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I'm, uh, where? Oh, that, as far as I'm aware, er, is all you would need to know, er, for MS for your finals. Uh, if you have questions as we go, the chats, but otherwise I'll probably do them all at the end if that's ok. Uh, so question two, I've put three scans up. Uh, this is three different head CT S. Um, and what I'd like is for somebody to essentially write down in order, uh, what they think each of those CT S show, uh, they're all types of bleeds as a hint if you go from left to right. Oh, and it said sub epidural something or other good. Anyone want to hazard a guess at what? There's something or others? Excellent. Excellent, good. Ok. Um, all really good suggestions. Sorry, I should say that this is pitched at finalists. Um, so if you're not getting ready to sit finals, then a lot of this will probably be, um, more detailed than you'd be expected to know for sort of specialty year exams. Um, but you're absolutely right. All of you. Uh, so here we've got a subdural hematoma. Uh, and the reason you can tell that is it crosses uh our normal borders, which means you can see it extends all the way along the curve here and you can see that it's essentially the way I would describe it is, it's just white and the rest of the brain is dark. So wherever you see these white bleed that crosses the borders, that's always going to be a subdural. Um I for some reason, uh have I, I've always called it unlimited sub caves. Uh It means absolutely nothing except it means it's, it's unlimited by suture lines. Um It's a subdural and it's called a concave shape. Um Obviously, that doesn't really work that well because you've kind of got to remember three nonsense words, but that's how I remember it. You're extradural. This is very, very classic. It's that normal uh lemon shape. Uh But what's important about it, an extradural if you can't pick it up from the shape is that it doesn't cross the suture lines of the brain. You can see that there is a degree of midline shift in all of these bleeds. So here you can see the ventricles are pushed off to the left and then you can see the ventricles are pushed off to the right. Um But absolutely correctly identified. The last one is a chronic subdural with an acute uh involvement. And the reason you can tell that is this part which is darker than the rest of the brain up here is a previous subdural that's essentially uh gone to sleep. So that part of the brain is now no longer working, but they then had another acute bleed on top of that. So this is an acute on chronic subdural. Again, with midline shift, all of these patients would probably have very poor prognoses because of the midline shift. Um But again, there are treatments for all three which we'll go through before we do that. Got another question uh which is somewhat related. Um This is a, so you're the F two on call on the acute medical take, it's an 83 year old man uh who's quite tachycardic and he's got an irregularly irregular pulse. And when you do his neurological exam, uh he's got reduced power in both the right arm and leg and a homonymous hemianopia. Uh He's obviously he's got an obvious dysphasia as well and his BP is 100 and 78/100 and six. So he's quite hypertensive. Uh The weakness started after he woke up three hours ago and he slept for nine hours and his left side is entirely unremarkable. Uh And his right side has no sensory deficits. So this is probably the most difficult question actually, which vessel was most likely occluded in this patient? Um But what diagnostic investigation should we be doing for this patient straight away if they come in with these symptoms? Good. Yeah, you get a CT head straight away um to be Frank uh as an F one. If you're about to start, if you have a patient with any neurological symptoms or any history of uh fall, you're gonna get them a head ct non contrast immediately. Anyway. Um And it's a non contrast ct that you do straight away because it will give you all the information you need. Um What treatment would this patient be eligible for Based on the presumed diagnosis? So, let's say that head ct uh comes back, not showing a hemorrhage. Uh And that we're probably suspecting this is an ischemic stroke. Uh What treatment would he now be eligible for? Good Aspirin. 300 mgs. I'm interested why you've gone for aspirin when there are other treatment options? Uh So Ella has said thrombolysis within 4.5 hours and it's non hemorrhagic. Um Good. So that's important. We've got a couple of varying answers. There is the aspirin. Uh because you think that he's outside the window for thrombolysis or is it because that's what you load him on anyway, you can also unmute by the way, if that's easier. Um But in the meantime, we'll say essentially yes, that we are gonna thromb this patient. Uh The reason being that he has presented within 4.5 hours, the sleeping for nine hours is an absolute red herring because this is a wake up stroke. He was well before he went to bed. Uh which means technically, uh, you have to give them the benefit of the doubt that they were. Well, right up until the minute that they woke up and that's when the thromboembolic event could have happened. And therefore he is within 4.5 hours and he's eligible for thrombolysis with something like ALP places. Uh, and Sophie's also said, could we consider thrombectomy as well? Absolutely. You could and he could definitely be eligible for it. Um And finally, what should we do about his BP? Because he's pretty hypertensive. Are we gonna control that or not? No idea. Yeah, not acutely good. Excellent. So, absolutely. Right. We're gonna get him a ct head straight away. Um We're going to get, we're gonna, he might be eligible, sorry, he's definitely eligible for thrombolysis. He might be eligible for a thrombectomy. Uh And we're gonna do nothing about his BP in the acute setting uh because it's less than 100 and 85/100 and 10. Um That's the target if you're gonna thrombo somebody. And the only other reason to acutely lower a BP in a stroke is if it's a hemorrhagic stroke, uh and the vessel that's probably occluded is a middle cerebral artery. So, again, super busy, sorry. Uh I'll go through it, but again, I just want it to be a revision slide for you basically. So, ischemic strokes rather than hemorrhagic strokes. What are your risk factors? Well, atrial fibrillation is one because you get clots forming in your atria, uh, which then when you've got a, um, a inefficiently pumping Atria essentially just blasted out. Uh, and it goes up to the brain. Uh, any sort of cardiovascular disease is a risk factor. Uh, and then essentially the way I would remember it is anything bad for your heart and your body is bad for your brain and it's going to increase your risk of a stroke. Uh And any thrombophilia or any sort of hereditary syndromes are also gonna be pretty bad pathophysiologically. You get the clots or the embolus which forms uh and then around that, you get this area of completely non viable, destroyed tissue from absolute ischemia, but the area around it, which is fine is your penumbra. Um And that's here. So you've got your core and you've got your penumbra and the aim of thrombolysis and the whole aim of the game in stroke is essentially to try and save as much of this penumbra as possible because the core is gone. So what whatever is damaged in the core is, is not coming back, the classification of stroke. There's a lot, we're not gonna go through all the syndromes because I don't think it's super high yield for finals. Um But just generally remember that you can get a, you can have a clot or you can have an embolus. So an embolus is something that comes from somewhere else in the body. Um a clot is something which forms in the brain and then occludes that vessel in the brain. Um But there are other types of strokes that you can get. So, for example, in a cardiac arrest where you've got absolute lack of cardiac output uh for a reasonable amount of time until CPR starts, uh you get absolute loss of perfusion to the brain. Uh And technically, that's a form of an ischemic stroke as well. Sinus thromboses are important to know about. Those are your venous sinus thromboses. So that's different. And those are treated with anticoagulation instead of thrombolysis. So you start them on a doac uh or treatment dose, low molecular weight heparins. Um And vasculitis is, are sort of rarer causes of strokes as well, which are important to know about in terms of your symptoms. You'll all be aware probably of the fast um sort of recognition for the public. Um But you also need to know about your Bamford classification which allows you to identify which vessel was probably occluded, which I'll talk about at the bottom there. Uh And diagnostically, you get them A CT head straight away, control their blood sugars, particularly if they're diabetic. Um And you need to get them a CT angiography or an MR angiography to work out whether they're a thrombectomy candidate, the place for them to be treated is definitely in a hyperacute stroke unit. There's quite a few of them, but when you're the f one in a few months time and your patient comes into hospital. Um, if you think that they're, they're suffering from a stroke after getting their CT head, you need to call your nearest Tau. If you've not got one, the hyperacute stroke unit and you need to get them over to there cos that's the best place for them to be treatment for stroke. It looks like most of, you know, that pretty well already. Um So if it's less than 4.5 hours, it's thrombolysis. If it's between 4.5 to 24 hours, uh they could be a candidate for a thrombectomy. Typically, we call it before six hours has to be a thrombectomy. But you're technically a candidate for a thrombectomy. If you've got an occlusion of your proximal anterior circulation, your proximal posterior circulation as somebody has stutely pointed out already. Um Or if there's literally anything salvageable because you don't need to get super academic with this. If you can get something, if you can essentially take like a um a clock retriever, put it into a vessel and pull it out, you can target it with thrombectomy. Um And that's the way I'd remember it. But absolutely for exams proximal anterior or proximal posterior just because you can reach them quite easily uh through IR approaches or interventional radiology approaches. If you've got a hemorrhagic stroke, uh most of the time it will be medical management. Uh reverse whatever their anticoagulation is and control their BP. But if they're super sick with it and they're a surgical candidate, uh, then you can evacuate whatever is hemorrhagic there as best as you can. Again, your golden words here. Um, I can't actually because I've lost this. There we go. There we go. Um, remember that if they're after 24 hours, they might still be a thrombectomy candidate. If there's something salvageable. Um If they have an irregularly irregular pulse, then it's probably af and you should be thinking about a stroke or a tia a remember and this is a really common pitfall. If they woke up with their symptoms, the clock starts from the point that they're awake because you have to give them the benefit of the doubt. Um And remember that everything in stroke is contralateral. Uh So if you get a stroke on your left hand side, then your symptoms are gonna be on the right hand side. Now, in terms of the different stroke syndromes that we have here, which are important to know. So I'm trying to minimize this. So I can see my own screen um good. So you can have strokes in various types of your vessels. If we start at the bottom, if you've got a small vessel stroke, it tends to be these weird pure sensory deficits, pure motor deficits um or sort of an unusual sensory motor pattern, but these are just small vessel strokes um but they can still have those facial groups. Uh If you have a total anterior or partial anterior, it depends on whether you have two or three of your Bamford Bamford criteria. So if you've got the criteria, a contralateral sensor, sensory or motor loss of the face arm or leg, a homonymous hemianopia or higher cerebral dysfunction. If you've got all three of them, that's a total anterior stroke and that's an occlusion definitely of either your middle cerebral artery uh or it could be your internal carotid as well. Uh You shouldn't forget the carotids. Um If you have only two of those, whichever two of them they are, it's probably an anterior cerebral artery stroke and we call it a part partial anterior stroke. Um and then posterior, to be honest, can be absolutely anything. Um Again, I wouldn't worry too much about learning all of the details. I don't think it's super high yield. Um But try and remember the indication for thrombolysis and thrombectomy cos that does come up a lot in finals and finally, to do with BP control, essentially, it will nearly always be a red herring in the final in finals because you normally don't treat ischem. Uh Sorry, you don't treat hypertensive uh urgencies unless it's an emergency. In which case, obviously, you have to treat it as usual. So that's um evidence of end organ damage. Um If you're going to thrombose them, you should try and lower the BP to less than 100 and 85/100 and 10. And the reason why is because in thrombolysis, your risk of hemorrhagic transformation. So, changing your ischemic stroke to a hemorrhagic stroke is quite high. Um And the higher your BP is, the higher that risk is, that's the only reason you try and lower it in an ischemic stroke. But in a hemorrhagic stroke, you should be more aggressive, uh, with BP lowering. Uh, don't drop it by more than 60. Um, and if they're gonna be a surgical candidate, then don't, don't even bother with the BP. Just take them to a neurosurgical center and they'll sort it out good. Uh, you can see stuff in the chat. Um, what medication would you use to reduce BP if it's over 100 and 85 or a hemorrhagic stroke? Acutely? Yeah, this is a really good question. It's really important as an F one as well because one of the most common bleeps you'll get is, uh, doctor my blood, my patient's BP is really high. Uh, what can I do and what you shouldn't do really is prescribe them any of your normal BP medications you're familiar with, uh, because they take way too long to work. So you're probably going to look at IV anti hypertensives. Um, and that's what's going to reduce your BP quite quickly. Definitely don't use CBS like amLODIPine they are rubbish and they take ages to work. Um, so you're probably going to look at IV antihypertensives to try and control BP. Good. It's important, you know, a little bit about TI A s because they're important. Um, we now use tissue based definitions rather than times why. I don't know because it's kind of crap because we don't get that much information from on a tissue level unless you, uh, MRI perfusion study somebody. Um But the important stuff for your TI A S is that it's a fully resolved episode of sudden onset neurological dysfunction. So, whatever the neurological deficit was, it has to have fully resolved. Otherwise, it's not ati A, it's an ongoing stroke and should be managed accordingly. Um If the TI A was within uh the last seven days, you need to refer them into Ati a clinic within 24 hours. If the ti A you suspect was more than seven days ago, then they need Ati a clinic within seven days. Kind of makes sense in terms of how quickly you need to load them with medications. Uh Don't use scoring criteria acutely like your ABCD S. Um And the advice and the exam advice is to get an MRI over the CT on the same day. Now, practically, when you're an F one, not in a million years are you get to get an MRI on the same day for a TIA A? But the exam advice is it's an MRI and again, technically, you should get an ultrasound of your carotids on the same day. Again, not in a million years. Is that actually going to happen in practice? Um, but, uh, that's the exam advice again, um, and the treatment for this uh is always going to be 300 mgs of aspirin quickly. Um, plus any secondary prevention, um, things which we've talked about underneath and you're gonna load them up with that for two weeks. And the secondary prevention er is cloy or aspirin plus dipyridamole if they are cloy sensitive, uh and you should start them on a statin really and you want to reduce their non HDL uh by over 40% if you can. And the other thing which often causes a little bit of confusion is when to do things for their carotids. So the guidelines in Europe are, if their carotid stenosis is more than 70% then you consider a surgical approach to that or if it's more than 50% in North America, then you consider a surgical approach to that to try and manage things because as we talked about earlier, if you do get really significant stenosis of your carotids, and you get, for example, what then essentially becomes an internal carotid artery stroke. Uh you get really, really nasty symptoms with that. It's a full anterior uh sorry, a a total anterior circulation stroke, any questions on tia S or strokes. Otherwise, I'll keep going. No, let's go. OK, next question. Um So here you're the F two. and for your SIMS, you've been put in the intensive care unit. Uh One of the nurses has asked you to see this 33 year old female patient uh who's on BIPAP and she's now got worsening respiratory distress uh but is still maintaining her oxygen saturations. Uh She was admitted to the ICU with an acute myasthenic crisis. She's been getting IV immunoglobulins as per your hospital protocol already. Uh And she's been heavily immunosuppressed already. So again, sorry, I should probably have changed the order of questions. I asked, I asked the first, the hardest one first. Uh So let's start with the second one along which is what antibodies does the patient most likely have. Uh So these are the antibodies that 80 to 85% of patients have in er myasthenia gravis. Good anticholinesterase. Excellent. Ok. Um We'll come on to the specifics of that afterwards, but let's leave that there for now. Um She got a CT chest Abdel s on admission for some reason. Um because she's 33 I don't know why you'd radiate somebody like that, but let's say it happened. Uh What is the malignant? Yeah. Very good, sir. What's the malignancy that you're gonna have? Yeah, it's probably a thymoma. Excellent. Um And what additional acutely does? Yeah, very good then. Um what additional acutely disease modifying intensive care treatment should be considered at this stage, I don't want you to tell me what extra ventilation she should go on to because I don't know the answer to that. But what's the, uh, what's gonna help her acute myasthenic crisis? She's already on immunoglobulins. Uh, and she's on steroids as a hint. This can, yeah. Very good. Sorry. This can only be done in the intensive care unit. Uh, there's one other thing you can give them as well. If they're already on steroids, you can deplete their immune system even more uh via another medication which is usually riTUXimab um in an acute myasthenic crisis. Um good. So it's plasmapheresis is the additional treatment which you're gonna get. Why? Well, essentially it's just gonna try and get rid and wash out of all of the er really nasty antibodies that are causing your problems. Um Absolutely right. Ben corrected it correctly. Um And we'll come on to the different sort of antibodies you get. Um, and it's a thymoma and Thymomas are really associated with um myasthenia gravis. You don't really see that robust in association with, with anything but this is about 30%. So again, if we look at this busy slide, uh epidemiologically, there's two peaks of myasthenia gravis. It's women under 40 men over 60 we call it a double peak. 10% of cases are in Children. And that's important to remember for your finals and there's this very strong association with di moments. Um It's I believe it's uh something like 30% of patients with a thymoma will have myasthenia gravis. And then 10 to 15% of patients with myasthenia gravis will have a thymoma. And it's just because of the relative like prevalence of both of those. It could be the other way around. II can't quite remember. Um pathophysiologically. Yes, you get this anti acetylcholine receptor antibodies binding to your post synaptic membrane for finals. Just remember what they are. Don't remember the pathophysiology that well, I just find that it helps to contextualize and understand the conditions a little bit better. Um So your symptoms are, you get this muscle fatiguability in the distribution of your diagram. So it's your small muscles of your head and neck. And that's why you get things like diplopia, your ptosis. A very weak swallow, uh chewing, fatigue, slurred speech. Uh and then it's your uh muscles of your proximal limbs as well, which is why it's difficult for them to stand up from a chair. Um And it's difficult for them to uh abduct their arms as well. Your symptoms are worse at the end of the day and that's because of your muscle fatiguability. Um For your diagnosis again, clinically, it's that classic one where you ask them, uh you put your, your finger in front of them, you ask them to keep looking up. Um and that worsens both their diplopia and their ptosis. But then most importantly, you need to get them an antibody test because you need to look for your anti acetylcholine receptor er antibodies. Um But also you've got those rarer ones. I don't know whether you need to know this for finals. I put them there because they do occur. Um and it's probably worth knowing about. But yeah, main one. Ach R um you should get them a CT or an MRI of their thymus or imaging that can capture their thymus because of the very, very close association with Thymomas. Um An electromyography is also important treatment wise. Um Pyridostigmine is typically what you start with, which is your long acting acetylcholinesterase inhibitors. The reason that's important is because your acetyl your cholinergic signaling uh at your neuromuscular junction isn't working very well. So what you want to do is try and stop the enzyme that's breaking down your acetylcholine cos that's just gonna compound the problem. So if you inhibit that enzyme, you get even more acetylcholine at your N MJ or your neuromuscular junction, which means that you're gonna try and reduce the symptoms or try and reduce the severity of that impairment. Um Again, as with most of neurology, corticosteroids and immunosuppressants have a place as well. Um And then quite interestingly, there's a lot of evidence that you should just take out the thymus for everybody. And there's a really cool clinical trial. Um the M GTX trial which showed the evidence for that, which is that patients do better if you take out the thymus um in the crisis setting, it's IV immunoglobulins, plasmapheresis, riTUXimab. And they will need an IC, they will need an ICU admission likely for ventilatory support as our patient was on bipap already. Um And the other thing which comes up a lot in finals is it's quite a difficult question is to stop any drugs which are gonna be exacerbating things. Um And these are the common ones that you need to know about. So your beta blockers, your penicillAMINE, lithium phenytoin gent macrolides and tetracyclines. Uh So those are the important ones you need to know about. Uh it's annoying but it came up in my finals. So it, it's, it's worth knowing about them. Um And then you've got uh the important uh distinguish uh the important way to distinguish between myasthenia bras and Lambert Eaton syndrome. Um And that is essentially just remember they're kind, they're similar, but in reverse. So you've got muscle fatiguability in myasthenia gravis, but instead you've got incremental muscle response. So the opposite in Lambert et syndrome, the type of antibodies that you see are different between the two of them and you need to remember that it's the presynaptic voltage gated calcium channel antibodies for Lambert Eaton syndrome. Um The distribution is different for both of them. So it's the head and the proximal limbs in myasthenia gravis. It's the totality of the lower limbs in Lambert Eaton. Um And then like I say, the association is different. So it's a thymoma and myasthenia gravis and it's small cell lung cancers or breast and ovarian cancers for Lamin. But the treatment is the same for both. Um because like we say, if you think about pathophysiologically, what's happening, it's the same thing for both but with different receptors. Um and therefore the treatment to clear it out is going to be the same good. So that should be everything you need to know about myasthenia gravis for your finals as well. Excellent. Um Fine. What are the differences between upper motor neuron and lower motor neuron clinical signs? This is particularly important for your Aussies that you're gonna sit in finals. Um So does anyone want to throw out some of your upper motor neuron signs? We're nearly there. But we've got three questions to finish the rest of neurology, Affin uh Good babinski positive. OK. Anything else for for up to neuron science? Hyperreflexia? Good alexander. Anything else for your up me? Excellent hypertonia? Ok. No muscle atrophy. Excellent, good. So my really quick way of remembering this is essentially upper motor neurone, upper, everything is up and lower motor neurone, lower everything is down. And what do I mean by that? Uh Well, for upper motor neurone, you get hyper reflex here, increased tone. So hyper Tonia, uh your plantars are upgoing um and you get minimal dys use atrophy. So you don't really get that much muscle loss. Uh Whereas in your lower motor neurone science, everything is down. So you get hyporeflexia, uh hypotonia, your plantars are normal. Um And you get muscle atrophy and essentially anything which happens in your lower motor neurone systems, you get things like twitches as well there. Um So for me, that's the quickest way of remembering upper motor neuron, everything's up, lower motor neuron, everything is down uh Good. What do I mean by plantars up, going and downgoing? So, do you remember the test where you, oh, sorry, plantar is no good. Um Do you remember the test in the neurological exam where you ask the patient to take their socks off and then you get the end of your tendon hammer. Uh, and you go around the outside of the foot and roll up towards the toes. Uh, if your toes go up when you do that, that's called an upgoing plantar response. If your toes do nothing or go down, technically. Um, then that is a normal, uh, slash. It could be a lower motor neurone response, but I wouldn't e essentially the main one here is your plantars being upgoing is an upper motor neurone response. Um, if they're, if they're downgoing that that's normal and all, I mean, by a lower motor neuron sign that they're normal is that you can't take a normal plantar as being a sign of anything. Does that make sense? Hopefully good? Um Cool. Ok. Uh The other thing which I just do want to point out for this because it's important for finals is what we mean by hyperreflexia. So, if you've ever tried to test your own reflexes out, which you would have, you would have found it's quite difficult. If you've done it on somebody else, you would have found it's probably a little bit easier. And the one we typically find easiest to elicit um is your patellar reflexes. Um But what we actually mean by hyperreflexia is that absolutely, everyone should have a reflex response under gravity. So that's why we have tendon hammers which look like, you know, it's got the or the, the queen square tendon hammer is the one which is long uh with the circular thing at the bottom. And the reason that neurologists are so um specific about you just swinging it under gravity is absolutely, everyone should have a reflex response under gravity. Now, if you slow down the tendon hammer, ie now you're physically trying to slow it down when you're hitting the reflex and they still have a reflex response, then, then we call that hyperreflexic or a brisk reflex. Uh And what you'll find is somebody with a really severe upper motor neurone problem is you can elicit their reflexes just by essentially hitting on it with your finger um at a low velocity and that's severe hyperreflexia. So that's what we mean by the difference between sort of a normal reflex or a hyper reflex. Excellent. Um This is our penultimate question. Um It's just a, a quick pattern recognition one around headaches because they come up a lot in finals. Um So you can put them in order of what you think each one is. First, you're an F two and GP 26 year old has a unilateral headache associated with photophobia and nausea. The second, you're the F one in the ed, 33 year old man has come in with his third really nasty headache of the day each last 30 minutes and he's got a red eye and he's crying from it. Um And in the third, you're in the A DC clinic and a 74 year old man with known polymyalgia. Rheumatica has presented with two weeks of a unilateral headache worse when chewing. So if you want to just write down in order what you think each of those headaches are good. Migraine cluster GCA fantastic, very good temporal arteritis is the last one. Everyone knows those which is excellent. Um I'm not gonna just in the interest of time. I'm not going to spend too much time on the treatment for each of those uh for anyone who has pass med, uh the treatment is uh explained very well for each of those, but it's important to know about them. Um And it's also important to know specifically about the treatment for cluster headaches in the acute setting. And it does require admission to hospital because they often need high flow 100% oxygen. Oh, yeah, you've, you've got this. All right. Fine. Our last question uh for neurology. Uh you're the F two in the EED. Uh, you've been asked to see an 83 year old man with known Parkinson's disease for more than 10 years. Uh He's been brought in by ambulance with sepsis secondary to an aspiration pneumonia. He's very confused, very agitated and he's got a completely unsafe swallow. Uh No, difficultly, he takes oral Cocca dopa for his Parkinson's disease. Um, his family who were there, uh, despite him being septic, secondary to an aspiration pneumonia are most concerned at the moment about his Parkinson's disease medications as his motor symptoms, uh have got much worse quicker than they did previously by that. I mean, previously, his co dopa meant that he was actually fine during the day. Uh, but now his Parkinson's symptoms and his motor symptoms get worse quicker than they did before. So first question is what should we do about his Parkinson's disease medications in this acute setting whilst he's septic? Can we stop them or is there any other option we have for him? There's a hint he, he can't have anything orally because he's got a completely unsafe swallow. Anideus uh, transcutaneous patch. Excellent. Yeah. Really good. So we're gonna put some sort of patch on him. Uh, do you know what med we normally put in that patch? You can't put levodopa in it frustratingly So it's usually a riot patch uh is what we use. Um One thing just to be aware clinically is that riot patches aren't great. They tend to make patients particularly with cognitive impairment. Um a lot more cognitively worse as well. So some neurologists are really against Ticotin patches in the acute setting. Um But as the F one on call, uh they do still need dopaminergic placement. Uh So you're probably gonna whack a patch on them in the interim. Um And what phenomenon of levodopa use is his family describing? So the fact that it, it's not working so well anymore, he essentially only gets a couple of hours of motor symptom relief. Um And then they get worse again. There's a name for that phenomena. It's not a particularly complicated name as it kind of says, what is it on the 10? No, it's your pen. Pee. No, there we go. Um It's your on off effect. OK. So you've got Riot Patch uh is what you're gonna do acutely. Uh And we describe this phenomena of levodopa as your on off effect. Uh really importantly for this NG tube. So you can put NG tubes down patients with unsafe swallows um to give them their oral medications. But the reason you're not gonna do that here, um The trick and the question is because he's super agitated and confused, which means he's just gonna pull it out. Um And it's, it's just gonna be really traumatic for everyone involved. So, Parkinson's disease and this is the final one, which we'll go through today. Epidemiologically associated with older age. Um less than 10% of the cases are autosomal dominant or monogenic and those are associated with your SNC uh genes most commonly. Um And we know that pathophysiologically, there's lots of gene environment interactions that contribute to it. 1% of everyone over the age of 60 will have Parkinson's disease. And that's, that's quite staggering actually. And a lot of patients that you're gonna see, particularly when you work in your district generals as uh as F ones sooner will have Parkinson's disease. Um We know pathophysiologically, it's the loss of dopaminergic neurons in the substantia, nigra pars compacta. Uh and you get these Lewy body deposits everywhere. Um But quite frustratingly, the onset of symptoms doesn't actually occur until you've lost more than 90% of all your dopaminergic neurons. Um So it's quite important just going forward in terms of research that we find ways of uh identifying which patients are at risk of Parkinson's disease. So, if they do become disease modifying treatments, they can get on them uh before they lose all those dopamine neurones cos once they're gone, they, they don't come back. Um your symptoms as most people are probably familiar, it's the classic triad. You get a resting tremor, usually unilateral. Um But the better word to describe it would be asymmetrical. So you can have a tremor on both sides, but one side will be worse than the other uh bradykinesia. So everything moves slowly and rigidity on the neurological examination. And we typically call that cogwheel rigidity. Um And the other things which you get are essentially remember, everything is just slowing down and smaller. So, hypomimia uh means an absence of facial expressions, basically uh micrographia. So they write really small. Uh They get a shuffling or a fascinating gait. So you've probably seen the classic Parkinson's gait where they're kind of stooped over and they struggle to get going as well and that's bradykinesia. Uh cognitive problems are really common smell loss, um RBD sleep disorder and postural instability. So, always remember patients with Parkinson's need to be screened for their falls risk. Uh not only because of their gait but because they can often get quite nasty orthostatic hypotension uh diagnostically, it's done clinically. Um But if you absolutely can't d differentiate an essential tremor from Parkinsonism, I say that you can do a spect scan for them, er, which I've put at the bottom here is there's a DAP spect scan and you can see the comma shaped um er the comma shaped areas around the basal ganglia here, which is more consistent with an essential tremor. Uh Whereas Parkinsonism is associated with these period shaped um areas around the basal ganglia and that's more suggestive of Parkinson's disease and that's a spect scan there. Um You also need to exclude your differentials. So, particularly if patients uh psychiatric patients who have been treated with antipsychotics for ages, which suppress your dopaminergic systems. Um If you take them off the antipsychotics, sometimes it's irreversible. Um but sometimes that can improve things quite a lot as well and treatment wise, the main thing I want you to remember is if you've lost your dopaminergic neurons, you need to replace your dopamine. Um and we can do that either via levodopa. Usually that's in the form of Co Carol dopa uh which also has another medication which stops the er breakdown of your dopamine as well, quite well, both peripherally and centrally. Uh And then you've got your dopamine agonists, your bromocriptine and your cabergoline, which are separate. So this isn't specifically dopamine replacement. This is trying to encourage your brain to make more dopamine. Uh And then you've got your monoamine oxidase B inhibitors which are selective inhibitors. So, your selegiline and your sag, the other syndromes that are important to know about are your Parkinson's plus ones. Again, I've not gone into detail cos I think it's quite high level and I don't think it's quite, I don't think it's too high yield, but you should know that multisystem atrophy, corticobasal degeneration and progressive supranuclear palsy are your Parkinson's plus syndromes which are all slightly separate. Um And they're all usually more characterized by their um er systemic problems, your orthostatic hypotension as well. Um And you get some gays palsies with some of them too, but I won't go into that. Good. I think we've run roughly to time. Um, so that is everything that I wanted to talk about. But I'm very happy to answer any questions. Um, and I'll also put my email in the chat so you can email me if you've got any questions. I'm always happy to answer anything about, um, careers or, uh, neurology, neurosurgery. Uh, if anyone's interested in those two, good, uh I'll hand back over to the ma Perfect. Thank you very much, Ash. That was very informative. Um I've put a link to the feedback form um in the chat. Um Ash, are you happy to share those slides? Yeah, of course. Yeah. So obviously if you fill out the feedback form, then we can get your um email address and we can email across those uh um those slides and then Ash has put his email in as well, but I'll hang about for a bit and Ash will hang about if anybody's got any questions other than that, that's all from us tonight. Um We got another event next Monday which will be rheumatology.