Computer generated transcript

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

tissue death because their blood isn't reaching the brain. It's it's floating around in the extracellular space, and there's two main types of hemorrhagic stroke. One is interest cerebral, so that's blood vessels within the brain or one is subarachnoid, which is underneath the arachnoid layer and around the brain. Essentially, those are two types of bleeds in the brain, causing a stroke. What are the risk factors for a stroke? So as it says, you've got non modifiable things like age ethnicity. Um, you've got gender, and then you've got other more risk factors. So health conditions such as atrial fibrillation, which we said can cause Stasis of blood in the atrium and that clock and then eventually dislodge and then fly off up into one of the carotids and cause a stroke. And then bolic, stroke, hypertension, diabetes, cholesterol, previous strokes or T. I s, um so all those kind of cardiovascular risk factors causing vascular disease drug use. So things potentially like methamphetamines and cocaine, or actually a risk factor for strokes. Polycystic kidney disease. Um, does anyone on a shoutout in the trap if they know why polycystic kidney disease is a risk for hemorrhagic stroke in particular any ideas for anyone in the track? So it cause, um, aneurysms in the brain. So polycystic kidney disease is associated with aneurysms, which are kind of dilations of the blood vessels in the brain, and that can cause, um, uh, subarachnoid hemorrhage. So that's a risk factor. Sickle cell anemia. Because the blood is more likely to clot, it's procoagulant vasculitis, where you get inflammation of blood vessels and therefore narrowing that cause strokes. Um, problem with the blood vessels, which is arterial venous malformations. And then any kind of clotting problem where if you're more likely to clot, you're more likely to get an ischemic stroke. And if you're more likely to bleed, for example, people with things like you know, hemophilia, for example, or, um, one of the hemophilia, hemophilia A or B that you're more like to get a hemorrhagic stroke. Hopefully, that makes sense. So the presentation of a stroke the key thing to remember is sudden onset. It's not kind of gradual developing symptoms, so it's sudden onset. So just like that, within a split second, they'll have their symptoms, such as whether it's loss of vision, whether it's numbness or tingling so a sensory loss, whether it's motor loss or weakness. It could be a higher function like speech, disturbance and the kind of slurred speech or inability to understand or produce speech uh, taxi, which is another word for poor coordination. If there's a bleed, it's more likely to cause headache or loss of consciousness. You're less likely to get those two symptoms if it's an ischemic stroke. But, um, different people obviously present differently. But the key thing with vascular picture, for example, stroke is sudden onset because it's the clock or the bleed happens instantly. And then there's an immediate loss of function. Um, so it wouldn't be, you know, gradual kind of weakness of the armed progressing over hours. It would be sudden onset, you know, one second it wasn't there, and then the next second. It is so sudden, one says, a key feature in the history for a stroke and any of these neurological symptoms, whether it's, uh, weakness, numbness, tingling vision, higher function could could be a sign of stroke, so you have to keep a lookout. This is a long list of differentials. I won't go through all of them, but it's quite useful one I found on I. C. K s about different differentials for for a stroke. So obviously a stroke is life threatening things, so that should be topical list. But you always have to consider other things. Is a person hypoglycemic? And that's that Causing them weakness, you know, is there is a drug use, so they're having a seizure. Have they got, um, sometimes you can get, um, paralysis along with the migraine. So there's all sorts of different differentials to consider. Um, but given your kind of history taking, which will go through in a couple of days time, um, you'll can tease out, given the risk factors in the onset of the of the condition, you can tease out which of these differentials should be higher on your list and which should be lower. But just bear in mind, these are things that can mimic a stroke. All right, So if people want to shout out or put the chat if you think somebody's having a stroke, So like the patient in the question sudden onset, left sided arm and face weakness. Um, what would you first go forward? You go for a CT head or would you go for giving them aspirin? 300 mg already, But people going for CT head. Um, noncontrast. Exactly. And so let's go through that. So correct. Um so, ct head, um, non contrast. So the first thing you don't need to give them intravenous contrast. So there's no restrictions in terms of g f r, that sort of thing. Um, so you have to rule out a bleed because obviously that you're not sure if that patient having a ski make or hemorrhagic stroke, And the only way to tell the difference is on imaging. Um, And if there's a bleed, then obviously you don't want to be giving them something that will thin their blood like aspirin. Um, so you have to rule out a bleed. And if this CT head is either normal or shows an infection, then you can start the aspect as this slide explain explains. So if there's no bleed on the on the CT head, um, and they've got symptoms consistent with a stroke, then from 4.5 hours, is the current cut off for thrombolysis? Um, so that's things like Alter Place, which will hopefully thrombo clot and license meaning breakdown. So break down that clot. So that's the kind of gold standard treatment, but it must be within 4.5 hours of onset, so it's very time critical. So the patient presents, you know, 12 hours later or they're unsure of the onset of their symptoms. Then it can be quite tricky. Um, and thrombolysis might not work. Um, and that kind of risks will outweigh the benefits if it's after 4.5 hours of onset of their symptoms. So say they woke up at nine AM with this left arm weakness, and it's now 10 PM in the evening. That's going to be 13 hours later. Then you don't go for thrombolysis. You go for aspirin, so 300 mg of high dose aspirin, along with a PPI for especially for patient to a high risk of any kind of gastric upset. Because obviously, aspirin's an NSAID can cause gastric irritation and ulceration so something like omeprazole or pantoprazole along with the aspirin. Um, and then you give them usually around two weeks of 300 mg aspirin, and then after that, you start them on, uh, clopidogrel, usually lifelong 75 mg the statin. The only exception to that is if they're in atrial fibrillation, because then after the two weeks of aspirin, they need to be started on anticoagulants. So anticoagulants things like warfarin or Duac such as apixaban, um to treat to anticoagulate. Um, for the A f, um, as opposed to lifelong clopidogrel. And remember the different clopidogrel and aspirin, anti platelets, um, and, uh, warfarin and do wax and heparin's anticoagulants. Um and so they used in atrial fibrillation or venous thromboembolism. Um, and then, obviously, the opposite. If there's a bleed on the CT head, um, so one of the ones you mentioned so subarachnoid or interest cerebral bleed. Then the patient will go to what's called his U Hyperacute stroke unit or neurosurgery, uh, for consideration of, uh, evacuation. If there's a large bleed, they need to control their BP. So you don't want BP to be too high because obviously, if they're running, you know, 200 systolic and they've got a bleed that's going to force more blood out through the open blood vessel and cause more blood loss and more bleeding. So that's worse. Um, you're gonna make the swelling in the brain worse. So you they came usually around 150 systolic or less, Um, in a bleed. Um, your observations are kind of your regular heart rate BP, temperature, etcetera, as well as G. C s and pupils and arm and leg power. Um, you to reverse any anticoagulants. So if they're on warfarin, you might be giving them things like, um Prothrombin complex. Um, and there's different reversal agents for the Duac drugs coming out when obviously you'd hold off the aspirin because that's going to make the blood thinner, which is the opposite of what you want to do. Um, so essentially depends on that CT head and that then it helps you decide which way you want to go down. If it's a bleeder, if it does that make sense. Any questions so far? Yeah, it's a bit more tricky if they're somebody wakes up with the symptoms. Um, you kind of Yeah, you can't be exactly sure, but, um, you kind of you have to take that as the latest possible time of their symptom onset. That's a good question. We'll come onto that a little bit later with head trauma, but Sorry. So CT head in ischemia can be normal early on, but after a few days after the kind of infected area of, um, brain kind of matures, it becomes darker on the CT head. Um, and so you might see a kind of darker lesion over the infected area, but it can also be normal. So normal ct ct head doesn't, um, exclude ischemia. It just excludes bleed, because I bleed. You will definitely see on a scan, but to answer your question, No. Yeah. You might have a normal CT head in the scheme. Eah, Or it could show a bit of a kind of darkening over acutely infarcted part of brain. Um, but the main. Yeah. The main thing. The CT is to look for the bleed. Good. Okay, so moving on. So other investigations management. So I like to split things up into bedside Blood's at imaging. So bedside tests? Um, this is kind of things to look for the kind of risk factors and causes of the bed person's stroke once it's been confirmed. And once you kind of treated the stroke acutely. So looking at the BP, the hypertensive e c g are there in atrial fibrillation or even a 72 hour tape, Um, is sometimes done because that is more likely to pick up if they're in, for example, paroxysmal a f or some other sort of, uh, arrhythmia, Uh, blood test. So you kind of your usual baseline blood for blood count using these LFTs, but also things like h p o N c. Checked for diabetes, their diabetic. That might be there might be an undiagnosed diabetic and need treatment for that and lipids to check their cholesterol. Um, and almost everyone after having a stroke will go on a statin anyway, um, and if they're young, a young patient with an unexplained stroke, they might be You might do a vasculitis screen. So, uh, a n a and hunker those sorts of blood tests, but that's a bit more specialist. And then imaging. Um, so an echocardiogram that can look for kind of any valvular defects or any large thrombus in the heart. Um, that could have caused a cardioembolic stroke. Um, a bubble echoes quite specialized test that they do want stroke units to look for a hole in the heart or kind of patent foramen ovale. And that's if patient's have kind of clot that travels from the right side of the circulation over to the left side. But that's very rare. Um, and that's but that's considered in again younger patient's um, where you're kind of hunting for a cause, whereas in older patient's, it's more likely to be either age of fibrillation or, um, they're gonna be a vascular path. A diabetic, hypertensive, high cholesterol Um, CT angiogram as well is sometimes done to, um, kind of further investigate which blood vessel is affected. Um, MRI can also be done. Um, so, like you said in the CT head can be normal in the scheme ick stroke. And MRI is more sensitive for picking up the kind of subtle areas of infarction. So sometimes if the CT head or CT angiogram is normal and you're still considering ischemia, then they'll do an MRI head, uh, later on. Obviously, MRI, though, um is not going to be the first line because it's much easier. And out of hours is much easier to get a CT head and more widely available and quicker to to do, uh, carotid Dopplers to look for a carotid artery stenosis so kind of plaques building up on the inside of the carotid arteries, which travel up, um, into the brain and into the through the neck and into the brain. Um and so if there's a critical kind of narrowing or atherosclerosis on the side that caused the stroke, then they might consider an endarterectomy. So removal of that plaque to clear out the carotids. And obviously, then you need, um, an M D T approach. So physiotherapy and occupational therapy for the patient's recovery, rehab, speech and language obviously, um, uh, swallow and swallow assessment, because swallowing can be affected a lot by in strokes, um, neurologists and psychiatrists, but as well because of the psychiatric burden of of having a stroke and the potential physical disabilities as well. So a lot of other things to consider, um, looking kind of going forward to help the patient and also to look for the cause of the stroke a few more questions before we move on. Um, if the patient has those same symptoms are sudden onset weakness or numbness, but they self resolve in 24 hours. What would the diagnosis be? Um, and then also thinking about a case that I saw in a and E the other day. Um, 72 year old patient with two episodes of short lived, uh, sudden onset arm and leg weakness that both self resolved in the last day. What would the diagnosis be then? And then finally, information has visual loss in one eye that self resolves within minutes. What would the diagnosis be? I'll give everyone a few seconds to have a think about these questions. Okay? Exactly. So people are saying t i a very good any thoughts for the second or third questions. So I'm sorry. I stop just checking the chat, so stop sharing. Um, hopefully I can see the slides now. Um, so yeah, very good. So t I a transient ischemic attack or what people call a mini stroke in non jargon medical. Have you got, uh, Amoros is who gets for the last one? Oh, yeah. Perfect. Excellent. Well done. Very good. Um, so yeah, So first one is t i A. So the symptoms resolving in Technically, it's less than 24 hours, but classically, it's within less than an hour. So they asked sometimes only a few minutes and then get better. Um, the case. The second case is specifically a crescendo. T I. So that's when you're getting multiple t I s within a short period of time. So that's even a higher, higher risk for a a stroke within the next few hours or days. And then excellent. Whoever said Amoros Few jacks, which is a t i a so transit kind of temporary, almost blood clot in the ophthalmic artery causing transient blindness. And it's classically described as, um, curtain, like so kind of descending down there. I you know, the black curtain and then eventually that that vision comes back. Um, so that that describes Amoros is for you x when it's describing a t I a ham bigotry management for a T I A. Um so they need to be referred to a specialist t i A clinic within 24 hours. If the t I was in the last week, um and then they'll be treated with aspirin 300 mg and the PPI if they have high risk of GI upset unless they're already taking aspirins. A nice actually advise is if they're already taking a low dose aspirin, then you usually won't give them the 300 mg that dose. But for everyone else, 300 mg of aspirin is the treatment for a T I A. To have those symptoms that are consistent with a stroke but have already resolved within less than 24 hours? Um, yeah, basically, the worries that they could go on to then have another embolic event or thrombotic event, which will actually turn out to be a stroke or another t I A. And so it's That's why you need to recognize and treat t. I is really early because of the risk it carries for, uh, that subsequent stroke. Okay. And just finally just cover the kind of, um, cerebral artery territory which covered in the question in the SBA. So kind of for the three cerebral arteries, you got the anterior cerebral artery, which runs through kind of the midline. Um, and then surprise the left and right kind of media X aspects of the cerebrum that you can see in the picture on the right. Um and that corresponds If you look at the homunculus, which is a kind of, uh, Corona cross section of the brain, you can see the medial aspect So if you imagine, you can see where the person's knee and foot is hanging over the side of the brain. That's the medial aspect of the hemisphere. We're just looking at the Left Hemisphere in this case, um, and that it supplies the feet and the legs, et cetera. So anything affecting the anterior cerebral artery you can imagine will cause more likely to cause leg weakness. Or, if it's in the sensory area, leg numbness or tingling, then you're moving kind of more laterally. You get the trunk, the head, the neck, the shoulders, the arms and the face and the hands on the kind of more lateral outer aspect of the brain and that supplied by the Middle Cerebral artery, which is the red shaded area on the brain, which is always kind of the lateral portion of the brain. Um, and it also involves speech areas as well. Um, so, like the patient in the question, um, they had face and arm weakness, and so that corresponds with the area supplied by the Middle Cerebral Artery. Uh, and then finally, posterior cerebral artery supplies a smaller part of the brain, which is at the back. The occipital area. Um, and that may need to do with the vision and the occipital cortex. Um, and so a stroke affecting the posterior cerebral artery will therefore cause visual loss. So it kind of helps to correlate the anatomy, um, of the brain and the homunculus, which is at diagram in the bottom and kind of the arterial supply of each of those areas. Um, and that's quite useful kind of classification. So the Oxford or Bamford stroke classification, Um, which you can look at in your own time. And this is a picture from geeky medics. Kind of is another way of classifying strokes. So anterior circulation. Um, uh, partial anterior circulation lack. You lack, you know, strokes and posterior circulation. Um, so not specifically to do with the, uh, individual arteries, but kind of the general kind of portions of the brain depends on the symptoms. So this is quite useful classification for exams and and for real life as well. Um, and finally, just remember that it might necessarily be something like weakness. Um, numbness or visual loss. You can get other symptoms in a stroke, so you have to be, um, aware of it's kind of a wide array of presentations. So one patient I saw, um, in any 68 year old lady with just with dizziness. So vertigo, the room spinning around and round vomiting. Any taxi? A. Since you woke up on the CT head, it turned out to be acute bilateral cerebellar strokes. Um, and then another patient with again sudden onset vertigo, nausea and, uh, tingling down one side of the face and the arm, um, ended up having a pontine hemorrhage. So a bleed in the brain stem. Um, so with this kind of sudden onset symptoms or patient's who woke woke up with those symptoms, um, and risk factor. So elderly af hypertension, diabetes, etcetera always have to think of a stroke because you've got these other sorts of syndrome. So lacuna strokes, which can cause, um, complete motor loss or sensory loss down one side of the body or a mixed picture. And then you've got brainstem or posterior strokes which affect kind of cerebellum ponds, medulla, etcetera because that's where the cranial nerves that originate. Then you get all sorts of weird and wonderful cranial nerve palsy. These things like Horner's syndrome, cerebella signs which will cover a little bit later. Um, you could get visual loss. Remember, that's the kind of back posterior side of the brink. Um And so, for example, one of those is Wallenberg syndrome. What lateral medullary syndrome, which affects the posterior inferior cerebellar artery. So the Peca and that one's quite favorite exams, and it's relatively common in real life. Um, is that presents with Horner syndrome? Um, if anyone wants to pop in the chat, remember what Horner's syndrome is. What the triad is also get dysphonia is the problem with speech problems with swallowing, dizziness, poor coordination and then loss of pain and temperature sensation on the same side of the face and the opposite side of the body. So that's a very specific kind of part of the medulla is infarcted, and so that affects certain cranial nerves and certain pathways that descend, um, and get receive pain and temperature. So just remember, with the posterior brain stem strokes, you're looking for those sudden onset acute cranial nerve palsies and cerebella signs. Very good. So Tosis drooping of the eyelid mitosis, small people and anhydrouse is so no sweating on that side. So that's Horner syndrome. So Yeah. Just bear these things in minds One for exams because they like to They might rather know kind of bond or one sided weakness or change in speech. They might throw one of these more niche to kind of syndromes at you and also in exams in real life as well. To consider these sorts of stroke is a different kind of patchy cranial nerve palsies. All right, I think that brings us on to the next one. Cool. So second s be a 19 year old female is hit on the side of the head by a cricket ball during the cricket match, initially blacks out and then comes around with a headache. After two hours, he collapses. Given the most likely pathology, what is the most likely source of bleeding near this patient? I'll give you a few seconds to have think. Cool. So I've seen a few of you put in the chat Option three. If you did well done. So it's a tricky question, little bit. Little bit mean. It's testing not only kind of what pathology it is, but also the kind of related vascular anatomy. So in this case, it's the middle meningeal artery, which is option three. So this is is an extradural bleed bleed, and we're going to Why? Why? It is, um So they had kind of quite high impact trauma. Lucid interval where they kind of come around and they wake up and they're okay for a couple of hours and then suddenly deterioration because it's an arterial bleed. So it's rapidly, um, exsanguinating loads of blood. So this section is on head trauma and the associated bleeds. So we've you can basically spit intracranial hemorrhage into four types. So one is extradural, which is just in this reduces just on the question. The next one is subdural. So underneath the dura, then subarachnoid. So you're going through each of the layers of the meninges and then the other one is even deeper. So intracerebral I within the brain Remember, we saw the bottom to earlier in as a type of hemorrhagic stroke, so subarachnoid and interestingly will bleeds. Also counters types of hemorrhagic stroke because they're essentially blood that's bleeding out from blood vessels that are meant to be supplying the brain tissue. Whereas extradural and subdural are not counter strokes, but they're hemorrhages. So these are all it can get a bit confusing the terminology. So just intracranial meaning within the head and then X. The first three tell you under which layer of the energy the blood reading is occurring and then interest to re rule means within the brain itself. So within the brain tissue, All right, so you got four types, so we'll go through each of those, um, in just a moment. So just things to consider Generally we'll come up. We'll go on the nice guidelines for CT head trauma, which is really, really useful things to think about. So, anticoagulants is the patient on warfarin a Duac heparin? Um, and do you need to reverse that agent if they're on it? And they're having a bleed in the head, Um, and a little bit related to what somebody has mentioned earlier. So in terms of a bleed on a CT head, it appears white, so really bright and hyperdense for around acutely until around three days time. Then, as the blood kind of degenerates, it turns ice so dense, so it's quite difficult to see because it's pretty much the same color as brain tissue. And then, after three weeks or so it turns hypodense as the brain as far as the blood breaks down, and so it becomes a bit darker. So you might see a dark patch where there was an old bleed that's more than three weeks old. Midline shift is the main thing that you're looking for as well. So is there so much pressure and swelling within the brain that it's starting to squeeze the structures across the midline? Um, and then the main thing is neurosurgical inputs. They might be doing things like burr holes or craniectomy zor craniotomy. Ease to relieve. Relieve that pressure because remember that the brain is a fixed box of fixed volume, it can't expand. And so if there's something actively bleeding into the brain, then um, you need to, you know. And if it's putting enough pressure towards midline shift, for example, or herniation of parts of the brain, then you'll need to evacuate part of that part of the blood or take some of the skull off. In some cases, which is craniectomy a craniotomy. In order to open that, um, expand that volume for the for the blood to fill, Uh, your observations that we mentioned so checking the patient's pupils. Um, and they're G. C s, um, and controlling the BP. Like we said, you don't want a rapid drop in blood pressure. At the same time, you don't want BP to be too high, in which case they'll start hosing out if their BP is 200 systolic. Um, and they're already bleeding. That's that's a bad thing. At the same time. Obviously, you don't want them to be really hypertensive, because then they won't be confusing the brain at all. So it's a It's a tight balance, Um, and sometimes they also give seizure prophylaxis because these patient's, um, are more prone because of the head trauma and the bleeding are more prone to getting seizures. So sometimes they'll the neurosurgeons would advise to give something like levertiracetam to prevent seizures. All right, so the first one, like in the question extradural bleed. So outside of the juror, this is always almost always associated with trauma. Really high impact traumas like in the questions will be a cricket back to the head or a road traffic accident and kind of sudden high force trauma, usually to the side of the head but can be anywhere usually associated because of the level of force trauma with a skull fracture. So in this case, for example, you can see on the right side of the picture, so the patient's left. There's a If you look at the eye of faith, you might be able to see a temporal bone fracture. Then you can see that kind of lens shaped lighter gray patch on the left on the right side of the screen. And that's the blood in the extradural space. It's not crossing the future lines because the juror is kind of tethered into the skull, and so the blood it will just collect in that lens shaped pocket it won't cross the future lines. Um, you get that kind of lens or, you know people call it different things. Lens shape on a CT head and it's acute. So it's going to be white, Um, and yet classically, it's if you fracture the temporal bone, then the artery under running just underneath that is the middle meningeal artery, and that's the one that classically lacerates and and that's hosing blood into the extradural space. And these patient's usually after the impact they might black out. They might be quite well, so lucid for a little while, an hour or two, and then suddenly they deteriorate because it's an arterial bleed, so that pressure is gonna be rising very, very quickly. Then all of a sudden, they'll they'll collapse or or become quite unwell or start herniating. Next. One is subdural, um, and so this one can be acute or chronic, so it's more likely in patient's who have smaller brains. So patient's, uh, with chronic alcohol use patient's dementia, elderly patient because this is caused by the share ing of the bridging veins. Um, which, uh, can bleed over a long time or acutely, depending on the mechanism of injury. Um, and if if you think about it, if the brain is smaller, there's gonna be a larger gap between the brain tissue and the, uh, skull. And so a longer way for the for these bridging veins to travel, and so they're more likely to be shared. And, for example, if with the head shaking or head trauma, you can imagine the brain moving to one site one direction really quickly. Then there's a sharing of those veins, and then you can get a venous bleed around the brain. This does cross suture lines, and so that's why it gives you more of a crescent shape. You can see on both of these pictures kind of crescent, as opposed to a lens shape on the one of the left is an acute bleed because the blood is is paler. It's more light, kind of white or gray or on on that left left side picture, whereas the one of the right you can see it's a chronic kind of old bleed because the blood has degenerated and has become a dark kind of crescent along the right side of the brain. So that kind of is the difference between an acute bleed and a chronic bleed. And you can kind of tell the ages as per the color, Um, and again, depending on you know whether there's midline shift. So this on the picture on the left side, you can see there's midline shift. If you draw a line straight down the middle of the scan, you can see that that kind of ventricle is the left hand ventricle is squished up, and the brain is kind of being squeezed over to the opposite side of the brain to the opposite side of the skull. So that's midline shift, so that would be an emergency. Okay, everyone happy so far. Any questions? Cool. All right, So subarachnoid hemorrhage. That's the next one. So these can either be. There's two types. One is traumatic. Um, you can get that in in in severe head trauma, and that's common, more common or spontaneous, which is when someone has, um, a predisposition to bleeding. It might be really badly controlled hypertension because you can imagine that force of the hypertension going against the blood vessels can cause, um, cause cause eventual rupture of the blood vessel in the brain. You can get an as a patient with aneurysm, so that's like we said, dilated kind of balloon shaped dilations in blood vessels associated with the polycystic kidney disease. Um, so they've got an association to have Barry aneurysms within the brain, and so they're more likely to have, um, subarachnoid hemorrhages via an aneurysm bleeding and then a VM, which is an abbreviation of arterial venous malformation. So any kind of dysfunctional blood vessel essentially, that's more week that's weaker or poorly structured and was more likely to bleed out. Um, the classic exam, Um, kind of s p a presentation of a subarachnoid hemorrhages, that sudden onset, severe, worst ever headache, usually in the occipital region, but can be anywhere associated with manages, um, because the blood is going to be irritating the meninges and so that it's going to cause that headache photophobia neck stiffness, which is the triad of meninges. Um, which you'll skip policy and meningitis. Um, so yeah, sudden onset, severe headache in, You know, some cases they might describe it as being hit on the back of the head with a cricket bat. That's how severe it is. And that's a classic kind of subarachnoid hemorrhage. Um, pain kind of picture a differential. Um, if you're interested for sudden onset. So the headache is actually pituitary apoplexy, which is infarction. So, um, kind of death of the pituitary tissue and that can present similarly but also has associations of low hormone so hyperpituitarism. But I think more common cause of the sudden onset headache and the one you want to rule out as a subarachnoid, um as well. And then you see blood within. You can see the circle of Willis, that kind of star shaped, star shaped, um, in the center of the scan. You can see that that's that white, um, star is the blood, and so that should that shouldn't be that shouldn't be there or there in the sulk I So within the kind of fishes on the left side of the picture here, you can see there's a kind of, um, almost l shape of white hyperdense blood. And that's blood in the fissure from the subarachnoid hemorrhage. And sometimes these patient's get nimodipine. So that's a calcium channel blocker, which will dilate the blood vessels and prevent vasospasm because the brain has a reaction to the bleed. Will call will, um, constrict the blood vessels to try and close down the bleeding. But obviously that might cause kind of rebound ischemia, so you don't want that to happen. And so that's why patients given nimodipine and then finally, interest cerebral bleeds. Um, so again, trauma hypertension problems with the, uh, blood blood vessels in the brain can all lead to bleeding with. And this is bleeding either within the tissue of the brain's brain. So intra parent time, all as you can see here or also intraventricular so you can see on the that large that space where it should be All black words yes, filled with CSF is filled with blood. So that's an intraventricular hemorrhage. And so this is kind of within the brain. Um, and so that kind of breaks down all the four different kinds of intra, um, cranial bleeds that you can get from trauma. This is just a nice summary. So, like you said Extradural, the thing to remember is does not cross suture lines and looks like that kind of by, um by con. I always get this confused by convex lens shape. There's extradural, as you can see on the right or the subdural is that crescent form. And that does cross, uh, suture lines subarachnoid within the fishes and within the systems and the and the circle of Willis and then intra powering high mall or intracerebral hemorrhage within the tissue of the brain. And here's a nice couple of summaries that I've picked from some handy websites. Take a look at those when you get the slides, but yeah, that's just a nice summary in comparison and that you it's classically in questions between extradural and subdural hemorrhage. They'll try and catch you out. But just remember the key features on imaging and the key features in the history. So the sub jewel's uh, L D Patient's alcoholics with shrunken brains and kind of more chronic picture, whereas Extraoral is going to be high impact trauma and then a initial lucid period and then sudden on a sudden deterioration because it's an arterial bleed. So it's going to progress. More and again, you can have a look at the nice guidelines for CT Head. So these are quite useful. Um, particularly exams they might ask you. Is the patient eligible for a CT head within one hour, eight hours? And so you just run through the kind of risk factors so measuring their G. C s either initial assessment two hours after the injury at the signs of a depressed skull fracture, any signs of a basal skull fracture? If you know any signs of a basal skull fracture, pop those in the chat. That's quite useful things to know for exams in clinical practice. Um, if they've had a seizure, if they've had more than one episode of vomiting or if they've got focal neurological deficit. So you know, hemiparesis or numbness down one side of the body or a facial droop that would indicate there's bleeding. And so they need an urgent CT scan performed. If they don't meet those, then there are kind of some more smaller criteria that would indicate they need a scan. For example, if they're on warfarin they've had. If they're old and they've got a clotting problem or they've had a lot of amnesia 30 minutes of amnesia after the head injury. Um, so, yeah, so basil skull fractures things like, um mastoid bruising. So battle sign bruising behind the ear, Um, kind of what they call raccoon eyes or kind of peri orbital bruising, Um, sometimes hemotympanum, which is blood behind the tympanic membrane when you look inside the ears or CSF leaking from the ears or the nose as well. So those are signs of a basal cell fracture. Um, so if you've got any of those signs of the signs mentioned here, then the patient needs an urgent CT scan. In real life, you tend to, um, I think probably scan more people than the guidelines would just suggest, Um, but Yeah, this is useful for kind of being strict with the guidelines and remembering, especially for exams. Who needs a CT head after trauma? And basically, these signs mean that patient's more higher risk or, more worrying, have an interest rebuild hemorrhage from from their trauma, and so they they need a scan. Okay, I finally just before we move on to the next topic, remember concussion. So even if the patient's got a normal scan, UM, no bleed or hemorrhage from their head trauma, they can still have mild traumatic brain injury, which can have quite debilitating effects usually lasting a few weeks after the injury, especially in sports, is a big push, especially in football nowadays and in rugby. For a while, it's been, um, talking about concussion and taking patient taking players off the pitch for after they suffer a head injury. Um, and really, they should be advised to avoid if they've got concussion, avoid sports for a few at least two or three weeks, and then once their symptom free kind of return gradually to to actions so kind of low, low level exercise and training and then building up as long as they're symptom free. Then they can return to return to sports, Um, and symptoms like confusion, depression and low mood anxiety. Brain fog struggling to concentrate fatigue Um, mild headaches, nausea and dizziness can all be signs and symptoms of of concussion. Obviously, if the patient then suddenly develops, you know, vomiting or seizures or hemiparesis, then they might need to be re evaluated. See if they need another scan if there's a bleed or a Dema in the brain. But these sorts of, um, quite kind of generalized symptoms can can be signs and symptoms of concussion, which is really, really common and something to look out for. So it's useful if you're saying patient's in an ER and G P. And they've had a injury head injury, and either they don't meet the nice criteria for a CT head or they've had a CT, and it's normal and your reassured. There's no kind of acute bleed or hemorrhage, but they've got these symptoms. You need to give them advice about kind of holding off sports and driving and that sort of thing until they're symptom free. Any questions from, um, from the stroke and head injury perspective? All right. Um, so we'll do this next question, then have a quick break and then move on to the second half of the talk. So, um, this third s be a 35 year old female with gradual onset. Can't spell numbness, tingling down the left arm. Four days similar episodes affecting her right leg last year that resolved she otherwise Well, her grandmother had a neurological it'll list, but she's not really sure what the name was. Which, which of the following signs is not consistent with the most likely diagnosis have I think this one's quite a tricky one. It's a bit of a mean question, so don't worry if it's finally get a bit harder. Second. So the correct answer here is option four. So recent campylobacter infection. Because that would indicate, uh, more in keeping with something called Guillain Barre syndrome rather than M s. So M s is the likely diagnosis in this case because you got a young kind of, uh, Milledge female with kind of gradual onset transient symptoms, neurological symptoms, um, in left arm and also having a previous episode of neurological symptoms that got better and the family history. So that's all pointing towards multiple sclerosis. Um, and these options 1323, and five or all six signs that you might see in in in M s. So you dose phenomenon is when symptoms get worse in the heat limit sign is pain kind of an electric shock pain radiating down the back and the neck when when they bend the neck. Um, relative afferent pupillary defect, um, is also seen in M s when, uh, the people doesn't constrict on, like, reflex. And then previous episode of, uh, painful, blurry, painful, blurry vision on one side might be descriptive of optic neuritis, which is very common presentation of so we'll talk in this section about demyelinating conditions. So obviously, myelin is the kind of, uh, insulating sheath that, uh, covers, uh, neurological, uh, neuron cells. Um, obviously demyelination meaning the destruction of that insulating sheath and that affects the conduction of the nerves and means that they're not able to conduct, um at all, or they may be able to conduct much slower than they normally would be. So that's the reason why these cause, uh, problems in the nervous system. So M s is, um, affects the central nervous system to the brain and spinal cord causing demyelination. It's a chronic condition. Um, and there are many different disease patterns, but common one is relapsing remitting. So patient kind of has period where they get worse, period where they get better, kind of waxes and wanes over time. Generally kind of gets gets worse. Um, but it's kind of comes and go comes and goes So they get episodes like this patient had, um, where they had this right leg, um, weak weakness last year ago. And then that got better. And then this is another relapse where they're having this numbness and tingling in the left arm. So that's that's a relapse and remitting part. So risk factors. Um, it's more common in females. Patient with the family history, those in temperate climates. Um, and it's been linked to those with vitamin D deficiency. Um, it's an it's an autoimmune condition. Um, how does it present? So optic neuritis. So inflammation of the optic nerve is a classic presentation, Um, and that causes kind of blurry vision and pain. Pain behind the eye and pain on the eye movements. Um, on one side, um, but kind of any any central nervous system lesion could could be the presenting feature. So it could be a cerebellar lesion and kind of, um, slurring of the speech or poor coordination. It could be motor a lot, so it could be weakness. It could be sensory. So numbness or tingling. So any of those combination of symptoms could be the presentation, um, in M s. So remember, it's an upper motor neuron lesion, so it's because it's affecting the central nervous system. So I things like hyperreflexia an increased tone. There could be sensory loss that could be, um, cerebella signs such as nystagmus that could be optic science such as, um, Afrin. People read effect. So it's a very broad kind of presentation. You know, diagnosis is based on key thing to remember. Is that what's called the McDonald criteria? So lesions differentiated in time and in space. So in time, meaning that, um, temporary, kind of differentiated. So having, for example, that right leg weakness a year ago which got better, and then how, having left arm weakness, that's differentiation in time and space, meaning to different kind of separate areas of the central nervous system. And so that patient would meet the criteria because they're differentiated in time having symptoms separated by, um, several months and space because one lesion was affecting the right leg. The other lesion is affecting the left arm, so they're in different, affecting different parts of the brain. So this differentiates it from just clinically what's called a clinically isolated syndrome, which the patient just gets one kind of one off episode of demyelination. And then it gets better. So the patient, in order to be diagnosed with M s, they need to have time and space. So, um, lesions that are in different parts of the brain or spinal cord and different happening at different times. And so that's how you diagnose M s. Um, And you look for those lesions on an MRI, which will show demyelination, um in the affected area. Um, and lumber puncture. Does anyone know what you're looking for on lumber, puncture and patient with M s? Feel free to pop into the chat. Um, and so once it's diagnosed, um, it's quite a tricky condition to manage. So there's symptomatic management because these patient's will get a lot of problems with pain. Um uh, kind of neuropathic pain. Spasticity. So kind of contraction and spasticity of the muscles from from the upper motor neuron lesions, they might have autonomic and bladder issues. Um, for example, and urinary retention. Um, they can have depression and and kind of mental health security of their their long term conditions. That's quite tricky to manage in that sense, Um, and for actually managing, Um, m s. There are There's research on kind of new treatments, but it's generally kind of immune suppressants and biological treatments. So and all this kind of antibody treatments against, uh, interleukins that will help dampen down the immune system. And if they're having a flare, then usually they'll get steroids to kind of dampen down the immune. Autoimmune reaction. Um, obviously things like physiotherapy input, occupational therapy. Um, uh, neurology specialist input and counseling and kind of patient support groups as well is key to the mountain. Um, oligoclonal bands. Very good. So somebody mentioned So the lumbar puncture in M. S you're looking for oligoclonal bands is the key kind of exam exam buzzword. They're looking for just a quick word about other conditions that are demyelinating. So I don't think that is kind of central nervous system or peripheral nervous system and acute or chronic. So m s fit in the Central's category and was chronic. Um, the so the kind of opposite is you might have heard of Guillain Barr syndrome. So that's a peripheral nervous systems. So it's causing peripheral neuropathy, and it's more acute and classically post infectious. So a few weeks after patient's had a bout of gastroenteritis or a chest infection or a viral infection such as E b v, mycoplasma, campylobacter, Um, even, um, covid. Technically, could be any infection. Um, they present with kind of an ascending weakness. Um, tingling. So motor and sensory loss. Sometimes they actually get back pain. Um, it's ascending. So it's starting, um, lower down and then ascending up. So starting in the legs and the lower limbs and then ascending up to the upper limbs. Obviously you have to check spyrometry. Does anyone know why it's important to check spyrometry in this kind of condition? Pop in the chat, Um, and you can actually get a rare variant of Guillain Barre, which is called Miller Fisher syndrome. So this is quite a niche exam one and one of my friends actually saw it the other week in a and it's quite interesting. Patient had a viral infection and then a few weeks later was complaining of really bad double vision and trouble with the walking. And it turned out they actually had Miller Fisher. So it was kind of ineffective flare of the demyelination demyelinating syndrome. Um, and they get a triad of a taxi, a support, coordination, no reflexes and ophthalmoplegia. So priorities of the eye muscles? Yes, exactly. So somebody mentioned the weakness and the respiratory muscles. So, like I said, it's an ascending neuropathy, so it might start with affecting the toes and the legs and then up to the thighs and the and the higher muscles. But then, once it reaches, for example, the diaphragm with the intercostal muscles, then it's affecting the respiratory function. And that can be really serious because they can get type two respiratory failure if if the neuropathy ascends that far. And so that's why I need to check the spyrometry for the patient and their things, like the vital capacity and F E V one. Um, check their in respiratory failure, um, and kind of get a baby or get a baseline in case they represent with a respiratory failure. Um, and then you they might get things like intravenous immunoglobulin to kind of treat the acute flare of their Guillain Barre. So the key thing with these neurological problems is you know, for example, the leg weakness or the tingling is not going to kill the patient more when it will become life threatening is when it started taking the respiratory muscles, because then they're going to type two respiratory failure, and they're struggling to ventilate because the diaphragm is paralyzed because of the neuropathy. Um, other conditions you can get peripheral and chronic. So this is, uh, that's called chronic inflammatory demyelinating polyneuropathy. So it's almost essentially like a chronic kind of form of Guillain Barr Reyes syndrome. So you're getting a peripheral neuropathy. So lower motor neuron. And it's chronic relapsing remitting, um, inflammatory disorder. Um, And then if it's affecting the central nervous system and it's a cute, it's something like acute myelitis. So that's kind of inflammation of the spinal cord. So that's central nervous system, Um, and that can sometimes be post infectious, or, I think, even autoimmune. Um, but the bottom two ones are pretty rare. Probably, probably not necessarily will come up in your exams where they're included for completeness. But the ones that will definitely be tested on is M s, which is relatively common. And Guillain Barr A, um, look out for that patient who's post infectious after a viral or gastroenteritis kind of picture and then starts having tingling or numbness or weakness in the legs. Um, that's the kind of plastic picture figure I'm direct. Cool. So that brings us around halfway through. I think, uh, feel free to have a few minutes for a break. Pop any questions from the chat, and then we'll come back two or three minutes to, uh, say 45 minutes to resume. Uh, the rest of the dog. Yeah, that's the name Draws Miller. Fisher. Um, yeah. So that's Miller Fisher. It's a It's a variant of Guillain Barre syndrome, so it's a type of kind of post infectious demyelination that causes of thumb or pedia. So paralysis by muscles, a ataxia so poor coordination and areflexia So lack of reflexes. Yeah, put your leg on the stride. Cool. Let's say she would come back around half past seven, uh, to resume There's about five more questions, but the last few topics are a bit shorter than the first few ones we've covered. Thank. Okay, let's make a start. Okay, cool. It's a question. Number four. You see a patient in G p who's brought in by their his partner, who's concerned that his husband has dementia. 74 year old male normally fit in well, and he's had four months of memory loss, confusion and hallucinations. Seeing small animals and his walking has also got worse, and it becomes slower. What's the most likely cause of these symptoms? Yeah. Mhm. We've got Lewy body dementia. Excellent. That's my mic on. Perfect. Um well done. Yep. So Lewy body dementia, Option three. And we'll go through the different types of dementia and these options And why, Uh, what kind of features in the history point towards one more than the other. So So commonest type of dementia is Alzheimer's disease. Um, and that kind of incorporates amnesia. So loss of memory aphasia. So troubles with speech later on a proxy a so practical difficulties agnosia. So loss of kind of recognition of common things and people. But the kind of main feature is cognitive dysfunction and that memory loss, which is progressive. And it's a condition that increases in incidents with age, and and it's progressive and and and, um, kind of irreversible. Essentially, um, we see they're supportive treatment. So, um, kind of involving the family and getting carers for the patient as well as. And then if there's medication treatment, so things anti cholinesterase inhibitors. So things like donepezil, galantamine and the river stigma for mild to moderate. And then if those don't work or country indicated, um, well, the patient goes on to develop severe Alzheimer's. Then drugs like memantine, um, can also be used. Mhm. So that's that's the commonest type of dementia. The what I think is now. The second commonest one is vascular dementia. So that's, um, as in the name kind of indicated by risk factors. So diabetes, hypertension and ischemic heart disease, cholesterol, high cholesterol. So all the kind of cardiovascular disease risk factors that think that put you at higher risk of strokes and T. I A s and heart disease and vascular disease also increase your risk of vascular dementia. So it's thought to be due to kind of micro infarcts and kind of progressive step wise, Um, infarcts of the kind of parts of the brain needing to decrease in cognition. And it's rather than a gradual. It's kind of a stepwise deterioration because, remember, vascular, um, conditions are gonna be sudden onset, so it's gonna have kind of a sudden kind of drop in their cognition, and then it'll be stable for a while. And then if they have another small, in fact, it's going to cause another sudden drop. And so it continues like that, any more of a step wise rather than a grad kind of continue a straight line. Um, and you just the main thing is to treat the risk factors. Um, so and that's another common, uh, cause of dementia in in the UK So three, which is the correct answer. The question is Lewy body dementia. Um, so that's a little bit more rare. And that's kind of the classic Triad is fluctuating cognition. So, um, pardon me, um, so cognition that kind of can get better and worse and changes with time, Um, and changing their memory and ability to understand things. Hallucinations and the classic hallucinations are of kind of non threatening small animals or Children is what they'll classically describe seeing um, and then parkinsonism, which is a movement disorder, and we'll come onto that bit later. And so this patient in the question here had, um, four months of memory loss. So that's kind of hinting at the, um, amnesia and confusion hallucinations with small animals and slowed walking. So with kind of bradykinesia slow movements, which is a feature of parkinsonism. So that's why that patient had Lewy body dementia, which you guys picked up, which is really good. Excellent. Um, and then number four, um, so the one of the less common types of dementia is frontotemporal lobe, and so remember the front front of temporal lobe deals with kind of personality and executive function. And so the patient's get more of a predominant personality change and behavioral changes and disinhibition um, compared to a kind of the classic memory loss of Alzheimer's. And but that's a slightly slightly rarer, rarer disease. Uh, you might hear it called Picks disease, which is a kind of subtype of frontal temporal lobe dysfunction that's picks disease. Um, so the key things with assessing a patient with dementia or suspected dementia collateral history. So, um, their partner or their family members and their friends who are really helpful to kind of describe the change in their behavior and the change in memory and personality change of the patient because they'll give you that kind of before and after picture, um, things like capacity. And considering advanced care planning decisions, so does the patient. Is the patient, um, able to make certain decision about their care? And do they want to put things in place for the future, for if their capacity gets worse? Sorry if they lose capacity rather and the condition gets worse. And it's the main thing is about supportive management rather than throwing drugs and psychoactive drugs. That these patient's and kind of, um, family support and care is is the main thing. Um, and kind of. There's different sorts of schemes and support groups and exercises that can help the patient, uh, to do with kind of reminiscence and helping the patient remember the past and kind of bring back those old memories and try to try to strengthen their their their their cognitive function. Remember, with patient who, assessing a confused patient, you also it's not necessarily going to be one of those four dimensions. There are other causes of confusion and cognitive decline. So medication, so it would be their recreational or prescribe drugs. Things like benzodiazepines and opiates and drugs of anti cholinergic burden can can cause kind of confusion in elderly, especially alcohol and and alcohol. Withdrawal itself can cause confusion. So, uh, sensory sensory loss. So things like hearing loss, visual loss, um, can make somebody appear to be confused when really they just can't hear or can't can't see what's going on. Depression can cause kind of pseudo dementia Picture, uh, can also coexist with dementia. Um, delirium is more of an acute kind of fluctuating, um, confusion picture in, uh, classically in elderly people and they've got altered consciousness and attention. Um, it can be hypoactive so kind of very almost drowsy and flat, very hyperactive and agitated. And there are multiple causes that were coming to in a moment for delirium. Um, that's something your commonly get your comment you see, especially if you work in a geriatric ward when you're doing foundation training. But on any kind of medical ward delirium is very, very common problem, and it can coexist with dementia, and it kind of goes hand in hand in that patient who have dementia more likely to get delirium. And sometimes delirium can kind of lead leave with the patient with a kind of permanent, long lasting confusion as well. But so that if it's a cute think of delirium, um, and then deficiencies. So things like Veronica's um syndrome, which is ophthalmoplegia ataxia and amnesia and as that be one deficiency and that can progress the course of course syndrome. And they get kind of confabulation. So that's, um, kind of almost essentially kind of hallucinations and making things up. So that's an irreversible syndrome of B one deficiency. Uh, that's classic and patient to alcoholics who, because they get fined me deficiency and also patient's, are malnourished and then other deficiencies. So B 12 and B three etcetera, Um, and then other things. The electrolyte abnormalities infections things to talk about. Early electronic subdurals can cause a personality change, um, Parkinson's disease, dementia, which is a specific type of dementia associated with Parkinson's disease, where they get the motor symptoms first, and then they get the dementia rather than the dementia, and then the motor function, which points more to Lewy body. Uh, so repetitive trauma, um, normal pressure hydrocephalus, which is a kind of niche condition that causes, um, expansion of the of the CSF containing ventricles. And they get incontinence, dementia and ataxia and then hypothyroidism and then general kind of age related cognitive decline is also a thing. But if it's kind of out of proportion, um, or kind of meets pathological guidelines, uh, kind of pathological criterion in the A M. T s or kind of cognitive assessment. Then obviously, you need to start looking for for one of the above diagnoses. And if you're seeing a patient, for example, on the ward or you're assessing a patient who is acutely confused, um, things to look for so kind of your confusion screen, um, so are they hypoxic? Are they hypertensive? Or, uh, I think an infection, you know, are there on any drugs that are compounding the confusion? Are they in pain, which can cause delirium and confusion? Uh, urinary retention or constipation? Um, are they having some sort of cardiac event or arrhythmia? Are they hypoglycemic? You know, look at all these kind of different blood test. So uh, Speed 12, Fire eight hyper or hypocalcaemia ammonia from encephalopathy. They've got an infection so high CRP, uh, causing them to be delirious. So there's a wide range of causes. And then if you're worried that they might have had an intracranial bleed or a stroke than CT head and then more detailed scans if none of these tests come back positive, then looking for things like HIV, syphilis, MRI of the head look for other sorts of encephalitis and, um, cause of confusion. Like I said, monitoring with an a m. T s so mini mental state exam. Um, And the 4 80 score, which you can have a look at online, is really useful way of assessing patients' cognition and on the ward. Um, and you mainly, it's about treating the reversible causes kind of supporting the patient, making sure they're oriented to time and place. Um, getting kind of familiar faces to visit, um, and using drugs as a kind of last line 104 confusion. So next one we bought, uh, you're in GPU. See, 68 year old male with six months of worsening mobility, tremor, postural hypertension, and you're on your attention otherwise fit and, well, what's the most likely diagnosis? Yeah, So this is a tricky custom. Don't worry. You didn't get it. Um, so this one is multi system, actually. So that's option one, because that involves a tried of parkinsonism, which is the kind of movement disorder, the worsening mobility tremor, autonomic problems. That's where the postural hypertension, uh, urinary retention comes into things, and they can also get cerebellum dysfunction. Um, so Parkins disease is very good shout, but it wouldn't necessarily explain the problems with the urinary retention or the severe postural hypertension. Uh, Wilson's disease is, uh, kind of inherited disease of copper metabolism where the patient gets excess copper. Um, and they usually get very early young, early onset liver disease and liver failure. Um, and they also have neurological neuropsychiatric diseases and parkinsonism. So a tremor, dementia, um, sometimes schizophrenia and psychosis as well. Um, and that's but that's usually present in much younger patient. So classically, it's young males in the age of kind of teenager or young twenties or so, and the drug induced parking is, um so this patient is on any medications that would isn't on any medications that would cause parkinsonism. So those kind of medications that antidopaminergic inactions things like metoclopramide antipsychotics like olanzapine and risperidone, etcetera. So what is Parkinsonism? Parkinsonism describes the syndrome that so a collection of these symptoms and signs so bradykinesia so slow movement is what that means, along with one of rigidity so kind of increased tone. A resting tremor. So tremor when patient's not doing anything supposed to an intentional tremor, which is cerebellar disease and then postural instability. So, um, they might kind of mean more prone to falls and have an unstable gait. So bradykinesia rigidity, a resting tremor and postural instability does the core features parkinsonism. That's the syndrome. That's what Parkinsonism describes the causes of parkinsonism, so this can get a bit confusing. So Parkinson's disease? That's when people say, uh, this patient's got Parkinson's or Parkinson's disease. That's idiopathic parkinsonism. So they get idiopathic degeneration of the dopaminergic cells in the brain. Um, that control movement, Um, and so they get motor problems like we mentioned on the on the previous slide as well as non non motor problems. So problems with their sleep depression as well. Um, in primary care, this one that you wouldn't necessarily start treatment for this. So you refer early on to a Parkinson's specialist who would diagnose either Parkinson disease or one of the following options of kind of the causes of parkinsonism, um, and rule out other causes and then treat with kind of the main line treatment is the levodopa, which is essentially dopamine. So replacing that dopamine. Um, but you've got other drug treatments, like dopamine agonists and monoamine oxidase inhibitors. Etcetera. Um, so Parkinson's disease from about is an idiopathic, um, cause of parkinsonism other causes of parkinsonism. So either so other causes of bradykinesia originally tremor and instability Uh, the Parkinson's plus syndromes. So progressive supernuclear palsy, um is kind of you get parkinsonism as well as, um, visual kind of, uh, eye movement defects. MSA. So multi system atrophy was a question, though, is what we encountered in the question. And so that involves parkinsonism as well as cerebella, an autonomic disease, and then quarter go basil degeneration. Um is another Parkinson's Parkinson's plus syndrome. So it's Parkinson's, plus just meaning that they get parking citizens. They get that triad as well as something else. Um um, as well as that kind of parkinsonism Lewy body dementia. We talked about where they kind of got more of a cognitive elopement and hallucinations. Wilson's disease we mentioned, is inherited copper problem. They get liver liver disease in in younger patient's drugs. We've mentioned you can also get vascular parkinsonism and trauma as well. Um, so I think back to Mohammad Ali had, uh, I think what was called, uh, type of traumatic kind of repetitive, traumatic inducing parking parkinsonism? It was thought, um, and the key thing to remember with patients who have Parkinson's disease or run Parkinson's medication so levodopa, etcetera. They're really critical medications. They need to be given very specific times so that sometimes for four or five times a day, um, does anyone know any options for prescribing a Parkinson's medication if the patient's know my mouth? For example, Parkinson's patient with Parkinson's commonly have swallowing problems so they might not be able to swallow the tablets if they're really unwell. So what is the other option you can use instead of a tablet Police patient's mhm so they can use patches So the rotigotine patch is another option for delivering. They're kind of anti Parkinson's medications via a patch. If the patient either can't swallow or isn't it by mouth for an operation. So that's important to know when you start, start seeing Parkinson's patients in the ward. Next question. So you're in a and e c. A 17 year old female or two days of fever, neck stiffness, confusion, seizures, headache and photophobia. So aversion to light otherwise fit and, well, what's the most? What's the best initial management given the most likely diagnosis, we've got two and four so far. Okay, good. Give you a few more seconds. All right, So correct answers for So this is another tricky question. So the syndrome, in this case, you're thinking about meningitis encephalitis, and we'll come in to what that means in a moment. And so the treatment for this patient would be ceftriaxone. So an anti broad spectrum antri of antibiotic acyclovir, which is an antiviral, um, steroids and anti clivia would not quite cover the bacterial element of meningitis. Ceftriaxone wouldn't cover the the encephalitis picture. Chloramphenicol, uh, could be used if it's if you're worried about meningitis. But if the patient's penicillin allergic and in this case they don't have any allergies, so you could go for kept track. So instead, for the meningitis cover and then amoxicillin wouldn't necessarily be adequate for common causes of meningitis. So talking about nervous central nervous system infections, meningitis, This is an exam classic, um, and much feared diagnosis, uh, in A and E in general practice. So how does it present presents with the fever? Because it's an infection. Headache? Um, really severe kind of pressure sensation. Headache all over, um, photophobia. So aversion to light. Um, vomiting as well they can get next. Stiffness is the classic, um, classic sign and symptom. Um, if they get more of kind of cerebral symptoms, so to do with brain function. So things like personality change, confusion, drowsiness, seizures that points more toward an encephalitis picture of than a meningitis picture, which is more the headache, headache and photophobia. But you can also get a kind of crossover of meningea and get colitis almost in the spectrum. Um, signs. Like I said, fever photophobia nuclear virginity is just next stiffness. Um, and these classic signs of uh, Brzezinski in Kernig Brzezinski, where you flex the neck and they get, um, pain down the back and kind of hip flexion and Kernig's sign where you, uh, lie them on their back, lift, uh, flex their hip and then flex the, um knee and then gets kind of neck pain. Sorry, I think you sorry. You flex the knee and then extend it and then you'll get pain in the neck and flexion of the neck because of the kind of inflammation of the energies. They're actually quite, um, poorly sensitive for meningitis, But they're quite useful to know for exams because they still like to test you on these kind of eponymous signs in exams sometimes, Um, and it's common kind of young patient's and especially patient's in big groups. So, for example, university students moving into halls, patients who are unvaccinated against the common causes of meningitis patients who are immunocompromised, um, and patients who have already got kind of untreated infections in the head and neck area. So it might be a sinusitis or, uh, really bad ear infection. And sometimes they can spread intracranially and then cause a meningitis or encephalitis picture or an abscess. Um, common causes. So viral viral causes the meningitis, um, quite common. And then when you get down to bacteria, it's things like Neisseria meningitidis Streptococcus Pneumonia? Uh, haemophilus influenza. Um, obviously, there's vaccinations, pneumococcal vaccine and the, um, meningitis vaccine as well. That kind of seeing the incidence of the first to reduce quite a lot, um, specific cases they might ask you about. So encephalitis is classically caused by herpes simplex virus, which affects the medial temporal lobe, Um, in neonatal. So newborns, when if you do a pediatrics rotation, they worry about things like E. Coli Group B strep and hysteria causing meningitis. Uh, during pregnancy. Listeria is one of the causes, um, is one of the feared causes of meningitis. And that's, for example, why patient's are advised to avoid kind of raw meat and dairy because of the risk of hysteria. Um, and the treatment for listeria remember, is amoxicillin uh, specifically for exterior meningitis and then patient to immunocompromised. You got to think about other causes, so as well as the steri, a TB, fungal and viral causes of meningitis and encephalitis. I'm just having to think if you've got a patient who is suspected meningitis and they've got a nonblanching purpuric kind of rash like any one of these, what would you be worried about as a kind of unifying diagnosis so that you worry about meningococcal septicemia. So meningitis mean the bacteria is just, in fact inflaming the meninges, whereas septicemia meaning the bacteria have got into the bloodstream and spreading and dividing in the bloodstream. And that's why you're gonna kind of a systemic sort of response. And that's that kind of bleeding under the blood bleeding under the skin. So that's why you're getting these kind of patiki eye and pop era, which are these little kind of purple, red, non launching spots on the skin. And so that's really worrying, meaning the infection's spread into the bloodstream. Um, finally, investigations for meningitis, obviously Bloods, including cultures and the CRP. So looking for infection. Usually they'll get a CT head to rule, um, to make sure there's no kind of, um, space occupying lesion or raised intracranial pressure before they get a lumber puncture. And then you'll send all these tests off on the on the CSF when you do the lumbar puncture. And that table is quite useful for distinguishing new team bacterial, viral and fungal causes of meningitis and um so, uh, lymphocytes point towards a virus, whereas, uh, neutrophils point more towards bacteria, etcetera. So this kind of differentiating features for each one, um, those that comes up quite often in exams as well. Um, so treatment is classically with antibiotics. So classically careful aspirin. Sometimes they give steroids as well to reduce the inflammation, Um, and then acyclovir. If you're worried about encephalitis and different complications of meningitis quite variable so they can become septic obviously, and get going to septic shock and disseminated intravascular coagulation. So D I c. They can get swelling of the brain that can abscess forms, formation long term problems of epilepsy. So seizures, deafness and paralysis. Uh and then remember also contacting a close contact at home who have had prolonged exposure to the patient. And they'll get they might get an antibiotics such a ciprofloxacin or rifampin, then, um, and those kind of things like public health notification as well, because it's a notifiable disease. Cool. Look onto the last time. Hopefully, you finished the five around eight. So yeah, this one you're in any, uh, this is a patient I saw on my one of my first weeks in any of night. 18 year old male with progressive tingling weakness and numbness in the toes in the last month. No other symptoms? No back pain or visual loss? Uh, no illnesses or past medical history? No. Um, Nonsmoker Nondrinker, they use much sock side over the last year. Uh, no family history of disease. And they've got reduced power sensation reflexes in the lower limbs. What's the most likely unifying openness is we're getting lots of threes, so B 12 deficiency. Very good. Excellent. Excellent. So that's correct. Answer. Well done. That's That was a really tricky question, actually. So So, um, so well done to those if you got it. So it's quite niche, but, um, nitrous oxide use. Um, prolonged use can actually lead to inactivation and deficiency of vitamin B 12, and that can cause internal peripheral neuropathy and degeneration of the spinal cord, which is what this patient of Scott has got, as well as the macrocytic anemia, which you can get a B 12 deficiency. Remember, it causes a megaloblast ick macrocytic anemia. So raised MCV, um, multiple sclerosis would more likely to cause upper motor neuron lesions, um, and would also be probably more patchy and asymmetrical. Motor neurone disease, um, doesn't involve any sensory loss So this patient has numbness and tingling, which the sensory symptoms so that pretty much excludes motor neurone disease, that the diagnosis and also motor neurone disease is classically in older patient's present slightly differently. Um, vasculitis is a potential, but they're more likely to have other features such as rash, uh, kind of vascular features such as claudications in the limbs and then uh, C d m degenerative myelopathy. That's kind of whether cervical bones squeezing on the cervical spinal cord, um, they would have more upper kind of limb symptoms. Um, and neck pain so quick run through of neuropathies. So the cause of neuropathy is I found this quite a useful acronym. So a B C D e A for alcohol, B for B 12 deficiency. It just talked about, see, for both CKD and cancer so you can get paraneoplastic neuropathies d Communist one diabetes, especially in the increasing prevalence of diabetes, the diabetes can cause lots of neuropathies and drugs. Um, you'll come across, uh, and then it is a bit of a, uh of how every vasculitis there are other rarer causes of neuropathy is that you can see at the bottom. So Guillain barre syndrome that we talked about earlier. Uh, and and CIDP, uh, Lyme disease, Sarcoidosis, which is an immune auto inflammatory condition. Uh, hereditary neuropathies and then weird and wonderful things like lead poisoning and acute porphyria. But don't worry too much about those ones. Just remember the ABC be ones. Um so remember, neuropathies can be the sense sensory causing numbness and tingling motor causing weakness, autonomic affecting the autonomic nervous system or mixed, uh, sensory neuropathy room about glove and stocking. So they affect the longest nerves first. So they start in the toes and progress upwards. So that's classic kind of like, for example, diabetic sensory neuropathy affecting the toes first, causing numbness and tingling in the toes. Uh, mono neuropathy is where one nerve is affected. For example, compression, carpal, carpal tunnel syndrome and then one on your artist multiplexes where multiple different kind of nerves in different parts of the body are affected. For example, if they had a facial nerve palsy as well as a common perennial palsy in the leg, So just remember the different kind of patterns. Um, New York, these moving on to the very last question Spn, about eight. Well, done for making it this far. Almost there. All right, so you're called to see a patient on the ward who's seizing. What? Which of the following is the most important initial step in management, assuming their airway is Is patent starting the timer Oscar stating the chest doing a CT head, getting blood sugar or checking phenytoin levels? Any thoughts in the chat? Good people are saying, starting the time, which is very, very good. I thought I might catch you out. This is a tricky question. Always stumble on, but it's starting the timer, so it seems contributed. But you need to know how long the seizure is going on for for it to to treat it, because that treatment depends on whether it's been going on for, for example, a lot more, more or less than five minutes. And it's useful to know how long the patient, just using for all of the other options, are really useful things that you would essentially would eventually get around to doing. Um, but starting the time is really important. So quick word about seizures. So, first of all, kind of the emergency, So status epilepticus when a patient is seizing from, um prolonged period of time or have a seizure and then come out of it and then don't fully recover and go back into another seizure. Um, obviously, as always, a B, C D E management. Um, And in real life, hopefully there's multiple people on the ward on the scene helping out doing these kinds of things at different times. Or one person setting the time or one person calling for help work person managing the airway, but in a kind of exam order. Fashion. Remember airway first, So you might be putting an oropharyngeal and nasopharyngeal airway in if they're. If you're worried about the airway, because remember that GCS is going to be low. They're not protecting the airway. Starting the timer calling for help. High flow oxygen. Um, because obviously, um, they might have some form of respiratory depression or an airway compromise. The oxygen will will do no harm at that point. Protecting them from injury, putting them in the recovery position, doing the full eight. We assessment, um, checking their glucose. Remember, ABC is airway bring circulation and D E f. G s. Don't ever get glucose because hypoglycemia very easy. Um to correct reversible cause of seizures and reduced GCS. So if it goes on for more than five minutes, when you start to treat the seizure so you give a benzodiazepine such as lorazepam, second dose and if they're still seizing after that, then you prepare things like melatonin or levetiracetam, which is more commonly used nowadays and call anesthetics because you're worried about the final step, which is information. If the patient's still seizing despite all of the above management, then they might need, um, information. So a tube down the trachea, um, and mechanical ventilation in order to terminate the seizure and control their breathing. Because there's there's also a risk that have respiratory issues from that prolonged seizure and, obviously, potential brain hypoxia. Quick word about seizures themselves. So see what is a seizure? It's sudden, uncontrolled electrical activity in the brain, for example, of a motor seizure, uh, manifest as a convulsion, so kind of uncontrolled jerking of the body. So there's multiple causes epilepsy, head injuries, um, not a space occupying lesion. So a mass in the brain strokes can cause seizures, infections, uh, metabolic things. So we talked about hypoglycemia, electrolyte problems, um, drugs alcohol withdrawal and associated seizures and a good way to to history. To tease out whether something is has has two seizures. Got a patient who's had a loss of consciousness so lateral tongue biting, so biting the side of the tongue. And a long postictal phase, which is when they're confused and drowsy for half an hour to an hour after the seizure. Whereas if it's another cause, for example, a vasovagal syncope where they've had a faint or collapse, they're more likely to have a rapid recovery and less likely to bite the side of the tongue, Um, epilepsy itself. You've got a lot very confused about epilepsy and seizures and what different differences. So epilepsy is just the predisposition to have seizures. So patients who have recurrent kind of idiopathic seizures essentially and that can be inherited due to a syndrome or required. And then again, it gets really tricky when you're kind of naming seizures and naming forms of epilepsy. So think about the hemisphere. It's affecting activity. It produces where in the brain and is the patient aware or not aware so you can get generalized seizures which affect both sides of the brain and cause a reduced consciousness. Or you can get focal seizures, which the opposite, which is affecting a focal one part of the brain to one hemisphere. And they can either be aware. So they're awake and alert, aware of what's happening or impaired awareness where they're not aware, Um, and then these focal seizures can also become generalized. It can spread from one to both hemispheres, and that's when it calls secondary. Generalized, then going down that route so generalized seizures can either be can be multiple, different types. If it's motor, it could be tonic um, which is that kind of, um, increased tone stiffness tonic clonic, which is that stiffness followed by alternating jerking clonic movements atonic, which is just a lack of tone myoclonic jerks absence seizures where the patient kind of is almost just not aware of what's going on. Um, and then focal seizures can are named based on the part of the brain effects. So if it's frontal lobe, it's going to be affecting the motor cortex, so on so forth. Temporal lobe seizures, for example, um, would affect the kind of senses and give patient's of taste or smell sometimes can be part of that or of that seizure? Treating seizures, Um, first of all, looking for an underlying cause or a trigger, whether it's an infection or, um, uh, space occupying lesion or a stroke starting them on anti epileptics. Um, there's a whole host of drugs with all sorts of side effects. Um, for example of interest, um, and the machine, which are more commonly used these days carbamazepine, which is more used in focal seizures. Um and then older drugs like valproate and phenytoin, which are teratogenic, can have a long list of side effects. And so we need a lot of tests before and after they've been started. Um, and then other things like lifestyle advice, for example, not locking the door to the bathroom when they go for a bath or driving advice because, um, to avoid driving, Um, if they've got poor seizure control, because obviously that's going to be a risk to themselves and others. Cool. So that's everything that we covered today. Um, few topics that we didn't manage to cover, Unfortunately, so spinal cord diseases, um, motor neurone disease, but we touched on a little bit, which is a progressive kind of motor. Uh, dysfunction presented with kind of fasciculation zones and weakness and muscle wasting. Um, and remember, it doesn't affect sensation so it won't cause pain. Uh, tingling or numbness. And there's different types of motor neuron disease that you can learn about, um, neuro muscular problems. So things like myasthenia gravis, where you get kind of blockage of the acetylcholine receptors and you get prolonged kind of activity causes fatigue and classic effects that I'm my muscles and that's an autoimmune disease. And again, like we said, you need to check the respiratory function. Okay, um, word on Huntington's disease, which is another movement disorder, causing choreiform kind of wild, uncontrollable movements. And it's it's a genetic disorder cerebella disease. Last question in the chat if anyone wants to. If anyone can let me know the signs of cerebella disease and the acronym is Danish, feel free to pop the answer in the chat, Um, and the classic causes of cerebella disease, things like stroke, alcohol use and multiple sclerosis as a preponderance for the cerebella. And then tomorrow Thursday will cover headaches. We'll go through with the differentials for headaches, primary and secondary, and how to take a headache. History um, and also cover how to do a full neurological examination on Thursday evening. Just do. And so just just in the chat perfect.