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Neurology Revision Session - Clinical years

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Summary

In this on-demand teaching session, medical professionals are invited to join Dr. Mark Walton, an internal medicine trainee specializing in neurology, and Dr. Gilla, a clinical fellow in urology, as they deliver an hour-long presentation on basic practices in their respective fields. This informal yet informative webinar will focus on identifying different patterns within neurology, understanding the mechanics of human neurology and interpreting complex patient symptoms. There will also be quick-fire questions for interactive participation. Listeners are encouraged to engage by asking questions during the live chat. This session offers a valuable opportunity to gain insights into adaptations in medical practice based on recent developments in neurology and urology.

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Description

Join us for a Neurology revision session led by Dr. Marc Walton, an Internal Medicine trainee. Designed for clinical year students and resident doctors, this session is open to everyone! Dr. Walton will review key neurological conditions and presentations, concluding with SBA-type questions to aid your finals preparation.

This hybrid event will take place on November 13th from 19:00 to 20:00, and you can participate either online on MedAll or in-person at the University of Aberdeen.

Attendance is free for Aberdeen Neuro members, while non-members will be charged £2 for in-person participation and £1 for online access.

Learning objectives

  1. To understand the difference between lower motor neuron and upper motor neuron facial weakness.
  2. To apply knowledge of neurological pathways to understand why certain signs and symptoms occur in different types of facial weakness.
  3. To understand the clinical relevance of distinguishing these patterns in clinical scenarios, such as acute stroke.
  4. To learn how to perform an appropriate and detailed neurological examination to identify patterns of facial weakness.
  5. To interpret and understand the significance of neuroanatomical diagrams and explain their relation to clinical symptoms.
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Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello, everyone. Can you hear us? Ok. Do you put a yes or no in the chat? I don't see. Oh, there we go. Yes. Ok. So, hi, everyone. Uh I'm Panos. I'm the vice president of Aberdeen Neuro with me is Michael, our one of their education leads and we also have for this evening uh Doctor Mark Walton and doctor G SIM. Uh they're an internal medi medicine trainee currently in uh Doctor Mark is an internal medicine trainee currently doing his neurology block. And Doctor Gilla is a clinical fellow also station urology and they'll be doing a quick uh one hour presentation on some ba practice. I'll let you guys take over. Thank you very much for being here. No problem. Um My pleasure. Um I, I'm Mark one of the I MT twos currently in neurology, but quite interested in neurology as well. So, um I thought it would be useful to run through some, some questions and, and Gia is interested in ophthalmology. So some of the more um eye or visual pathway oriented stuff she'll, she'll kindly run through. Um I guess overall it's a pretty informal session. I'd say a few disclaimers you know, I don't know what's in the exam. I don't, not that familiar with the Aberdeen curriculum. So this is more of a, just a general overview of stuff that I think is pretty important, likely, I guess to come up in any exams and useful in real life clinical practice. Um, there's a mix of content, some of it is kind of the types of things you might see in MC QS though, I would emphasize that the, you know, they've not been rigorously tested these questions. They do have surprisingly high standards when they put them in exams and they have to meet all sorts of criteria that's kind of just been made off the cuff. And then a few, I think last year they were quite popular, some kind of quick fire questions. Uh just to get used to recognizing some of the important patterns within neurology. Um I'd say at any point, feel free to stick questions in the chat. Um I'm not sure if this platform lets you guys talk, but if you want to type, please do and I think we'll make some polls as we go along as well. So just fire in with any questions and equally it's useful. Um We're running a similar session in a couple of weeks time. I've got questions ready for that, that are all different. But if there's anything you'd really like to cover, just put it in and I'll make sure there's stuff relevant to that anyway, enough kind of rabbiting on, I'll get to the, the, the meat of the questions and to start off with something I think's pretty important and common to come up in any kind of neurology level, whether that's second year or later on. Um, a bit of a busy slide. But if we just talk through it and I should say throughout the, the patient names all have a little story behind them or a wee clue as to what might be going on. But uh we'll, we'll get to that after. Um, so you've got two people there. You've got Mr Holmes on the left of the screen and Mr chime on the right, the right side and you can see there if you ask them both to, you know, show me your teeth and the top row is what they do when you ask them to do that. Um So you can see there's perhaps a problem there with both of them and after you've done that, you ask them to, you know, close your eyes and see what they can and can't manage. So take a little time to just look at that the question. As I say, it's a bit of not very well worded. I'll apologize, but it's just asking for which of those two things there is the, the, the correct answer. And I'll give you a wee minute to just kind of look through it and see what's what feel free to vote on the polls in the chart. Thank you. So, maybe six responses so far, I'll give you another wee bit of time and then we can chat through uh the answer and the sort of the relevant pathways behind it. Fine. So there might be a few more trickling through, but just to talk through it and how I sort of think about it. So if we walk through Mr Chime, for example, on the right hand side, you asked me to, you know, show me your teeth and on, on his left, you know, i the screens, right, but his left, he's, he's able to show you his teeth pretty well, but on his right, he can't. So, you know, there's a problem with the, the, the musculature sort of in the lower half of the face in terms of facial expression. Um and then you ask him to close your eyes and he can close them perfectly well on his left, but you can see on the right there, he's just not able to close his eye at all. Um Where is it slightly different with Mr Holmes? Similarly, he can't show his teeth on his right, but he is able to close his right eye. So there's sort of a, you know, upper and lower face is involved in Mr Chime, but only at lower half of the face is involved in Mr Holmes. And so to me that would suggest that Mr Chime here has a lower motor neuron pattern of facial weakness. Mr Holmes has what you'd refer to as an upper motor neuron pattern of facial weakness. Um So B would be in, in, in my view, um If we just skip forward there, these are just, I know last time people have asked to get the slides with answers on them. So it's just the, the bold answers to sort of, you know, correct one And it's maybe helpful just to talk through this to, you know why that is. Now this is AAA diagram that I always find quite helpful. And I was trying to understand this. The terminology is a bit clunky as well. But if you're talking about uh it's easiest to start with a lower motor neuron pattern of facial weakness. So what do we mean by that? So look at this, I don't know if you can see my cursor actually on the screen, probably not, but looking at the sort of normal normal labeled diagram. And you can see that, you know, the sort of lower motor neuron essentially, if you knock out the whole lower motor neuron um nucleus that provides your uh seventh cranial nerve, you're going to affect both the upper half and the lower half of the face. Um So that's kind of a lower motor neuron pattern of weakness is when you've got both the upper and lower parts involved. Whereas an upper motor neurone pattern of weakness is when you only have the lower part of the face involved. And the reason for that is a little bit tricky. Um but essentially your motor cortex, when it comes to providing eye closure, both your uh your right. Uh let's say your right motor cortex will provide the left side of your face with closing your eye, but also your right. So for example, if you think about controlling your arm, your right motor cortex will only provide input to your left arm. It won't do anything with your right really. But in the upper half of the face, it's a bit different. Both cortices provide both sides. So you've got a lot of redundancy in that system. And I suppose the reason for that is, is you think it's so important when um humans and you know, related species were evolving to protect your eyesight. So if any damage happens on one side of your brain, you still want to be able to close eyes on either side. Anyway, it's maybe digressing slightly. But the point being upper half of your face gets bilateral cortical innervation. Um So both Creon nerve seven nuclei get input from the motor cortex that provides eye closure and raising of your eyebrow. So if you only knock out one core side of the cortex, the other one's still going to provide both sides. Therefore, you can um still close both eyes. The situation in the lower half of the face is more you know, it's more in line with what happens in your limbs. So, for example, the right cortex will only provide um lower half of face expression uh to the left side, it won't give anything to the right. So you get this situation where if you have a upper motor neuron or, you know, essentially a cortical lesion, um your eye closure will be spared but your um you know, lower half of your face will be affected. D does that make rough sense so far? It's something that, you know, you get so used to thinking of you kind of lose track of whether it's clear or not. But um hopefully it doesn't, we can always come back to it if not because it is a bit clunky. Um So I suppose you can hopefully see from that that if you affect the, the peripheral facial palsy, that diagram on the right, that's just another term for a lower motor neuron pattern of weakness. So the lower motor neuron sort of bundle is being struck out. So you can imagine on that side, he's not able to do anything with eye closure or smiling or raising his, his mouth. Um Whereas in the upper motor neuron or also known as a central pattern of facial palsy, um there's a sparing of of eye closure. So hopefully, that makes rough sense. It's a helpful diagram, I guess is the main thing. So be familiar with it and be comfortable with um you know, what's what in terms of upper and lower motor neurone patterns of, of facial injury. Um And the classical situation that you might be asked particularly if you're in earlier stages is if you, if you were in A&E and you had two people, you know, which one would you want to see more urgently if one guy had um you know, I'll put it that way. Who would you want to see more urgently? Mr Holmes or Mr Chime on the, on the balance of probabilities? Are you going to be more worried about someone who's got an an upper motor neuron pattern or a lower motor neuron pattern of facial weakness? I don't know if anyone wants to hazard a guess. It's, it's not a perfect answer to it. But would there be one who you think probably has something more serious going on? It's no problem. We come to it. Yeah. Yeah. So generally people would say upper motor neuron, the, the reason being, you know, you're, you're really sort of thinking, have they had a um an anterior circulation stroke? Whereas the pathologies that cause lower motor neuron uh patterns of weakness are more likely to be something a little more insidious, but we'll come on to. It's not important. I don't want you to construe that as saying it's impossible. You, you do get strokes that cause a lower motor neurone pattern of facial weakness, but you're right on the whole you're usually more worried about an an upper motor neurine pattern of weakness. But just for argument's sake, those little dots in the brain stem sort of represent the facial nerve nucleus. If you have a stroke that affects your brain stem, you can have a lower motor neurone pattern of facial weakness. So just bear that in mind, you'll have a lot of other stuff going on as well. You'll have sort of crossed hemiparesis and all sorts of other things, cerebellar signs. But um it's worth seeing your strokes can cause that too. But yeah, no, agreed. Generally you and men are more focused on. So last wee bit about seventh nerve. Um I suppose that that first question is maybe a bit difficult to, to, you know, go through or maybe just answer it myself and instead of um putting you through the, the, the typing thing, but maybe worth just thinking, you know, Mr Chime had this lower motor neuron pattern of weakness. Could you see that he has a Bell's palsy? Um Does he? Yes or no. In fact, let's make a poll for that. Does it, would you say Mr Chime has Bell's palsy? It's a bit of a, but maybe a bit of a leading question, but it's one that I think both in exams and in, in real life, uh people can get a bit tripped up with or I suppose I shouldn't say, you know, based on the info you've got so far. Um, does he have one? Interesting. So, I suppose the, the trap I'm sort of laying here and it may, is being a bit pedantic, but I don't think it really is, is so a Bell's palsy by definition is someone who has a lower motor neuron pattern of facial weakness, which we agree Mr Ch does have, but a Bell's palsy by definition is also, it's essentially idiopathic. So they've had 1/7 nerve palsy for no one really knows why it happens. It might be related to some weird viral infection, but it's idiopathic and it progresses, you know, usually it'll reach its worst point within a certain defined period of time, then it improves over a certain period of time. And essentially what I'm saying is there are other things that can give you a seven, a lower motor neuron pattern of facial weakness which aren't Bell's palsy and you need to make sure you're not missing them before you manage. Someone has a Bell's palsy because there's some pretty serious things you could, you could miss. So a couple of examples there. So that first one, you know what, what might the diagnosis be if someone had a lower motor neuron pattern of facial weakness. But also you had a look at their ear and you saw that photo on the right and I guess I read a script here description, they've got some vess on their article and then they all three canals and we want to type in the chat, you know, what, what might the diagnosis be there? Yeah. Agreed Ramsay hunt. So, sort of VZ V infection affecting your, your seventh nerve. Um, which isn't a Bell's palsy. It's not idiopathic. There's something else causing it and you're going to have to manage the, the, the varicella. So you can see here you can have a lower motor neuron pattern of facial weakness. The temptation is always to say they've got a Bell's palsy, but actually, if you're being proper about it, they don't because Bell's palsy, you, you're going to manage differently. So it's important that you don't miss these other things. Um And yes, you've jumped the gun, Philip. But the next one, I suppose they are showing you a, a rash that's sort of typical for Lyme. Um And I guess the stem, they are suggesting if they had, you know, sore joints, a bit of a stiff neck and this bulls eye rash. So Lyme disease certainly often causes a bilateral seventh nerve weakness. But again, it's a lower motor neuron pattern. And you, you know, you don't want to miss that and call it a Bell's palsy, give them steroids and miss the fact that they've got Lyme disease that then progresses and becomes problematic and maybe the most cryptic one is to last. But any thoughts for that, if someone had a lower motor neuron pattern of facial weakness, and they were also a reflexic and had sort of ascending sensory symptoms and weakness in all four limbs that was kind of progressing over several days. It's probably one that if I didn't mention the seventh nerve palsy and just said that aflexia, ascending sensory symptoms and weakness, people would probably jump at the answer. But the seventh nerve that maybe puts you off slightly any thoughts. Yeah. Agreed. Uh So GBS certainly causes, can cause commonly causes even um seventh nerve weakness. Again, it's often symmetrical. So you might miss it if you're not really testing their power. Um You know, you know, if you just looked at their face, it looks symmetrical. But if you try and open their mouth or getting to close their eyes and open it, you'd see what's actually weak. So again, it's just labeling the point, not all lower motor neuron sevens and weakness is Bell's palsy, a large subset of it is, but you need to make sure you're not missing these other things anyhow. Um that's just highlighting the, the things again there at this point, I'll, I'll hand over to Gilla to chat through some um things about visual fields. So Gilla over to you. Oh, hi, everyone. I'm gla I'm gonna talk you through about visual field defects and the visual pathway. So we're gonna start off with some questions. What, how can you des describe this visual field? Um There's a pole, I'll wait for some answers. The the first pole is for the image on the right, on the left. Sorry, I'll wait for a few more responses. So this is left Hormon name as Hemianopia because the visual field defect is on the left side of the visual field. I'm not sure if you're able to see my cursor. What do you think the lesion would be if there is a left ho name as hemianopia or which part of the visual pathway you can use a check uh function? Mm So if there is a left home, her name as hemianopia, usually the lesion would be on the right optic tract in my next slide, I'll just go through the visual pathway just for a bit of understanding. So in the second question, so that would be your picture on the right hand side. Um So what would be? Um Sorry, I think there's been a bit of uh change in the poll. Yeah, sorry. It's the, the last one posted. That's OK. Um I'll So yes. So this the photo on your right hand side, that's uh right monocular visual loss. So the complete visual loss of the right eye. Um I'm not able to change to the next slide. I'll go to the next one for you. Thanks, Mark. Um This is a bit of a busy diagram, but this is the visual pathway where the visual information is carried from the retina via the optic nerve and it ends at the occipital cortex which is where the primary visual um center is. The different components of the visual pathway would be the retinal fibers, optic nerve optic chiasm. So that's where the nasal retinal fibers will cross over and we will be forming the right and the left optic track and the sensory fibers will synapse at the lateral geniculate nucleus. And from here onwards will form a lower optic radiation and an upper optic radiation and finally will terminate at the occipital lobe which is the primary visual cortex to understand. So if there is a lesion anywhere in this visual pathway, it would cause a visual field defect. So to understand the visual field defects, the nasal retinal fibers will carry the visual information from the temporal lobes and vice versa. So the retinal fibers in the temporal lobe will carry the visual information from the nasal visual field if we look at level one. So if there is a lesion at level one, it's gonna affect the right optic nerve that would lead that would cause uh right monocular visual loss because the fibers have not crossed over at the optic chiasm. So in a prechiasmatic lesion, it will cause a complete right visual right eye visual loss if we look at level two. So that's the optic chiasm. Now, this is where the nasal retinal fibers from both eyes cross over. Now, the nasal retinal fibers will correspond to the temporal visual fields. So if there is any lesion that's compressing the optic chiasm, it's gonna cause uh temporal visual field loss. So a bitemporal hemianopia, what what could cause a bitemporal hemianopia. There's no poll for this. So you can just write in the check correct. And craniopharyngiomas can also compress at the optic chiasm and that can cause a bitemporal hemianopia. Moving on. We are gonna look at the postchiasmatic visual field defect. So it's anywhere beyond the optic chiasm. So if there is a lesion at level three, so that would be the right optic tract. So the the reason why the nasal, the reason why the crossing over happens at the optic chiasm is to ensure that the inflammation from the same side of the visual field ends up on the same visual cortex. So the right optic track will now carry information from the left side of the visual field if we follow this purple pathway. So you've got super purbal pathway to the left eye. So that's where the nasal retinal fibers that would correspond to your left eye, temporal visual fields. And we go back um to the level three and follow the purple pathway to the right eye. So that is your temporal retinal fibers, temporal retinal fibers will carry information from the nasal visual field. So, on the right eye, you've got the nasal visual field defect, how would you? Um So if there is a lesion at level three, what visual field defect, um would you get there's no pa for this. So um you can use a chat function. So if there was a lesion at the root optic tract, it will cause a left-sided homonymous hemianopia. That's shown below the postchiasmatic. That's the photo that's under the postchiasmatic. So to understand moving on, so you've got these sensory nerve fibers, adverse synapse at the lateral geniculate nucleus and then form the lower and the upper optic radiations to understand the visual field defect. If there is a lesion in the optic radiation will divide the visual field into four quadrants. So f there was a lesion at level four that depicts the lower optic radiation. So we're on the right optic tract. So if there was a visual field defect, it will give uh left um hormones and to determine whether it's superior or inferior quadrant that's affected, we'll need to understand a bit more of anatomy. A com a pneumonic that I tend to use to understand to see whether it's an inferior or a superior visual field defect, it's pits. So the parietal will give an inferior visual field loss and the temporal will give a superior visual field loss. That's because the lower optic radiation loops around the temporal lobe and the upper optic radiation will loop around the parietal lobe. Where do you think the lesion is if someone's got a left hormone, a superior quadranopia, is it the parietal or the temporal lobe? Yes, it's the temporal lobe because the temporal will give a superior visual field loss and it would be the opposite if there was a lesion at the parietal lobe. So I've got, so we'll move on to level six. Be before that. Can anyone tell me where would be the lesion? If someone's got a left homonymous hemianopia with the macular sparing, you can use a check function for this as well. Any guesses. So if there was a left home, her name as Heia with macular sparing, the lesion would be in the occipital lobe. The reason why it's left hormon, that's because we are. So if there is a lesion at the right occipital lobe, it will cause a left homonymous hemianopia. And the reason why the macular is bad or the central vision is preserved is that the occipital lobe has got dual blood supply from the posterior cerebral artery and the middle cerebral artery and the visual cortex is in the occipital pole which is supplied by the middle cerebral artery. So I'll hand over to mark to continue. But if you do have any questions, let me know. Brilliant Gina, thank you for um for talking through that. It's always a a really high yield topic and one that's um uh often difficult I found to get my head around when I was learning it. So, thank you very much and very well done. Um Skipping on to some kind of more, this is kind of quick fire stuff. So this one isn't really a an M CQ per se. It's more maybe just put it in the chart uh, as we go through or have a think to yourself. Um, I won't dwell on them for too long. Some sort of headache, uh, things, it's pattern recognition. So let's say you meet someone who had a gradual onset unilateral pulsating headache, which lasts, it lasted about eight hours and it was associated with some nausea and vomiting. Um, made the patient want to lie down in a dark room before the onset of the headache, maybe half an hour prior, there were some flashing lights and zig zag lines in one half of the visual field. Um With all that, what's the kind of type of headache that's jumping to mind? Perfect. Yeah, migraine with aura, migraine. Brilliant, good. It's good. Just getting used to that sort of those things coming together. It's probably pushing you towards migraine, isn't it? Uh, won't dwell on that too much going on to the, the next thing then, what kind of process or what kind of pathophysiological process makes you think is going on. If you had a, let's say there's a 30 year old female, I suppose it could be an age. But let's say the 30 year old female, they've had a continuous headache for two weeks. It's generalized. So all over worse with lying down, coughing, straining and it's worst, you know, when they work, wake up first thing in the morning and they've got papilledema on fundoscopy. What kind of process do you think is going on? Not, not a diagnosis as such, but what's going on inside their brain or inside their skull? Ok. Tumor. Yeah. So tumors can absolutely, it's an appropriate thought because it can certainly cause what's going on. But I suppose raised ICP S some, something causing raised intracranial pressure and you're absolutely right. Han, a tumor is one of them but there's other things always to think of too. Um Yeah, so for example, space occupying lesion, again, that covers quite a broad range of things. There's some other things that aren't space occupying lesions but very good, very good. So then under that there's two different um headaches to sort of continue on that theme. So this first person, they're also 30 they've had this continuous headache, you know, worse first thing in the morning fundoscopy. But then you're told um they were also admitted to A&E following a seizure at home. They've got some left sided arm and leg weakness. Um They've had a history of recurrent miscarriages and they've got livedo reticularis on their legs. I've not put a photo of that there, but it's that sort of blue purplish hue almost looks like a neck sort of rash. Um And again, they've also got papilledema and fundoscopy, but you knew that already, what specific cause of this person's raised intracranial pressure is going on? What, what do you think is causing this particular patient's raised CP based on the exam findings and history. A bit of a bit of a tricky one. Ok. Good suggestion is a possibility. I suppose. You know, you're right. That could give people seizure, it could give them, uh, weakness. It's completely, you would completely investigate for it. Meningitis too could give you seizure, left sided arm and leg weakness. Um, I suppose the thing that's a bit harsh here, it maybe is more a post graduate um thing. Um is the, what do you think the recurrent miscarriage is in livedo reticularis? What might that suggest in a female of this age? All these other things are completely possible, by the way, you're absolutely. Yeah. So anti fossil lipid syndrome and what would that cause? How would anti fossil lipid syndrome cause raised ICP. It's always one of the sort of raised p headaches. II never really thought of as a student, but in real life you think about it and some see it and not unreasonable amount. So it's worth having on your radar. How would antis lipid syndrome cause this picture? So, a a cerebral venous sinus thrombosis. So it's a bit like getting a DVT but in your brain sort of thing. So, um antiphospholipid syndrome puts you at risk of that, II suppose. Yeah. All the other suggestions are entirely reasonable though for, for a lot of that history and you would investigate for them. So very, very good. The second one. So the same initial bit of the stem. But this time, um, they were referred from ophthalmology and they've had a CT head, a plain CT head and act venogram that are normal. So they've not got a, a clot and they've got an elevated BM I, and they've recently gained some weight and they've got a, let's just say, a completely normal neurological examination. So, what do you think might be going on there again? 30 year old female? So, um I suppose this is something you might go on to the suspicion would be idiopathic intracranial hypertension. So it's a cause of raised intracranial pressure. Usually in, you know, females of this age, usually who have a raised BMI. Um And you know, to confirm that they need to have a lumber puncture showing raised pressure. They need to have completely normal CSF constituents. But that's the thing that you might think of in that context. Both of those I'd say are a wee bit, you know, in second year, I wouldn't worry too much about them, but it's worth knowing about them. The main thing from those ones are, are thinking about features of raised ICP. Anyway, the one at the bottom of the, the, the slide, someone's had an excruciating unilateral headaches around the right eye, they last about an hour and happen twice per day, roughly at the same time of day as well. For the past two weeks, the eye was really red in waters during the headache, any thoughts as to what that headache syndrome might be again, maybe slightly niche, but finals probably worse than the one. Um, so it's a pretty good growing story for a cluster headache. They're, they're rare. Um, but the main feature is it's unbearably sore. Whereas in migraine people want to lie down in a dark room, people are often said to sort of want to bash the head of a wall, It's that kind of feeling. Um And they get these autonomic features on the same side of the headache can occur like clockwork sort of thing as well. And as the name suggests, they often come in clusters, there might be, you know, a month where they're there a couple of times a day, then they go away the next year or two years later, get the same thing again. So um there you go, worth thinking about headaches for a wee bit these, I'll maybe skip past for now. There's some more kind of maybe slightly low yield headache things, but we can come back to them if there's time at the end. Uh The other headache questions, I think where maybe pretended in saying that are maybe slightly more useful, particularly think. Oh, the slides have disappeared. What slide are we on now? Can you see the one that starts with? I can see the Mr Mr Perfect. Yeah, that's the one can, can you still see, I'm not seeing that slide? Oh on the eye side, let me see. There might be a bit of a lag. Yeah, sometimes there's a bit of a lag with these things as you see, eye slide. Is that the one with the photos of people's eyes or is it the ones that g was doing? Oh, all right. Ok. Sorry. Um So you've missed a, a few bit of the recent ones. Um I'm not sure how to rectify that. Sometimes it just gets a wee bit upset. Let me see. I tell you what if I just pump this off presenter mode. Um I'll just give me two minutes, I'll edit my master copy and I'll just put up the later slides. Maybe it doesn't like it when there's more than a few. So I'll stop presenting market. It might also be worth just sharing your screen at my work as well. Yeah, very good point. Um Give me two ticks. I'll fire up the, the presentation and as you say, it might be that that works a little bit better. I'll just skip through to the relevant bit and then uh let's give it, I'll give that a go. So show on my screen. There you go. So hopefully there are you seeing a slide with Mr Koenig on it? Ok. So I'm gonna put it on the chart if they can see that. Perfect. I should say, II can no longer see the chat and stuff. So just keep me right if anything's coming up there. Yeah, I'll let you know. Brilliant. So, um, where were we? So, let's say Mr Kigs, a 21 year old man, he's come to A&E with fevers and a gradual onset of headache over the past day. So, fevers and gradual onset headache. Um, he's also photophobic. He's got a stiff neck and he's drowsy and kind of wakes up to loud voice but not much else. His examination is unremarkable. Apart from some mild left upper limb weakness and swollen optic discs, his blood sugar is normal and his observations are stable routine. Bloods and blood cultures have been taken and sent off. You're still waiting for them to come back. What's the next most appropriate investigation to perform? Um And again, it's something this is also about learning a little thinking a little bit about your strategy and a multiple choice question. It's asking you, you know, what's the the next most appropriate investigation to perform? Um So what do we reckon out of that? Maybe just let me know once there's kind of a healthy number of answers there, we can chat through so far. There is a bit of an even split between. Oh, now the majority is voting for city head first and then there is an lumbar puncture and then there are also a couple of people voting for an MRI or an ABG. OK. Yeah. And so I'd say in this, the question they've asked you, I'd say the appropriate thing to go for would be a ct of the head. Um I mean, I'm, I'm assuming there are most people are thinking, oh, this sounds like uh you know, bacterial meningitis. So lumbar puncture completely, you, that's the test you really want to do because it's the one that's going to help you guide microbiologically what you're doing. But in terms of the next most appropriate investigation, you've got a 21 year old man who's got quite a lot of, he's got evidence of raised ICP. So he's got swollen optic discs, he's got upper limb weakness. So he's got focal neurological abnormalities too. So I suppose you want to make sure it's safe to do a lumbar puncture. That's sort of the, I don't really want to call it a trick here because it's, it, you know, it's something that you need to think of in your life. So it's not really a trick, but it, you've got to make that cognitive jump and go, actually, essentially you'd have to do a CT head before doing a lumbar puncture because if he's got a raised ICP, let's say this was, you know, it was a meningitis, but he also had a collection, like sort of a um uh collection of pus in his meninges. If you did a, a lumbar puncture that you can cause him to cone if there's sort of the raised ICP there. So that's the reason for doing the ct head so you can only really safely do a lumbar puncture without doing imaging first if someone isn't obtunded. So one, he's obtunded two. If they don't have papilledema, which you know, he's got papilledema, you don't have a focal neurological deficit, which again, he does, there's a few other criteria you can argue with as well, but you'd have to do a ct of his head before proceeding. So worth just having that in mind. But beyond that, completely agree, lumbar puncture is a really useful investigation because it sounds like bacterial meningitis. You're gonna want to know what's causing it and to try and confirm that diagnosis and see what antibiotics are kind of going to work. Um again, like MRI if you had it available there and then great, but actually CT is just always gonna be more available. Um And arguably for some of the other differentials here like acute collections of blood, the CT is going to be better. ABG you're almost certainly going to do as well and someone this unwell, but it's not really the next most appropriate thing to perform, you know, you could argue um fine. So in a similar kind of vein thinking, still of headache and sort of tricky worded questions. There's another young man who's 21 comes to A&E with a sudden onset headache which is 10 out of 10. So reached its worst ever headache within a few seconds of onset, he's also photophobic and he's got neck stiffness. Um The headache started seven hours ago. Um, examination and routine bloods are unremarkable and that plain CT is normal as well. So, what's the next most appropriate investigation to perform here? What do people go for? Just give me a couple more seconds so that most more people can reply. So now the majority seems to go for a lumbar puncture as soon as possible and that there is a three way split between MRI C head with contrast or lumbar puncture in five hours. OK. And this one probably is, is, is, I guess, probably tricky question. And I'm aware that there's a lot of debate in the past couple of years about whether the paradigm in this might change. And, but essentially the, the, the what you want to exclude here really is a subarachnoid hemorrhage. Now he's had a plain ct of his brain. And some people would say that that's enough when you present quite early on to fully exclude a subarach. But even the strongest proponents of that would say only if you do it within sort of six hours. So you can't say for sure, this man hasn't had the subarach yet without doing a lumbar puncture. Now, the difficulty with lumbar punctures for diagnosing subarachnoid bleeding is that they, they don't detect blood itself or they do. But you, when you're doing a test for a subarach and a lumbar puncture, you're not looking for blood itself, you're looking for the breakdown products of blood. So you need to give time for those to develop and for the blood to be broken down. The reason really you do this is because when you do any lumbar puncture, you're going to catch a little blood vessel somewhere. So you often will have some blood cells under the microscope. So you want to see is there any evidence of blood, you know that appeared there when this headache started? So you really need to give it about 12 hours before doing the LP for it to be a useful test. So in this person, a lumbar puncture as soon as possible, isn't going to be sensitive enough to rule out a Subra. So you're going to want to probably wait five hours MRI brain and you know, you could make an argument for, but it's one, you're probably not gonna get it in that time frame and, and two, it's not going to be, you know, it's not going to definitively exclude a Iraq. No further investigation. I don't think you could defend. I think, um you know, you've not proven that he doesn't have a, a ct of the brain. With contrast. Again, you could argue that's like doing a CT angiogram. But again, that's not going to fully exclude a nonaneurysm bleed or a small aneurysm that's bled and this sort of covered itself over. So I think here, the learning point is sort of get familiar with the the, the timings of diagnosing, uh, a sub, I should remember. You came up in exams and stuff. So worth knowing about. There you go. Um, this is just again, some kind of quick fire but random jumping onto other topics but just getting used to pattern recognition, particularly, I suppose, second and stuff. Um, but it's just taking a wee minute to, to look through and think, let's say the blue bits are the bits that people are weak in the non blue bits, people are fully strong. So you've examined them and you've sort of mapped out, where are they weak? And it's just thinking of the options below. For example, for patient, number one, what's the most likely localization of his weakness? Is it coming from a cerebral hemisphere? Is it coming from a peripheral neuropathy? Is it a spinal cord problem? Is it a brainstem problem or is it, you know, a muscle problem? Um So just we'll give you a minute to think through for, for each of them. So, in the first one, I mean, how would you describe that? It's a, it's a symmetrical proximal weakness in all four limbs. Number two, I suppose it's a, a unilateral hemiparesis involving the face, arm and leg. Number three, it's what I would describe without using buzzwords. It's sort of a, it's, you know, symmetrical and distal about using the, the tempting buzzword, but symmetrical and distal all four limbs. Number four is sort of a, um, you know, bilateral lower limb weakness with some involvement of the lower trunk. Uh, number five is a bit more of an interesting pattern, but you've got sort of a crossed weakness involving ipsilaterally, the arm and leg and contralaterally the face. Um, and for, you know, going back to that horrible slide about seven or palsies, it's both the upper and lower face, which I guess is relevant. Anyway, we've probably giving you enough time to look at them there. So jump into the next one. I agree that a bit of an odd way. But picture number one, I'd say is most likely to be a myopathy. So a muscle problem, they're classically uh symmetrical and proximal. There are exceptions to each of these, you know, there are some demyelinating neuropathies that I'll give you that pattern. But by and large you should be thinking, oh, could this be a myopathy? Um Picture number two is most likely to be coming from someone's cerebral hemisphere, it sort of face, arm and leg all on the same side. It just kind of makes sense. That's the most likely uh single lesion to cause that pattern. Number three is most likely to be a peripheral neuropathy. It's kind of length dependent and symmetrical. So you can see how that comes about, you know, it would be very unlikely to have a cortical lesion given that you need to have four ones that are equal size in different bits of the cortex. So it's not impossible, but it would just be a bit odd, wouldn't it? Um Number four, again, the most likely thing is probably a spinal cord issue. If you've got bilateral lower limb weakness, though, there is one other spot that not uncommonly can give you it to. And if you look at the diagram on the bottom of the page, sort of the motor homunculus, you can see where someone's foot is in the middle. Um and their legs sort of goes down that central sulcus. So you can imagine if you have a big lesion like a meningioma or something, right, uh right on the central sulcus, you'll also be catching the contralateral central sulcus. So sometimes midline lesions in your cerebral hemisphere can cause a um bilateral lower limb paralysis without affecting your upper limbs. So, spinal cord is the most likely but bear in mind. Uh um sort of central um cerebral issue over the cortex. And five is sort of suggestive of a brainstem problem. You know, your seventh nerve um nucleus is in the pons. So if you have a pontine lesion, you can get 1/7 nerve weakness, lower motor neuron pattern down one side. But that will also catch the pal tracts that are traveling, you know from your cortex and then they cross in the medulla which is lower down. So you get a, a contralateral hemiparesis, it's difficult to show without a diagram. But if you see that kind of crossed pattern always think is this a brainstem issue because lots of stuff's crossing from side to side in the brainstem. Um, anyhow, I'm trying to see how we're doing for time. We, we've still got like, four or five minutes. Um, I'm happy to run through a couple of others and then we can sort of see if there's any burning questions. Maybe I'll, I'll skim back quickly to the, um, the chat. And just see before we do, are there any kind of burning questions people want to ask? I'll maybe jump out of this endless, uh, is she nothing? Nothing? If anyone has any questions, you can post them on the chat. Maybe just in the, the two minutes that are left. I think the last slide is a quick one. So maybe just go through that, um, with you. I'll just share the screen again very quickly. Two. Ok. That one, maybe that was quick. So this one is gonna quick fire again. Which of the following wouldn't give you a positive Romberg sign. There's another thing that often gets a wee bit muddled and we have time to make you go through it. But, um, people often say, oh Romberg's, that'll be a cerebellar issue. But in fact, a cerebellum problem doesn't give you a positive Romberg sign. Um The best way of thinking about that is, is if you're, if you've got a cerebellar problem that's making you unsteady on your feet, you're going to be unsteady, irrespective of whether your eyes are open or closed. The Romberg's test is really screening for if you're steady with your eyes open, but you become unsteady when you close your eyes, that must mean you've either got a problem with your vestibular apparatus or with your pro receptive apparatus. So all those other lesions can give you a positive Romberg's, but a cerebellar lesion doesn't give you a positive Rhomberg sign. Yes, it can make you unsteady on your feet, but you'll likely be unsteady even with your eyes open. So that's often something I used to get sort of um, well, trip up on to find the pump. Um and then the sort of lower down one here, you've got a patient who suffered a stroke affecting one of her cerebellar hemispheres and she's got a completely normal neurological examination apart from some dysmetria. So, an intention tremor in her left upper limb and left lower limb. And it's asking you which of the patients cerebellar hemispheres has been affected. So, if she's got cerebellar signs in her left arm and leg, um which side do we think has been affected? And again, I patient probably don't have time to do polls and stuff like that just now. But long story short, it's going to be the um the left side. So cerebellar control is sort of ipsilateral. It's one of the exceptions where most things are kind of crossed over Cerebellar is ipsilateral. So it's quite a good, a good one to know as well. Um, anyhow, I'll scunny back over to the, the main page and again, to see if people have any questions. Um, oh, I see. You actually a poll for that. And, well, like most of them maybe learned something hopefully from the last question anyway. But it's just kind of looking back. I think I made these slides not long after I'd done sort of finals and stuff and you just sort of remember the things that you went. Oh, actually I didn't realize that when I was first reading through. So, II hope none of that puts people off neurology. They, they are, I think on the whole fairly difficult questions but stuff that certainly can come up and I guess I've just tried to pick out things that are a bit trickier. So if, if you did find that tricky, please don't be disheartened. Um, it's just, you know, there's no point in going through stuff that people are already going to know anyway. Um, if you see what I mean? So, uh thanks everyone for, for engaging and coming along. I'm very happy to hang around and go through some extra slides. We've got or answer questions if people have any. But if not, it's, uh what's, that must be about eight o'clock now. Um But yeah, thank you. Thank you very much. And that was an excellent presentation. Uh If anyone has any questions, you can put them in the chart, we can stick around for a couple more minutes. And so I would like to let, let the audience know that you'll receive a feedback form after the event. And after that, you can, you'll receive your certificate after you've Yeah, thank you. I just, I just sent out there. Thank you. Oh, yeah. So the link to the feedback form has just been put in the chat. So yeah, we'd be very grateful you could fill that out. Thank you. Uh Oh do uh mark, we actually have a question uh just asking uh confirming that they're going to get the slides. I'm, I'm, I'm happy to send them out. It was one of the bits of feedback from last year was if it's possible to get them. I've, I have no problem with sending them. I don't know what the easiest way of doing it is is whether we send it to yourselves. The other thing is, I don't know, last year a session very similar to this one was recorded. So I don't know if people who weren't at that one can navigate back to it because the slides are also recorded there. But whatever is easiest. I'm happy to send a PDF of them to an address. I don't know. Just let me know after the event. I don't mind. Yeah. No, I just pop and we can, we can sort it out through the social media, um put a link for it through that. Sure. Thank you. Similarly. Again, if there's stuff that folk weren't covered in, I think it's the 22nd we're doing another sort of similar thing. There's a few other kind of themes, there's a bit of a stroke theme to the first half of it and then a few other kind of just a random bunch of other neurological stuff. But if there's anything that that's not been covered or that people want to be gone over, very happy to tailor it to that as well. So now's your chance um to put it in. Yeah. Uh Also there was a question from Nicola. Yeah, we'll, we'll discuss it with Mark. And what might happen is we might get the slides from Mark and then forward it to the people who attended and then you can share it with with your class. Hope that works. Uh Yeah, we, we'll have them emails um under the attendees. I think so. Yeah, we should. Yeah, we'll do that. That, that works best actually. Um So yeah, we'll just, we'll just send it out to the email which you signed up your, your um medical account with. So if there aren't any questions, I would like again to thank Mark and Jua for coming tonight and for your wonderful questions and your great teaching. And I would also like to let everyone know we have another teaching plan for next week, the 22nd for it is more so focused on preclinical years. But again, we'll have uh more questions and practice BS and stuff like that, which can also help for our revision as well as fourth years and third years. So thank you very much. Again, Marin Ju I don't know if you'd like to say anything else, but yeah, thank you. No, all good. Thanks for coming and thanks for organizing it. Much appreciated. And uh thanks Gilla as well. Just please make sure you do do fill in the feedback one to make them better as we go on and two for, you know, for portfolio purposes, it's so useful for me and Gilla as well. So I know it's always a hassle, but please do. I just wanted to say thank you everyone um for organizing and also for everyone for joining. I hope that was useful. Yeah, absolutely. Well, thank you, everyone. Have a good night. All right, cheers guys. Thank you. Goodnight.