Computer generated transcript

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

So the recording has started. So we'll just continue with the presentation. Um So welcome everyone to um a nearest spotlight which is a high yield revision series on neurological disorders and clinically relevant neuranatomy. So as you've seen in the previous emails and posts that we've put out, it's essentially aimed at final year medical students as well as fourth years um in the op and special censors block as well as first or third years with a keen interest in Europe. The slide basically just says what I've just said. Um and so um it's just to reassure you that we all these sessions will be run by doctors. So today, we're very fortunate to have a consultant who's an expert in the field um discussing the topic with us and other sessions will subsequently also be delivered by doctors to assure you that we our best to make sure you're getting the high old information from people that have, you know, gone through the same process as us and know what's relevant to know and what's applicable to clinical practice to enable us to prepare for foundation training. Um And so in terms of the team, I'm I'm very grateful um for the support of the team members. Um So, including Sad Franz and Sola. Um And so, and as you guys might know from my uh many emails, so I'm Ololade and I'm very grateful that you guys have um just joined us for today. Thank you. And so today we'll be joined by Dr Mistry. Um He's a strict consultant at UHL and he will be introducing himself and letting us know a bit more about him. But yeah, we're very grateful as we say to have um Dr Mistry speaking to us about strick today. So I think with that, I'll hand over to him and then we have some announcements at the end just before we send out the feedback links. So if you could just stay till the end to make sure you get your certificates and access to the recordings after that would be great. Thank you. So I just stopped sharing and let doctor MRE. So you OK. Yeah, perfect. Yeah, excellent. Uh I won't be able to see the images of people or any text while I'm talking. So um thank you all for inviting me. Uh II. It's a high level challenge to give you a high yield revision information, but I'll do my best to live up to that challenge. Uh My name is ah I'm a consultant uh at the University Hospitals of Leicester in Stroke Medicine. I'm the current Head of Stroke Medicine and I also have some other roles uh including an seniorship with uh University of Leicester. Um I'd like to put a little plug just before I start. We, we won an international award for doing some virtual simulation training for stroke. Uh and the links are there. Should you wish to have ever have a look at it? Um Certainly for Leicester people, it's uh uh East Midlands uh people, it's visible on UL he.com. So today is brief, we will try to cover, let me just that slightly. Um We'll look at the epidemiology of stroke. Uh just talk quickly about a competency grid. So you have an awareness of where you stand in the overall scheme of things, explore the types of stroke in the assessment and then time allowing we might go to uh a further session on stroke mimics and or management. So let's um just focus on why we want to talk about stroke. Stroke is a serious lifethreatening condition. And you might be disappointed to know that the lifetime risk of stroke in anyone who is over 25 is one in four. It's very high indeed. And a quarter of strokes happen in people of working age. So uh there is also loss of income and wider family impact as a consequence. If you look at UK figures, there's more than a million stroke survivors in the UK and there's a stroke in the country every five minutes. And this amounts roughly to about just close to 100 and 50,000 total strokes per year, mostly due to first strokes. And the cycle cost is quite significant. If you look at the Leicestershire patch, uh they call it the integrate integrate care board now. So the LR IB, we have a population of about 1.2 million people covered by university hospitals of Leicester with about 20,000 stroke survivors in the community. And we see uh and treat about 1000 strokes every year in the ul. So uh I suppose it's good to look at the strategic side of things. Where are we with stroke mortality? And hopefully, you can see the graph and the trends here showing that mortality from ischemic heart disease in the green is coming down significantly at the same time, stroke or cerebrovascular disease related mortality is also coming down. So there are successes in the field of vascular disease. And what you can see is a dramatic rise in the red line which reflects dementia and Alzheimer's disease. Perhaps more. So because of correct coding of dementia as a cause of mortality as well as the vascular element of contribution to dementia. So just put this puts this into the right trend and in the bottom right, you can see the 2018 ranking with regards to cause of death, dementia, first, ischemic heart disease, second chronic lung disease and then cerebrovascular diseases. So, cancer now ranks fifth in the cause of death. Um particularly important is the future contribution we expect of cardioembolic or a related stroke. And on the left panel, you can see uh depending on which study you look at the Atria study or the American Mayo Clinic data af is on the rise and certainly from now to about 2050 we'll see at least a doubling if not even a tripling of the number of AF patients. So you might ask, well, if is rising, we expect that because people are getting older, having more comorbidities and we're getting better at detecting air. Even our Apple watches can now detect if, if we really want it to. Well, the impact of AF is primarily due to the stroke that results from it. And if you look at the trend, uh this is a, a projection of UK figures based on data from provided by the FAF study group in the under eighties. The the trend is really quite flat. There is an increase but not so much. But in the over 80 age group, the increase is staggering in the next 10 years. We'll see doubling of af related stroke and tripling in the subsequent 20 years of a related stroke. So a related stroke is going to be an important thing that all of you as future doctors will be seeing. And overall the annual cost is quite high. And this just is a slide from the Stroke association that shows you that most of the cost is not actually health related. There is an about a third of the cost attributed to the NHS itself, but about 60% almost 60% of the cost is from informal care that follows because of disability consequent to stroke. This is one of the key discriminators between stroke and heart attack. Stroke can cause mortality just like heart attack, but most people who survive a heart attack, some of them have heart failure and symptoms, but mostly people can manage without symptoms and without loss of job, et cetera. But in stroke patients and survivors, there is a substantial proportion of disability that results in a lot of informal and ongoing care that is sort of captured there. So now that we have said the same about stroke, this is an informal uh and not not a University of Leicester approved document, but in the stroke service, we use this as a basic guide as to what level of knowledge we expect at appropriate levels. So you can see your future here. Medical student column on the left going on to foundation core and specialty training and it's worth spending just a couple of minutes on this. Uh There's a second half to this on the next slide. So causes of stroke, we'd expect medical students to list causes of stroke, a foundation doctor to start thinking about which might be the relevant cause a core doctor to talk about the to classification of stroke which I'll mention later on. And a specialty training to be able to do much more comprehensive, uh identify the likely cause of stroke. And then of course, think about further steps. Similarly, if for example, if you look at investigations of a stroke, we'd expect medical students to list the common investigations used for stroke patients, the foundation doctor to make some initial investigation choices about blood tests and scans, perhaps call medical doctor to start interpreting some of these scans and especially training to be able to do a comprehensive overview of the scans of the results, perhaps some of the interpretation and initial management. So you can see we are talking about step increase in knowledge and all the slides that I present today, talk about the basic stuff, but there is opportunity to discuss more detail. Should you have any questions on the matter? So one of the further examples that might be worth highlighting here is reducing risk of stroke. So we expect medical students to know the risk factors for stroke risk factor is relevant to the individual patient for the foundation doctor, initial management of risk factors by the co trainee or a medical sort of uh initial training medical doctor and the specialty trainee to give us a definitive comprehensive prescription and a management plan for patients. Similarly, for anticoagulation indications for anticoagulation, consider the complications and the discharge aspects of anticoagulation, start anticoagulation and give a comprehensive plan and discussion to a patient. You can see we propose a sort of a graded increase in knowledge, which if you happen to end up in the field of stroke or cardiology, you'll be looking for anticoagulation and building your knowledge step by step. So, coming down to the core of today's topic, let's start with the stroke types. You're probably all familiar with the fact that it's either a block or a bleed. Now, you might use different terms for that. Clearly, the commoner variety of stroke, about five and six strokes, roughly around the 80% mark are due to ischemic or clot variety of strokes where a clot goes and finds a vessel that matches its size and blocks it. And if this happens in the brain, of course, you get an ischemic stroke and persistent ischemia can result in a cerebral infarct or infarction. Conversely, about one in six strokes is because of a bleed and this is due to a leak from a blood vessel. So a problem with a blood vessel causing blood to leak into the brain matter, irrespective of either cause. The presentation is largely similar in that an area of brain is damaged and you get a corresponding clinical problem. Just to be clear about definitions, a transient ischemic attack is a sudden onset of a focal disturbance of brain function with the presumed vascular origin. So they don't have a medical other problem like for example, hypoglycemia. And if this resolved completely within 24 hours and the imaging is normal, we call it a tia conversely, if it lasts more than 24 hours or the imaging shows evidence of brain or tissue damage, we call it a stroke. Now, this is a slide worth thinking about in more detail. If you look at the two types of stroke, the infarct side and the hemorrhage side, the underlying pathology can be quite diverse. Whereas myocardial infarction or heart attacks are quite uh monotonous in terms of their cause. They are largely due to atherosclerosis causing plaque rupture, thrombosis and sometimes embolism in the coronary arteries. Conversely, cerebral infarcts come in a lot of different varieties and this is uh covered in the toast classification. So the groups in terms of how common they are are large vessel disease, which is due to atherosclerosis, cardio embolism, small vescent these and then there are two other categories. One is other known etiologies. So for example, someone known to have a prothrombotic condition who then goes on to have a clot causing an ischemic stroke. And finally, it is cryptogenic. You do a, a comprehensive list of investigative workup and find no cause as such underlying the stroke. So that's the sort of the five step or a five category classification of cerebral infarcts. And it's important to know that the top three cover about 75 to 80%. Uh So you should be well versed the management of that as you go through your training on the other side, intracranial hemorrhage. Uh as we mentioned, one in six strokes are less common, but primarily this is due to a vascular abnormality. Uh commonest being microvascular damage from hypertension, which covers pretty much 80 to 90% of all intracranial hemorrhage. There is increasing recognition of CAA which is cerebral amyloid angiopathy as a cause for intracranial hemorrhage. Also. Now the other uh conditions that cover most of this are anticoagulant related bleeding where there is a bleeding tendency, which is iatrogenic, of course, anticoagulation as we've already talked about is given for patients with atrial fibrillation. Other conditions leading to bleeding include macrovascular issues like aneurysms, arteriovenous malformations or other sort of developmental abnormalities of the blood vessels where the blood vessel wall is thin and fragile. You might have an underlying parenchymal abnormality in the brain like a tumor, someone undertaking an operation or indeed a prior stroke, which makes the brain tissue very fragile and f and friable and live like liable to have hemorrhagic transformation. And of course, if you give someone a bleeding tendency, whether it's due to drugs due to indirect effects like bone marrow suppression and thrombocytopenia or sort of uh um uh uh drug abuse like cocaine and amphetamines. Uh you can get vascular problems or vascular spasm causing ischemic and sometimes bleeding kind of stroke and alcohol excess is specifically a risk factor for intracranial hemorrhage rather than ischemic stroke. And of course, there's a traumatic variety of intracranial hemorrhage, you hit anything hard enough, there's going to be some bleeding. If we cover the toast classification, just in a few slides, large vessel disease is essentially atherosclerosis of the blood vessels. Um If you get carotid atherosclerosis, you get stroke, aortic atherosclerosis, stroke or systemic embolism. And that's simply the direction of the vasculature. And hopefully, you're all familiar with the pathological process underlying atherosclerosis. There is uh excess LDL in the blood, uh lipid accumulation in the blood vessel wall leading to an inflammatory response and consequent steps leading to atherosclerotic plaques which may rupture or simply cause a significant degree of stenosis. And you can get thrombosis and embolism causing artery to artery embolic stroke. That's a large vessel disease, cardio embolism uh is essentially 50 to 75% if not more of the time due to atrial fibrillation. And essentially, we expect uh all of your medical students to be checking pulse and any irregular pulse on a pulse check should lead to an ECG to diagnose or confirm af uh one of the interesting questions is, do you need an E CG? Well, the problem is there are several other causes of irregular pulse which perhaps we could discuss some other time. And so an ECG is a must to confirm atrial fibrillation before you start treatment. There are of course, other cardioembolic sources and the common ones are listed here. Post M I valvular disease, infective endocarditis and of course, patent foraminal valet though you could debate whether it should fall under cardio embolism or a more systemic cause. Um I think recognition of atrial fibrillation on an ECG is a basic sort of medical student skill and I hope all of you will easily recognize that this ECG shows fast atrial fibrillation. There is a variable or, or interval, no clear discernible P waves and it's quite fast. So if you count all of them, there's about, I'm doing a quick count about 24 times six. So we are running a heart rate of about 100 and 44 already per minute. So this is fast air and those of you who are even more skilled at ECG might even notice some changes that might suggest an inferior M I. So we won't go there, but this is fast atrial fibrillation. Uh Finally, small vessel disease. This is a gradually progressive condition where you see uh steady progression from mild, moderate to severe disease in the context of risk factors, chiefly diabetes and hypertension. Often in early stages, it's subclinical and all you see are subtle white matter spots or T two hyperintensities on an MRI scan. And as the spots start to stick together, you start seeing larger areas. So moderate disease and it progresses onto a geographic or widespread sort of T two hyperintensity, that's the severe burden of vascular disease. And as you get to moderate and severe stages, you start potentially developing some symptoms like cognitive impairment uh leading on to vascular dementia gait instability, incontinence issues. Just to be clear. This is at two weighted MRI and you see the lesions as white on this. If you look at the standard CT scan, it looks dark as shown on the bottom left. And this is a severe case of small vessel disease with geographic widespread hypoattenuation. Of course, uh small vessel disease is punctuated by events like lacunar stroke. So you can see a small sort of established lacunar infarct there on the le on the um left side of the brain and a slightly larger infarction there. On the right side, a subcortical infarct there. And of course, uh small vessel disease is also associated with uh increased incidence of other conditions because of shared risk factors. So you can get atherosclerotic large vessel disease as well as a as af which can then result in a large stroke. And you can see there's a large sort of approximately wedge shaped uh MCA territory infarct on the right side of the brain. So you would have a slowly progressive condition that goes in steps and you might find dispersed lacunar events or even large vessel events um that complicate the progression of that disease. So the last two categories, other known etiologies, um you hopefully have heard of these etiologies have not seen patients with this, but arterial dissection is a reasonably uh well documented cause of uh embolic stroke. There is a tear in the internal endothelium of the blood vessel wall causing a clotting cascade which results in thrombosis and then embolism. And often there is a typical precipitating history, but that is not uniformly. The case antiphospholipid syndrome happens in young women of the primary variety or secondary to other autoimmune diseases. And then there are the vasculitis conditions or the vasculit disease like large vessel arthritis uh that can cause uh thrombosis and embolism. Finally, less commonly, you see hematological conditions that cause an imbalance between pro and antithrombotic proteins leading to a thrombophilic or a clotting tendency, which can then go on to cause a stroke. And there are also hemodynamic strokes. Uh These are typically uh associated with a sudden drop and a dramatic drop in BP, which might happen, for example, perioperatively with large amount of blood loss and you can get watershed territory. In fact, essentially, watershed refers to the, the territories between the AC A and the MCA or the MCA and the PCA. Uh apologies for the abbreviations. It's anterior middle and posterior cerebral arteries. Hopefully you're familiar with this anyway. And finally, uh this is a sort of snapshot of the to stratification. You can see this online. If you like in our cryptogenic stroke guideline from Leicester, you can just Google it. So if we get people with cerebral infarction or ischemic strokes, we consider the common large vessel disease, small vessel disease and cardio embolic aspects. Often they already have a diagnosis of a condition like vasculitis and that might be the cause of the stroke. And we have a, a locally derived label, this is not a uniformly accepted condition of pcs, presumed cryptogenic stroke. And we have a standard battery of investigations that may allow us to classify them back into any of the other causes. And if not, then we call it a confirmed cryptogenic stroke. What about the tests required? Well, if you go back to that previous slide, atheromatous disease is picked up quite easily on a carotid Doppler. So we do that for most of our admitted patients and ti clinic patients, small vessel disease is seen on the brain scan as I've shown you earlier and cardio embolism is largely an ecg diagnosis of atrial fibrillation. So that leaves us with more advanced cardiac tests to do. And we have to give due consideration to when an echocardiogram, cardiac monitoring or P fo detection and screening tests are appropriate. And often we do a CT angiogram to look for aortic arch atherosclerosis, which ultrasound Doppler cannot detect cause it's deep in the body. Not everybody gets all these tests, but it's quite common to do a transthoracic echo and a 24 hour cardiac monitor in a large number of uh stroke patients. Finally, this is just a selection. But if you want to see the full detailed work up that we do for our stroke patients in Leicester, you can look at the guidelines. We would certainly encourage a full coagulation profile, blood cultures, often severe blood cultures. And hopefully, that will make you think about endocarditis as an underlying cause autoimmune conditions and vasculitis. We do a standard screen, a standard battery of tests. And for thrombophilia, we do a lupus screen and an anticardial antibody homocysteine level assessments are falling out of favor because there is really no evidence for effective treatments in that uh situation. And so there's a question of whether we really need to treat uh sorry, we whether we really need to diagnose elevated homocysteine levels or not and so on and so forth. And II should stress to mention the last two conditions, alpha galactosidase levels of Fabris disease. This is quite, quite rare. Uh I don't think I've seen a patient yet, I've provided shared care and that one of my colleagues has diagnosed a couple of patients. The importance here is that Fabris disease can result in progressive disease, but it's entirely preventable if you can give them the enzyme that they are deficient in virtually normalizing their life. Um And of course, ct chest abdomen, pelvis, looking for a malignancy that sometimes underlies a stroke. Ok. And then if you look at the bleed side of things, we talk about hypertension and cerebral amyloid angiopathy as the two common underlying conditions uh that result in cebral hemorrhage and, and uh recognized feature of both these conditions is microbleeds, which you see on special T two sequences called gradient echo or T two star on MRI. And you'll notice the small circular black sort of drop in signal areas uh that represent microbleeds. These are not seen on a CT scan, they're only seen on MRI scans and they are indicative of early hypertensive or amyloid disease if the microbleeds tend to be central. So in the center bit of the brain, as you can see quite a few here, we tend to consider them to be of hypertensive origin and they can sometimes present with hypertensive bleeds. So a deep bleed in the sort of right putamen um that you can see on the panel on the left of your screen, an amyloid disease can go on to produce sort of convexity, subarachnoid hemorrhage. You can see those cous structures, it's called superficial SCDs. And there are other sort of criteria that can lead to a diagnosis of CAA uh called based on the Boston classification. Uh It's usually only used by specialists, but you would, you would see sort of over 60 year olds with multiple bleeds in the brain classified as probable cerebral amyloid angiopathy. Uh A definite diagnosis requires brain biopsy, which is sometimes done but not a common thing uh amongst the stroke investigation. Then we talked about parental abnormalities that underlie a bleed on the left panel. You can see a series of different types of brain tumors that can sort of present with bleeds as a sudden acute presentation. And on the right side, the series of six panels shows you sort of various types of uh hemorrhagic transformation of infarct. Essentially. That means that the underlying pa pathology is ischemic leading to infarction. And then there's a secondary bleed uh on top of the ischemia in the top panel, you can see very subtle bleeds. In which case, the management is still directed towards the ischemia. In the lower panel, you can see somewhat larger sort of bleeds where you would be cautious about giving anything like aspirin even until the bleed has started to settle, sometimes needing a repeat ct scan to confirm things have settled. Finally, we talked about coagulopathy. This is a scan, a series of scan slices from one patient who had thrombolysis for ischemic stroke and ended up having multifocal hemorrhage. So, hemorrhage in multiple areas is suggestive of a bleeding tendency caused either by drugs or treatment. And sometimes this is also multi territory bleeding or infarction is indicative of malignant uh meta metastatic lesions. And on the right, you see sort of different varieties of bleeds caused by trauma. And you will note that there is a uh sort of extradural bleed here, a subdural bleed here, an intraparenchymal contusional hemorrhage here as sort of different manifestations of traumatic hemorrhage. And you will know the traditional teaching about co co injury. Sometimes you may see a bleed on one side but an external sort of bleed or a skull fracture on the other side. Uh I'm not, I've not got a typical scan to show you that. So hopefully you've started to get an understanding of the stroke types of the underlying sort of battle, logical or a battle physiological classification of both types. And you've seen a few of the scans to get an understanding of stroke. We'll talk in the next phase about assessment of stroke and some of it you will be familiar with and hopefully some of it will be new to you. So you would hopefully have heard about the fast test, face arm speech time to call 999 test where you see a facial droop on one side. And if you lift both arms, one arm falls down because of weakness, difficulties in speech and any of those or hope more than one of those are highly predictive of stroke. And the positive predictor value of the fast test is about 90%. So nine out of 10 who are positive are likely to have a stroke and it's got a reasonable take on the negative predictive value. Also these days, uh we moved on to do what is called the be fast test. And that's because we recognize that an acute onset of balance problems as well as eyesight problems is also indicative of stroke. So loss of balance, eyesight changes and then the face arm speech test with a time to call 911 or 999, depending on which country you're in. And usually for predictive tests, the way to uh address them in stats is positive and negative predictive value. But this test that developed BA S looked at sensitivity and specificity and it shows a better specificity for the BSA. So you are not missing that many. Once you get to the emergency department, there's a dedicated school called Rosea and it's got a similar positive predictive value as the fastest. But the negative predictive value is quite high. So you don't miss um if you, if the test is negative, there's only one in eight who turn out to have a stroke. And the reason this is better is because there are some negative predictors and presence of syncope or any seizure activity give you minus one point each. So your score will range from minus 2 to 5 and anything uh that is a positive score is assumed to be a diagnosis of a stroke. So we have evolved from using fast to be fast and now rose in the emergency departments. Essentially, these are all simplistic mechanisms to try and identify focal neurological symptoms, which hopefully are indicative of stroke and that allows us to trigger our pathway to early imaging and early intervention. So going back to basics in terms of the assessments, what would I expect from a medical student coming to an exam in terms of the history I'd expect uh some awareness of the importance of symptom onset. So, a date and time if you can get one the suddenness of the onset, whether there's been a fluctuation or a progression of symptoms, I'd be looking for a specific inquiry about neurological symptoms. So, which parts of the body were affected? Was it motor sensory? What other sensors were affected? And particularly important is the distinction with between positive and negative symptoms, referring to extra symptoms added on, for example, involuntary movements or pins and needles or negative symptoms, referring to loss of motor power. So, weakness or loss of sensation, numbness or typically termed hypoesthesia and stroke typically is uh represented by negative symptoms quite often rather than positive symptoms. And positive symptoms might suggest other differential diagnoses and expect an inquiry about other symptoms that might suggest bleeding, for example, raise intrarenal pressure or indeed some sort of cardiac etiology or other etiology like a history of cancer. And it's important to be wary of atypical presentations that may not be picked up by the standard fast, be fast or even Rosier scores. For example, what they traditionally used to call the geriatric giant delirium confusion, collapse, acute incontinence. All are possible in the context of a stroke. And so you often find a CT scan as part of the workup of these presentations. From the specialist perspective, I'm particularly interested in time of onset, the suddenness of the onset, a key summary of symptoms. And that might be right-sided weakness, speech disturbance, and rightsided hemianopic visual disturbance. I'd like to uh be told if it's a clear focal neurological deficit and uh try to establish the urgency so I can triage my decision making with regards to imaging and acute interventions. And when you do your neurological examination, I've purposely skipped the general examination which hopefully you're all OK with. But when you do your neurological deficit, the importance is to recognize patterns of neurological deficit that represent focal brain dysfunction. And by that, I mean, unilateral hemiparesis, sometimes monoparesis. So isolated, limb weakness is due to stroke but important not to neglect. Possible peripheral nerve causes there a unilateral facial palsy. And there is an important distinction to be made between upper and lower motor neuron lesion, which hopefully you're all familiar with and you need that sensory deficit. And when we are looking for higher cortical features, we're looking for a dominant sort of uh dominant brain. And as we already know, most right-handed people have dominant brain on the left and as do most left-handed people, but the prevalence of right dominance is uh sort of commoner in left-handed people. So the dominant brain results in problems like dysphasia, dysgraphia, and dyslexia and non-dominant, cortical lesions produce visuospatial disorders and neglect. So, unawareness of one side or the other. And of course hemin or quadranopia and these are homonymous binocular visual field deficits. So they're exactly the same sort of area in both eyes when you do visual field testing. But important to note it's not a single eye problem. It's a binocular problem. And if you look for it carefully, you should hopefully be able to detect that. And of course, common cranial nerve signs and cerebellar signs. Oh, I thought it would be a good juncture since I've been talking about focal neurological deficits, referring to problems in the part of the brain supplied by the blood vessel To refresh our knowledge about the major cerebral arteries. You might find this somewhat monotonous, but it's important to know roughly some uh areas and some blood vessels. So we'll go uh and step by step. Uh Usually we like to distinguish between anterior and posterior circulation. Anterior circulation being the carotid territory, which is marked with that dot dash line. Most of the blood from the uh ICA goes into the middle cell artery. The MCA, the smaller branches are the AC A and the posterior communicating artery or the PCOM. As some people like to call it, the posterior circulation starts with the two vertebral arteries. They merge at the bottom of the brain stem to form the basilar artery. And this bifurcates roughly at the top of the brainstem to the two posterior cerebral arteries. So this forms the circle of Willis at the top. So you can see there are four main arteries supplying the circle of birth. Roughly these are not scientific figures but roughly 40% of blood supply for each of the carotids and 10% of blood supply for each of the vertebras. It is possible to have no problems whatsoever by blocking one of these vessels or maybe in two of these vessels. But usually you start seeing problems uh if there is significant blockage in these major blood vessels and just to go in individual detail here, the terminal internal carotid artery, uh the branches are the ophthalmic artery, which is why we get uh monocular presentations with carotid disease, which are called transient monocular blindness. Traditionally, morros is fuga but that term is now out of favor. And then the posterior communicating artery and the antoral artery which causes typical lacunar infarcts involving the internal capsule. The MCA is the uh continuation of the ICA and this is where most strokes happen. And this is why hemiparesis and hemisensory problems are well documented features of stroke. The AC A uh is a smaller branch and supplies the medial surface in adjacent convexity. Hopefully, you've seen some diagrams where the vasculature of the brain is split up into different colors, making it easy to understand. And in terms of the motor supply, the ac A typically supplies the distal leg power. So isolated leg weakness at the knee and below could be due to an ac a infarct. The vertebral arteries actually arise from the subclavian arteries. They have a very tortuous course and often there's an asymmetry in both sides and the largest branches of these are the posterior in fetus cerebellar arteries. And you will know these uh the pika arteries because they cause quite dramatic Wng syndrome. As its term, the lateral medullary infarct. The basilar artery over the pons supplies most of the brainstem. And uh unfortunately, it's a single artery where a blockage can cause dramatic brainstem, uh stroke and death. And there are several important arteries. The two of them being the superior anti inferior cerebellar arteries which cause distinct cerebellar syndromes. Uh If you were able to go into the field of neurology or stroke, you would learn more about the detailed cerebellar sort of pathology. Finally, the PCA, uh both PCA S arise from the bifurcation of the bacillar artery. However, a significant proportion actually get their supply from the anterior circulation and the PCA typically supplies the occipital lobe and the visual areas. And the problem with a PCA causes contralateral homonymous hemin. So that was a whistle stop about the blood vessels, hopefully, revision rather than new knowledge. Finally, um when you've done your clinical assessment from the history and the examination, hopefully you should be able to arrive at an O CSP category that helps us decide the severity of the stroke and the potential prognosis. So, if you look at the total anti circulation stroke, this is the most dramatic type of stroke which has all three features as we call it a contralateral motor and or sensory deficit, a contralateral visual deficit and higher cerebral or cortical dysfunction. And the importance of the tax presentations is that there is quite a high 25 to 30% mortality in the first month. So it's important to recognize that people who suffer from attacks have a high mortality in the hospital. And the vast majority of those who survive going to have significant disability and are often discharged to a nursing home or a residential home requiring significant help with their activities of daily living. A is a partial anterior citation stroke. So a branch of the MCA is occluded and results in more restricted infarction and lesser neurological deficit. Unfortunately, this seems to be balanced out by a higher early recurrence rate. So we focus our efforts in finding either underlying atrial fibrillation or uncontrolled risk factors which you can treat to reduce the risk of recurrence. Lacuna. Strokes are of very specific pure motor or sensory variety. And there are some other rarer features and often these can be silent in some cases if they don't have any associated symptomatology and the posterior circulation strokes have typical brainstem cerebellar or occipital patterns. They tend to be difficult to diagnose. Sometimes they can present dramatically sometimes with a collapse and a very low G. And there is a preponderance of thrombosis and air in the, the posterior circulation, the tax and the PAX groups. Finally, if you should uh enter the medical field and or the neurology stroke field, you will become increasingly familiar with a stroke scale that has been widely used for the last 20 years or so uh called the stroke scale, which provides a newer sort of estimate of the severity of neurological deficit across various domains of neurological symptoms and signs. Ii appreciate this is small print. You can Google I stroke scale at any point uh and find the information online. It's essentially a 42 point scale and you can see the severity is judged by an increasing severity with increasing sort of risk score. Uh important cutoff here might be uh more than 20 is quite severe stroke, usually seen in total anti circulation strokes and 0 to 4 is quite mild severity. And you have to think carefully before you give them invasive and aggressive treatments with potential side effects. So once you've reached a sort of reasonable conclusion as to whether you think this is a possible stroke. Uh it's important to consider urgent brain imaging. Now, I've skipped through the basic investigative work up like checking for glucose, BP, doing some basic blood tests for renal function, anemia, any blood count abnormalities, et cetera and jumped straight to brain imaging because if the criteria are met for either thrombolysis or mechanical thrombectomy, apologies for the empty abbreviation. Uh We would want what we call a next on CT scan in our hospital where the stroke team would wheel the patient to the scanner, which is just a short distance away from the resuscitation room or er as they like to call it. And the CT is designed to rule out bleeding any other stroke mimics. And it's important uh to then conclude whether you think this is an ischemic stroke. Uh just a key thing to mention. Most early CT scans do not show any signs of ischemia. So a normal CT scan or an apparently normal CT scan is entirely consistent with the diagnosis of ischemic stroke or in fact, and then there is a selective use of MRI uh later on in certain scenarios, if we feel that it's going to add to the management. So what's all the fuss about? Why do we have such a focus on stroke on call? We have stroke consultants on call all the time. Uh Some logistical sort of preclinical studies suggest you lose almost 2 million neurons a minute. So a lot of brain is lost if you're going to be sitting around twiddling your thumbs. So it's very important to get to a CT scan as soon as we can to facilitate the interventions listed at the bottom. Clearly, the most dominant uh interventions depend on the type of stroke. So if we cover the less common bleed, there is what is called the ABC approach A for anticoagulation reversal. If the patient is on anticoagulation, B for aggressive and intensive BP lowering, often with intravenous labetalol and C for care in the right place, which is almost always a stroke in it. But in select situations, you might end up in it because you cannot maintain your airway or you have recurrent seizures or you go to neurosurgery in select circumstances. Meanwhile, for the ischemic stroke, again, the scan is there to facilitate thrombolysis and mechanical thrombectomy if appropriate. And if you're not able to give those major interventions, you move the patient to a stroke unit, give them aspirin and in very rare circumstances, neurosurgical options are available for complications of ischemic stroke rather than the ischemic stroke itself. And when we start thinking about thrombolysis, uh uh stroke units are very uh keen on seeing strokes, giving them the treatment. Uh We should make sure that before we give uh intravenous thrombolysis, for example, which has got a 5% risk of major life threatening bleed as a complication that we don't thromb obvious non stroke presentations and that's where the scan is useful. So hopefully, I'll give you 20 seconds to just think about what you see on these scans from left to right and we'll talk about it. Scotland. OK. Hopefully you've given some thought to what you might see and hopefully it'll be proved right when I kind of point to the right abnormalities. So first scan, you can see there's an asymmetry seems to be something on the right side of the brain that's squashing the ventricle inwards, there's ventricular replacement with mass effect and you can see external to the brain there is sort of an area of darkening with a small amount of white hyper attenuation. Posteriorly, this is an acute on chronic subdural hematoma with uh sort of a chronic collection of blood which is darkened already, but there's an acute element of blood there, but it's causing mass effect. And this would be something that shouldn't be thrombo clearly but potentially is amenable to neurosurgical intervention. The middle panel shows you a a five pronged star uh at the bottom of the brain with hyperattenuation. Now, if you saw a normal scan, that should be dark because that's where CSF lives. And in this case, there's a significant subarachnoid hemorrhage. These are often aneurysmal subarachnoid hemorrhages which present very dramatically with acute drop in g in young otherwise sick people. You also noticed that there's a little bit of blood in the fourth ventricle of the back. Finally, the scan on the right shows you what is called in the literature. Dawson's fingers, fingers sticking out. Uh and that is typical of sort of edema vasogenic edema secondary to a tumor in these circumstances, we would not want to go towards the stroke pathway. We would not want to deliver thrombolysis or thrombectomy, etcetera. But just to um round off with the discussion around the acute interventions that we offer intravenous or clot Buster as it's called, as stated, is delivered intravenously. Uh you get 10% of the dose as a two-minute bonus and the remaining 90% as an infusion over an hour. The license for this remains at 4.5 hours from documented onset. And of course, the CT head is required to exclude bleed and other mimics we just talked about in the previous slide and it needs to be a clinical diagnosis of acute stroke as evidenced by a sudden onset no other cause. And it's not actually getting better really quickly, which might indicate that it might be at and often junior doctors find themselves doing on call. And the stroke consultant is sort of remotely available on the phone and says, yes, you've got the right patient. You should go ahead and throb and you get into a situation where the conversation can be difficult if you have not dealt with the situation before. So just figures for your awareness, uh I think the green panel is the kind of figures that I use at the bottom out of 20 people treated six people are better off because their neurological deficit is significantly improved. One person is worse off because they've got a significant major hemorrhage and 13 people really don't have a significant benefit or harm from the treatment. So they are unchanged. And if people want to consider percentages, you can always multiply this by five to make it easy to understand. There is a link uh below to a useful information leaflet that can be given for people if they want some written information to stroke thrombolysis. So it's an example, we don't use written information because of the time constraint within this decision making. And also there's uh you can access virtual simulation training which talks uh which has videos about consultant, discussion with patients and their relatives on the phone about decision making around thrombolysis. So I suppose is there something more than thrombolysis and thrombolysis is now becoming old hat? It's got a 5% risk of major hemorrhage. We now have a better option. We have something called mechanical thrombectomy or clot extraction. The advantages of this are you can do it for six hours from symptom onset. So you've got a little bit more time. However, you do have to do an additional test, a CT angiogram to demonstrate that there is a clot in the proximal blood vessel. So what we call LVE or large vessel occlusion because it's really difficult to get to more distal vessel effusions and large vessel proximal occlusions are the ones that are amenable to clot extraction. Interestingly, there is there is evidence that you can continue with the thrombolysis to try and maximize benefit whilst you're waiting for transfer to a unit that provides empty. And for Leicester, that's in Nottingham. And we have got good relationship with our colleagues there. We've got a hotline, we've got some artificial intelligence being piloted in the CT scanner that picks up people with large vessel occlusion. If you do a CT angiogram and alerts Nottingham directly So we have a two way conversation about transferring patients without delay, I must say um during my career with a stroke physician, this is the intervention that has changed lives for every three people we treat. Um one person has a dramatic improvement from what we would call a disabled existence, potentially to uh walking out about four or five days later from hospital. So if you can give this treatment early enough, uh this is very, very effective. This is just an example, if you do a CT angiogram, the panel on the bottom right shows you that the on the right side, the middle c artery is being filled appropriately. That's the yellow arrow. And on the left side of the image, the green arrow shows that there is no filling of the middle cell artery suggesting a proximal large vessel occlusion. And if you don't treat this, uh as in don't do a thrombectomy, you get a major stroke that is shown on the CT on the top left of the panel. And that is a dramatic version of right total anterior circulation stroke, potentially going to cause severe deficit if the patient survives their hospital admission. Unfortunately, this is not available 24 7 in the country. There are some areas London, Manchester where you can get it 24 7. But for example, in Leicester at the moment, it's not available 24 7 and and the whole system is working towards trying to uh provide this 24 7 because of the very fact that it is so effective. Finally, don't forget about uh differential diagnosis where features in the history or examination are atypical. Please consider alternative causes of such a stroke like presentation and I've listed the common ones there. I put hypoglycemia in red because you all you have to do is see one patient with hypoglycemia who treat with a dextrose infusion and you miraculously improve their stroke with no risk whatsoever. So always make sure that acute presentations, there is a check of the capillary blood glucose. I think I might stop there. We've reached eight o'clock. Um I will stop sharing my slides and my email and I'm happy to answer any questions and if people are inclined, I can talk a little bit more about stroke mimics um to finish things off. So I'll hand back to the organizers for a moment. Thank you so much doctor M I really appreciate that. Um I've definitely learned a lot and I hope that everyone on the group as well is learning from this. Um So if you do have any questions, um please feel free to pop it in the chat. Um In terms of um going forward, I will just put some announcements and some um and feedback forms. So anyone that's here, as I said, can fill in the feedback form because that's how you get access to the recording. So I will just share my screen, um just one second, bear with me. So while she's doing that, um Yeah, it's feedback is very, very helpful for anybody who organizes the program like this. And I'm very impressed by the, the, the group that I've shown commitment to organizing such a program. Um And I think of course, as a speaker, I very much appreciate feedback on things that were good things that could be done differently. Uh So that we can tailor our talks and improve it for future presentations. Thank you very much, Doctor MRE. Um So I will just put up the announcements just before I share the feedback. Um And so if, yeah, so um a few announcements before we go um again, so we have one of the things that we would like to let you know about is a *** conference, which I've sent some emails out regarding if you attend the University of Leicester. And so essentially, if you don't know about *** um it's a neurology and neurosurgery interest group and it's essentially tailored to medical students to improve your accessibility to neurology, neurosurgery and even more recently expanding to neuroradiology. And so for this conference, if you just scan the QR code, you go to the meal where you can sign up for your tickets, but it's been hosted online and in person. So if you prefer to watch it from the comfort of your home, you're happy to do that. But if you do come, you will have a great experience because there's a great speaker lineup and the team have put in a lot of effort to make this a success. And there are workshops such as abstract writing. So if you're not familiar with the research and you want to present your work and make sure you maximize your chances of getting your work accepted at conferences um to boost your CV or for personal development, then this would be great. So, as well as abstract writing, there's a lot of conferences that will be announced on the Nancy Instagram page. But then there's also things for people that are interested in neurosurgery. So like intraoperative monitoring and so, you know, there's really something for everyone. So whether you care about neurology, neuroradiology, neurosurgery, um then this would be a great place for you to come to and just have an opportunity to um also present your abstract. So the deadline for abstract submission, if you have done a project in neurology surgery, neuroradiology, um the abstract deadline is the 29th of December. So if you just scan that QR code, it takes you to the middle page where you can get some tickets and also submit your abstract with the hope of presenting on even winning prizes which can, you know, boost your confidence and add to your portfolio. And the second thing that I'd want to shout out also is the ABN undergraduate Prize. So the ABN is the Association of British Neurologists. Um and essentially, they have um an undergraduate prize every single year, which for this year will be closing on the 12th of January 2024. And so you can either present a clinical case um or a basic or clinical research related to urology or some audit or healthcare improvement that is related to neurology. And each category actually has a chance of winning 200 lbs. So either category that you apply for, you're bound to win something you're only allowed to um one submission per person, obviously. But you can choose either of three categories, which I think makes it really nice because if you haven't been involved with an audit, you might have seen a patient on your neurology placement or somewhere else that's neurology related and you can write about them pretty much with um just adding some clinical detail and um following the guidelines that they set on their website and, you know, you have a chance of winning 200 lbs. And also those who are considered to have high quality work would also be invited to present their work at the ABN meeting, which has taken place in Edinburgh in May 2024 which I think would be a great experience of, you know, presented at a national conference as well. So that would also just be a benefit. And what the ABN do is every year they have a student day, which is just a Wednesday afternoon, usually where they just go through different neurology topics. I've attended a few of them and honestly, they've always been amazing. Um And so I would highly recommend checking out the ABN become a member. It's quite cheap to be a student member and you can attend, you know, the national meetings as well as an autumn meeting, which I recently attended. And it was just amazing to just learn about the advances in neurology and even neurosurgery as well. So that was really great. So I'd highly recommend and then finally the feedback form. So please, please, please, our speakers have put in a lot of effort to make this possible. And so we're very grateful for that and they've given up their time to teach us. And so please please please fill in that feedback form. Um You shouldn't have any issues with the QR Code. So hopefully everyone can scan that. But if there are any issues, let me know, I will try and put the link in the chat now as well. So just bear with me while I do that. And if you have any questions, please pop them in the chat. Thank you. Yeah, I'll be happy to answer any relevant questions or any general queries about stroke or neurology. Uh If anybody wants to put in the chat, if they're shy or just ask, I guess. Yeah. Oh yeah. And then the final thing, of course, we want you guys to keep coming back. And so the next session is scheduled for the eighth of January 2023. So we're covering different things from cranial nerves and clinical correlates to neur anatomy, motor and sensory pathways. We have people that some of you at Leicester might be familiar with like Dr Steve Jakes, Dr Lisa Quinn and a lot of other junior doctors who have been part of neuros. So, and are interested in you in a career in neurology, neurosurgery who will also facilitate some of these sessions. So we can guarantee that there's going to be a lot and a lot of them are lesser grads for those that want to Leicester, so or teach in Leicester. So it will be quite tailored to the lesser curriculum. But again, the aim is to, you know, make this relevant to everyone regardless of what med school or health care institution you attend so that you can be prepared in your clinical placements as well as pass an exam. So for further details will be posted on your Instagram. So um just to make sure that you follow the Instagram to be updated with the details and the the link is always the same. So every Monday from the eighth of January, just join on the same link or use the same um joining ID. So thank you so so much for coming. We really appreciate your time and please fill in the feedback. Thank you. Thank you for your patience and attention. Thank you, bye-bye. Thank you. Um Let me just copy the.