before you start. I just like to remind everyone if you do want to speak up. Um Just to put your hand up beforehand, so we don't have too many interruptions. Okay. Thank you. All right. So, our objectives today, I'm hoping that today you'll be able to differentiate true motor weakness from what we call lassitude and poor activation to recognize certain patterns of motor weakness that localize a problem to a particular place in the nervous system and then to avoid some common pitfalls in tone power and reflex testing. So here's our agenda for today to define true motor weakness and look at the different distributions of weakness that can help us figure out where in the motor pathway the problem is happening. Um We may not have time for pitfalls of the motor exam, but um I'd like you to be able to test your knowledge at the end. So just so that you, you have this ready, I'm going to give you this link that we're going to use at the end for some, some quiz questions. Okay. So if you can copy that down or screenshot that right now, that would be great. Okay. So our first task is to define true motor weakness. So weakness means a lot of things to different people. Um It could mean lassitude and you'll hear this all the time when a patient comes in and says doctor, I feel weak and when you ask them what they have difficulty doing, they just say everything, everything feels weak. Um interesting. The interesting point is when they use this term week and talk about this, it's not so specific for true motor weakness. So lassitude, it could be just a general feeling of tiredness and um inability to do anything. And so that could be from for many other medical reasons um or psychological factors, um things like anemia, um or sleep apnea. Uh so they could be mixing it up with, with sleepiness. Uh There can be pain or poor activation. And so these are the typical patient's who have M S E M S K pain and they'll say ouch. And when you start doing power testing for them, they'll be able to give you some effort at the beginning, but then they'll have too much pain and then they'll give way. Um So what we're really looking for um in neurologic weakness is this category in the red, true motor, true muscle weakness. And so muscle weakness, it's defined as reduced power in a muscle group. And so usually if you um really ask these patient's, they will be able to tell you a particular task that they find difficult to do. And that's what's helpful. Um If you can start to identify the tasks, the very specific um muscle groups that are weak that um uh that allow you to figure out what is, what is their pattern of weakness? Okay. So let's look at different distributions of weakness. Um So what parts of the body are we, then we can start to um look at the different patterns. So this next part is interactive. I need you to tell me what sort of symptoms patient's will have, who have proximal arm weakness. So weakness in these muscle groups over here. Yeah. Is that uh lifting of the arm, lifting, lifting of the arm? Great. And so sometimes patient's will even say, oh doctor, I need to use my other arm to lift this arm over. Great. Anything else? Uh any word, rotation, inward rotation. Yeah. Yeah, for sure. Rotating my arm in. And so these are some other kinds of things that patient's can tell you I can't lift my arm doc here. I'm using my other arm to lift my bad one. A lot of times people just say it's heavy, that's a very common one for patient's, for example, with myasthenia. Remember any time you need to hold your arm out for long periods of time, showering's shaving, combing. Um Then they find that their, their arm is weak. Okay. Let's talk about distal arm. Now, what about distal weakness? What types of things will people complain? Uh Grip, grip strength. Yes. Yes. Anything else? Al comma Yes. Inability to lift an object. Yes. Yes. So manipulating objects with their hands. Any other specific activities I'm going to show you a list here. Okay. So things like writing, I'm, I'm finding difficulty writing or typing, using my phone buttoning things, tying my shoelaces, I'm dropping things, um, fingers seem to start to get curled. Now, this is a pattern that I've started to notice in a lot of patient's with neuro muscular weakness that their hand starts to look Claude instead of pin cering. And that's because if you start to have some weakness here of the first dorsal interosseous, like you're not able to spread your hand out, like in a star Faith up, you start to kind of get this raking quality. So um I've noticed this a lot in patient's who start to have weakness either from a bad ulnar neuropathy or from motor neuron disease. Their hands starts to look like this and you can see some of the wasting of the intrinsic hand muscles, see how prominent these extensor tendons are because some of the muscles in the hands are getting smaller. OK. Proximal leg and trunk. This isn't a uh normal walking. Yeah, difficulty walking, okay. And this one in particular. So stairs are hard getting up from a chair. Um I really want you to pay attention to this one, lifting my leg with, with arms. So using my arms to have to lift up my leg, I think that's a very helpful piece uh that suggests proximal leg weakness, getting into a car, right, stepping into the bathtub, a waddling or Trendelenburg or Myelopathic Gate. That's what you may have heard of. I'll show you some examples afterwards and doing sit ups is hard if we're talking about trunk, okay. And finally distal leg, these are the patient's who have trouble clearing uh, the floor. So, tripping over their toe, dragging over the toe and walking on tiptoes, um, and he'll, and he'll walking is hard. So, um, these patient's will often have a characteristic foot slap. So, um, another group that I've lumped together because when one is weak, we're starting to worry about all the others is facial or bulb er, weakness around the face. Uh So these are patient's who have a flat smile. I'm going to show you an example of that in a moment. Sipping is hard. I start to drool or cough on my food. I can't close my eyes completely orthopnea. That's an interesting one. Does anyone know why orthopnea is a symptom of respiratory weakness because of the vehicle tone of the like while sitting? It's different. Uh Yes, I saw him. This is him vagal tone. Is it? That's interesting. The vagal tone, you know, I may need to look into it to see how much the vagal tone changes. Um There's also a simpler explanation which is just the help of gravity. Okay. You can imagine a week diaphragm with the help of gravity, it's a lot easier to breathe, sitting up than it is uh lying down when you have all of your abdominal viscera, all of your intestines pushing against that diaphragm. So just mechanically even it's harder to breathe. And so I remember a patient with severe myasthenia gravis with respiratory muscle weakness, diaphragmatic weakness, who became severely orthopnea, couldn't sleep at night. So remember that's just a different reason why someone can have orthopnea aside from pulmonary edema. And then headline, we've seen that in our kids, for example, with a proximal weakness. Okay, what do you think is happening with this woman here? Um I just want to point your attention to a few things. Um This is an example of bilateral facial weakness. Okay. Look at her style. She cannot bring up the corners of her mouth. She has a uh oh, that's a great thought. Who said that? Uh Sorry, Angelie? Sorry Anjali. Thank you. Thank you. Um That's a great thought. It could definitely be a bilateral Bell's palsy just to give you a bit more information. So she has a little bit of respiratory weakness. She has a tracheostomy and there's a mild bit of right sided tosis. So this was actually somebody with a my aesthetic, a myasthenia gravis crisis. So she has by facial weakness, strict osis and respiratory weakness altogether. So I just bring this up, please memorize this face. Okay. If you see patients who are not able to bring up the corners of their mouth, start to think about bilateral facial weakness. I find it notoriously difficult to see facial weakness, especially when it's on both sides. Um So look for that. Um again, I'm sorry, that this is zoom thing is uh cut off some of your view at the top. Um But here we can see some patient's with a form of muscular dystrophy called facioscapulohumeral dystrophy. They start to get weakness of the face. So you can see when these patient's on the left hand column are milder cases on the right hand column are more severe cases. For example, this patient here when trying to close the eyes firmly, really can't scrunch the eyes. So the orbicularis oculi is not so strong and in a more severe case, they're not able to close their eyes completely. Okay. Um So uh that reminds us for our patient's with bells policy who cannot close their eyes completely that you really need to give them eye drops so that their cornea does not dry out when they're, when they can't close their eyes. Um Look at this part of the, uh look at this panel here pursing the lips. So uh in a milder case, they can really only purse their lips a little bit on this right side of the face. Um but with a more severe case, really have difficulty or bringing the lips together. So these are all examples of facial muscle weakness. And then our last category is ocular weakness. So I've just lumped in tosis diplopia and forehead of wrinkled, okay, a little tip for you how to pick up tosis in someone from a patient who has non um non organic or functional tosis. So a patient with true tosis, as we see in this page, they will try to compensate by activating their frontal is. So you see how wrinkled his frontal this muscle is. That's because he's trying to compensate for the tosis by lifting up some of the muscles, lifting up some of the tissues around the eye to compensate for this week. Levator Palpa brie superiorize. So look for that. Okay. I'm going to pause right. There. Are there any questions about those distributions of weakness that we talked about before we match them with the anatomy? Okay. Well, let me know if throughout if there are any questions. All right, this is the summary slide of the talk. If you don't go away with anything else, please memorize this because it really does help serve as a key and it's crucial to basically every area of neurology. If you even have this framework, um you can start to make diagnoses or at least narrow down your differential diagnosis quite a lot. Okay. So what is this showing? It's basically showing you the patterns of weakness. We already went through the different um areas that can be weak but the different patterns of weakness in patient's with different types of lesions. So let's look first at the first three. Okay. These are all lesions in the central nervous system. And the one common feature we see it here is that they involve at least one half of the body. Okay, there's a split down the midline. Um So we involved, if we have damaged the corticospinal tract, we get a hemi plegia brain stem lesions are characterized by cross deficits. So one half of the face and the other side of the body, spinal cord lesions, we think about that in anybody who has bilateral symptoms. So that could be bilateral leg weakness or bilateral leg parasthesia. Okay. Okay. Now let's turn to the peripheral nervous system. These four over here and the one distinguishing feature about the peripheral nervous system is those areas that are affected um by sensory symptoms that helps you really clue into there being some nerve involvement, nerve root involvement. So you're in this one of these two categories, nerve root polyneuropathy or polyradiculoneuropathy. Okay. Um The pure muscle, um pure motor symptoms are myopathy. So you get proximal weakness, proximal arm, proximal leg, neuromuscular junction. The characteristic features you get ocular bulb, er respiratory as well as my uh like proximal muscles involved. We all know the stocking glove pattern and diabetic polyneuropathy that's here. And then ridiculous opathy. It's key is that you can involve both proximal and distal muscles at the same time uh as your facial and respiratory muscles. Okay. So, remember this pattern, we're going to go over it again and um you'll see how useful it can be for narrowing, narrowing, your differential diagnosis. Okay. Um This is just in verbal format, what I was mentioning to you before about the central versus the peripheral nervous system. I like to tell people this is basically all I know about neurology summed up in one slide. So let's go on. Um I think you'll have these slides for reference afterwards. So where's the motor lesion? So um just around this is just a reminder about our motor pathway from primary motor cortex. It travels all the way down through internal capsule through to the pyramid in the medulla where there's a decussation in of our motor tract um into the lateral corticospinal tract of the spinal cord, then to the anterior horn cells in the anterior uh spinal cord, then you have in the peripheral nervous system, your nerve root, the peripheral nerve, neuromuscular junction and muscle. Um So as we've seen before, some of the helpful things include the distribution of the weakness, it's symmetry and asymmetry. And then we get a lot of other clues from the nervous system about where the problem could be by all the associated symptoms. The company that things keep okay. All right. So let's go through these motor primary motor cortex. Um This is probably the most helpful clinical tool I can show you. So everyone I want you to um show me how you test for pronator drift. So this is a test for subtle uh motor weakness. So if you just bring out your hands in front of you, um like you're holding up a tray, you've gotten your patient's to close, they're close their eyes and gradually you start to see a slight pro nation as well as the week arm going down. Okay. I want to show you a much um less well known but very helpful tool for looking at very uh subtle strokes, for example. So the reason I shown you this motor homunculus is to remind you how much space in the cortex, your, your brain dedicates to your hands as well as to your face. So when people are um looking for subtle weakness on one side, playing the piano fast, so moving your fingers very quickly, you'll find that patient's with strokes in the motor cortex, there are a lot clumsier on the one side at moving their fingers. And so I find that very helpful just to get your patient's to play the piano fast and see the clumsiness on one side. My favorite sign in neurology is a satellite sign. So what is this? It's the forearm rolling test, you can try it out for yourself. So if you spin your both take both fingers and you spin the spin both hands around each other very quickly. What you are looking for is a satellite sign where a week arm will get uh satellited by the stronger arm. Okay. And this is sometimes a way you can start to see very subtle weakness, okay. This is the type of corticospinal tract weakness that you may not even be able to tell on power testing. Um But these are helpful um signs to improve your sensitivity for that. So you'll get upper motor neuron signs which will review in a moment and all the associated cortical symptoms. Okay. Let's see how we're doing for time. All right, good. The internal capsule is where the highway of all the motor pathways comes together in a very small white matter region seen here on this axial ct scan and here in this axle MRI scan. And so because all the motor fibers are so close together, you get all of your face, arm and leg being paralyzed at the same time. Okay. The brain stem here, you have crossed face and body symptoms. So why is it that you get one side of the face and the other side of the body being affected? Well, if we um consider this lesion here. So if I have a lesion in the brain stem right at this location, then I've interrupted this motor pathway that's coming down all the way from primary motor cortex. So my left cranial nerve five, for example, gets taken out and my left face is numb and the left side of my face, left cranial nerve seven is taken out. So the left faces week. But remember that this same motor pathway is the one that also crosses over to the right side of the body. And so the right leg here is also week. So we have left face and right leg being weak. So remember in our brain stem, all of the bull bar muscles, what I like to call the DS. So diplopia, dysphagia, dysphonia, and the V's vomiting or vertigo. These are all brain stem type um problems. Ok. Spinal cord, there are lots of different spinal cord syndromes, but the key takeaway from this is that they involve both legs or all of the extremities in general. Okay. Um So we're looking for patient's with bowel or bladder dysfunction. So these are patient's with bilateral something, bilateral um weakness and numbness or even sometimes just bilateral um bilateral tingling in the central cord syndrome. OK, parameter weakness. Um If you have not seen this before, um very helpful to be able to pick up the gate that I'm going to demonstrate now is democratic gate. Um This gate, if we were to uh to demonstrate it, we need to be able to show the extension of the leg and internal rotation. So the leg is too long, we have circumduction in with the paretic side, but very importantly, as well is that the upper extremity is very much involved. And so there's adduction of the shoulder flexion of the elbow, pronation of the wrist, the thumb is tucked under and a cortical fist. So this is the position uh the hemiparetic gate with the other side being normal, heavy, normal associative movements. You can actually hear the pattern of the gate as well as we have circumduction for the credit side. Again, watching upper extremity postured into the decorticate posture, more extremity is actually circumduction did coming around. Great. So, a really helpful gait pattern to recognize in patient's who have any damage to the corticospinal tract. All right. So these are the patient's who will be spastic or hyperreflexic will have a positive babinski sign and not any muscle fasciculation zones. Compare and contrast that with patient's who have lower motor neuron damage, uh where you no longer have trophic factors to the muscle. So it starts to atrophy and have spontaneous fasciculation zones. Um Here's an example of just some spontaneous fasciculation. So these are just activations of individual, more motor units. So it can happen when there's damage or d innovation, but it also happens very commonly in normal individuals after exercise, especially in the cats. Ok. Sorry. Um Quick question. So the people that I've had um Akimoto neuro damage there, um spinal cord damage or should we say the damage is devastated from one side to the other, correct? Whereas the lower motor neuron goes, haven't decorated. Is that right? Or? Um that's a good question. So, um as you can see from this diagram here, the cortical spinal tract, any time that upper motor neuron connection with its lower motor neurons. So you see the upper motor neuron, it's axon all the way in the pink. Here's a lower motor neuron in the ventral spinal cord, the anterior horn sell okay. So anytime the corticospinal tract is damaged, you will see the upper motor neuron sign. So that could be above the level of the declaration here. But it can also be below the level of the deck ization. Okay. And so we can see that patient's even with spinal cord damage, they will have this parameter pattern of weakness because the uh the upper motor neuron um has lost its connection with the lower motor neuron so that the lower motor neuron has no longer has it's inhibition of it's spinal reflex. So it's a really hyperreflexic reflex. Does that make sense? Okay. So we can damage right hand side and it can affect the left. Is that correct? That is correct. So, so for example, here a damage to the upper motor neuron at the level uh that's contralateral, that's a very common finding and stroke, right. So if I damage here, the left motor cortex, I get right sided upper motor neuron signs, right. However, if I had um for example, uh if I had multiple sclerosis affecting the right side of my spinal cord at the level of the neck, I will still have hemiparalysis on the right side. Does that make sense? So it's, it's affected the right spinal cord and it affects my right side of the body because I'm down here below the level of the decolonization. Mhm Thank you. Okay, good. Um Assad. Yes, it was regarding the stipulation, uh it could also be regarded as a muscle twitch, yes, a muscle twitch. So, um it's important to um uh ask patient's what they mean by muscle twitching because sometimes patient's are actually confusing maya clones. So usually fasciculation, ts do not actually involve movement around a joint. Usually it just looks like a bag of worms um moving um uh within the muscle itself, okay because their individual motor units and it's not enough to, to actually move the foot. For example, in this gastro, how could we differentiate from it? Like as a muscle cramp? Yeah. So a true muscle cramp. Um It usually implies d novation and these are really painful for a single for, for a, for a moment. So, um for about a minute, patient's say, uh doc, it really hurts for about a minute and then it relaxes and they tend to happen in the evening. You know, both of those I think where it's helpful is that, is that both of those, a cramp and a fasciculation in, they tend to signify the same pathology, meaning denerve ation somehow. Um You're um you're having some kind of damage to the nerve, supplying a muscle. Um So fasciculation zones really are not painful, cramps are okay. Are there any other questions here? Ok. Damage to the Yep. Uh It's not a, regarding a clinical question, but it's uh it's something a child might ask. It's regarding the crossover. We've seen that the nerve innovations or the, the signal coming from the upper neuron, the cross over at the uh basin, basin region. Is there any reason for this crossing the world? Or is that the evolutionary reason why the crossing over has occurred in a human brain or it's common in the mammalian brain? Uh That's a good question. Um I wish I knew the answer to that. I don't have a good answer for why the crossover happens. Um Because it could be, I thought it would, uh it's a evolutionary advantage or something because we could have the same by lab when we say the same innovation could go to the same side. But some, for some it's crossing over. I just wanted to know why this crossing me. I don't actually know why there is a crossover. And keep in mind this diagram is not 100% accurate in that there are some fibers usually more for Trunkal muscles that stay on the same side. Okay. It's not 100% crossing over. Um Similarly to the um the axons that come from your retinal ganglion cells to go all the way to your occipital cortex. Um many of them cross over um from that um from the nasal side of the retina to the other side. Um Some would argue it would be evolutionarily advantageous to have bilateral innovation of everything so that when you have a stroke, you don't get unilateral weakness. So I I think that it may not be advantageous to have a complete crossover of any kind, but maybe multiple crossings over might be helpful. Um Okay, let's go on lower motor neuron. I want enough time for questions and maybe maybe the quiz lower motor neuron. So again, no sensory abnormalities. And look at this patient who probably who has A L S. Again, the wasting in the muscles and the very characteristic extreme wasting of the first dorsal interosseous that muscle that allows you to abduct the finger. Um So in this patient with A L S here, there's actual movement of that first dorsal interosseus. Now it's a little bit atypical, this type of fasciculation. In the very small hand muscles, you can sometimes move the joint. So actually see a, see a move, but most of the time it's just a little movement of the muscle. Ok. Nerve roots, okay. This is a very typical pattern for Guillain Barre syndrome, which you're seeing here with enhancement of the Kata equina. Uh with contrast because it's inflamed. But the characteristic pattern you need to memorize is that nerve root weakness um causes both proximal and distal weakness. Okay. So it's not just the reason why they, these patient's have difficulty walking is because the nerve root that inflame's um L2 and supplies their, their hip flexors is also supply, supplying some of the distal muscles at the same time. Um So they quickly have difficulty walking. You can get facial and respiratory involvement and you tend to have some sensory symptoms with it too. Okay. Finally, peripheral nerves. So I'm going to show you a patient who has or an example of someone with distal leg weakness. Okay. So let's look at this video demonstrates too common patterns for those that have a foot drop or dorsiflexion weakness. First of these patterns is a step educate note here, the patient is hiking, their hip flex, their need to clear the foot that has weakness. The second pattern is a foot slap. Listen, all the weaknesses not visually apparent. The audible foot slap is your sign of this weakness. Okay. So, very good to listen for this as well. These patient's will start to have atrophy and loss of reflexes in their most distal muscles as you can see here, um usually symmetrically neuromuscular junction. So just remember that these patient's the key feature is fatigueability. So initially, when looking all the way around there, extraocular movements look full, but with prolonged upward gaze, they start to get tosis and uh and or diplopia. Okay. Finally, muscles. So you may remember, um, gowers signed here. So patient's who have severe proximal weakness, they can have problems here lifting their own bodies up. And so here's a boy with Duchenne muscular dystrophy trying to stand up. So you can see how he first has to crawl, go um, in the crouch position and really get his weight underneath him. And really walk up his legs that's called gower sign. So that's quite severe proximal muscle weakness and then the Trendelenburg Gate, okay. This is a patient who has a myopathic gate and I'm sorry, it's not so easy to see here, but it's, this is also known as the supermodel gate. Okay. So, so you kind of have this waddling characteristic because your hip abductors are weak. And so whenever I put my plant, my foot down on my right side, plant my right foot down, I'm really relying on my right hip abductor to keep my pelvis from falling down. So in these patient cases, their pelvis will fall down and in order to maintain balance, they really compensate by using their upper body to swing, swing there, center of balance over to one side. And so people will liking it to kind of uh walking like a super model with that pelvis tilting downward or waddling a lot. So you'll see that in this patient here. Okay. Now, we have gone through all the patterns of weakness that help you figure out where in the nervous system, um the problems are happening. Um And the localization really helps you with your differential diagnosis. You can see um there are only uh it's a much smaller list of problems once you know where the problem is happening and it can help guide your investigations um to know what part of the nervous system we should be investigating. So let's see what time it is. 7 43. Okay. I want there to be enough time for us to have questions. And so I'm going to skip through the motor examination, which you can review, um, unless you have specific questions. Now, I'd like you to write down one topic that you learned from today that you'd like to explore further. I'm going to give you some time and I'm also going to open it up now to some questions, any questions you have before we try our quiz together. So are there any questions about what we reviewed today? Yeah, just um um wondering. Hi doctor. Hi. Yeah. You know, we were doing the, I think it was the carnation like when their hands are out like testing the was it a pronation pronator drift? Yes. Yes. Uh Does that matter if patient is sitting down or standing up or what was I think it's best when the patient is sitting down just because in the lying down position? Um it's a lot easier for or you don't have the benefit of gravity um challenging the patient? Yeah, but it is possible to see it in a patient who is supine, you get them to raise their, their hands maybe 30 degrees off the bed. Yeah. What about standing up if you can also do it? Standing is fine. Yeah. Standing is fine. All right. Thank you. Any other questions? Um Just also just sorry, I'm sorry guys. Um in, in terms of the lower motto neuron um um issues. Does it always um originate from the, it will always originate from the spinal cord, right? The lower motor neuron? That's a great, great question, Lola, I'm glad you brought it up. So, the lower motor neuron um whenever it has. So it's a very although it lives in the spinal cord, remember that it's axon is sent all the way out to through the the nerve root, through the plexus, through the peripheral nerve to the neuromuscular junction, and then finally to the muscle. Okay. So all of those signs that we talked about the atrophy, the fasciculation zones, um and the reduced reflexes with lower motor neuron damage that happens not just when you damage the, the the the motor neuron in the spinal cord, but also in the peripheral nervous system. Okay. So, for example, patient's with a ridiculous opathy due to a slipped disc that's pushing on their L5 nerve root that will lead to atrophy fasciculation zones. And um uh over time of all those muscles supply like the tibial is anterior and posterior. So, um anywhere along that whole tract of the lower motor neuron will you find um whenever there's damage to any part of it, you're going to see all those lower motor neuron findings. Okay. And Hannah says, please complete the feedback form. Yes, that, that's very helpful. Okay, if you don't mind. All right, let's move to our quiz questions then. Um and you, so we can uh and please feel free to interrupt me if you do have other questions. Ok. So in order to participate, I need you to navigate to um this website here. Oh, it's very difficult to show. Okay. Can you see my screen here? You'll need to navigate to this. It's called Paul ev dot com slash Jeremy Zong 454. So you can do that on your browser or on your phone. Um Doctor, would it be possible for you to copy and paste that into the chat? Oh yeah, let me just put it in the chat for you. Just a second. Q okay. I'm gonna give everyone just one more minute. Taiwo says, please. I would like us to discuss radiculopathy. Taiwo, is there something in particular you wanted to ask about ridiculous opathy? Yeah, maybe think about it and then um let me know afterward the pathogenesis of the symptoms. Okay, for sure. Um Ridiculous opathy. It means a problem with the nerve root. And so there are many um problems that can occur. I would say the communist that you will see in clinical practice is uh just related to degenerative disease of the spine. So, osteo fights or even um slipped discs can herniate and protrude backward and just push on various nerve roots, causing a lot of ridiculous er, pain along those dermatome and weakness along the myotome tomes that are supplied by that particular nerve. Um I think we think there's some local compressive cost but ridiculous apathy can be from many other reasons. Um uh The other reasons can include inflammat inflammatory diseases like Guillain Barre syndrome that particularly affects nerve roots. We think because there's less um protection around our usual blood nerve barrier. Just at that nerve root area scenario, we are just going to do a few quick quiz questions um related to weakness about the talk. So let's let's die right on it. OK. Which of the following patient's is most likely to have true weakness? Good. Okay. So this is the patient. Um So just uh the pearl here was to remember that patient's who actually give you something concrete um in a task that's difficult are more likely to have true weakness good. What is the most likely distribution of weakness in a supine patient who takes an exceptionally long time to sit up and reposition 180 degrees in the bed good. It is proximal leg and trunk. Okay. And so those patient's um um our next question, what is the characteristic pattern of weakness in a patient with weakness due to a nerve root problem or ridiculous empathy? In other words, Brad didn't very good. Okay. So the correct answer was proximal and distal weakness. Okay. So these are the patient's because so for example, think of the L5 nerve root, which is a very common one. These are patient's because of the myotome all distribution. They get hip abductor weakness, which is a proximal lower extremity as well as a foot drop, dorsiflexion weakness and inversion weakness. So it's all along that myotome. So, remember proximal and distal for patient's with nerve root problems and that's to distinguish it from just those with a peripheral nerve problem, which usually affects the distal legs the most. Okay, an 85 year old woman with rheumatoid arthritis and carpal tunnel syndrome develops one month of occipital headaches, hand clumsiness, four falls and new bladder urgency. Where in the nervous system must you look? So, what's the most appropriate investigation? Excellent up lumber spine. Okay. 11 thing to remember about this um um maybe a little bit tricky is to um the correct answer here was MRI cervical spine, MRI lumbar spine. That's a very reasonable thing to think about for someone who has falls. Um I guess I should have, we we could be a little bit more specific. She started to have a lot more hand weakness. Okay. And so remember with bilateral symptoms, were thinking about the spinal cord patient's with rheumatoid arthritis are especially predisposed to getting atlanto axial joint arthritis and cause and causing a cervical myelopathy. So just think about that, we routinely need to screen patients with rheumatoid arthritis for degenerative disc disease in this cervical spine. Okay. A 78 year old woman, she has a history of hypertension, poorly controlled diabetes and hyperlipidemia now presents with vomiting, vertigo, dysarthria, unsteady, gait and numbness of the right face and left arm. Where is there most likely lesion localisation? Good. The brain stem. That's right because we have crossed body symptoms. We have all of these symptoms referable to the brain stem, vomiting where to go, dysarthria. The other ones would be diplopia and dysphagia and we have crossed findings right face, left arm. Okay. 67 year old man has five months of progressive difficulty climbing stairs and rising from chairs. His CK is 15,000. He was advised to stop rosuvastatin and did so two months ago. But the weakness has worsened. His anti signal recognition particle antibodies are positive. What is the most likely diagnosis? Okay. We didn't talk about this particular disease today, but this patient has what's called an immune mediated necrotizing myopathy. And so these are the patient's who have really high ck's sometimes they, they have been exposed to statins, but the key is that they continue to worsen in terms of their weakness, even when you stop the statin. So that helps differentiate it from a statin myopathy. Um And he has a very characteristic antibody. The other one being an antibody against H MG Coetzee reductase. Good. Okay. Which of the following would be a typical for a large right emcee a stroke. Okay. And the answer here was fasciculation in, in the left face. Okay. The fasciculation zones are a feature of the lower motor neuron. Um And so here in an M C A stroke were damaging the upper motor neurons. Babinski sign an upgoing plantar response. We would see because we've damaged the cortical spinal tract. Okay. So you see that with any damage to the upper motor neuron. Okay. This is a 21 year old woman. She presents with three days of fatigue, a bill tosis diplopia, dysphagia, nasal regurgitation. Meaning she, when she coughs, actually, the food comes out of her nose drooling and head drop, she can't lift up her head after starting moxifloxacin for pneumonia. What's the most likely site of her symptoms? Excellent. The neuromuscular junction, okay. It's fatigue. A ble she has occulopar Albar involvement and she started on a fluoroquinolone which is a very typical trigger for my aesthetic crisis. Okay. This is a myasthenia gravis patient. All right. What would not be typical of the most common pattern in polyneuropathy? So, for most patient's on chemotherapy. Okay. So the correct answer here was weak, knee extension and strong toe flexion. Okay. Because polyneuropathy, it affects the long longest nerves in the body. We expect muscles that are very, very far away, the toe flexors, for example, to be weaker than ones that are more proximal. The symmetry is very common because usually toxic effects to nerves from chemotherapy or from diabetes. It affects both sides exactly the same. So the right would be similar to the left. Sorry doctor, we do have a lecture starting now. Okay, let's stop right there then. Um Thank you very much, good job to al comma and thank you for everyone else for participating. Thank you doctor. Thank you doctor. Thank you all the best. Thank you very much. I will stick around if there are any other questions that you have. Um I am going to have to end the meeting. Okay, so sorry, sorry about that, but thank you very much.