Computer generated transcript

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

The introduction. Uh So, hi, hi, everyone. So as I said, my name is Ahmed. Uh just finished medical school at Cardiff University and I've just started to work as an EENT doctor. Um, so as medical students, you think, you know, it's, it's never ending, but honestly time fliess. So uh you'll be in the same position as me very soon. So, so today we're gonna be doing uh neurology teaching just mainly focusing on high yield questions that you um are likely to uh encounter in your examinations, especially progress test. So just um a uh stop to through some of the important to topics in urology. Uh So we're gonna be starting uh with stroke and just moving our way down as you can see here in this list. So next slide please. That's all. Uh So we, we want this session to be quite interactive with you guys. So we're gonna be presenting with a series of uh multiple choice questions. So this is the first question for you. Uh So ha have a go and let us know your answers in the, in the, in the chat or you can speak up as well if you would like to, I'll just give you another 30 seconds. Any ideas. What might, might that be? Ok. Right. Uh Give you guys under 10 seconds. If not, we'll reveal the answer, just have a go, just have a go. Ok. We have someone saying a ok provider. Anyone else, right? Ok. So let's, let's have the answer. Yeah, so a was correct. Uh, so this question, we see that this is a gentleman that has come in with a couple of s with a couple of symptoms. Uh So the, the important things here to look at is the left sided uh facial sensory loss and also uh the motor weakness as well. And uh and yeah, and, and also the uh homonymous seminal here as well. So this is partial anterior circulation infarct. So if, if we go through the, uh we're gonna, we're gonna now go through the Oxford stroke classification, which will help you a lot to identify uh the kind of strokes. But before we do that, we're just gonna go through the pathophysiology quickly of stroke. Uh So just in terms of the causes of stroke, it mainly happens due to ischemia and that constitutes about 85% of why people have strokes. And that could be due to a couple of things including uh you know, atherosclerosis, infective endocarditis and thrombosis as well. Hemorrhage can also occur in a, in a minority of patients. And that's basically the bleeds that you get in the brain including subarachnoid hemorrhages and intracerebral hemorrhage. Next slide, please. Uh So here we come to the Oxford uh show classification system. Uh So if we, if we here mm oh let me get including posterior circulation stroke and lacuna stroke. Uh So in terms of the tachy, uh there needs to be at least uh or there needs to be 33 symptoms as you can see here, unilateral hemiparesis and or hemisensory loss of the face, arm and legs. So basically uh a motor loss or a sensory loss in one side of the body and also homonymous heia. And you, and you can test that by doing a cranial nerve exam and they would usually have a loss of visual fields and also higher cognitive dysfunction. Uh So, for example, they will appear confused or they will have uh you know, other higher cognitive dysfunctions. Uh in terms of the PKI, it's basically the same as, as the TKI, but you only get two out of three. Uh So if you get two out of three of them, then we call it a package. Uh in terms of the other types of stroke, we have the posterior circulation stroke. Uh and they uh they typically present with these symptoms here. One of them including loss of consciousness or they would come in with homonymous heia by itself or Cerebella or Barring stem syndromes. Laguna stroke is also another type of stroke, which is a bit rarer and uh it presents with one of the following pure sensory stroke, ataxia, chemic reis or unilateral weakness of the face or uh and or, or arm. Basically. All right. Next slide, please. So I think it's very important for uh for you guys to understand the uh anatomy of the stroke and uh to be able to understand where the stroke is isolated. Wh where, where the stroke is, is is localizing to. And I think it's important to do that because basically by, by looking at a patient, you can tell exactly where the stroke is originating from. And to be able to understand that we need to understand the um hormonal of the brain. So if you can see the figure here on the left hand side that describes basically which parts of the brain control the sensory uh or the uh the the, the uh the sensor or actually this part is the motor homonal, there is also a sensory homonal. Uh But the one with uh we're seeing here is the motor hemono chus. So the medial aspect of the brain controls the legs and then as you go more laterally that controls the upper limbs and then the face. So that explains why in anterior cerebral artery, for example, you get uh the the lower limbs are more affected because it usually affects the medial part of the brain of the brain. As you can see here in, in the diagram on the right. Uh In contrast, the middle cerebral artery affects the uh upper limb more than the, than the, than the lower limb. And uh you can see that as well from the diagram here in terms of the posterior cerebral artery, this this artery innervates a lot of things. It in uh it innervates the occipital lobe, the cerebellum and also the brain stem. So you can get a lot of symptoms with the uh posterior cerebral artery strokes, including uh as you can see here, uh contralateral um contralateral hoop uh and uh also with macular sparing as well. Uh There's also another type of stroke that sometimes comes in progress tests. Uh It stands, it, it stands for PCA or posterior inferior cerebral artery, also known as lateral medullary syndrome and that usually presents with Horner's Syndrome. So if you see a, you know, a, a multiple choice question uh with the Horner's Syndrome, that's a clue that it's basically it's posterior inferior cerebral artery. Uh But in addition to that, you also get temp temperature loss and also facial pain uh as well. Next slide, please. So now moving on to the second question, you can have a go at that as well. So Daniel is a 67 year old man presented to Ed with some right sided weakness on examination. He has five out of five right wrist extension, elbow, flexion and shoulder abd abduction. Two out of five power and right hip flexion, knee extension, and ankle plantar, flexion that is equal reflexes bilaterally based on the clinical presentation, which of the following blood vessels is most likely to be affected gate. So we have, we have right, the same D ok, that's fine, which is in fact the correct answer. Next slide. Ok, great. Um Any questions regarding the, uh, the we we covered so far? Ok. I'll take the silence as a no, right. In terms of stroke assessment, there are two ways of assessing stroke. Er, one of them is the quick way and that's what they us usually in the community and er the acronym for it is er fast and that stands for face on speech time. So, so that basically it, it uh it says it says what you need to look at. Uh so if there is any facial droops, arm weakness or speech changes, you need to call 999 as soon as possible because uh stroke is basically it's time. If you, if you, if you miss, if you miss the time then you know. Yeah. No, no, no, no. Yeah. And to is another score that you can u that we can use and it's um it's mostly used in ed and uh as you can see here in this diagram, I'm not gonna go through it the whole er through the whole of the score but er basically you can use it on er, apps like me Talc er, and then it, it calculates the score for you. Er but if the score is one or greater than one, then stroke is very likely. And that you should, you should do a non contrast CT head uh as a first line investigation. And that is important because you need to rule out er, if there is a hemorrhage er, first before you give any anticoagulants or antiplatelets like aspirin. Nextly please. Uh so in terms of imaging, what you would see on a scan, er, if you see like a hypodense region that, that then that can suggest ischemia and we're gonna go through the different kinds of, er, imaging as well. You see with, er, you see with hemorrhage as well on the next few slides, next lab, right? So in terms of the management of a stroke, uh so I think another important thing to know, especially for acies, er, if you get a stroke station, the most, one of the, one of the important things to, to mention is to exclude hyperglycemia because hyperglycemia can actually mimic stroke and it can cause motor weakness and it can cause speech disturbance and it, so I think it's, it's very important uh for, for us to exclude hyperglycemia first. And as we said before, uh if you suspect a stroke, you should be a, you, you should do an immediate ct head just to exclude hemorrhage before you're able to give uh the medical management for a stroke. Uh which is usually aspirin 300 mgs as a stat dose uh to, to be given after CT and that is usually continued for two weeks. And then that is usually switched after that to 75 mg as uh for uh for a lifelong. Uh So in terms of uh the timing of a stroke, uh and what we said before that it's very important, you know, to call 999 as soon as possible. And that's one of the reasons. Um So if the symptoms occur within the 1st 4.5 hours, we're able to thrombo er to, to do th thrombolysis. Er, but if the symptoms are within six hours, we're also able to do thrombectomy as well. So, if a patient presents within the f uh within the 1st 4.5 hours, then we can offer a combination therapy with thrombolysis and thrombectomy as well. If there is evidence that there is that the tissue is still er salvageable from the CT scan, this time window can be actually extended to 24 hours, but that depends on the imaging melas. All right. So as we said before, er nice guidelines recommend, you know, as we said, aspirin, you can give that for two weeks and then after that, you can switch to clo clopidogrel, 75 mg. And it's important to know that if clopidogrel is not tolerated, uh then you can give aspirin and also um Diol uh and also uh in terms of the uh in terms of the long life uh treatment for a stroke as well. Patients can be given uh atorvastatin. It's usually 80 mg and that is started if uh C cholesterol was greater than 3.5. Uh and then obviously, there are other risk factors for stroke, including diabetes and hypertension. And it's very important to control these factors in stroke patients and to offer suitable therapy for diabetes and hypertension. Uh stroke can also affect other things as we saw in the uh um Monus. Oh, so we have a question here. Yeah. So yeah, there there's a question here. When is clopidogrel not tolerated? Ok. So some patients have certain side effects of clopidogrel. Er there are a number of side effects of clopidogrel that will be that you know, that can happen with, with clopidogrel and if they occur, then we can switch to another medication. But also uh there, there are another important thing to note as well is that in some patients, uh clopidogrel is not effective. Uh So there is an enzyme called CIP two C 19 and some of the uh so, so clopidogrel is uh is, is a pro drug that needs to be activated by this CIP enzyme and some patients are not able to uh to, to metabolize this for. Mhm. Mhm. Mhm. It stim. Mhm. So in now uh some studies in the NHS um to basically try these uh we call it Pharmaco pharmacogenetic testing and mhm. I think that will happen in the future. Does that make sense? Ok, great. Next slide, please. Um hi, everyone, please do put your answers in the chart. Um And like I said before, if you don't want to message um publicly, you can privately message uh Mohmed as well. We just encourage you to kind of um you know, just think about the answers and contribute. Ok. Yeah, even if you are not sure, just uh just give it a guess. So on to the third question, Ellen is an 85 year old woman who presents to hospital with left-sided arm and leg weakness. These symptoms resolved after 55 minutes, she has had a ct scan of her head and has been diagnosed with having a tia A or transient ischemic attack, which statement is most applicable to this diagnosis, right? This is more of a uh of a, more of a difficult question but just, just have a guess even even if you're not sure. Ok, so you, ok. So actually, so the uh the who, who the, the people who said be the definition is based on duration of symptoms. This used to be the old definition of ti A but now we have um more uh uh like a newer definition, er which basically states that ati A should be based on tissue appearance and not the duration of symptoms. N las Yeah. So as we said before, T ra were based on the, the timing uh and the timing of the, the duration of the neurological symptoms. Uh and it was, it was defined as less than 24 hours. However, a new definition now is based on uh o on, on the tissue. So if the tissue is showing uh survival, then, then, then, then, then we can define it as a tia in terms of the, er, management of ATR A, it's, it's very similar to a stroke. Uh So we, we also give aspirin 300 mg, er unless there is a bleeding disorder or the or a patient is taking anticoagulants already like Warfarin, for example, for patients with af already taking uh anticoagulants, uh that's fine. We don't need to give them uh aspirin in that case. Uh And then uh also uh with ti a patients, er an urgent assessment uh is, is required by a specialist within 24 hours as well because sometimes it can also be very hard to differentiate TI A with other uh syndromes. Like for example, migraines can also uh closely present ti A s. So it's very important to get that specialist assessment within 24 hours. And also another, another important thing to know as well in patients with TIA A. Uh 111 investigation that we do for them is uh carotid artery ultrasound. And uh if they have steno stenosis greater than 70% then we're able to offer them uh endo endarterectomy, which basically means taking out uh or breaking, breaking down the, the clot and also with any, uh with, with any patient as well that you see in OSC, it's very important to talk about conservative factors, you know, diet exercise. So in these patients, we also try and offer them a lifestyle advice, uh especially that, you know, things like diabetes and hypertension can increase the risk as well. Lectotype on to the fourth question. Yeah. So we have an answer here. B anyone else? Yeah, I have another answer be OK. So uh the clue here from this question is uh here here at the back of his head. Uh She, she, she felt that this was a hit at the back of her head as if someone hit her with a baseball bat. This is a typical uh terminology that is used in these kind of questions and it is the biggest clue uh for subarachnoid hemorrhage. So, yeah, B is correct. Yeah. Next lower please. Yeah. So in terms of the pathophysiology of subarachnoid hemorrhage, uh it's basically a hemorrhage into the subarachnoid space within the meninges. And as you can see here in this diagram uh between the meninges, which is the layers of the brain, you get a bleeding there. Uh And uh and it's typically caused there, there are two main causes of subarachnoid hemorrhage. It can be due to trauma and that is the most common cause or it can also be due to a, to a spontaneous uh cause as well. And one of them is very aneurysm and this is associated with conditions such as polycystic kidney disease and is done those. And the reason for that is that these conditions affect the connective tissue and it increases the risk of arteries bulging and then, you know, causing an aneurysm and then causing a bleed. Then uh also a v malformation or arteriovenous malformation can cause uh spontaneous subarachnoid hemorrhage. And as we said before, the clinical features of subarachnoid hemorrhage patients would usually say that they have pain at the back of their head. It's as if they're be be being hit with a bat uh at the back of the head and also sometimes uh they have nausea and vomiting and also men meningism as well. Uh which is photophobia and neck stiffness, which is very similar to what you have in meningitis. So, yeah, it's something uh to keep an eye out for. So in terms of sorry, uh just going back quickly to the investigations for sub arachnoid hemorrhage. Uh it's uh it's, we usually do a CT scan uh to look for the bleed and we're gonna go through the scan as well in a, in a few slides. What, what it usually shows, uh it's important to know that if the CT scan is negative, then we do lumbar punctures. Er, and an important thing to know is that lumbar puncture must, must be done twen uh 12 hours after symptom onset. And that is to allow the time for blood to appear in the CSF. And the, and the medical term for that is xanthochromia. Uh So that is something to look for as well. Next slide piece. OK. Yeah. So in terms of the management of subarachnoid hemorrhage, uh as with any uh intracranial bleeds, referral to neurosurgery as soon as possible. Um OK. To the way they manage it, it's usually done by a uh it's usually done by interventional radiology and they usually treat it with a coil. As you can see here in this diagram, the other alternative is to clip it. Uh but the majority is treated with a coil and these patients are usually also sent with a 21 day course of niMODipine uh to prevent vasospasm in the brain. And also they're advised to uh to conform to strict bed rest as well. And BP control just to avoid uh the BP increasing and potentially causing further bleeds. Uh So, complications for subarachnoid hemorrhage. Uh This is something that I remember. Um it, it, it could come up in an OS. Um you know, as with any, as with any presentation, they can ask you what the, what, what the complications is. Uh So in terms of the complication of subarachnoid hemorrhage, there is a couple of complications to be aware of. Uh one of them is uh vasospasm and that's why we give niMODipine for 21 days afterwards. Another complications include uh uh si A DH as well causing hypernatremia and also hydrocephalus. And unfortunately, a quarter of the patients uh can die after they have subarachnoid hemorrhage within the 1st 24 hours. So, these, these are some complications uh to be aware of as well Meloy. So, in terms of uh the imaging of subarachnoid hemorrhage, uh it's the most important thing to know about it is the star sign. Uh So usually patients with subarachnoid hemorrhage have that star sign on their uh ct scan. And that basically is representing blood in the subarachnoid spaces. That's something just to be aware of next to please. Right. Moving on to the fifth question, 28 year old man is brought to the emergency department after a fall from a ladder, hitting his head, he initially lost consciousness for a few minutes, but then regained full consciousness and reported feeling fine. However, after one hour, he began complaining of a severe headache, nausea and feeling increasingly drowsy on examination, he stent but arousable with a dilated right pupil and left sided weakness. Yeah. So we have a couple of answers here. All all pointing, all pointing towards me. So the biggest clue in this question is the history of trauma uh which is usually, you know, what happens before someone has an extradural hemorrhage, for example, in an accident, someone riding a motorcycle fell off, um or someone you know, climbing a ladder, like in this case, fell, fell off his head. Uh So yeah, trauma is very, is, is, is the biggest clue here for um exou hemorrhage. And also another another big clue here is that they have regained consciousness. Uh So they were feeling absolutely fine for a bit and then they deteriorated again and that this is what they call the UC period. So if we go over to the next slide, I will be able to explain. So yeah, as we said before, so clinical features of extradural hemorrhage classically uh you know the the lucid interval or the lucid period. Uh this is why the patient briefly regains consciousness, feels absolutely fine and then they deteriorate again. And also another thing to note here in the previous uh in in that last question that we did, the patient had a fixed and dilated pupil. And that's an important sign to look out for, especially in ed when patients come. Er for example, from an accident, it's very important to look at their pupil er to look for any dilation and uh to look if they if they have a fixed pupil. And the reason why it occurs in uh in in hemorrhages including extra hemorrhages is that the hemorrhage can press uh in the brain and it can cause the temporal lobe to herniate uh specifically the oncle region of the temporal lobe as you can see here in this diagram. And it can actually compress on the oculomotor nerve and the oculomotor nerve. Uh the motor nerve is responsible for eye movement. And also uh it's also important for it to control the pupil construction as well. So if it's, if it's compressed, then it can cause dilation and it can cause fixed, fixed pupil. Uh Also another thing to note here for ural hemorrhage is that it's caused by an artery in con, in contrast to other bleeds, uh which subdural, for example, which is caused by a vein here, it's caused by the middle meningeal artery. And it's usually, as we said, it's, it's caused by trauma. The definitive management for hemorrhage is also a referral to neurosurgery and they can consider things like rio basically to take out the hematoma. Next one, please. So in terms of the imaging, what you would expect to see from exo uh hemorrhage, you would see a lemon shaped uh bleed here, usually also with midline shift. Uh as you can see here in this image. Uh sorry here, if you just press on enter as well, it will come with the description. I think there's a bit of an animation here. Yeah. So as we said here, there's a bit of a midline shift. Uh It, it's a lemon shaped lesion. Yeah. So these are the most important things to look out for to be able to differentiate it er to other types of er intracranial hemorrhages. Next slide, please. Right. 76 year old woman presents with episodic confusion and headaches for the, for three weeks. She has a history of alcohol excess, frequent falls and type two diabetes. Her daughter reports that she has been having frequent spells of confusion over the past few days. Neurological examination is unremarkable and her blood sugar is 6.7 had, is done which reveals the bill, which reveals the below. Yeah. So, er, actually the, I'm not gonna, I'm not gonna show you the, the, the diagram unfortunately, because I think I've, I've put it in the er in the answers by mistake. But from the um from the history, if you were able to tell what is going on, just put it in the chart, please accurately. So can you, we'll, we'll go to the next slide. Yeah. So in, in this case, you actually needed to see the image uh because to be able to differentiate between acute and chronic. Uh So in terms of the uh of the chronic subdural hemorrhage, uh this is usually a hypo dense uh hi, a high p dense uh hemorrhage and I will show you a diagram in the next few slides how to different, how to be able to differentiate between acute subacute and chronic hemorrhage. But uh in in contrast to extra hemorrhage, the uh subduer hemorrhage is usually uh banana shaped as you can see here and it's uh not restricted by suture lines as well. So, next slide please. Yeah. So another thing to note for subdural hemorrhages is that it's, it's caused by uh veins and it's, it's caused by the bridging veins between the dura mater and arachnoid matter. Key risk factors to take note of, especially when you're in ed. Uh It's usually more common in uh in elderly patients, patients who are using uh you know, alcohol and also patients who are on anticoagulation. But the, the, the biggest clue really uh to look for in the history is, is alcohol because alcohol can affect the veins. Uh c it causes basically fragility of the, of the veins. And that, and that is one of the reasons why uh rupture in these veins can occur easily. Oh, just a quick figure to show you guys how to differentiate between acute subacute and chronic. It's usually hyperdense and that is usually the case if patients present within the first three days afterwards. So if you just press on enter h Yeah, after that, if they present after three days, it's usually isodense or gray. And that is between four days and 21 days. We call that subacute subdural hematoma and then post 21 days, it then becomes hypodense if we just show the figure, please. Yep. And uh that is usually a black hemorrhage as you can see here, a hypo dense uh after 21 days and then uh sorry, h if you just press on enter again. Um Yeah, sorry. One second and it's not usually not restricted by suture lines. Any questions at all, any questions before we move on to the next question? Ok. That's fine. Uh We'll move on. Then a 37 year old woman presents with a two month history of marked fatigue. She has had an initial tired all the time, blood test two weeks ago were, which were insignificant alongside. She also describes a two week history of paraesthesia to her legs. Bilaterally she attended today because of worsening right sided eye pain on eye movement and some lo loss of color vision. What is the most likely underlying diagnosis? Ok. We have, you have to be here. OK. Any anyone, any other answers? OK. So in fact, yeah. B is the right answer. So uh the, the, the key clue here in this question is that a patient has presented uh it's, it's a relatively young patient uh woman as well, which is a risk factor for um uh for multiple sclerosis. They're usually uh younger females that present to the clinic and they have multiple system, uh multiple symptoms that occur in different areas or different locations over time. So, as you can see here in this question, she had paraesthesia to her legs bilaterally. And then after that, she had a totally different symptom to her eyes. So that's a big clue that it is um uh multiple sclerosis. So, moving on to the next slide. Yeah. So uh a a key feature of multiple sclerosis is that it's disseminated in time and space. So, symptoms occur in different locations over time. Uh Sometimes it can occur in the eye. It can occur in, in the eyes cause causing visual symptoms like optic neuritis and uh s phenomenon, which is an interesting phenomenon which basically patients have worsening of symptoms during uh hot temperature. For example, if they have a shower or if they go to hot countries, their symptoms can become more severe. Uh Also they have sensory symptoms including paraesthesia, pins and needles and also motor symptoms. They usually have leg weakness as well. So these are some symptoms to look out for uh in terms of uh how to diagnose multiple sclerosis. There is the mcdonald criteria. Uh It's, it's, it's a big table. We're not gonna go through it completely because it's out of the scope of this uh lecture. Uh But just a simple way of diagnosing. It is patients that have two or more relapses and also uh objective clinical evidence of two or more lesions in the brain. So there are three different types of uh MS, one of them is relapsing, remitting and this is the most common cause. This is why patients uh relapse. So their disease deteriorate and then they actually improve after that. And then so they basically keep uh improving and falling, improving and falling. Uh Unfortunately, there is another type of uh MS primary progressive, which is only 10% of the patients and they basically go downhill from the uh as soon as they get diagnosed with MS, they just go downhill. There is no up and down secondary progressive is when uh relapsing remitting patients after they fluctuate, they then move on to a more progressive phase. Uh And then they have sustained uh disability. Next slide, please. So this is an a very important investigation for uh MS. Uh and that is to do MRI scan. Uh It's, it's the most, it, it's, it's, it's the most accurate scan we can do for the brain to look at, you know, soft tissues. Uh And what usually appears in MS is what we call dow and fingers and these are white matter that are per perpendicular to the corpus callosum. And this is indicative of uh MS helotes, right. So, in terms of investigations for MS, uh we said uh Mr, we said MRI scan, uh we can also do a CSF analysis to look for uh legal clonal bands. And uh also we can assess for action potentials as well and that usually er the the results of that shows er delayed visual auditory and somatosensory er potential. So, unfortunately, there is no cure for MS. Uh The management is focused on s symptoms and trying to reduce the er relapsing er phases. Uh So, for acute relapses, uh the management for that is steroids, oral prednisoLONE or uh or IV methylpred. Um And then moving on, there are also more advanced medications that we can use as well, including, uh, Natalizumab II. Don't think we need to, to like to know exactly the, uh, the specific names, but I'm just giving you some ideas of, uh, what, what, what they use in clinical practice, uh, spasticity as well is one of the symptoms that can occur with, um, MS. And for that, uh, we can use baclofen and gabapentin for fatigue. Uh The nice recommends er amantadine, which is basically like an off label treatment for fatigue. And the way it works is they're not really sure how it works. Uh But there are some theories that suggest that it uh reduces uh glutamate neurotransmission in the brain. And glutamate is like an exci uh it's an exci it acts on the uh excitatory pathways in the brain and by reducing the excitatory pathways, it can help reduce the fatigue, the central fatigue in the brain and thereby reducing the fatigue in general. This is one of the theories. But yeah, um bladder dysfunction uh as well as one of the symptoms as well. And that can be assessed by doing an ultrasound next slide, please. Sorry. Sorry. Yeah, great. So, moving on to epilepsy just uh a quick uh uh Yeah, yeah, here we go. Yeah. So we're just moving on to epilepsy now. Uh So epilepsy is uh is a disease basically caused by aberrant currents in the brain and there's a lot of causes for epilepsy. Uh One of them is basically op lesions, cancers uh in, in smaller kids, er febrile convulsions is more common uh due to pyrexia. Also, alcohol withdrawal can cause epilepsy as well. And also in the major in, in a, in a lot of the cases as well as idiopathic. We don't have a cause for epilepsy. Unfortunately. Uh so there, there is a, a lot of ways how we can categorize epilepsy. Uh a simple way is to uh categorize it into focal seizures and a generalized seizure, which we can also divide further into uh we can divide further the focal seizures into focal aware seizures, which is basically when the patients have uh full awareness during the seizure. Uh in con this is in contrast to focal impaired awareness seizure. And this is when the patients have impaired awareness during the uh focal seizure and then uh also focal seizure can turn into bilateral seizure. So usually focal seizures originate from a specific part of the brain, usually at, at one side of the brain and that can spread into bilateral uh or generalized seizure by spreading through the whole of the brain. Moving on general right seizure can also be split into uh uh more groups. One of them is the tonic clonic seizure and this is where patients have a tonic phase followed by a clonic phase. So the limbs would usually stiffen and then jerk after that. And there's also usually tongue biting in these patients as well. And incontinence, there are some myronic seizures which is basically when patients have a sudden jerk of the limbs, trunk or the face and then also absent seizures, which is more common in Children. This is where the child would for a brief period of time, they would appear as if they've lost consciousness for about 10 seconds. And then, yeah, they would then come again and wake up again after that next slide, please. Yeah. So uh we can actually we can actually localize uh a seizure based on the symptoms. Er So temporal lobe is a lobe that is important in memory and also important in the limbic system. And uh so patients that have a temporal lobe seizure, they have uh they can have a lot of emotional symptoms and they can also have hallucinations because they can activate the memory centers in the in the brain including the hippocampus which is started in in the temporal lobe. Uh And also the uh these patients can have uh automatism basically like lip smacking and also other strange symptoms that they have. Uh and they can also have dysphagia as well. Frontal lobe, uh frontal lobe seizures can affect uh the pre uh uh so frontal lobe uh seizures can affect uh the the the the motor uh movement uh in the body, including the head leg and the. Mhm. Mhm. Mm. Mm. Mm. Mhm. Mhm. Mm mm. Yeah. And that is cited in the frontal lobe, whereas the post central sulcus is important for the sensation in the whole body. And that is cited in the parietal lobe. And that's why they get a lot of uh sensory symptoms. The occipital lobe is responsible for vision. And uh in this case, patients have visual symptoms that can be split into a positive phenomena and negative phenomena. Next slide please. Yeah. So uh in terms of investigations for epilepsy, uh MRI is quite important for uh for epilepsy. Also, eeg s uh user needs to rule out any um metabolic causes of uh epilepsies and also a drug screen as well including alcohol. And to see if they uh the patients are potentially having like an alcohol withdrawal and also a CSF analysis to rule out meningitis. It's important to know and that that is a common uh M CQ question that comes uh so pa uh patients especially women who are taking anti epileptics trying to conceive. Uh we usually increase the dose from 400 mcg into 5 mg, folic acid once daily with regards to the management of epilepsy. A very simple way of putting it is uh for generalized tonic chronic seizures and absent seizures. The first line is sodium valproate. Uh that is in men in uh females, it's preferable to use lamoTRIgine because sodium valproate is uh genic for focal seizures. Uh The first line is uh carBAMazepine. And uh yeah, in terms of the er, policies regarding driving. Uh Also that is a bit, it's quite common as well in M CQ questions. If a patient comes in with an isolated seizure, first episode, then they must not drive for the first six months. Whereas if they have recurrent seizures, er, they, they must not drive for 12 months until they become sei seizure free. And then after that, they can drive again. Exide, please. Ok. Status epilepticus is something that is seen quite commonly in Ed and as F ones and F twos, you'll see a lot of them. So I think it's very important to be quite familiar with this pathway. Uh So status epilepticus is um technically defined by a single seizure lasting more than five minutes or two or more seizures within a five minute period er without recovery in between. And that is very important to know because if you don't manage these patients uh promptly enough, it can, it can lead to irreversible brain damage. So the way uh we can manage these uh patients is just to approach them in ABA B DCD er manner. Uh So if the seizure is lasting more than five minutes, it depends in the community, we can give rectal diazePAM uh us uh 10 mg or we can give IV LORazepam 4 mg and then we'll see how the patients are. If they continue to uh seize uh 20 minutes, we repeat uh the step above. So IV Loraz or rectal dipam and then 30 minutes in, if they are still seizing, it's very important to alert the, the anesthetics in this case because you might need them later. But at 30 minutes, if the seizure continues, you can give phenytoin infusion and then in refractory cases at one hour, if they still have not responded, then the anesthetist would then need to come and actually put them uh they, they need to intubate them and put them under general anesthesia. Next slide, please. OK. We're coming to the end guys. So uh Zahid, a 72 year old man is brought into your GP clinic by his wife who is concerned about his mobility and behavior. Over the nine months, his wife has noticed that Zed's movements have been much slower. He walks to the chuckling gate and has had a few recent falls on examination. You know, that Zahid has a tremor and on assessing tone, you know, cogwheel rigidity, given the most likely diagnosis, which answer best describes the tremor. You are most likely to see any ideas an OK, let's review the answer. OK. Right. So, so th this, this M CQ is a typical of Parkinson's and uh Parkinson's uh typical presentation is a unilateral tremor and that is uh w which improves or movement. So these are quite important uh features to look at when looking at the question. So in this question here, we know, we know that the patient has a shuffling gait and has had a few holes and uh that is due to the autonomic dysfunction that Parkinson disease patients have. And we're gonna go through that in the next few slides as well. Uh So if we can move on to the next slide, please. So Parkinson's disease is u usually characterized by a triad of, of symptoms, including natural tremor rigidity and bradykinesia. Uh And the way uh I wa ii remember in my placement in medical school, um how to assess bradykinesia. So ask the patient to do this movement. And if, if they're, if they're able to do it slightly, then you're able to uh you know, tell for a certain that they have bradykinesia because they have reduced range of motion. Uh So Parkinson's disease is more common in men. Uh It's, it usually occurs at the age of 60 it's, it's important to know that it's a clinical diagnosis as well. There is not a single test that can help us with diagnosis. So it's just based on symptoms and as we said before, the clinical features, er in addition to the triad that we talked about patients also have no, no facial expressions. And the, the, the medical, like they call it the medical term for it is like mask like faces. They also have micrographia, which basically means that er their hand writing is quite small as well and that is due to the bradykinesia, the bradykinesia that they have, they're unable to have the full range of motion to be able to write properly. And then there's also psychiatric symptoms as well, including depression and dementia. And it's important to monitor for them to see if they require any antidepressants, for example. And also autonomic dysfunction is, is quite debilitating for patients and that can cause things like constipation and also postural hypertension as well. So in terms of imaging for these patients, the most important thing to consider here is a, a CT scan or an MRI. Uh but the, the another diagnostic test is the SPECT D at scan, which is basically a pet scan that looks at the to the dopamine uh receptors and neurotransmitters in the brain. And uh these, these basically light up. Uh So if there is degeneration of the dopa dopaminergic neurons in the substantia Migra of the brain, uh there is this area would not light up as much and then you were able to diagnose Parkinson's disease. Next slpi. Yeah. So uh Parkinson's disease is usually managed by a specialist. Uh There are drugs, some drugs that you should be aware of including levodopa, which is uh a pro drug, it's converted into dopamine basically and A a and acts the same as uh dopamine. Uh And then unfortunately, the efficacy of this medication reduces with time. So uh I think usually neurologists leave it as a as a uh like one of the last results to use. And uh levodopa works more effectively if you give it with, er, COMT inhibitors. Er, and, er, so that, that's why you can sometimes use COMT inhibitors uh with Levodopa as well. Dopamine agonists as well. Er, neurologists can use uh a side effect to note with the dopamine agonist is uh impulse control disorders which is quite common in M CQ question. Usually a patient with, with uh would, would be in the M CQ question uh as like unable to control their spending and uh uh these kind of impulse control disorders. So that that's seclude that they're on dopamine agonists. Other other options as well include monoamine oxidase uh inhibitors. So, the management of Parkinson's disease involves a multidisciplinary approach with uh neurologists and also psychiatrists and physiotherapists and other team members as well. Uh So levodopa, sorry, just a quick note on levodopa and also anticonvulsant medications. These are quite important medications and you should never forget to prescribe them when patients come uh on admission. And but also LEVODOPA should never be withdrawn suddenly. Uh becau because it can cause uh dystonia and neuroleptic malignant syndrome. Uh patients are are unable to take levodopa orally, we can give them uh patch, uh we can give them dopamine agonist patch. Next. So there are some other symptoms that you should be aware of as well. Parkinson's plus syndromes. Uh The first one is PSP or progressive supranuclear palsy. The, the differentiating the easiest way to differentiate this palsy is, is that in the MC questions they would present as a patient that are um that doesn't have vertical, unable to move their eyes vertically. So vertical, eye gaze palsy uh and these patients usually have a symmetrical uh onset rather than like unilateral onset and they have little tremor as well. Uh M SA or multiple system atrophy. Uh These patients have an early autonomic feature uh including postural hypertension incontinence and they usually have more rigidity in compared to tremor, Lewy body dementia. Er, also, er, it, it's quite common in MC three questions. A differentiating factor for them is like patients who usually have hallucinations and then Parkinson's would come later on. So in Parkinson's usually the motor symptoms start first and then after that, they can actually develop dementia. But with Lewy body dementia, they have uh hallucinations first and cognitive impairment and then they develop Parkinson's later and that's how you can tell the difference between them. Cortical basal degeneration is another also Parkinson's Plus syndrome. And these patients have akinetic fragility uh involving one of the limbs and