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Um Hey guys my name is Johanna, I'm one of the recent period graduates and I'm working currently than a fun at whipps cross. Um Before I start can someone say something in the chart. I have to screen so they just want to make sure that I can monitor the chat appropriately if someone can just type in or someone they let me know if they can hear me see me and just so that I can test the chat perfect. Thank you daniella okay um So let's make a start because we have quite a lot to cover um So today we'll be covering. Um I think what is most important for your neurology revision for your finals okay perfect um just monitoring the chat um so obviously, I'm not able to cover every single detail that you know that you need to know, but I'll try to focus on the most important things so now that for many of you neurology can be a bit complicated and confusing, but I think what's most important to do really well in your exam is to be able to identify where a problem in the nervous system is exactly caring is it in the central nervous system, is in the peripheral nervous system, where exactly and if you identify where the lesion is in the neighbor system, then there are only a handful of pathologies that can affect each part of the neighbor system and you know a little bit about them, you can do really well so try to provide you with the framework of how to approach most of the uh questions for your neurology finals and paces, um and I have have included quite a lot of questions. Uh. I'll be monitoring the chats, so if you have any questions, please feel free to, to interrupt me, so let's start with a basic introduction to the nervous system. So as we hope you will know the nervous system is comprised of the central nervous system and the peripheral nervous system, so the central nervous system includes your brain and um uh your brain and spinal cord and your peripheral nervous system includes the peripheral nerve that start from the spinal cord uh They go to I either your muscles or your your organs and your visa. I also hope that we can all identify the difference between an upper and a lower motor neuron problem, so an upper modern urine problem will classically cause increased tone, reduce power, increased reflexes, and upgoing planters, whereas the lower motor neuron pro, problem will on inspection, Have a circulation and wasting. You will have reduced own reduced power, reduced reflexes, and downgoing planters and the main pathologist that cause an upper motor neuron problem and that come come come up a lot in finals is stroke, m. S, brain, humor, or some sort of course pathology which we're going to speak about later, whereas the main lower motor neuron problems are usually due to prefer nerve uh prefer neuropathy such as Giambra syndrome, due to other prefer neuropathies or do the problem in the neuromuscular junction, which we're again going to cover and if someone has both upper and lower motor neuron problems, then you have to think a little bit about motor neuron disease, so this is just a revision uh slide uh so that we can think about the main areas of the central nervous system and the pathologist that affect each of the different areas, so let's start with the brain meninges. We just cover your brain and the main things that can go wrong with them is meningitis and subarachnoid hemorrhage, which will cover later. Then we have the cerebral cortex, which is divided into magical lobes and the things that can go wrong and can affect the cerebral cortex and the cerebral hemispheres are mainly strokes, m. S, humor, brain bleeds and venous thrombosis, which is to betray but we'll talk about it as well. Then underneath your cortex, you have the basal ganglia, which are subcortical structures, which are mainly involved in motor control and things that can affect those is mainly parkinson's and parkinson's related conditions, huntington's and lacuna strokes, which are small strokes which we're going to talk about. Then you have your cerebellum and the main things that can go wrong with it is again stroke, alcohol related cerebella, degeneration, and parkinson's then we have the brain stem and the problems again are due to stroke or parkinson's, parkinson's plus disorders uh and spinal cord. The main things that can affect it is again m. S, hemi, section of the spinal cord, syringomyelia and cord compression, So this just a summary slide now going on with the brain. Um If someone has a brain lesion um On examination the main things that you're going to find our increased tone, reduced power, contralateral e, contralateral sensory loss, and increased reflexes, so the thing that used to confuse me quite a lot um as as a medical student was what we mean by increased tone and it actually means to think it's either spasticity which is also called class knife or rigidity. No specificity is usually what your cortical issues will give you and what we mean is a velocity dependent uh resistance to movement and it's and it's actually the resistance that you feel will be different in flexion and extension, your rigidity. You'll mainly see that in the extrapyramidal conditions, so the things that affect your basal ganglia in the subcortical structures that we talk about and it's described as either lead type, which essentially where you have a resistance, which is the same throughout. The movement is the same in flexion and extension and cog wheeling, which essentially means rigidity and tremor. Together, Now thinking of those of the small introduction, let's do a couple of questions, and then we'll go through the answers together. Um I couldn't really sort out the mental meters, so um if you just put them on the chat and I'll be more entering it, so I'll give you 30 seconds for the first questions and if you can type your answers in the chat okay um any answers I can't seem to see any answers in the chat okay, we have a c okay, I'll go in with the next one. Again, please be, uh you can put your answers in the chat. I'll give you 30 seconds for this one as well, any volunteers. Thank you. Hair if thank you daniela okay, I'll go into the next question. This is a bit of a difficult one okay let's start with speaking about strokes, so a stroke by definition is a sudden onset focal neurological deficit of presumed vascular origin lasting for more than 24 hours. The main symptoms that uh we usually want public about how to recognize its facial drooping and weakness and speech difficulty. Now thinking it what caused the stroke. Most of the strokes are skipping but about 10 to 15, 15 to 20% of strokes are hemorrhagic. Now ischemic strokes are caused by a lack of blood flow in your brain and they're either caused by thrombosis, which happens when you have a vessel, which has a bigger atherosclerotic plaque, which narrows, this affects the flow of the, of the blood within the vessel, and then a thrombus can easily form and block the blood flow to the brain. Ischemic stroke. Can also be caused by embolism, which is essentially when a blood clot forms somewhere elsewhere in the body, usually the heart in someone with a f, and it just travels through the circulation and blocks an artery in the, in the brain and they can also be caused by systemic hyperperfusion, which is essentially when you for another reason such as a cardiac arrest or very low BP, you don't refuse your brain very well and hemorrhagic strokes are caused either by due to a bleed inside the parenchyma of the brain, so an intracerebral hemorrhage or do you to a bleed in between the manager of the of the brain, so there's a barcode hemorrhage. Now another thing that's quite important to know is the Bamford classification, so this device strokes into total anterior circulation stroke, partial anterior circulation stroke, posterior circulation, stroke, and lacunar. In fact, uh in order to um understand this, we have to do a bit of of an anatomy revision and remember that the blood flow to the brain is supplied by your vertebral basilar arteries, which are for which come from your subclavian artery in your or to and from your cerebral arteries, which come from the internal carotid arteries and now uh the middle cerebral artery, which comes from the internal carotid artery and the anterior cerebral artery uh together from the anterior circulation, which supplies the area, which is shown in the diagram as blue and orange and the posterior circulation uh supplies uh the area which is uh shown in yellow and white, so your occipital lobe, mainly your brain, the brain stem, and the cerebellum, now going back to the bomb for classification. Um We'll talk about what the anterior circulation uh stroke. The anterior circulation is essentially your anterior cerebral artery and your middle cerebral arctic, so in order to for stroke to be classified as a total anterior circulation stroke you need to have all three of the following symptoms so contralateral motor or sensory deficits, homonymous hemianopia and higher cortical dysfunction which is manifested as dysphasia or neglect um and the total idea circulation stroke means that you have both your theory and your meals. Terrible artery's blocked. A partial anterior circulation stroke is actually uh you need only two out of the three ones of the three following symptoms and it means that either you're on tier or your middle cerebral artery is blocked um So, if someone has a partial uh anterior circulation stroke, it's also important to understand whether it's the anterior cerebral or the middle cerebral that is blocked or or blood or whatever so in order to differentiate between those two. Uh We need to remember the motor homunculus, which is essentially this map where your whole body is represented on the brain and in the motor cortex. So if you look at the motor homunculus, the anterior cerebral artery uh supplies the more medial part of the homunculus, and in the modern homunculus, the leg is represented more immediately than the arm and the face, so an anterior circulation stroke which applies the medial part of the modern homunculus will affect the leg more than the arms. The miserable artery, a miserable artist, stroke on the other hand, will affect the hands more than the legs and the arms, the the hands and the arms more than the leg, sorry, and this is because the mode in the modern home oculus, uh the hand and the arms are represented more laterally than the leg. Another thing to remember is that anterior circulation strokes uh can also cause sometimes behavioral changes because your anterior cerebral artery will also supply parts of your frontal lobe and also that the middle cerebral artery can also cause quandary copias, because will affect your optic radiations and also aphasia because your speech centers are also supplied by the middle cerebral artery. Any questions so far okay, um now moving on to the posterior circulation strokes so that the posterior circulation supplies mainly the occipital lobe, the brain stem, and this uh cerebellum and so this is why you get the following symptoms. You have mainly um occipital a lesion symptoms such as hormone emus control, ago, hemianopia, and visual agnosia, can anyone put in the chat, what visual agnosia so to make sure that we are all in the same page um Essentially visual agnosia is when you can see things, so your visual pathway works well, but you can't recognize them exactly, so this is so almost so prosopagnosia is a type of visual agnosia where you can't really remember faces, but can also be with objects depending on which part of your visual cortex is affected, and so typically people with visual agnosia would be able to copy images if you ask them, but they won't be able to recognize that this is a glass. This is the pen, um and then on the posterior circulation symptoms. You also have um you can also have cerebella uh symptoms, which are classically remembered by your acronym danish so this diet coke in asia, ataxia, nystagmus, intention, tremor, slurred speech, hypotonia, and important thing to remember is that cerebellar lesion lead to ipsilateral signs, so the signs on on the same side of the body and now brainstem lesions will affect consciousness. Because you have all your all your important life centers, any of the brain's then we'll cause the cranial nerve damage because from the brains and remember you have all the all the cranial nerve nuclei and all your cranial nerves start from the brain stem and you also have the most important bit is that you have crossed signs, so you have contralateral signs in the arms and the legs, and the body, and ipsilateral signs in the face, uh which is kind of what this picture shows and this is because if we look at here, the contralateral motor signs will be caused by the damage in the corticospinal tract. By any so you get control lateral asians, by contralateral signs and symptoms by any lesion that is above the above the pyramids where the corticospinal tract um cross and you sorry these are the corticospinal tract and you also get contralateral sensory signs. Because again, if you remember from your your anatomy, the dorsal columns and your spinothalamic trucks that can that carries uh sensory inputs from the peripheral to your brain also cross. So this is why brain simulation lead to contralateral motor and sensory signs uh in the arms, legs, and body, but the same time you have ipsilateral cranial passes because you have your your cranial nerve nuclear in the brain stem which uh innovate deep sea lateral part of the face is that clear. It's quite important so if you have any questions, let me know in the chat okay and the last bit of the bomb for classification are lacunar, in fact which essentially are small strokes that involve small perforating our arteries, which supply mainly your basal ganglia, internal capsule, and thalamus, so because smaller smaller, milder symptoms, so you have either pure motorhome, empiricist, pure sensory uh stroke, a toxic hemiparalysis, sensorimotor stroke, and in general, because they they involve subcortical structures, they generally lack cortical uh signs such as the agnosia. We spoke about the the hemianopia, the a proxy, a so, this difficulty in initiating movements and initiating actions. If you have brains and liver do, you have multiple cranial nerves affected, um so you can have multiple brain uh you can have multiple cranial nerves affected uh. It depends on where in the brain stem uh the lesion is, so if you remember from your from your second year in your anatomy in your mid rem, you classically have the 3rd, 4th, and 5th nucleus, then in the pond you have another set of nuclei and in the medulla, you have another set of nuclear, so it depends exactly where uh in which part of the brain stem it ease. It also depends on if it's the lateral brainstem or the, or the medial part of the brain stem. So classically you have, I've not included the slide, but uh I've kind of hugh donated my presentation because of uh time, uh but you also a classical brain stem stroke is the lateral medullary, in fact which um which supplies the lateral part of the brain stem and you have uh you can have for example, uh swallowing things because from from that bit your ninth and 10th cranial nuclear start, so it really depends, you don't have all of them apart you unless you have kind of a lesion affecting your whole brain stem and so going back to the first question, we have a 70 year old man who was admitted with the facial droop and slurred speech. His arm is kept in a flex position. So this is your classical upper motor neuron posture because your extensor is weaker than your flexes, and the power on the right side is too, whereas on the, on the, in the upper limbs and four out of five in the lower limbs, visual fields are intact, so this as most of you said is the left is a lesion of the left middle cerebral artery uh because essentially you have it's left sided lesion because your right side of the body is affected and it's middle cerebral artery stroke because you have symptoms in your um arms being more pronounced the symptoms in your legs, it's not a total total anterior circulation stroke because your visuals, two pills are intact, so you would need all those three criteria which we don't fulfill right now uh. B. N. D. R. Wrong because they would call left sided uh body symptoms and it's not a brain from stroke because we don't have really crania, Cranial nerve passes, or anything like that now moving on. When you suspect that someone is having a stroke, the first thing that you need to do is order a noncontrast ct head uh scan of your head, not your head of the patient's head, uh and you need to get that within one hour and the reason why you do the city head is not to make sure and prove that there is an area of the brain which has a ski mia, but it's it is to rule out a bleed through that hemorrhage. Once you've done, that you can start treating as an ischemic stroke and the reason why you really need to rule out the hemorrhage is because the treatment that you're going to give for an ischemic stroke are things that will make your clot burst and your blood thinner, so they will actually make a hemorrhage worse, so first thing you know you do is you do a city uh scan of your head and then you start treating for an ischemic stroke now how we treat for an ischemic stroke, so you've included um you, we've excluded hemorrhage and the next step depends on how much time has passed from symptom onset, So if the patient presents within 4.5 hours of symptoms onset, you can you can give thrombolysis and we usually do that with intravenous alteplase, Then you after Turnbull acid they'll most likely do another scan again make sure that there is no bleed and no risk of hemorrhagic transformation and they will give aspirin 300 mg for two weeks. However, clinical trials have shown that if more than 4.5 hours have passed since symptoms onset, the risk of thrombolysis is actually greater than the benefits because there is a greater chance of hemorrhagic transformation and bleeding of the stroke. So if more more than 4.5 hours have passed, you don't give thrombolysis and you just start with 300 mg of aspirin for two weeks and then you switch the patient to clopidogrel 75 mg um And this is life long as a secondary uh preventive measure. You can also do thrombectomy, would you use it, which essentially is a mechanical intervention to remove the clot and you do that. If you have a large um essentially artery occlusion on the city or the MRI angiogram now an important thing to understand is why we we do those reperfusion therapies, so why do we do the thrombectomy normalizes so a stroke by definition is an impact which is essentially that you have brain brain cells which are dead. This is irreversible, however, there around the dead cells, there is an area of ischemic penumbra which is essentially means that the that there is reduced blood flow. There is ischemia, but the cells are still alive and this is reversible. So the aim of the profusion therapy is to reduce the ischemic penumbra, which is the area that is a scheme ick, and it is at risk of becoming infected, but it's not yet infected, so that's why it's really important to start treatment early on and as soon as we can for stroke now moving on to the next question here we have mrs smith who woke up this morning and she looked a bit funny hella. The last time that she was seen to be fine and normal was last night, so actually the duration of the symptoms here is unclear. Now they suspected the stroke Based on her symptoms, um a city head has exclude the hemorrhage, so now we have to treat for an ischemic stroke. The correct answer here is to give 300 mg of aspirin because we don't know how long she's had we, we can't be sure that she's had symptoms for less than 4.5 hours, so we can't crumble eyes, so e is wrong for this reason. Um No carotid doppler you would do in anyone with suspected ischemic stroke, but you it wouldn't be the first thing that you do you would of course do a carotid doppler after to see if there is uh reduced blood flow in the carotid arteries, in which case uh if it seems that there is more than 70% of a stenosis, uh you would discuss whether that patient is a candidate for karate, then Doctor mix and Doctor ectomy, but it's not immediate treatment, 75 mg of clopidogrel um is that you would again do, but after two weeks of 300 mg of aspirin, so it's the secondary prevention and e. C. G, you would again doing a any as part of your 80 assessment, but I would hope that that at that time that the patient has had the city head as someone has done in sed, as well in any, no what is a transit ischemic attack. A transit ischemic attack is a transit episode of neurological dysfunction which is caused by a focal brain, spinal cord, or retinal ischemia without acute infection, so usually patient's with a. T. I. A. Will present with with in a and e, but by the time we've seen their seen by a doctor, they won't have any symptoms because essentially there is no there is no infection, but there is a ski mia. There was an area of the brain that had reduced blood flow, had some symptoms, but for some reason blood flow again improved and their symptom free, so what's done in uh t. I. A. S. The first thing is to treat a stroke, so you give straight away your 300 mg of aspirin unless contraindicated, so, unless you think that someone has increased chances of bleeding because of his past medical history, um and then you need to refer them to the t. I. A. Clinic within 24 hours, then they will be assessed by a stroke specialist and they'll usually have an MRI done, which will demonstrate the area of ischemia. Remember, MRI s are more sensible than cities to identify ski mia and once uh ischemia is confirmed, they will start secondary prevention 75 mg uh for life lifelong Now. The important side note is that actually in the, in the TIA, you wouldn't you wouldn't really do a city head before um giving the aspirin and I think the reason is that they think that it's not cost effective, and they think that uh it's been demonstrated that if someone has presents and his symptoms have resolved, then it's likely going to be some sort of ischemia and not and and it's not going to be a bleed, but because the symptoms wouldn't resolve and so there is not a great risk of bleeding by giving the aspirin does that make sense. If not, I'm happy to answer questions now, I'm not, then this slide is about vertical. I'm not going to go into great detail uh into vertigo because of time, um but I think it's quite important in order to answer the last question that we had in the first step. So very tikka essentially is a sensation of spinning and movement of the room around you and it's either do two central causes, so problems in your brain stem or sell cerebellum, mainly which are most likely a stroke or an m. S. Affecting um the cerebellum and the brain stem or it can also be due to a peripheral problem, which essentially means that the labyrinth, which is responsible for balance is affected, and the main difference between central and peripheral um Cause of vertigo is nystagmus in peripheral uh causes of vertigo. Nystagmus is usually horizontal, whereas if it's multidirectional or vertical you you have to worry about a central cause. Now the different peripheral causes a vertical, the main one to to be aware of is benign positional paroxysmal vertigo, where essentially you have it's due to movements of the otoconia, some some crystals in your ear which, and the, and the and bppv last for seconds because it's as is due to this movement. This transit movement of the otoconia and it's worse with head movement. Another cause to be aware of is Meniere's disease, which causes usually unilateral symptoms. They last for a bit longer than bppv and you can also have associated tinnitus and sensorineural hearing loss. Then you can also have labyrinthitis and vestibular neuro nineties, uh which essentially inflammation uh of the your labyrinth or your vestibular nerve, and this usually present after an infection and the way to differentiate them is that in labyrinthitis, you can't have hearing loss. Because in your library through your library, you have your cochlear nerve whereas in your vestibular neuro nineties, it's only your vestibular nerve that's affected and you don't really have hearing loss. Um. Then you can also have a stimulus sonoma, and vestibular migraine, which usually someone would have a past medical history of lots of headaches. Now keeping this in mind, let's go and approach the sec, the other question, so here we have someone who has very good associated with nausea and vomiting. He does have some risk factors for stroke such as hypertension, obs, are fine, and he also has some clumsiness in the right arm, which is a bit suspicious for ataxia. Uh There is also some droopiness in her right eye and multidirectional stand rooms, so multidirectional nystagmus as we've said it means that we have to worry about a central cause, so from those answers, from the options below, the only central causes are cerebellar and brain stem stroke, now how do we differentiate between those two, that was a very difficult question, um a very tricky one but the correct is it's not a it's a sorry, which is a brain step stroke, and the reason for that is that the droopiness in the right eye together with the nystagmus could hint toward the cranial nerve palsy. I made it purposely hard, uh but that's so that you're aware of it, let's move on with the next question. Again, uh if people can put in um their answers to the chart so that I know so I can explain previous again yes, uh so are we do, we all agree that this is a central cause of vertigo, so it's either cerebellar or brains them, and I think the the question is extremely tricky and difficult, and but the droopiness in the right eye could mean that they have some sort of doses and you see a doses with the cranial nerve three pulses is that clear. It's a small hint towards the cranial nerve policy but like cerebella, stroke, wouldn't really cause droopiness in the right eye, whereas a brain stem stroke if it affects the cranial nerve three nucleus can't cause a cranial nerve policy, but it was a bit of a very tricky question okay moving on to the next one, If people can put their answers to the chat. Thank you thank you okay, let's move on, so let's speak about parkinson's, so parkinson's is a neurodegenerative disease which affects the basal ganglia and as we said the basal ganglia are those subcortical structures, uh which are a group structures that are involved in motor control and motor coordination. So what happens in parkinson's is that you get an abnormal accumulation of a protein called alpha synuclein oh in this area here, which is called substantia nigra from this area here, the substantia nigra you have some dominatrix neurons, which traveled to the stray atom, which is another subcortical structure, which is part of the battle nausea, and so it affects the uh nigrostriatal pathway, So this pathway you don't need to know details, but essentially for your understanding is a pathway that is involved in a motor in a complex motor loop, where essentially it sends signals and it increases the activity of the motor cortex, so because you have loss of this pathway uh essentially, you have less activity in your motor cortex and it all leads to a hyperkinetic phenotype, so hyperkinetic. It seems more like difficult to to, to initiate movements, more rigid, more bradykinetic, more difficult to control your movements as well, so that's why you have the classic triad of Reddick in asia rigidity and tremor, and quite importantly again I didn't, I hadn't really realized when I was examining patient's until quite late last year, but you don't really have weakness, which makes sense because you the the neurons that travel from your brain to your muscles, so that your classic corticospinal tract is not really affected. So you the main symptoms of parkinson's is the classical pritikin, asia rigidity and tremor. The rigidity can be described as a lead pipe or coke wheeling as we said before and you also get the tremor, which in parkinson's is unilateral and it's addressed. It's a pill rolling resting tremor and if it's bilateral, you most likely have to think about other causes and in terms of non motor symptoms, you can get lots of nonmotor symptoms. Um You can revise the slide with a little man at your own time, but you can get other symptoms such as sleep disturbance, depression and also economic symptoms such as special hypertension. Parkinson's is a clinical diagnosis uh and you don't really need to do any further tests, uh but I'm sorry, I think there is a small log with my screens. Um Let me know if there's any problems. Uh in terms and you don't need to do any further images. Imaging However, if there is any diagnostic doubt, you can do further imaging settles an mRI or a dopamine transporter scan, it's called that scan, and usually if someone suspects it has a very strong suspicion of parkinson's, they can give a trial level levodopa, which is usually the first medication that you would give form other symptoms in parkinson's and if it's a good response, it's a good enough explanation too, and it provides strong evidence that this is parkinson's now in terms of other differentials to think about what someone presents with a tremor, We have other cause of tremor apart from parkinson's as well, so we have intention tremor, which essentially is when the tremor is not addressed like parkinson, but it's worse at the end of purposeful movement and this is usually due to cerebella damage, so you can see that in a mess in stroke in alcohol people, uh and you can also have postural tremor, which is essentially worse by sustained posture and the main causes of partial tremor as are essential tremor, thyrotoxicosis, better battaglia n'est added differences to, to think about a drug drug induced parkinsonism, which is caused by any medication which, which can interfere with department transport. The main big one is antipsychotics and especially first generation ones, which are potent dopamine antagonists members, schizophrenia. You have lots of deployment activity, so you give dopamine antagonist to reduce this. Um this activity and other medications that can cause a drug induced parkinsonism is metoclopramide, metoclopramide is an anti emetic, which also works as a pro kinetic in the gap, So that's why in the question you, it's very good for gastroparesis, but it does cross the blood brain barrier and does cause extrapyramidal side effects. Don't paradigm is a similar medication, which doesn't cause a cross the blood brain barrier. It doesn't cause extra parameter side effects. So this is why when someone has a past medical history of pakistan's, you would never give them at the copper might, if they have nausea, vomiting, and uh when they are made in the hospital, but you can't give them the paradorn and the difference between parking, so the classic idiopathic parkinson's disease and drug induced parkinsonism is that um drug induced parkinsonism usually has symmetrical symptoms. At the differentials include parkettes and plus syndromes, which are a group of neurodegenerative diseases, which presents with the main features of parkinsonism, but they also have other features that differentiate them from typical parkinson disease, So this one these parkinson plus syndromes include progressive supernuclear policy, multisystem atrophy, dementia with Lewy body and corticobasal degeneration. I don't think you need to know anything you need to know this in a lot of detail. I think the only thing i would remember is that psP has vertical gays problems, msa has lots of autonomic problems, dementia with new louie bodies, resembles a lot of parkinson's, but in dementia with Lewy body, the cognitive symptoms start before the motor symptoms, whereas in parkinson's the opposite and critical based on the generation, it affects the cortex, so it has loads of those of praxis, agnosia and you also get those alien in phenomenons which are interesting, but I don't think you need to know in great detail, so Parkinson disease is asymmetrical and drug induced, is asymmetrical exactly and in terms of treatment for parkinson's the first line treatment is levodopa, that is the first thing that you would do that you would give if the motor symptoms affect quality of life, and this is a drug that when it's it's decarboxylate, it's metabolized into dopamine, so it essentially increases the amount of dopamine you have in your brain and it's usually given together with another drug called carbidopa, so it's usually called cockerel dope or something like that, uh where essentially carbidopa is a peripheral uh dopamine, the carboxylase inhibitor, which means that levodopa cannot be metabolized in the periphery. It can only be metabolized in the brain and so this reduces the systemic side effect of levodopa, uh But you still still levodopa has quite a lot of side effects and the main ones that you need to know is the end of those in wearing off on and off phenomena, which for some reason, sometimes you get your symptoms that were sometimes symptoms are better, dyskinesias, dry mouth, anorexia, palpitations, and partial hypertension. So going back to, uh to this question, I think we can do, went through it uh as as we're speaking about parkinson's essentially we have someone who has parkinson's like symptoms, but it's not classical ideopathic parkinson's, unilateral tremor, so we have bilateral symptoms, so we have to think about a typical parkinsonism. Importantly, they were also started on this really nice for kinetic, which is metoclopramide, but which causes again extrapyramidal symptoms, so the best way to treat that is to switch from the metoclopramide to something else that doesn't cause the blood brain barrier reassuring discharge doesn't solve any problems at all trial of the levodopa, we would do it if we were suspecting ideopathic parkinson's, entropy, know, and selegiline are also other medication that can be used either as monotherapy instead of levodopa, or they can be used in addition with levodopa, but usually if a dopa is the first one that you would give it more the symptoms are affecting quality of life. Next, question you would only do the levodopa trial yes. If you have a strong enough reason to suspect that it's parkinson's and if they respond to it, then you have enough evidence that what you're doing is working, so you can diagnose as a, you cannot diagnose the parkinson's, so it's just because the clinical diagnosis as way towards your clinical reasoning that this is parkinson's and you would do um you would do those imaging. If you had suspicion that was something else as well, no worries anyone else okay, so we have quite a lot of different answers here, okay, let's go through it, so we've talked a bit about central nervous system problems, let's move up into the peripheral nervous system, no wait see, I think it seems, but we'll see um so and so peripheral nervous system problems will have lower more than you're in science. On examination, This is a very simplified way to think through it, but I think it can be quite helpful for your face is so so you have someone on your paces who presents with lower motor neuron signs on examination, so think so the first thing that you think is does this follow a specific nerve distribution, so the ones that I would quite that that would know is carpal tunnel, so your media nerve, radial nerve policy which will cause your risk group and um loss of sensation in the back of your hand and common peroneal nerve policies which will cause you classically your foot drop. If no then think does it follow dermatomal might normal distribution and if it if yes, it's usually due to nerve root impeachment from at the side of the exit of the nerve from the spinal cord and then if not, it's usually a peripheral polyneuropathy, which is when multiple peripheral nerve roots are affected and usually the symptoms are symmetrical and worse distally, and if you think about it makes sense because it's worse distally, because the nerves have a longer way to travel to go distally. So if the blood flow, for example, do the diabetes is poor, uh it will be worse at the distal bits of the, of the, of the nerves that make sense and you can differentiate them into those that cause, predominantly not modern, not monitor sorry modern symptoms, and predominantly sensory symptoms. Motor polyneuropathies is mainly jamboree, uh CIDP, which essentially kind of the same thing but more chronic uh polio, which damages the anti a horn, but it's quite rare now and charcot marie tooth, which is again rare, is hereditary because of uh motor and sensory uh poly neuropathy, but many mother and the predominantly sensory polyneuropathies is diabetes, alcohol p 12, amyloidosis, or CKD. So starting with guillain barre, Guillain barre is an acute autoimmune demyelinating polyneuropathy that affects the peripheral nervous system, and so we think that this is happening because of a molecular mimicry, so what essentially happens is that you have an infection and you're let's say you have a gastroenteritis and your body uh makes antibodies and against the campylobacter that cause you cause this gastroenteritis, now the campylobacter for some reason has some antigens, which look a bit like myelin and then what happens in jamboree is that after your after the acute infection for the gastroenteritis. For some reason, your body confused the myelin for some sort of Campylobacter antigen and it attacks your antigen. You're the mailing in the peripheral nerves and then therefore you have peripheral demylination and you have uh the following symptoms, so you so you have your infection classically Campylobacter, but can also be at some sort of like upper respiratory infection gastroenteritis and then two weeks after you have a peripheral neuropathy, which is symmetrical and it's assenting and it you can also it's mainly model you can also but you can also have paraesthesias and pain and you can also get economic nervous system, never symptom system symptoms as well so as incontinence and the important thing is that it's quite dangerous because, as the sense it can affect your respiratory muscles and little respiratory paralysis. So the investigations to investigate this uh we do nerve conduction studies, so nerve conduction studies are very useful for parade from neuropathies in general, and it will have reduced conduction velocity mainly so your peripheral nerves are damaged and it it affects your myelin. If it affects your myelin, remember that the myelin is what makes the nerve signals travel faster, so if you don't have enough myelin, you're amplitude will usually be okay, but your velocity will be lower. Um There are forms of jamboree that can also affect the axons, so you can have also reduced amplitude, but the main one is reduced velocity and then uh you can also do a lumbar puncture, which causes alby alby amina psychological association. This means that you have high protein in your csf because you have an inflammation, but you're normal, but you have normal glucose and normal cell count. Because you don't have any sort of infection. It's really important to do spirometry because you assess for progressive respiratory weakness and if you see that someone has worsening uh parameters, then you then you'll need to be linking with liaising with ICU for ventilatory support and you can also find some antibodies. There is also a miller fisher variant which called mill, official miller fisher, which cause of salma plegia, where you have specific antidotes and the management Because it's an autoimmune condition, you would give immunoglobulin plasma exchange to remove the antibodies, antibodies, and supportive supportive management such as intubation ventilation for someone who has respiratory paralysis. So going back to a question, we have someone who presents with pins and needles so sensory signals and also uh mainly motor symptoms that progress and they are sending two weeks ago they had diarrhea and vomiting. So this all makes us think that it could be something like guillain barre, and we just said that uh the main thing that you find in Guillain barre is race protein with normal cell count's, normal glucose, which called Algemeen a psychological dissociation now d. N. E, which most which a lot of people went for you would actually find reduced um amplitude and velocity, mainly velocity because um myelin damage, but you could also find reduced amplitude. If it's if there is actions, axonal damage, and your a and b are things that you would find in bacterial and viral meningitis. Next, question sorry, I've included the answer here, but we'll go through it, so let's peak about problems at the neuromuscular junction, so the the junction between the peripheral nerve and the muscle. These are mainly caused by myasthenia lambert eaton, and botulism and they have all quite a bit of of common features, which are obviously lower modern urine. You only have modern symptoms because it's the connections from the modern urine to the muscle that's affected. Your tone would be normal um and you need the usually affect proximal muscles more than the um uh than the different muscles, So myasthenia gravis is a tunnel autoimmune disorder affecting the acetylcholine receptor at the post synaptic side of the neuromuscular junction, and it's important to remember that it's associated with famous hyperplasia or thymoma and this has important implications for treatment. The main presentation is a muscle fatigability, which which means that symptoms get worse as time passes and this is because you in my sonograph is you have antibodies which attack the receptors at the post not thick membrane, So the more you have to use it, You have less binding signs available, so and you know and you actually need more binding sites sites, but you don't have them because of the antibodies and that's why symptoms get worse as time passes, so typically they are worse in the evening. I masses are affected the lots because doses and importantly you get normal reflexes because we spoke about fatigability, which means that symptoms get worse by the end of the day and so the reflex are normal. If you just check the reflexes because did not have enough time to get fatigued and so important investigation again, mg which will show this decremental response, so the more you test the worse it gets you can test for antibodies and usually they also do a city chest because to see if they have a thymoma, which is a mass in your thymus, which could be malignant, and also it has been shown that for people, must in the graph is if you remove the thymus gland, it actually improves some for some people, it improves the symptoms, so there is a whole theory that the pathophysiology of myasthenia originates from the times and in terms in terms of drugs, you usually give a period a stigma as I told your in my previous question, uh which is uh acetylcholinesterase inhibitor, Essentially you have your seat alkaline it gets released into your sign ups and then you have this acid cholinesterase, which is an enzyme which breaks down acetylcholine into the sign ups. If we inhibit this enzyme, then we have more um more set alkaline in the sign ups, and because it's an autoimmune um disorder, we can also give steroids, plasmaphoresis, and i b i g uh to reduce the attorney in response and you can also have a thymectomy as we said, which for some people it improves the symptoms. An important differential is lambert eaton myasthenic syndrome, where which presents a bit similarly, but they're also features we can use to differentiate with myasthenia, so here you have antibodies against the casio channels at the neuromuscular junction, which are in the prison optic nerve and essentially you have less um ast alkaline being released. It's usually manifested as a paraneoplastic see uh syndrome, so it's associated with cancer, especially small cell lung cancer like myasthenia lambert Eaton syndrome, again presents with proximal muscle weakness, however, um while we said that in myasthenia, symptoms get worse with repeated use here, weakness improved with repeated use because you can get more of the dalkon, I relief because released because more calcium channels are engaged and instead of having normal reflexes now you have reduced reflexes so going back to the previous question, um So we have someone who's complaining of fatigue and double vision. Double vision is caused by problems in the eye movements and the closest um and she has noticed that her symptoms are worse at the end of the day, So this is classic for myasthenia. She has hypothyroidism and the link is that it's a not a immune disorder and therefore people with autoimmune disorders have more are more likely to get either or the immune problems, and there's also my bilateral tosis, So this is my sonograph is the main thing to do is pre, the stigma, uh interference is completely random, you would just you usually give it an m. S, um increased level thyroxin, those again nothing atropine would cause the opposite things, so it would cause symptoms become worse because atropine would make you have less acid alkaline and stop levothyroxine. Is again a bit of a random one. Uh I have a couple more slides about spinal cord compression and headaches. If you're tired, I've kind of prioritized them in the things that I thought they were most important so we can stop, we can have a break or we can continue straight away. Any preference is I'm completely fine with anything okay. Let's continue anyone else break. I'm aware that they've kept you for a long time, so do we say okay, let's do a three minutes break so that everyone is happy, I'll start at 32 past oh okay, good luck everyone with the estate is um it's 32 past is everyone happy to continue uh. I know that s. J. D. Is a bit stressful, so you let me know are people happy to continue more break, continue okay yes, Please let's continue okay fine um so um just have 30 minutes, 30 seconds or 30 minutes and read through the question and put your answers into the chat, anyone else okay, well done, so next, we'll we'll speak about cord compression and code equina, so first starting with the spinal cord compression. The problem is in the actual spinal cord, so cord compression is an injury to the spinal cord and the symptoms and the extent depend on where the delusion is and at which level in the spinal cord. The problem is it can happen acutely usually after trauma or chronic and the main thing that I've seen it in the hospital is due to tumors. Especially you have tumors that you have tumors that metastasized to the bone because lytic lesions, you have fragments in your bones in your vertebra and this push and compress the uh spinal cord and you get spinal cord stenosis, but can also happen after osteoporosis, called the cost cortical steroids. How it presents you get linguist nous, and because you're nervous haven't divided, it affects both sides, so you get hemiplegia or paraplegia. Your arms may be affected or may not depending on the height and the level of the spinal cord that get affected, so and you get upper motor neuron symptoms below the level below the lesion because you kind of damage all the descending um corticospinal tract so we're still in the spinal cord, upper motor neurons below the level of the lesion and lower motor neuron symptoms at the side of the lesion. Because you also damage the nerves that exits and symptoms are symmetrical. You also have sensory law lost below a specific level. You have back pain and you also have autonomic uh symptoms of this constipation, urinary tension, erectile dysfunction because of damage of those lumbosacral nerve, uh which uh is involved in all of that. So this is where your for example your problem is and what do you do. Uh So you need an urgent mri, response spine to confirm uh the stenosis and then you need to refer to a neurosurgery orthopedics um depends on the hostel which he manages it. Sometimes it might point they might give dexamethasone if there is suspicion of malignancy, because it reduces the surrounding inflammation in the surrounding edema, but the ultimate management will be surgical decompression already a therapy, and it depends really on the fitness for surgery, So you need to know the prognosis of that of a patient before you uh think about surgical intervention, So for example during the weekend, I wasn't called I was doing port cover and there was a patient who had land cancer with bone meds uh with, but for some reason we did they didn't really know the prognosis, so they so they waited for to find out the prognosis. They had impending spinal cord compression, and they wouldn't do anything with a vertebral fracture unless unless they knew the prognosis, so what they were asking me is to come to go and do a new exam every day to make sure that they don't have spinal cord compression symptoms, So you do mri, you referred to the team, you can give the mometasone if there is malignancy and then you can do surgical decompression already therapy as definite treatment depending on the fitness for surgery. The code now let's think about kodak wanna, so what is the code equina, so your spinal cord ends at around the level L1 and L2 and below that you have cardiac wanna, which literally means the tail of the horse, which is which is a branch of uh peripheral nerves that are in the spinal cord uh sorry that are that are where where the spinal cord ends uh and there's a group of of profile nerves together it's nerves so you don't get any upper modern neuron problems, so they are usually the big, so it's in the end of the spinal canal they become compressed and usually it's because of the compression or stenosis of the spinal canal usually caused by disc herniation. Um It presents with lower motor neuron symptoms, perianal anesthesia, bladder retention, leg weakness and because it's the lower motor neurons and it's usually like one side is affected more than the other so thinking through the uh the answer we have someone who has metastatic prostate cancer who presents with weakness in both legs and urinary incontinence now prostate cancer. Um as you might know is one of the cancer, which causes bone lesions and boldly so bone metastases and therefore you can have bone lesions and then four you can have spinal cord compression uh and you have upper motor neuron problems and like weakness. Um Ask it is uh due to a malignant, the spinal cord compression is due to a malignancy. You the most appropriate immediate management is to give to start the dexamethasone and then you would think about spinal decompression or spinal radiotherapy now. I have a couple of slides about headaches um I'll give you 30 seconds, okay, well done, next, one, next one, and last one the boy daniela. This one is a bit of a difficult one, anyone else for this one. It's a bit of a main one yeah I'll wait for one more response and then I'll move okay, so headaches, we can divide them into uh one second okay okay. I'll give you 10 seconds, 10 987654, wait what okay, so headaches uh We can divide them actually maybe be uh so we can divide headaches into primary headaches and secondary headaches, so primary headaches are uh when there is primary headaches are when there is not usually an underlying disorder that's causing the headaches, but it's due to the function and the wiring of the nervous system that you get the headaches, where secondary headaches are have an underlying cause. I'm just going to cover the ones in a pink, do, to treat you to time pressure uh Essentially I've tried to cover the ones that you might find more helpful for your ps, PSA as well, so what is a migraine, migraine is a chronic condition that causes a tax, of headaches. We don't entirely know really why but um there is a theory that it could be due to inflammation of the trigeminal nerve, which change the way that the brain process stimuli and remember that the trade general nerve gives you the sensation in your, in the, in your head, So maybe there is a link between that usually migrant, has commentary years that just chocolate hangovers, organs apparently cheese, caffeine oil contraceptive, lions, alcohol travel, exercise, um bright light, light of sleep. All of that, I guess you know most of it anyway. Uh In terms of the symptoms when you get a history, the headache is usually unilateral. It's parks is small and it comes on gradually. Character is positive, it'll and throbbing timings. They usually last for 4 to 4 72 hours. It's exacerbated by physical activity, stress, noise and light and it's usually really relieved by lying in a dark room and in terms of severity, they're usually moderate to severe associate the symptoms people some people might have an aura, which is like flashing lights or tingling for the phobia, phonophobia, nausea and vomiting, visual changes, tingling, numbness and usually it interferes with current activities and people sometimes do to take time of work. Risk factors is family history in terms of how we manage it. First step is usually conservative measures such as a headache diary or avoiding the triggers, um and so usually gps, ask people to put down a diary, what brings it on and try initially lifestyle management to avoid the triggers. If someone has an acute attack, the first step is either paracetamol, ibuprofen or incense, and the second step, if this doesn't work, you have to escalate and start triptans and then if someone has recurring attacks of migrants, you have to think about ways to prevent people from requiring attacks and usually you give propranolol, which is a bit of lucky or topiramate, which is an anti epileptic or amitriptyline can also help. Sometimes, if it's not, if the other measures are not effective, so going through uh these options um we have someone who comes in with a headache, it's unilateral and it's usually relieved by sitting in the dark. In terms of management, they've already tried ibuprofen and and set, but this wouldn't help, so the question asked about the management of an acute migraine attack, so they've already tried ibuprofen it and sets so as you previously said here we need to escalate and start with the treatment with the triptan, so there is a bit of a lag, I want the previous slide okay, so uh Nsaid and paracetamol we're not effective, so we escalate, so correct answer is uh Treatment sumatriptan is a type of treatment. Um the coffee nick. He's already had an inset, coding You don't really give it for migraines and the other two's are given the attitude a preemie and amitriptyline are for prevention of recurrent migraine attack. Next, one is trigeminal neuralgia, which essentially you get facial pain in the distribution of one or more branches of your trigeminal nerve, and we said that the trigeminal nerve and is it responsible for um the trigeminal nerve is responsible for carrying sensation in the face, so a colon is asking, so you wouldn't give her a panel in unless treatments don't help no, uh it depends on the question so propranolol is given to prevent people with recurring attacks yes, exactly so as I had said, so per panel wouldn't do anything in an acute attack, but this salmon has migraine attack weekly. Let's say this obviously is affecting the quality of life, so you need to do something to prevent them from from from having recurring attacks, but triptan is for the acute attack, so that they get their symptoms get better, does that make sense okay going back and I thought you could prescribe both as a g. P yes, you can't go prescribe. I think I'm not entirely sure about what you please kind of kind of prescribe, I think yes, but the question was more about the acute management, sorry that if I didn't face very clearly um so going back to trigeminal neuralgia, so we said facial pain syndrome in the distribution of the trigeminal nerve and it's usually caused by compression of the trigeminal nerve by loop of an artery or vein and it's associated with a mess. I don't think it's completely understood why so you have triggers, which is essentially things to do with like touching your face, so washing your face, um washing your teeth speaking, eating shaving, and in terms of how someone would present on what you would find on taking a history. In terms of your socrates, yes, the side would be unilateral, it would be along the trigeminal division, which if you remember has an ophthalmic zone, a maxillary zonana mandibular zone as you can see the picture. Uh it's paroxysmal and it lasts only for a second. It's kind of neuropathic pain, it's shopping and shooting and it's worse by brushing teeth, speaking, shaving, talking you can also have associated numbness. It's a clinical diagnosis and in terms of management, carbamazepine, which is an anti epileptic is given first line and this comes up sometimes near piece a so just learn that for trigeminal trigeminal neuralgia. Um you give carbamazepine. I think the way it works is because antipill like we're gonna work some sodium channel just changes the signal and some sort of neuropathic pain. I'm not entirely sure the thing is completely understood why people give it now going on. Two meningitis, so we spoke about, we've spoken before about the meninges which cover the part of your brain and so uh meningitis, inflammation, infection of the meninges, and obviously it can be life threatening, so it is an emergency, so it can be due to bacteria, viruses on our TB uh and the bacteria actually kind of change the distribution of the bacteria you get depending on your age, So young people and babies usually get a cola in group B strep because uh I think it could be colonization of uh like the flora. They don't know the where they they've been growing up neisseria meningitis. This is seen in um young people. Uh Aids influencing strep pneumoniae in children and all the people also get listeria and strep pneumonia and viruses include enteroviruses, hsv, uh varicella zoster, and hiv. In terms of the history, the headache that yet is usually acute and severe and you also get meninges um which is the symptoms you get of neck stiffness and photophobia, youtube irritation of the meninges and you have can have associated fever rush classic classic non biologic uh rush vomiting and seizures, and risk factors is living in close communities and being below five or above 65. This is the classic uh particular nonblanching crush where you also do the classic glass test to see if it's blanching or not. They teach like I think mom's like to do them when the children have rushed just to make sure that they know how to identify an urgent rush and then you can get carrying signs and read this design, which essentially carrying signs. You get you kind of flex, you try to extend the knee with the heat flex, and you get pain in your I think next and which is a sign of me and jason and in brewed in ski sign you flex someone's neck and then the hips and knees flex together. Um csf is very important uh to invest in that, in investigating for meningitis, and it's hard to remember that before anyone put the needles in in the patient's back, we need to make sure that they don't have raised intracranial pressure, so you do a city head before lumbar puncture. If they have any focal neurological deficit or reduce consciousness, because those symptoms can potentially mean that they have some sort of increased intracranial pressure and the csf has a characteristic appearance and analys, depending on whether the meningitis, bacterial viral all to be related, so bacterial meningitis. You have lots of neutral fields because these are the cells that you that you that you used to fight bacterial infections, low glucose because bacteria consumes your glucose and high protein. Uh You also you also have n viruses, low lymphocytes, uh sorry high lymphocytes because essentially these are the cells that you used to fight viruses, glucose normal and protein is normal or high and TB again has high lymphocyte, low glucose, and high protein. So the this is this is something that you just need to learn and it's quite important it comes up a lot and in all of them, you can you have high pressure in your csf and I think it's because of the inflammation. Your um violet that absorb the csf work less well because of inflammation, so you don't absorb csf as well and therefore you have increased pressure in your csf pressure. I'm not sure if you know how to measure pressure, but clinically when you do a lumbar puncture, you have a manometer on top and then the cerebral spinal fluid flows and fills up the manometer and where it stops. This is your opening pressure, so what do you how do you manage it. The main antibiotic that you use is kept reaction iv, and because we said that in immunocompromised or people who are above 60 years old, uh list era is a common cause. Uh You can add amoxicillin uh in the community, Obviously because you don't have access to intravenous antibiotics, you give ben, dependency in which is intramascular those and then you send them to a any and if you have suspicion of encephalitis, for example, if someone has uh most most common people who have HIV video immunocompromised, or they have behavioral change. You would also cover with acyclovir. You can also give dexamethasone and the reason for that is that it has been found in clinical trial to reduce the long term consequence of meningitis particularly here in law's uh and you give it if there is evidence of bacteria infection and uh and we said it's because you it reduced the complications, however, if someone has meningococcal septicemia and and they are in shock, you wouldn't give dexamethasone, so it's quite important as well, so going through the answers. Uh Salmon has fever, head headache, and confusion, impossible to leave the head from the pillow, so this is a sign of meningism, neck stiffness, um abs are not super fine. They have their tachycardic, they are, they're the temperature is high, so they're a bit septic, so this is most likely to be bacterial meningitis, given the sepsis and the and how unwell we are with it, so it's we said bacteria meningitis. You would have high pressure race, protein, excess neutral fields, and low glucose because the bacteria consumes your glucose now were briefly going to speak about. Uh Please why would be many many meaning going to feel like this because of the confusion yes, I get it um you could cover with you could cover with acyclovir as well. Confusion could also be part of sepsis, though and I think the main thing as bacterial is more urgent. If you have any yeah, I got the just it's acute answers are just bacterial. Also they have a greater fever, they look more septic, they are more and well. The bacterial meningitis is the most dangerous thing you could cover with acyclovir as well, but the main thing here is to treat the bacterial meningitis because it's more urgent more and well be our septic. The whole picture is more bacterial meningitis, but some people could cover with acyclovir as well and I've seen people covering with acyclovir For any if they are a bit of the g. C. S. Is a bit of that. We don't no one knows what's happening some people in. I have seen hopes hospital they cover for um identified as well. Um We're not going to speak about uh brain bleeds. I'm going to do it quite quickly because I'm aware of taking a bit long, does fever makes you think of bacteria in this case. Usually when someone has a bacterial infection, the fever will be higher, and there will be more septic, so the whole fever, the tachycardia, the fact that they are well with them. It could be viral as well, but you want to make sure that you don't live and bacteria meningitis saturated. If you have any suspicions of bacterial meningitis, so let's go about, let's speak a bit about bleeds, so you have extradural subdural exam. Barak noid bleeds, so this depends on where in the brain the bleeder cares no problem, so extradural is a collection of blood in the potential space between between the dura and the bone, so this is your bone. This is your europe and this is a potential space because usually you're you're is well attached to the bone um So when you have a trauma, it can you have some you have some arteries between the dura and the bone they can and they can if there is a lot of force, they can bleed and blood can collect and this is an extradural hemorrhage and usually it's the middle in, in jail artery that's affected and you need quite a lot of force. It happens in young people who place contact sports. So in terms of the symptoms, it's usually acute following a lucid interval, so you have someone in the classic either you have someone he falls, he has a big big force accident default they are on the floor, some they get a lucid interval and then they drop that you see us again. It's a it's increasingly severe in severity, so it gets worse and worse and worse because you have more and more and more blood collecting and associated with decreased dcs, symptoms of increased intracranial pressure, and the main risk factor here is head trauma. You do a non contrast city urgent scan of your head. You can also do an mRI, but cities are more widely available. Fresh blood is white because it clots and it's usually has a lemon shape because the as we said, this is a potential space and it's limited by the fault of the dura, um and so you only have a limited space where blood can collect and so this is why it looks a bit more like it has a bit of a lemon shape in contracts with the subdural, which we're going to speak about now, so the sub Bureau is a collection of blood between the bureau and the arachnoid uh uh layers of the meninges in the brain. Now, we said that extradural is usually due to an arterial bleed. Subdural now is due to collect due to rupture of the bridge in veins, so it's a venous bleed and it usually happens in the elderly alcoholics due to brain atrophy, now because it's a venous bleed and because blood in the veins has less pressure, the symptoms are gradual and some people don't notice it until weeks and weeks past. The headache is usually continuing, but you can have fluctuating consciousness, confusion, personality changes, and symptoms of increase intracranial pressure. We've spoken about risk factors, head trauma, falls all date alcohols and uh people who drink a lot of alcohol and anti coagulation because obviously you're more successful to bleeding and the main reason why old age and alcohol use is a risk factor is because your brain atrophy, so there is more space for force and bleed to accumulate, so we're talking about how the epidural hammers. Extradural epidural is the thing is the same thing has a lemon shape because there is not a lot of space because of the sutures. Um of the brain, the subdural has more space, so it's usually described as a banana shape, so again it's an emergency uh a. B. C. D. E. And you do in your refer to neuro surgeons and then they will decide they might do a bare hole craniotomy, bare hole or craniotomy, if they think it's large enough or significant, or they might wait if it's small enough, do nothing and observe for, for the brain to absorb the bleed and subarachnoid is a bleeding into the subarachnoid space, most commonly due to rapture of a secular aneurysms. So remember aneurysm is when there is a bulging in one of the blood vessels and then it bleeds, it dropped just and it bleeds, so it's usually uh side is usually occipital, it's sadden, it often inscribed that Thunder Club, and this is because it corresponds the onset of the headache corresponds with the rupture of the aneurysm, and people describe it like the worst pain that they the worst headache that they ever had or like they've been hit by a ball. It's continues it's very severe and it reaches the maximum intensity within seconds because it's in the suboxone space which is between the ministries. You can also get symptoms of mini genes, so neck stiffness and photophobia, symptoms of raised intracranial pressure and risk factor is polycystic kidney disease because you get brain aneurysm and then more chance of some of an aneurysm rupturing alcohol smoking, and hypertension. So again you do the most important thing is to do an urgent, again non conscious ct scan of the head within 12 hours, however, the problem is that as time passes, the sensitivity of city of the city for a PSA barclay bleed decreases, so your chances of identifying it are less and less so as you can see. If you do it within 12 hours, you're almost 100% likely to pick it up on the city, however, if you do it more than three days after your most likely not not going to find anything, So if you don't find anything, it doesn't mean that you don't have a subarachnoid hemorrhage. It means that you have to do a lumbar puncture to check for xanthochromia, knocks hemoglobin, and these are apparent in the lab apart, in the csf from 12 hours after symptom onset and essentially these are byproducts of billy ruben metabolism, which billy ruben is released from from your red blood cells when he lies and when there is a bleed and this and please give the csf a kind of yellow appearance, so some 1000 greek is kind of blonde um so it has this blonde appeared. This is a summary slide for your revision to differentiate between the different types of hemorrhage. Um Test question so we have someone who comes to A and e, after a very bad headache. We started last evening she collapsed and vomited, signs of minimalism. We are we are worried about a very severe headache. The city head is normal so very severe headache. City head is normal, could space a bark, not hemorrhage, uh What we said we need to do islam, a puncture to look for xanthochromia, laughing, uh cerebral sinus venous thrombosis. It's second to last slide the promise, so I thought that this was a very minor thing and I didn't read that we didn't really need to know about it until it came up in our faces. So the only reason I've included in in my lectures because it came actually up in my face is we had a station with some with a woman who had a headache and the diagnosis was terrible sinus vein thrombosis. Uh I thought it was everything but it's actually something that you investigate in the work up for headaches. So as a hint, we know that the Astrazeneca vaccine causes um because it uh increases blood clots and you can't have introducing three boxes, so they found that multiple cases were reported after the Astrazeneca vaccine. In general, presents as a headache. You can have nausea and vomiting and then you can have specific symptoms depending on which venous sinus affected, so the venous sinuses those those collection of venous blood in your brain, and essentially what happens is that you have a thermos iss in your venous plexus. I that drain the blood from your brain to your entire now jugular vein, city is not always sensitive enough to pick it up, so you have to do an m. R. Venogram and because it's a venous thrombosis, you need to give an oX, a parent and then you'll give warfarin, so you give treatment doesn't appear in the same way that you would do for DVT or a p, which are venous thrombosis. Because remember you give aspirin and, and uh chlamydia and all of that for your arterial bleeds, but for your venous bleeds, you need any coagulation, so you'll give treatment those enoxaparin and warfare. So this last question, I think only harris, got in the end uh So it's a 60 year old woman who comes with a three day history of headache. Initially, she thought it was due to the side effects of the astrazeneca vaccine risk factor for thrombosis. However, uh this morning it goes worse and she had someone associated nausea and vomiting with it. She complains of right pain behind her eye, which can happen with sometimes some types of venous thrombosis and she also said she has has, she has some very vision. Examination of her eyes reveals popular edema and see the head is normal, so cervicitis venous thrombosis. Treatment is an x apparent aspirin you would give for stroke there salamat you would give in glaucoma and multi place you would give in a stroke if it presents between 4.5 hours of symptom onset agent referral from your surgery is for pain gets. Um so I think this was everything thank you very much for listening, sorry, for overrunning slightly. Let me know if you have any questions and good luck with your finals and your face is, I'm sure you all the great you've gone very far, so you're almost there good luck, let me have you have any questions. Thank you. I'll send all the slides um how to get the slides. Um I'll speak with hair if, and I'll send him the slides in, He'll sort it out how, if do you want to reply for that, mhm, I think it's the med det, that will deliver the slides. I'll speak with him. I think if you feel your feedback and you give your email that should be fine how if can you confirm uh huh give me a second, give me a second. I'll reply ah It'll be applauded perfect.