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Right. Um So welcome back everyone. My name is Doctor Taba Khan and I am an fy one and our topic for today is going to be um neurology. Um So here's some of the topics that we'll be covering today and we'll be running through some of the most um important aspects of neurological conditions, um which would be relating to um, stroke, epilepsy and seizures, um Parkinson's disease, cranial nerve palsy, multiple sclerosis, um guillain-barre syndrome, um peripheral neuropathy. Um and we'll also be learning how to localize um some neurological diseases, um and how to choose the appropriate investigations and treatments and also to run through some of the common misconceptions that you come across in neurology as well. Um The session is going to be question based. So I would appreciate it if you guys try and participate. Um I've set up some polls, um which I will try and see um if I get, I can get them to work um with the slides. Um So here's the first questions um for you guys to read. OK, you can put your answer into the pole. Mhm. Four. And can you see the questions now? Oh, is that OK? All right. Um So we'll try again. Um have a read of the questions and, and put in your answers into the pool so we can start discussing it. All right. Um So the answer is a total anterior cerebral infarct and more specifically the right anterior and medi middle cerebral arteries. Um So this is a 65 year old male who's presenting with um sudden onset, left-sided weakness. He has a past medical history of type two diabetes and hypertension. Um We've done a physical exam and that showed us that there's reduced power in the left arm and left leg. Um There's a left sided uh homonymous he heia um and left-sided neglect as well. Um There's no facial weakness. Um So which one is the most likely diagnosis? So, the likely diagnosis here is an acute ischemic stroke. Um The point is to correctly try and localize the um um stroke to the correlating area. Um So you'll know that when we localize the right side of the cerebral cortex, we supply the left side of the body and vice versa. So that's why it's on the right side. Um The next aspect to look into is whether or not um it's a total or if it's a partial uh anterior infarct or if it's a lacunar stroke. Um usually with lacunar stroke, it's less likely to give you such widespread symptoms and more likely to um lead to some focal motor or focal uh sensory disturbances. So therefore, it's less likely uh to be a lacunar stroke as for the other options. So, if you look at the total or partial anterior cerebral infarct, um you can see there's a lot going on here. So there's a reduced power in the left arm and the left leg, there's left-sided, um homonymous hemin noia and left-sided neglect. So even if you were to sort of he your bed, you might consider it to be total rather than partial. And then, so you can narrow your answers down. Um And so that would make it the correct answer. Um But you also might be aware other than what we've just discussed, there is something called the Bamford classification or the Oxford classification of um the acute stroke. We'll go through that in a minute as well and that might sort of help you localize the stroke further. Um OK, next slide. So there's different types of strokes. Um As you know, there's two different types, broadly speaking, um there's ischemic, which is about 85% of the strokes that we see. And there's uh hemorrhagic strokes, which is about 15% of strokes. Um So you can see on the left hand side, there's uh this hypodensity um on the left side of the brain. And you can see that that's a very large ischemic stroke. Um Whereas on the right-sided image, the right hand side, um um you can see there's um sorry, on the left hand side of the right-sided image, you can see there's hyperdensity and that's, you can see it's consistent with a hemorrhagic stroke. Ok. So discussing the risk factors, um as you can see, there's multiple and they tend to relate to um vascular risk factors and equally they're similar to um to some extent to cardiovascular disease risks, um as well, um such as um the age that matters, uh male having a male sex, um female history, if you've got of ischemic stroke, uh if you have a history of um sorry, I said female, I meant family history of ischemic stroke, hypertension, smoking, diabetes, high cholesterol and atrial fibrillation. Um And the main bit that I've highlighted here is um af so af is a very important risk factor for ischemic stroke. One reason is because um there is a treatment for it. So if you are to treat someone with the anticoagulation, it reduces the risk of the patient having strokes further. Um So it's something you always need to look out for in the early stages and you'd want to anticoagulate the patients, um who had a stroke, um who also have af and you can do that by looking at the ECG and you can see that um I've given an example here, I'm sure you all know, um if there's an irregularly irregular heart rate, um there sometimes can be a lack of P waves as well and that's how you recognize your classic, um, af um, so with hemorrhagic strokes, next, um, we have similar vascular risk factors but also there's others such as being on anticoagulation in the first place. Um So that's a contrast with our EF ones where we're starting them on, um, anticoagulant. But for hemorrhagic strokes being on anticoagulant already is a risk factor. Um, are less important risk factors. Um, would be, um, the ones that are mentioned here, but it's again important to ask anyone with a hemorrhagic stroke. Um whether or not they have had any recreational drugs and also if they have any family history of vascular malformations. But again, this, this is a smaller subsection of patients with um hemorrhagic stroke. Ok. So this is um going back to the Bamford or the Oxford classification of stroke, which we were talking about earlier. Um You can roughly divide it into anterior lacuna um post and posterior stroke. Um I've sort of just left these here to show you um what each of them represent. You can have a good read of it. But roughly speaking, um your anterior circulation uh stroke can be either total or partial depending on how much of the brain is affected. Um therefore, with a total, you would expect sort of the anterior uh cerebral artery and the uh medial cerebral cerebral artery to be affected. Um Whereas with partial, it's either anterior cerebral or middle cerebral. Um and equally with lacunar stroke. Uh you would have expect that it affects essentially the very deep sort of perforating arteries. And you would expect um pure motor, pure sensory and sometimes a sensory motor stroke. Finally, with the a posterior stroke, and they're more difficult to localize because they can be quite variable in their presentation. So this can lead to uh cerebellar dysfunction. Um can also have problems with the brainstem um subsequently leading to sort of eye movement disorders. You can have cranial nerve palsies have uh cortical uh blindness if it affects the occipital lobe. Um and these are secondary to um occlusions to your vertebra, basilar arteries and their branches. Um Again, these are less common than anterior circulation stroke, but they can cause a significant amount of disability. So you definitely need to have a high index of suspicion um in anyone who has a sudden onset neurological syndrome of uh any sort um because it could be anterior Laar or posterior stroke. Ok. On to the next question. So please have a read. Um I'm going to release the Maxol for you all to uh try and use. Um OK. So here we have a 72 year old male who's presented to A&E with sudden onset difficulty speaking um and inability to raise the right arm. And he has a past medical history of hypertension. He was last known to be functional three hours ago when his daughter spoke to him on the phone. Um physical examination, you can see he has a receptive aphasia and a right arm paralysis. Then you look at the BP, you see it's quite high, it's about 1 45/95. But otherwise, um he's quite OK, you do a CT scan and you see there's a hyperintense lesion in the left middle cerebral artery, um vascular territory. Um So you given the diagnosis, what, what would be the most appropriate acute management? Um So the answer for this, I will reveal it now is BM. So the main thing to notice here is that this is sudden onset. Um and then you can see what the CT scan is revealing very clearly to you, which is a hyperdense lesion in the left middle cerebral um artery. So, looking at this, as we said earlier, when we have a hyperintense lesion, that's more likely to be hemorrhagic other than ischemic stroke. And so if you keep that in mind and look at the answers, so if someone has a hemorrhagic stroke, um and you give them IV all to place and that's not appropriate as that, that's the treatment for ischemic stroke. Um when you are trying to break down the clot um with option C um the aspirin um that's again, usually used with ischemic stroke as well cause that's an antiplatelet agent and that will help us um with breaking down of the clot as well. So it won't be helpful then option D um with the clot retrieval um is usually used for large vessel strokes. So again, that wouldn't be appropriate because that's for ischemic strokes. Um And then finally, our option E Ivy labetalol. So that's a bit of a red herring. Um labetalol is very often used in patients who have hemorrhagic strokes. However, we would normally try and maintain a BP of about 1 40/90. So, in this particular scenario, the BP, although it is quite near that number, um we still wouldn't want to reduce it even further by giving labetalol. Um but in patients who have a very high BP, um say if it was 160 or 180 systolic, uh we might want to reduce it in the early period because that reduces the disability moving forward. So the answer is um supportive management in this particular case and that would be you doing e to e analysis um doing a fluid resuscitation, making sure the patient is safe and not um hemodynamically unstable. So, trying to stabilize them. Uh and you would do a neurological referral as well. And for that reason, um because it's hemorrhagic um stroke, uh you would require neurosurgery to be involved and you would want them to be assessed by the neurosurgical team to see um if there's any surgical interventions that that may be required, um that might be in their best interest. Yeah. So the next one, if you look into the different types of bleeds, we said earlier, um that we have different types of strokes, but there's also different types of bleeds that you can come across in your um practice. So, on this slide, you can see on the left hand side, there's some slight white aspects throughout the brain and that's sort of consistent with uh subarachnoid hemorrhage. Um So that would be when you have a bleed in the sub subarachnoid space and that often leads to an uh it, it often tends to be related to an aneurysm. Um for example, but it can also be caused by trauma. Um It's less um obvious compared to other bleeds that you'll see on here. Um So you need to sort of typically look into the middle of the brain to see if there's any evidence of hyperdensity, um which you can see is pointed by a nice little arrow. Um And that can be quite consistent with subarachnoid hemorrhage. Um If you look at the picture on the right, you can see that there's some movement of the brain um in the middle, which you'd call a midline shift, but there's also a hypodensity and there's a hyperdensity at the top as well. Um So on the bottom is hypo and on the um top, it's hyper as you can see. Um So you um would want to basically um look at it and you can try and figure out that there's something more chronic and there's something more acute going on here in terms of bleeding. So this is actually an acute on chronic um subdural hemorrhage. And it's sort of this um way classic concave shape. Um and that's more equivalent to a subdural hemorrhage. And if it was just an acute subdural hemorrhage, the whole thing you would see uh would be sort of um lighter in color, more white um rather than how it is now with a bit of white on the black. Um So on to the next. Um So in this slide, you can see in the left, um it's uh um in the left, it's a hemorrhagic uh stroke. And usually these types of strokes tend to be um more towards the midline rather than on the peripheries because um this sort of bleeding is related to um bursting of small arteries and therefore, it's more likely to be in the middle. Um And then finally, um on the right side, you can see a CT scan of um this epidural hemorrhage and epidural hemorrhage typically relates to um trauma. Um And because it's in the epidural space, um it can't quite push. Um And that sort of makes it look like um this um convex shape um and it's bound by the dura as well. Um So, classically, if someone, let's say, has a baseball bat to the heart, to the head, um or maybe they've come after a road traffic accident, for example. Um And that can be quite severe and um this sort of bleeding can be quite severe because of this sort of um trauma and the vast majority of these kind of bleeds, you will be expected to discuss with neurological uh team or neurosurgery. Um And you would need to discuss with them to see if they require a surgical intervention. Um So please make sure you have a bit of a read on the different types of bleeds and make sure when you discuss these um with neuro that you note down the G CS score for the patient that you're calling them up for. Um because the G CS score will basically help dictate um if surgical intervention is required or not. So the next slide and this is just something uh that was a bit silly that I used in med school. It doesn't make sense 100% but it does help me remember things. So um I would always be confused between subdural and epidural hemorrhage. And um so this is just what helped me uh remember. So subdural has bee in it, so banana and if it looks like a banana that's um subdural. Um and then epidural. So you think about a pie. Um And so you somehow remember a lemon meringue pie and, and that's how you can differentiate this. OK, on to the next um the acute management of stroke. So, the most important thing about stroke is that you make sure that you're quickly um acting on it and making sure that your patient is stable. So, as we mentioned, you do an E two E assessment um and then you do a CT head as soon as you can, if CT head is normal, you can treat it as an uh ischemic stroke. So the idea is that CT scan is not quite diagnostic um for a stroke, it just helps you to rule out any evidence of a bleed. Um, so if it's within 4.5 hours, um, and there's no contraindications and then you'll consider thrombolysis with alter place. But if, um, CT is with bleed, then you need to discuss with neuro. Um, and you also might, uh, want to do a BP control, as we mentioned before, um, which you should try and keep it, uh, at 1 40/90. But if CT is normal and you're not in a 4.5 hour window, um, then, um, if they have another reason to have a stroke, maybe you're thinking about af then you shouldn't be, um, giving clopidogrel, you should start them on, um, anticoagulation in the form of a Doac such as Apixaban or Rivaroxaban. Um, further investigations that you might want to do as to why they've had a stroke. Um, finally, um, normally you get this done by a neurosurgical, um, specialist. Um, sorry. Ok, sorry about that. Um, so you will, uh, need to do some, um, PT or OT, um, along with further investigations, um, to try and figure out why they've had a stroke. The PT and OT is quite an essential part of, uh, stroke units if you've been to one, because you want to help them, uh, sort of get back to their normal life as soon as you can. Um, and then, um, down here you can see in at the bottom of the screen, um, the contraindications to thrombolysis. So recent trauma, um any sort of a recent surgery, high BP, low plate platelet count, um any high inr anticoagulation, um things like that would be um complete contraindications. Um So you would look into that um, and deal with it appropriately. Ok. So if it's a chronic stroke and then the management is slightly different, so you can use the mnemonic uh halt to remember. So, um, if there's any hypertension, you're going to treat hypertension. Um, as we said, if there's any af then you treat with anticoagulation, otherwise you would treat with clopidogrel. Um You would use a lipid lowering therapy such as um using a statin, you'll advise the patient for smoking cessation if they're smoking. Um, if they're uh diabetic, then you would screen them for diabetes or manage them if you know already that they have diabetes. Um, if a patient who has a carotid artery stenosis to a significant degree, um, you can send them in for surgery, um, and send them for carotid endarterectomy, um, there have been a lot of trials um which show you that if you have a stroke or a tia a for example, and that's secondary to carotid artery stenosis, then having interventions such as endarterectomy will significantly reduce um your risk of strokes or tias going forward. Ok. So here's our next question. Um Please take your time. Have a read and I will release the next poll for this as well for you to answer. Ok, well, this question, um we have a 23 year old who's got an acute uh onset of weakness in the um left side shortly after returning from holiday in Spain. Um over the next few days, she's got worsening weakness in the legs and in both arms. So, depending on what the diagnosis is, what would be your um initial investigation. Ok. So the answer here is um c vital capacity. Um The question here basically is trying to ask you to figure out what the most likely cause of her weakness is. And the key here is that she's had it over a few days rather than a few minutes, um, or a few hours or whatever. So that should help you narrow down the diagnosis to something that's probably not vascular like a stroke. Um Other than that, she's a young person, she's just 23. So that makes it less likely for it to be stroke as well. Um So the thing that we are thinking here is that she's back from a holiday in Spain. Maybe she's eaten something or been exposed to something that she normally wouldn't have been. Um, maybe she's got some, uh, sort of a tummy bug. So you need to ask her more questions about her travel history. Um, and see what she's, uh, what's been going on preceding, uh, these symptoms. Um, so she's got gastroenteritis probably from her holiday, um, to Spain. Um, and in that case, you would think about um if this is GBS um or guillain-barre syndrome. So that's our working diagnosis here. And then the question is really asking you what, what's the most important clinical investigation. So, with GBS, it's an acute polyneuropathy and it can lead to weaknesses um in your arms and legs and it can also lead to respiratory failure and it can happen very, very quickly. Um So you really need to be on top of it and make sure you refer the patient to IC ASAP. Um So you need to make sure that you uh find a way that you can monitor this patient so that if they do deteriorate, um you can escalate quickly. Um So doing a full blood count might be important, but it's not the most important initially um because it's not quite reel terribly like as relevant. Um In someone with GBS, um peak flow tends to be typically used for asthma. So it doesn't really give us much information about lung capacity and how well they're doing in terms of oxygenation cause that's really what we're looking for. Um serum potassium again, is useful as sort of a general medical thing to do. Um but not the most important initial investigation in this scenario. And finally, the difference between um ABG S and um uh vital capacity is something that causes a bit of confusion amongst medical students sometimes. And the reason is that we, so the reason for why we're doing EB GS for it for a lot of patients. And I think that's typically what um sort of leads a lot of people to this answer. Um But the question is why is vital capacity more important than doing ABG S? Um And because E BG will show us evidence of hypoxia which is useful when the patient is very, very unwell. Um But what happens is in patients with guillain-barre, um they have quite significant reductions of vital capacity and that happens much, much earlier than any changes that you will see on an E BG um result. So it's more sensitive um to help us understand if the patient is deteriorating. Um and it catches that um more quickly than ABG S would. Um whereas ABG S by the time, um there's something that goes wrong on them, it might be too late to escalate um if the patient's already getting hypoxic. So the answer here is going to be a vital capacity and that's the most important um investigation and you can have a vital capacity monitor sort of by the patient's bedside, um and make sure that your patient is being monitored correctly. So, with guillain-barre syndrome, um because it's uh an ascending polyneuropathy, and basically, you have these antibodies that are directed towards the myelin sheath. Um as you can see in the diagram, um and therefore, you'll get sort of slower times where the nerve impulse is generated. And therefore, you can get motor dysfunction and sensory dysfunction. Um It's very typically associated with lower respiratory uh tract infection and also um gastric sort of gi infection. Um So, my mycoplasma and Campylobacter are going to be very important organisms to look out for here. Um especially when you're asking about your um history. Um make sure you ask them where they've traveled recently. Um So that becomes very important in this case. Um The risk of respiratory failure as we've discussed is very important. So you're going to do bedside spirometry for uh checking the F VC. Um And the treatment would be um plasma exchange and IV uh immunoglobulins um to try and dilate antibodies against these nerves. Um And always, always in these groups of patients, you need to assess whether or not you're going to escalate this to it because these patients can definitely deter deteriorate very, very quickly. And so make sure you keep an eye out and escalate appropriately next question and I'll release the next poll as well. Ok. All right. So here we have a 54 year old uh Russian man who's complaining of altered sensation in his feet for several months. He has a past medical history of essential hypertension gout pulmonary TB, which was treated in Russia a year ago. What's the most likely cause of his symptoms? Ok. So the answer here is going to be b um so we have a lot of things going on here in this question. But basically, this is a question that's asking you um about the causes of altered sensation in the feet. So when we have someone who has altered sensation in the feet, we need to consider whether or not this is a peripheral neuropathy. So when you think about a lower motor neuron lesion that could be either motor or sensory and we can't really see much motor going on here. Um We can mainly see sensory. So in this group of patients, we would try and screen for sort of simpler things such as diabetes, for example. Um But in this particular scenario, there's no past medical history of um diabetes. So that's going to be less likely. Um And then we've got uh vinCRIStine toxicity. Um and that's a chemotherapy drug and that does often cause um peripheral neuropathy. But in this scenario, again, there's um no evidence of cancer. So that's going to be less likely. Um And then we've got motoneuron disease. So as you can see in the name it says motoneuron. So it's less likely to have uh this sort of sensory functional um issues. And so finally, you have your Guillain Barre syndrome. Um that's going to be less likely to be this slow um and go on for sort of several um months. So you may want to consider a motor component um as well rather than just sensory on its own. So that would make GBS less likely. And so the unifying diagnosis you find here is that you have someone with TB who is often treated with um I saw um iso mm isonide and um that is often uh associated with peripheral um neuropathy. So, if we just talk a bit more about peripheral neuropathy, it's um as we've mentioned, tends to be either sensory or sensory motor or just motor. Um certainly in most cases that we see in clinical practice, it's a sensory um peripheral neuropathy. Um just to make it clear that although we talk about a bit more rare things in this uh previous case like um isozide. Um And we also talked about the chemotherapy. Um the most important cause of peripheral neuropathy um is sum summarized in this uh Pneumonic here, the EB CDE Pneumonic. So you've got alcohol, um B12 and FOLATE, you've got C KD, you've got diabetes and you have E for everything else. And so the E bit is sort of more niche aspect of peripheral uh neuropathy. So you've got um Charcot Marie tooth disease, you've got vasculitis and lead toxicity. Um but I wouldn't start off with e if someone asks um you a question about the causes of peripheral neuropathy, but see if it comes up in your exams, um or if it comes up in your acies and you have to give differentials a try and go for the more common things. Um So typically that would be alcohol and diabetes that you see most often. So when you're investigating, um you should always check for vitamin b12 and folate, um, check for a full blood count as well to see. Maybe they've got a macrocytic anemia which they might have developed uh secondary to alcohol use. You will also check the renal function um in to. So you can screen for chronic kidney disease and you also might, mm perhaps want to check for HBA one C um just to make sure that they've not been undiagnosed diabetics and, and that would basically cover most things for you. Um And you may also want to do a vasculitis screen as well. Um And if you're looking for shaky tooth disease or CMT, you might wanna do a genetic testing as well. But um, typically you're not going to be, um, asked much about it uh about the treatment of it um, at your level in terms of further investigations, um, you would do nerve conduction studies because that would accurately tell you which part of the nerve is um affected. And if that particular nerve is corresponding to the clinical picture that you've seen, sort of um the subjective aspect of what the patient is telling you. Finally, um we talk about the Romberg's test and that causes a lot of confusion for most med students as well. Um because it's often incorrectly thought to be um in something that only happens in cerebellar dysfunction. But in fact, Romberg's is used for sensory loss or sensory ataxia. So if you remember that um Romberg's is for sensory, then that will really help you a lot. Um So the idea with Romberg's test is you ask the patient to stand up, you ask them to um keep their eyes open and you see if they're stable, you sort of put your hands around uh them to make sure um that they don't fall over or anything just for their safety. Um So you ask them to keep their eyes open, you see they are um quite stable. Um So then you ask them to close their eyes and then you check if they're unstable as well. Um If they're only unstable with their eyes closed, that's what a positive Romberg sign is. And it's therefore likely to be related to sensory loss. But the this is happening because of uh lack of sensory input and that's what's causing the patient to be unstable and sort of get a bit wobbly. Um But if you have a cerebellar dysfunction for example, then you would expect them to be unstable if their eyes are both open and um closed. So with Romberg's test, um uh positive is when you have a patient who's unstable, only um when their eyes are closed and that's going to be due to a sensory loss or um sensory ataxia or peripheral neuropathy. So, we're on to our next question. I'll drop the next poll for you guys. OK. Yeah. All right. So here we have a 45 year old man um who is complaining of double vision. And when you do your examination, you note that his right eye is abducted downwards and his pupil is also larger than the other eye. You do an MRI scan of the brain and uh orbits and you find a tumor is pressing on it. So which um structure would it be pressing on? So the answer here is d it would be the oculomotor nerve. Um So there seems to be a tumor. We're trying to find out what structure is affected here. And this would, the answer to this question is basically related to your understanding of neuranatomy to a certain extent. Um But it's also related to how you would localize a lesion. Um So you might remember that in someone who has a right eye abduction that goes downwards, um that tends to be related to the syndrome, uh We would sort of refer to as a down and out pupil, which is a very typical um question a down and out pupil which tends to be related to third nerve palsy. Um So that's the oculomotor nerve and that's why this answer is correct. But if we were to look into a bit more detail, the other aspect that's important is that the pupil is larger than the other eye. So the pupil is also affected. Um So this comes to the other important concept um which is if you have a surgical, the uh third nerve palsy or a medical third nerve palsy, which is what I've explained here in this diagram. Um And this is related to which aspect of the third nerve is affected. So, if we look at the top of the diagram, there's something that's affecting or pushing against the third nerve on top. Um So maybe like a tumor that's pushing on it and it would tend to affect the parasympathetic neurons which um o overlie the um motor neurons of the third nerve. And we call this uh um as a surgical cause because it's dealt with by the surgical team. So things like tumors and aneurysms would be involved here. Um So when they affect the parasympathetic neuron, they cause a dilated pupil. Um and that's why in this example, you're seeing the, the sort of dilated pupil as well. Um In contrast, when you have um medical third nerve palsy, um that tends to not affect the parasympathetic um neuron. Um because nothing's really pushing on them, but it's more affecting um the intrinsic motor neuron of the third nerve. So, medical causes would be like diabetes and vascular disease. Um that would affect the motor fibers and will not affect the pupil. So, if you have someone with a third nerve palsy, it's important to see um if their pupils are affected. Um and that will help you to localize if it's a surgical cause or a medical cause and then you can direct your treatment accordingly. So, if we talk about um ophthalmoplegia, so we've talked about uh the third nerve palsy and it's important to rule out surgical causes because they might need urgent treatment. Um And medical causes will typically require further investigations for the most part. Um There is this phenomenon called internuclear ophthalmoplegia. And that's basically when um the medial longitudinal um fasciculus is affected, it sort of just distract um um where all these um nerves are going. Um and it tends to be related to the inability of coordination um between the 3rd, 4th and 6th nerve uh that go into your um crane into your cranium. Um So the tract is formed by the 3rd, 4th and 6th nerves and this sort of phenomenon is created when there's poor coordination between them. Um And here you can see it's um typically caused by things like MS. Um that's the usual cause especially in exams. Um But it can be also um a number of different things and that might be affecting this region. So, stroke and tumor uh are other causes as well. Um And you can see in this di diagram on the left, that's what we're trying to um show. Um otherwise you have the sixth nerve palsy, which is um related to the abduction or the abduction of the eye. And it can be related to something that's locally affecting the, the brain stem. Um But because the sixth nerve in itself is very long, um it can also be caused by um intracranial pressure. So, if you have someone with um someone that acutely become unwell, who's sort of come in bleeding or um has an intracranial hemorrhage. Uh and they have 1/6 nerve palsy, then it's um possible that they also have a raised intracranial pressure. And this is the only sort of obvious examination finding and that will lead you to treat them very urgently and refer them to the neurosurgical team um to consider if they need an intervention or not. And then finally, you have the fourth nerve um palsy, um which is typically um difficulty in looking down or a ducting ad ducting. Um And that's less common, but it's typically either associated with um trauma or MS, but essentially, it's caused by anything that's affecting the brain stem or the fourth nerve um itself. Ok. So, here, you can see, um I have mentioned some more details about um the cranial nerve three which supplies um the extraocular muscles. And this is a mnemonic to remember. Um So cranial nerve three supplies all extraocular muscles except superior obliques, which is cranial four and later, um Rectus, which is C can nerve six if you remember. So, four LR six, if the eye can't move laterally, then you're thinking about cranial nerve six lesion. If the eye can't move inferiorly, whilst the patient is sort of looking forward, and there's a cranial nerve four lesion. If the majority of the eyes movement is impaired, but the eye is sort of in the stereotypical down and out position, then that's going to be a cranial nerve three lesion. And this pneumonic should sort of help you um through your exam questions and also through a um if there's um any sort of abnormal eye movements which aren't fitting a particular nerve lesion and you should think about complex ophthalmoplegia. Um And the causes for that would typically be things like graves, um Myasthenia, gravis, um brainstem lesion, all of those. Um OK. Next question, have a little read and I'll release the pole for you to answer as well. OK. So we have a 55 year old man here who's presented to his GP, he's got a unilateral facial droop and weakness. Um And then you find out that it was sudden onset that happened six hours ago and wasn't associated with any other symptoms like pain or any sort of recent illnesses when you do an examination, you find out that there's um forehead sparing on the side of the facial weakness. So, what would be the single most likely diagnosis here? All right. So I'll reveal the answer and it's going to be a acute stroke. Um So this question is asking you to differentiate between the different causes of uh facial nerve palsy. Um So, the most important thing here is to see if it's a lower motor neuron, facial nerve palsy or if it's an upper motor neuron, um facial nerve palsy. Um So when we're talking about upper motor neuron and lower motor neuron, an upper motor neuron lesion is going to typically be in the central nervous system. So typically your um brain and spinal cord. Um and when you're doing your neurological examination, the typical signs of an upper motor neuron lesion would be um sort of things. So you think about up, so it's upper motor neuron, everything is going up. Um So you're thinking about increased tone, you're thinking about um hyperreflexia, you're thinking about upgoing plantas. Um So those sort of things should help you um to sort of um just a little cheat that I use um to help me identify if the symptoms I'm seeing are um upper or lower. So, similarly, with lower motor neuron lesions, um that's a lesion that's affecting anywhere from the anterior horn cell to the muscles that sort of line um that goes and again, similar to the upper motor neuron when it's low motor neuron lesions, um, the typical signs will be think going down. So you'll see muscle atrophy, you'll see fasciculations, you'll see reduced tone. Um You'll see weaknesses. You'll see either reduced or absent reflexes. You'll see downgoing plantas or you'll see there's an absent response. So that's again, a cheat sheet. Coming back to the question, the key aspect of this question we're talking about is for head sparing. So if you've got evidence of um forehead sparing, it's more likely to be upper motor neuron lesion. And in the answers here, if you take a look at them to distinguish which one's upper motor neuron uh lesion and which one's lower motor neuron lesion. So we will talk about Bell's palsy, that's typically lower motor neuron lesion. Um You talk about um cholesteatoma um and that's typically an ear infection. Um and that's local. So again, that's going to be lower motor neuron lesion, then we were talking about the space occupying lesion. So that can likely be upper motor neuron in the brain. Um But it won't be causing the sort of sudden um onset which happened six hours ago, sort of um quick facial droop like that. And then we have conversion disorder and that basically relates to a patient who has no obvious um physical dysfunction on examination and is less likely to cause a facial droop. Um And that also tends to cause motor weakness. Um as well. For example, so acute stroke is our only answer um which is of the upper motor neuron lesion and which is also sudden. So the forehead sparing is important because um in ap motoneuron lesion, it's the forehead that's applied by both sides of the brain. So if you have a dysfunction on one side of the brain, there's also a collateral supply um from the other side, if it was low motor neuron lesion, then the forehead is not bad because the facial nerve in its entirety is not bad. And so you would expect there to be a forehead, um droop as well. Ok. So in this particular scenario, um where we've discussed the seventh nerve, um palsy and this is what we're trying to showcase as you can see in the diagram. Um there's no crinkling in the forehead. Therefore, the facial nerve is affected um in itself and, and this is a lower motor neuron lesion. If it was upper motor neuron, it can be a lot of things um such as uh stroke, um MS, it could be a tumor, for example, but the other aspect is a low lower motor neuron lesion that can be related to Bell's palsy, which is thought to be an idiopathic, um low mod motoneuron, um seventh uh nerve palsy and that sort of tends to get better on its own as well. Um For Ramsay hunt, it tends to be related to these vesicles that you can see in the ear um and it's secondary to the herpes um virus. Um you can also get a differential um sorry, you can also get different infections um such as Lyme disease, sarcoidosis, um GBS and malignancy in the parotid. And that can be invasive and it can also affect the facial nerves. And the other aspect that comes up um often is this correlation between 57 and eight dysfunction and that's related to uh cerebellopontine angle tumor. So, basically, you have a tumor which is close to the cerebellum and it can be invasive. Um but it could also be benign. Um It can be uh malignant as well. Um But the point being that this tumor affects 57 and eight nerves. So if you're doing a clinical examination and you notice they have a facial palsy, it's important that you cover all other nerves, but definitely also um hone in on the 5th, 7th and 8th nerve. Um and see if hearing is also affected. Ok. So we're on to our next question and I released the pole in the chat. OK. So in this question, we have a 74 year old um who's a righthanded woman and she's uh presented to the clinic with a resting tumor um in her right hand and she has a history of frequent falls over the past year, um which she's attributing to having poor balance. Um And then you note bradykinesia and it's worse on the right side. Um There's a resting, the resting tumor that we see is also present on the right hand side. Um There's no postural tremor that's noted. So, what would be the most appropriate, um, medication to help with her symptoms? So, I think this is an easy one. So yes, the answer is B levodopa. Um So we've got resting, resting tremor, we've got bradykinesia and we've got falls. So the most likely diagnosis here is definitely Parkinson's or Parkinsonism. And that's a representation of the number of symptoms that we've um sort of had described here in the question, the most common cause of parkinsonian um syndrome um is Parkinson, Parkinson's disease. Um or you also call it idiopathic Parkinson's disease. And there's a number of different treatment options that are available as you can see. Um Levodopa is the one which is used most often. There's some other aspects that you might consider as well. So if you look at the choices, we've got propranolol, mm propranolol is not really used in this particular scenario um for advanced treatment um for Parkinson's. So what you can do is um with propranolol, sometimes you can give it to people who have a resting tremor, for example, and that might help, but it's not typically used in people who have um Parkinson's tremor and then we've got deep brain stimulation. Um But you typically use it as a very advanced um treatment for Parkinson's um when it's at its later stages and then you've got um epimorphin. So these epimorphin injections are also used in later stages. So that's not going to be the correct answer either. And we've got the final, an uh final option. Um ropinirole, um ropinirole is a dopamine agonist. Um And in the past, it was used more often um in Parkinson's disease um in order to reduce the amount of levodopa uh that they have, so it doesn't wear off and start causing all sorts of side effects, but we don't really see it being used commonly anymore. Um The issue with ro ropinirole is that it can lead to a loss in different um effects in dopamine transmission. So it can lead to all these sort of behavioral disturbances, um which can be quite harmful to the patient. Um And therefore, we don't really use it anymore and people are now treated with levodopa, particularly if they have um motor features. And that's uh typically the one that you will see in your exams as well. So, Parkinsonism is a syndrome, as we've said, um there's um some specific key features. So we've got tremors, we've got rigidity, bad kinesia, we've got postural instability, um resting tremor is typically going to be a tremor that's worse at rest. Um When we talking about rigidity, we're talking about this sort of um movement where you, if you try and passively move the patient and they're going to sort of resist it. And so that's what we mean by uh rigidity. And then bradykinesia is the slowness of uh movement. So, the key here is that there's um differential diagnosis within Parkinsonism itself. We've talked about Parkinson's disorder, which is the idiopathic cause, but we've got other things like um vascular parkinsonism, um vascular parkinson's, which can be related to um a lot of vascular events, let's say, which have happened in the brainstem. Um So it might be secondary to a stroke or sort of a stepwise progression of uh motor dysfunction over a period of time. Um And then drugs can cause this as well. Um So, antipsychotic drugs in particular is important and that can cause um parkinsonism. Um You have also got this uh syndrome called Parkinson's Plus Syndrome. Um And that's basically a group of these sort of rare diseases. Um And that can sort of look like Parkinson's, but they have a different path of uh physiological cause of parkinsonism. Um And that can be um sort of certain disorders um such as progressive um supranuclear um palsy, what can be a multisystem atrophy. Um And basically, um this isn't quite um sort of med school focused. Um But I would just keep it in mind um if you see any uh Parkinson's patients, but they sort of looking a bit different to you. Um For example, if there's any patients who've got very severe Parkinson's with um sort of early falls who have Um for example, a symmetrical uh tremor or symmetrical features um that might make it more likely to not be idiopathic Parkinson's disease. And you might want to think about um all these other things. So the key in Parkinson's disease um in itself, you have to remember that it's asymmetrical to start off with um the other aspects to differentiate between essential tremor and Parkinson's disease. Um So how you can do that is by making them right? So, if you've got an essential tremor, you'd have a patient who has this very difficult tremor. And what happens is when you ask them to write or sort of draw, let's say um this spiral, for example, is going to be this really large and really wiggly spiral. Um But on the other hand, with Parkinsonism or Parkinson's disorder, um you will have a small spiral and it's going to be more stable and not has frigg and that's um what's called micrographia. So very small handwriting. So that would help you differentiate between essential tremor and Parkinson's um dis uh disorder. So finally, um although often people focus on sort of the more motor aspects of Parkinson's disease, there's also other aspects that can be quite distressing for patients and families. Um the common complications of Parkinson's disease will be dementia which can be quite progressive and can be related to um things like Lewy body dementia and it can also coexist um as a spectrum um dementia with Lewy body disease. Um When we talk about that, that's a type of dementia that's associated with features of uh parkinsonism. It's basically a progressive cognitive decline and the patient will have uh symptoms of visual hallucinations, delusions. Um They'll have rem uh sleep disorders, they'll have this sort of fluctuating consciousness. Um So that's what we mean by Lewy bodies. Um There's also a depression that you can consider as a complication of uh Parkinson's disease. So, depression itself can either organically be linked to Parkinson's or it can be just related to the fact that the patient is quite upset and they aren't able to cope with sort of their own condition and what's going on with them um because they were fine and one day things just started going downhill and that can have an effect on their lives, their careers, their family members. So it's difficult to say if Parkinson's can cause depression or if um it's the fact that they have Parkinson's that's causing them the depression. So when you see a patient's a patient with Parkinson's, you might want to screen for these things and treat them appropriately. So, another thing we've discussed for Parkinson's um is the bradykinesia. So, Bradykinesia is when the movements are getting slower and smaller and that sort of a thing presents in several ways as you can see in this um nice diagram. So we've already talked about micrographia where it's getting smaller, but there's also small steps when they're walking and that's what we called a shuffling gait. Um, and in order to sort of compensate for these, um, small steps, right, um, in order to compensate for these small steps, they're going to, um, take more steps. So the frequency of the, the steps increases, um, and that's called a fascinating gait. Um, they'll also have difficulties in turning around when, uh when they're, um, sort of standing and they'll have to take tons of um little steps in order to make a turn. Um So when you see a patient like this, um just when they're walking in through your door, you can um look at and identify a lot of these symptoms. You also see they'll have um reduced facial movements and facial uh expressions which we call hypomimia. And that's what causes this sort of uh masked face. Um They'll also have difficulty in initiating mo movement. So if they've been standing still and they need to start walking, they'll have a lot of difficulty in doing that. So that's um bradykinesia. Ok. Um Other features for Parkinson's, we've discussed already will be depression and, but there's also sleep disturbances and insomnia in these patients, they can have a loss of the sense of smell. Um And then they have postural instability. So you'll have these patients who've come in with um high risk of falls. So even whilst they're admitted on the ward, they'll continue to have these increased risk of falls so that really um sort of constricts them um and their independence, they'll also have cognitive impairment and mem memory um problems as well. So this is a neat diagram to help differentiate um very common exam question will ask you um to differentiate between a tremor and you have to then figure out if it's a tremor of Parkinson's disease or um essential tremor. And so this table here will sort of give you some tips to remember. So, always remember Parkinson's typically is going to be asymmetrical. Essential tremor is not. Um You can also try and memorize the Hertz. If you, if you wish to some questions do ask the Hertz and they'll or they'll give you that the tremor was you that you noted was um five Hertz or whatever. Um And then the next would be that Parkinson's um their tremor improves while they're just sat around. Um sorry, the pro in Parkinson's, it becomes worse while less at around but essential tremor, they are going to be nice and relaxed. Um Parkinson's with an intentional movement which you can examine is going to um improve but essential tremor is not in that we can see with the handwriting, the spiral example that we've uh given um Parkinson's, you'll have other features as well to help you identify but essential tremor will not have any um typical Parkinson's features in it. And then the last one is the that there's no change in the symptoms with alcohol in Parkinson's tremor. Um but in essential tremor, it's going to improve with alcohol. That's not to say that you start giving alcohol to your patients. Um in uh clinical practice to try and differentiate it is just a fun tidbit to remember and it is interesting as well. Next, we have the management of Parkinson's disease. So Parkinson's is diagnosed clinically based on the history that you take and your examination findings. Um but typically this sort of diagnosis should be made by an experienced specialist. Um So the treatment um as well is typically initiated and also guided by a specialist. And the specialist then will tailor the treatment um to each individual and they'll see the responses as well to the different medications. Um With Parkinson's, I'm sure you all know there's no cure. Um The treatment is typically focused on um controlling symptoms and on trying to minimize the side effects of Parkinson's. So levodopa is um the main option here. Levodopa is basically synthetic dopamine and you take it orally. Um typically you will combine it with a decarboxylase um inhibitor. So for example, uh copy dopa um which will stop it from being metabolized in the body before it reaches the brain. So you'll see that's the main um sort of um treatment plan for uh Parkinson's disease is that when you start giving them dopamine, for example, with Levodopa, it's very, very effective as a treatment because the synthetic dopamine really works well, um, to help with the, uh, treatment of the symptoms, but it's becomes less effective over time, unfortunately. And, um, people develop this sort of on and off phenomenon where they can have these sort of sudden symptoms and they'll freeze up and, uh, things like that and then all of a sudden the symptoms will go away, um, until eventually they're just always symptomatic and rarely having these non symptomatic periods because the medication has stopped working. Um And also, um if you're giving them dopamine agonists, um it can also lead to changes as we've mentioned before and sort of other aspects of the dopamine pathway. So things like gambling addiction, for example, behavioral changes um can start happening, which is quite distress, distressing for the patients and their families. Um So it's often reserved for when other treatments um are not controlling their symptoms anymore. So, we've got examples here of um combination drugs. Um So we've got corbinal dopa and coc dopa. So anything dopa that you see, um typically is going to be our exam. Um The main side effect of levodopa is dyskinesia, which you can see in the image there. Um, dyskinesia is basically abnormal movements, um and that's related to this excessive motor activity. Um So you will see symptoms like dystonia, chorea, um and uh aosis. So, dystonia is this sort of excessive muscle contraction, um where you'll have this abnormal um, posture or like exaggerated movement, chorea is um the sort of jerky and random um abnormal involuntary movement and athetosis is the sort of twisting and writing the movement of your hands or your fingers or your feet. And you can see that um in the diagram very clearly. Um And then just a little tidbit is you use um amantadine to um help manage the dyskinesia that's associated with uh levodopa use. Um And that's a glutamate agonist. So that's how it helps other aspects of um Parkinson's disease are typically much more specialist. Um And they focus around the same principle to try and increase the dopamine release or the dopamine present in the brain. So, we've got um COMT inhibitors uh for example, anti Capone. Um and they are inhibitors of the com T um or the conti enzyme. Uh And that enzyme basically metabolizes levodopa in um both your body and the brain. Um And you take it with levodopa to sort of slow down um the breakdown of levodopa in your brain um and extend the effective duration of uh levodopa. Um And then we've got dopamine agonists, they will mimic the action of dopamine in uh the basal ganglia and they will start stimulating the um dopamine receptors. They are less effective than levodopa typically um in reducing the symptoms. And typically, you're again just using them to delay the use um of levodopa. And then once you've delayed the use, then you start using it in combination with Levodopa. So that you are not using um as much as the dose of levodopa. And then once you've sort of maximized your dose as well, um Then there's uh not many options remaining. Um But with dopamine agonists, something to remember is pulmonary fibrosis, that's a um side effect that's associated with uh long term use. Um And we've got um our mono um monoamine oxidase B inhibitors and they again, um will block the action of monoamine oxy oxidase B enzymes. Um And they're again going to help increase the circulating dopamine. Um So they're going to break down neurotransmitters like dopamine, serotonin adrenaline that are present. Um But um monoamine oxidase B is more specific to dopamine. Um It'll delay the use and then you start using it in combination. Um And it's the same principle essentially. Um We've got subcut apomorphine. So that's basically a Parkinson's drug um that falls under the category of dopamine agonists as well. Um But unlike the name, um what it suggests, it, it doesn't actually contain any morphine in it. Um So it's just a dopamine agonist. And the only reason I've specifically and separately mentioned it on the slide is because it was in the question that we just sol solved before. Um And then your last step is deep brain stimulation um which can be used. Um And that's not really related to dopamine release. So, unlike the rest of these options here, um But it's going to work. Um if there's an unknown cause. Um and you require neurosurgery and sort of long term um follow up as well um by the neurosurgeons or the neurologist to just to see how people are doing. So, in deep brain stimulation, you have these electrodes that send um electrical impulses and they help to control the motor symptoms um that you have in Parkinson's. Um it's most effective with motor symptoms, but it can sometimes improve some nonmotor symptoms like um any problems with your sleep, um pain urinary, um problems like urgency. Um Again, DBS is or deep brain stimulation is not um a cure for Parkinson's. Um It doesn't slow down the progression of Parkinson's either, but a lot of people basically um go for it to because it helps them um control the motor symptoms. So that's how it works. And it's not even a 11 time surgery. It's sort of like an ongoing treatment that patients will go for again and again. So we are now down to our next question and I'll release that in the pool while you guys have a read. All right. So in this question, you have a 30 year old patient in A&E who's been teasing for more than five minutes. Um He already has a longstanding history of tonic clonic seizures and he's taking sodium valtrate for it. He also has a history of um alcohol excess and he's been uh well in the few days prior to his um admission. So if he's already on the medication and um he's already being treated. Now, you need to think about why um he's still having the this problem. So, which is the most likely cause of a seizure? And we've got the option B here, which is epilepsy, which is the correct answer. Um So in this question and this is to show you sort of the effects of antiepileptic drugs and how they can be used. Um and how they can be affected by different things as well. So if you look at the choices, um a acute stroke is going to be less likely, this is a 30 year old man and we don't know much about his risk factors, but just because of his age and other things, I think it's um less likely um for it to be a stroke induced um seizure and then you have um subdural hemorrhage. Um It's also less likely to cause seizures. You could get a subdural hemo hemorrhage. Um If you bump your head during a seizure, that's true. But it's less likely that you have a subdural hemorrhage um without having a history of trauma. And then, MS um that's a very common cause of seizures as well. Um Sorry, that's a very uncommon cause of seizures. Um And then you have meningitis and again, we don't really have any um typical history of meningitis. Um So it's going to be less likely as well. Um Because we don't have any symptoms that would indicate um meningitis. Um So this question is really pointing to the idea that we have somebody who has epilepsy, they're on sodium valtrate. Um And they're having seizures in the past. Um But they're also drinking a lot. So, as you might already know, um there's a number of enzyme inducers. So, chronic alcohol users can induce the P 450 or P 450 enzyme. Um and that can lead to reduced activity of certain medications. So, in this scenario, that's probably um what happened. Um and you can use this mnemonic um crap GPS induced me toh. Um And you can see all the different options here. Um So we've got carBAMazepine, um Rifampicin alcohol, uh phenytoin and all these others as well. Um So it, for our scenario, it's going to be alcohol. Um That's um sort of the culprit. So the less activity or the reduced activity of his antiepileptic drug is going to be secondary to his um alcohol use and that's basically what's causing a seizure and he has epilepsy. So that's um going to be the most likely cause um for this particular um question compared to other differentials. Um So we've got different types of seizures. So you have focal seizures. Um So they can be complex or simple seizures and they tend to be um related to um if patients will lose or not lose their consciousness while they are seizing. Um they can also be secondary um generalized um seizures where they become generalized after the initial stage and then you have generalized seizures. Um and they can include absent seizures. That's why patients uh become sort of blank, they start staring into space and then they sort of by abruptly come to come back to normal. Um absent seizures are typically seen in Children. And during the episode, the Children are just not aware of their surroundings and they stop responding to you. Um And when that happens, often enough, that's when parents sort of start realizing it um that there's something wrong and that's when they'll come in. Um absent seizures will last maybe about 10 to 20 seconds at best. And most of the patients will stop having these seizures um as they get older, which is a good thing. And then we've got tonic clonic. Um we basically consider tonic clonic um as the classic seizures that we're told about. Um patients will have tonic and clonic movements. So, tonic meaning where their muscles are going to become really tense and clonic is where the muscles are going to be sort of these jerky movements. And it's also associated with a complete loss of consciousness. Um tonic clonic seizures, you can also call them as grand mal seizures. Um typically before the seizures, a la lot of the patients sort of experience this aura um which is like an abnormal sensation that gives them the warning. Um that a seizure is going to occur a lot of the times, uh, with these patients that can be tongue biting, um, incontinence, that can be, um, sort of groaning and, um, irregular breathing. And then after the seizure has passed, there's going to be this really long, um, period, um, which we call as a postictal period and that's when the patient is quite confused. They're really tired, um, they're really irritable, they're feeling really low and um they basically just want to go to bed essentially and just not talk to anybody. Um And then you have myoclonic seizures which present with this sort of sudden um but brief muscle contractions. Um So it's like an abrupt sort of jolt or like a jump, sort of jerky movement. Um um but they remain awake. Um And myoclonic seizures can occur um as part of um sort of juvenile myoclonic um epilepsy in Children. And then you've got atonic seizures or you also call them drop attacks. And that involves this sort of sudden loss of muscle tone. Um And basically, the patients usually have a fall because you suddenly sort of um your muscles just lose their sort of tone. Um These sort of atonic seizures will last very briefly and patients are usually also aware during the episodes and these sort of atonic seizures very often begin in childhood. Um But they're less commonly seen in sort of general medical environment. Uh So talking about triggers, it's very important that you ask the patients that these kind of patients, when you see them about the um quality of life, how they're doing in day to day life. Also ask them about alcohol and drug use. And if they're having any withdrawal symptoms, because these are all the things that will um trigger the seizures. So you should definitely ask about that. But other things can also be triggering these seizures. For example, you've got stroke, um you've got intracranial hemorrhage. Um if someone has risk factors or um if they're a bit older, then you definitely need to think about these. Um It's also important to do a CT head to check if there's nothing other that's causing um the seizure. And then finally, um it's important that you check for electrolytes because metabolic disturbances like hyponatremia can cause um seizures as well. So it's important that you do sort of a general um screening. Ok. So for management, um so the first thing that you do is going to be an MRI um of the brain. So you do your eeg that's the first thing that you do. Then you can do the MRI to um sort of help you with any structural pathology that you might want to diagnose, for example, um any tumors that might be um causing this and then you can do other investigations to exclude pathology as you can see on the top. Um bar. Um So you might wanna do ECG, you might wanna do um ec check for electrolytes. So you'll do sodium, potassium, calcium, magnesium, all of the regular ones. Um You might wanna check for uh the blood glucose and see if the patient might have hypoglycemia or if they might be diabetic. Um And you might also want to do blood cultures, urine cultures and a lumbar puncture if the patient is sort of septic or if they're coming in with symptoms where you're um suspecting encephalitis or even meningitis. So, it's quite um difficult to manage seizures. Um And that's quite often done by a specialist as well, but there's a few rules of thumb, um which you can take into consideration. And a lot of these rule of thumb is not actually very important um in med school. But the only aspect for this one that you should take into consideration is um that sodium valproate is extremely teratogenic and therefore you shouldn't be starting any woman um especially a woman um who is um sort of um able to have Children who to start on sodium mate, who's on uh who's a childbearing age. Um It's a difficult decision to make um typically, and therefore you need to um sort of adequately have a discussion with the woman, have them consent, discuss the risks and benefits of sodium valproate. And there's this whole conversation about um contraceptives that you need to have, they need to be on something very permanent. Um So they can, it's done to basically make sure that they, they definitely don't get pregnant um, while they're on sodium valproate. And if they want to get off of sodium valproate, then that's a whole different, um, consultation where you need to sort of wean them off. And that's something that's very important um, for you to know, um, in terms of your exams and even your sys, um, because you might have scenarios where that's covered. So typical rule of thumbs. Um And we've got this really nice table here which you can use for reference um to help you as well. So typically, um lamoTRIgine um Levier um uh and valproate are going to be good for all seizure seizure types. And then you've got carBAMazepine, gabapentin and phenytoin um which will be better for focal seizures. And then you've got um um for um absent seizures, um oxamide, um which is the drug of choice. And then you've got carBAMazepine, which you can definitely not use in uh myoclonic seizures. So just some of these rule of thumbs, if you remember, it might help you with your exams. But um mostly for treatment of these seizures, you aren't really expected to um know that much detail. So the thing that you should definitely know about um is status epilepticus. Um This is one of the more important sort of acute emergencies um in seizures. So status epilepticus is a medical emergency and they are typically seizures that last um for more than five minutes, they're typically very dangerous and can lead to hypoxia and if they deteriorate, um can also lead to death. Um So it's important to deal with it quite early. Um Status of plexus will also have sort of, other than it lasting more than five minutes. It can be multiple seizures and typically, it'll be without sort of regaining consciousness um in between those multiple seizure episodes. So to manage um status epilepticus, you're going to do your A two E approach to make sure you're stabilizing the patient. So um you're going to secure the airway, you give them a high concentration um of oxygen and check the blood glucose levels and you start correcting that if there's anything wrong. Um And then you also definitely have to gain IV access by um inserting a cannula. Um and you try and get both arms if you can. Um because um then it makes it easier to give them the medical treatment. So for the medical treatment, you're going to give a benzodiazepine as the first line. Um if the seizure is continuing, then you repeat it in 5 to 10 minutes. Um If that still doesn't work, then you go for second line. So after two doses of benzodiazepine, at least you go for um the IV option, which is IV either um Levetiracetam or Phenytoin or sodium valproate. Very typically, I've seen it be phenytoin and then um third line option. If that doesn't work is going to be PHENobarbital. Um And if that doesn't work, you can even go for general anesthesia. So, anesthesia will only be considered if all these treatments aren't working. But typically, if there's a patient with status epilepticus, you will want to involve the anesthetic team very early on because they'll help you with um securing airway and they'll help you with the treatment um options as well. So when we're talking about Benzodiazepines um to be used here, there's three options that you can use for Benzodiazepines. So you can use uh Midazolam. So Bal Midazolam um which you give 10 mg or you can use a rectal DPAM. So if orally they are, they've clenched their teeth and they aren't um and they aren't sort of going to be able to take it and you don't have any IV access. Um then you can go for Rectal and that's 10 mg of rectal Azep um as well. So both Midazolam and diazePAM were using 10 mg. Um But the most typical option when you've got your IV access as first line is going to be um 4 mg of LORazepam. So the top right corner, if you see the Pneumonic or just something to help you remember is Laurie Laurie funny called it. So the first line, Laurie Laurie being the two Benzodiazepines um or basically IV LORazepam um that you might want to give. So two doses of that and then funny is for Phenytoin. So if that doesn't work, that's your next option to go for IV Phenytoin. And if all else fails, call it UI Tu is your anesthetic team. So I'm going to ask them to come help you. All right, final question. And I have released the final poll. Mm This is a bit of a mean question to be honest. So if you don't get it, don't worry about it. Um we'll discuss it in detail. All right. So we've got uh not a 600 year old man. We have a 60 year old man who's attending the clinic with a three month history of leg weakness. Um On examination, the tone is going to be normal. That's what you find out and there's reduced power bilaterally um in the distal lower limbs. Um You also find out that ankle reflex is absent bilaterally, but knee um reflexes are present, you find out plantars are upgoing. Um So it's a bit of a mixed picture. Um So which of the following clinical signs is most keeping with this um diagnosis? Sorry. Ok. So let's work it out one by one. The correct answer here is going to be the with the small hand muscles. So there's one key aspect that you need to look at here. Um So you need to think is this upper motor neuron lesion or lower motor neuron lesion and anyone who has evidence of um limb weakness or not. So, you can see there's normal tone and reduced power bilaterally, which doesn't really help us that much in terms of. Um is it upper motor neuron versus um lower motor neuron? But you see the ankle reflexes absent bilaterally, but knee reflexes are present. Um and you see plantars are upgoing. So, in, in summary, essentially, you're seeing both upper motor neuron and lower motor neuron lesion signs. So the key aspect here is to think about what could possibly cause a mixed upper motor neuron and um lower motor neuron lesion. And in this scenario, it could be caused by M ND or uh motor neuron disease, which is most likely. And M ND, as you can see, we've mentioned it on the top. Um If um there M and D present is going to have a mixed picture of both upper motor neuron and lower motor neuron. Um So you can also look at it. Um The, you can also look at it in another way if you look at the choices here one by one. So going for the first one, the pale optic disc, we know that's related to optic neuritis. Um And that's typically related to MS. So this can be MS if you have just low motor neuron lesion um equally with the bottom internuclear ophthalmoplegia. Um That as we said is most likely related with MS and also oculomotor nerve is not affected in M ND. Um The other aspect is this um positive um Romberg sign um as we mentioned already, Romberg sign is a sensory sign, so it won't be affected in um M and OK. Um And then option C um postural hypotension um is autonomic rather than motor. So, again, uh in this scenario, you can sort of work out um in the sense that, you know, this is M and D but knowing that it's a mixed picture sort of upper motor and lower motor neuron signs. So wasting of hand muscles is um lower motor neuron signs. So it's keeping with this sort of mixed picture. Um Although it's also um common in uh motor neuro um motor neuron disease, there's also another way of working it out in the sense that um it is sort of a continuation of this lower motor neuron sign. Um I guess to summarize this question, the learning point is um when you're looking at any question with any sort of uh limb weakness, try and ask yourself, is this upper motor neuron? Is this lower motor neuron or is this mixed? Um now that you know, um mixed is related to motor neuron disease? So that's a good plus. Um but don't worry, most questions will be a lot sim simpler and they will help you differentiate between these two upper motor neuron um in terms of MS or lower motor neuron. Um in sort of um for example, um Guillain Barre syndrome um and alter and peripheral neuropathy which we've discussed today. So that's basically the key to um localizing neurology in this particular um scenario. OK. So to summarize, you can um you can have a read of this later as well and we're going to um put up the um powerpoint presentation. It's already on the um deck if you want to have a look. Um and that can help you sort of as a short hand for remembering the top three differentials for each one. So think about certain scenarios. Um for example, here, the spastic um paraparesis where you will have bilateral upper motor neuron lesions. So, MS um called compression and stroke, that will be the examples. And similarly, if you have spastic hemiparesis, um which is an upper motor neuron syndrome in um let's say one leg, for example. Um And so that's more likely to be um caused by stroke, tumor or MS. Um So just have a read and think about it in detail, but you can definitely keep this as a reference source. Um And then right at the bottom of this list, you can see what we discussed earlier. Um So we've got our motoneuron, uh neuron uh motoneuron disease. Um But we also have cervical spondylopathy. Um And we also have sac D or subacute uh combined degeneration of the cord and that usually happens as um secondary to um B12 deficiency. So, and that's why you also um would screen for that. And then you can see this really nice um link at the bottom of the screen. You can either try and copy, paste it or take a photo of it whatever would work um or just put it on your Google, try to check for osk stops. Um Neurological Differential diagnosis. And they have a very nice, if you have the book, then that works as well. They have a very nice list of differential diagnoses that you can sort of go through. And what I did in med school was memorize the top three of them. Uh of uh examples of um upper motor neuron lesions, lower motor neuron lesions, if it's unilateral, if it's bilateral things like that. Um And I found that to be extremely helpful for me um to remember all of these things. OK. So we've come to the end of um our session today. Um If you have any questions, please leave them in the chart and I'll have a read. Um We will release the feedback as well. Um So please make sure that you um give us a nice feed feedback. Um And we ask you for your um email address for from your uni just because if you come from a specific trust, then we can basically get certificates for teaching that particular trust if um we're also working in that trust. So that would be helpful if you're not from the UK, that's fine. Don't worry about it. And if you have any further questions, um Please leave them, um Please leave them here um or send me an email and I will try and get to them later on. Thank you. Um She was asked if a brain lesion can cause uh mixed symptoms. Um So brain lesion will typically cause ap motor neuron her symptoms. But if a brain lesion is for example, present in the brain stem, um then it may cause a mixed picture. So I hope that answers your question. I'll just hang on um until you guys all leave. If there's any questions, I'll hang around and answer them. Um Sorry. So there's another question in the chat box asking how do you differentiate between a posterior circulation, stroke and vertigo? So that's a very good question because uh posterior circulation stroke and both vertigo can present with quite similar symptoms. So you'll have dizziness, imbalance, nausea, those kind of things. But some differences you can look out for will be. Um So vertigo, for example, will last for a few seconds up to a few minutes. Um but the symptoms of uh um posterior circulation stroke are going to be sort of more persistent and severe. Um You can also look for um other symptoms. So if you have weakness, um numbness, slurred speech, um double vision, um or maybe even difficulty swallowing, those are typically stroke associated symptoms. So, ver vertigo will not have um these symptoms. Um and then more specifically, vertigo is also positional. So if you have a stroke, then that shouldn't be positional. Um So if there's any specific head movements that are making your symptoms worse or any changes in your position, that shouldn't be a posterior circulation stroke either. Um And then vertigo is going to be very acute, very sudden onset, but posterior circulation stroke will be a bit more gradual. Um However, I can appreciate that a lot of the times that stroke is quite acute as well. Um So it might be hard to distinguish it just based on the onset. And then you can also sort of look for things like um the patient's past medical history. Um So if they've got any risk factors for stroke, um for example, what we've discussed like hypertension diabetes, um even smoking. So those kind of things can provide you clues as to what's going on exactly. Um Or if they've got past medical history of um other previous strokes or um they've got tia S things like that will sort of point you towards a more stroke picture. Um So essentially you need to um do your due diligence, ask them thorough questions. Um And also you would want to um further have more confirmation by doing scans. So your CT scans, um or even if you wanna get a detailed picture with MRI S, um that would be sort of quite um important here to make sure that you have the correct um correct diagnosis. Um So, I hope that helps.