Pre-Clinical Lecture Series
Summary
This on-demand teaching session will present a comprehensive overview of ischemic strokes, which account for 85% of all strokes. It will cover topics such as the types of strokes, risk factors, pathology and clinical features. Participants will learn about the anatomy involved, as well as non-specific symptoms that indicate a stroke. Differential diagnoses, such as seizures and psychiatric disorders, will also be discussed. With an extensive list of clinical features presented, medical professionals will gain an understanding of how the effects of an ischemic stroke depend on the region of the brain involved.
Learning objectives
Learning objectives for this teaching session:
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Identify the difference between strokes and syndrome.
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Recognize the modifiable and non-modifiable risk factors associated with ischemic strokes.
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Describe the pathological responses of brain tissue to ischemia.
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Differentiate between the clinical features of an anterior circulation and posterior circulation stroke.
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Recognize common neurological and non-specific symptoms associated with strokes and rule out related differentials.
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Computer generated transcript
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So today's open ultimate lecture today is gonna be about a skim it stroke. So it should be quite helpful for an HB a gyn a home. So if you're studying these modules, hopefully would be quite helpful. But I think it should be an interesting lecture and I'll let you get going. I guys Oh, my name's Greta. I'm one of the four years are clear. Um, on I'm gonna be presenting Ischemia street today. Strokes is quite a broad topic, so I tried to narrow it down a bit. Um, didn't think you're all preconstruction. It's at the moment. So if anything, don't worry too much about the details. It's an introduction to the topic and to the type of knowledge you will need to know in clinical years. Um, it's quite high. And your topic. That's why I thought was an interesting want to talk about. But if any of it doesn't make sense, feel free to email me or just put it into the chat now as I'm going on and I'll try to answer your questions. And if I use any acronyms which don't mean anything to you, Yeah, just let me know and I'll clarify what I mean. So I'm sure you've seen that picture before at the bottom. The face arms speech time. Now we'll go into a little bit more detail about strokes. So so. Strokes. The most common cause of adult disability on be 100 25,000 strokes occur in a year in the U. K, which accounts for 6% of the NHS expend show, which is massive. Um, a stroke is an acute neurological injury caused by a scheme. Your hemorrhage. You can see the wh definition that up on the screen the most interest, the most important take away from this is that stroke the syndrome and not a disease. So the difference being a syndrome is a group of symptoms that might not always have a definitive cause, whereas the disease usually has a defining cause, distinguishing the symptoms and the treatments. So the different types of strokes that you will encounter Ah, transient ischemic attack, which is a temporary focal cerebral ischemia that results in neurological deficits without acute infarction or permanent loss of function. And then we have a scheming stroke which will be covering today versus a hemorrhagic stroke. You can see the table for a comparison. So you get this power point after this teaching session today, you can have a look at the differences between the two. A brief summary but basically an ischemic stroke. Is it the cerebral infarction due to insufficient serial blood flow? Hyperperfusion, which results in a ski mia and your old injury was a hemorrhagic stroke, is also cerebral infection, but it's due to the hemorrhage. It's, uh, down to only ischemic strokes, which account for 85% of all strokes. You can see the risk factors on the screen, which are divided into non modifiable and modify. Also, quiet off them are the same. Uh so for many diseases, such as increasing age of female sex, African Americans later Americans, family history of cerebral vascular disease and cardiovascular disease. Genetic disorders history. On an off course, you have the modifiable, while such a systemic hypertension hyperlipidemia and diabetes as the most common ones. Yeah, now we can break ischemic strokes down even further, based off off what is causing it. As I said, it was a syndrome, no disease. So today I'll break it down into forming categories we just seen on the screen. Um, the one I will discuss in detail histologic strokes, as this accounts for 50% of all strokes. So all this came extra Sorry. So you have the large vessel after sclerosis, which is the rupture or an arthroscopic clock and exposure of some endo feeling or collagen, which causes the formation of a thrombus, most commonly which is commonly occurs at branch for in arteries. Then you have the small vessel occlusions, which which account for 20%. So we'll go into, um, from the pathology off these in detail and then you can get and bullet strokes such as cardiac Campbell I close by atrial fibrilation or rheumatic heart disease. Onda Other amble I call it was by internal corroded artery ambulance. So aortic arch ambulance and a part of this is the paradoxical amble is, um which is we have a venous thromboembolism, especially duty DVT in patients with the right to left cardiac shung, such as a persistent form in a body or atrial septal defect causing strokes. Then you can get a global cerebella ischemia caused by systemic hyperperfusion. So this is where the shock or bilateral large artery arthrosclerosis causes decreased effective oxygen delivery to the whole brain. It's a very common during cardiac surgeries or hyperglycemia, in which repeated episodes increase the risk off cerebellitis Kenya on severe on a chronic hypoc see as well, which just causes global tissue hypoxia in the brain. Other causes, which account for about 20% are such as hypercoagulable states, which can be inherited thrombophilia polycythemia hormonal contraceptive, sickle cell or vasculitis or arterial day it dissection. Then we moved on to pathology. So this is probably the part that you guys will know most about at this time. Hopefully in your, uh hey today on an HB. So in general, the in fortune causes a lytic Factive necrosis, which causes this cystic cavity formation. So there's two main responses to brain tissue ischemia. Selective neuro necrosis on partner crosis. You can see, um, the heaviest allergic Allfirst's. Cher's basically all the time from the start of ischemia. Um, you won't need to know as much detail about this in clinical years. They all smoke questions about it and Prefontaine. But basically selective neuro necrosis is where selective destruction of nurse als happen, sparing glial cells so transient ischemia causes subsequent Reapra fusion, which increases metabolic demand and releases toxic exploitation. Neurotransmitters causing ischemic injury so certain ones are more susceptible to ski McKendry, such as the pyramidal cells of the hippocampus, which damage causes enter great amnesia. Also, Kinji cells of the cerebellum off which damage causes intention tremor this tag massage and a taxi, uh, and pyramidal cells off the neocortex, which causes symptoms depending on the affected brain region. Then you have panic crosis which is the death of ulcer types in a group in region of the brain, including neuron glial cells on vascular cells. This causes this is caused by power an ischemia. So if your first year don't worry about the anatomy, you will learn this all in the next year. But for the 2nd and 3rd agents here, the areas and cells most wonderful typography Here are the neocortex hippocampus for Kinji cells on the water shed areas which are, as you can see, that the regions of the brain that received your blood supply um which is the brown point, um off two main arteries, so clinical features of strokes off very varied. These next few size will cover extensive detail on the anatomy and specific signs you do not need to learn all of this. I just wanted to include it for completion so that you can look back on there. Um, after lecture when you get the power point. Basically, what you see on the left off the slide is the most important clinical features. So the sudden onset off focal neurological deficits to the sudden is key on weakness. Paralysis passed easier. A failure. Dysarthria. Those are what we are looking for in terms of neurological deficit examples with either just examples. Um, the fact that then non specific symptoms make it make a strike more likely than it's differentials. So these include impact consciousness, nausea, vomiting, headaches and seizures. Third point is that the symptoms dependent medication of the strokes we'll go into the small. This in more detail on the symptoms could suggest a specific etiology, such as aortic dissection, which could have been the cause. So I'll go into the different types of clinical features based off whether stroke happens with the anterior circulation posterior circulation, or it'll look in a streak. The difference between these, uh, that the stroke therefore anterior onda posterior circulation, the stroke symptoms, our bases of the vessel was for a coon stroke is basically for what affected region. So, second marriages, I'm sure you will remember the circle of Willis. Pictured that at the bottom, if you don't mind. Um And this is where what's gonna affect what kind of symptoms we see. So, first of all, discussing an anterior circulation stroke, you can see the circle list there of the bottom again. We have the middle cerebral artery on the until a cerebral artery occlusion or the store. That should be oh, occlusion of the I see a can result in a skinny and both, actually, and the Middle cerebral artery is the most common place for there to be an ischemic stroke. So you can see here away the different types off clinical features we will see in an emcee. A whether it's left. All right, emcee. A stroke. Lots of different types. If you're not a stroke specialist, you will not need to know the difference. Then we move on to anterior. So about all three again a little bit different compared to the middle. Take your time to read these. If you are revising hey today or an HB once you get the lectures on a posterior, a cerebral artery. This again You can see a picture there at the bottom walk vessels this involved, um you can further divide these basal for Paris. See a sip. It'll lobe the medial temporal lobe with Tomic infarct on. Then you get brainstem, which involves the midbrain Pons medulla on each of those will again have different clinical features. The important thing to know is probably all that they're all involve symptoms which are non specific. So that coming back to that second point again off the impaired consciousness, nausea, vomiting, headaches, seizures they're very non specific and then finally cerebellum off the posterior circulation. So here infarction causes a demon resulting in mass effect herniation and compression of the fourth ventricle, which can lead to rapid to Terry a shin uncle. And she's nurse And surgical decompression is often necessary with these type of strokes. And then you have the lacuna strokes, which are dependent on the area off the brain that is involved so you can get pure motor. Pure sensory sends remoter a Texex and clumsy hand. Uh, dysarthria. You will only need to know these 4/5 and sixth year exams? No, in huge amounts of detail, you never need to be able to tell the difference. Basically all clinical features. Um, an extensive list where the influx has happened. But I think what's your learning and not to me is quite nice to see that if there is a pathology in the area, what features are affected? Because that directly linked. So just to summarize the most common clinical features off these thrombotic strokes a category of ischemic strokes dependent on where they happen you get these non specific symptoms weakness dysphasia Uh um, a nap. It hemiopia on neglect. And you can have this life table to show whether it happens based off the region where the stroke cut. Okay, so moving onto differentials the differential of strokes for are very extensive, probably because of the non specific symptoms on stroke should be ruled out. This specifically impatience, presenting the first time epileptic seizures on subsequent neurological deficits as the seizures may have been caused by an acute cerebella. A follow gee, So you have all sorts of different categories going from neurologic Such a seizures, even Teo ent, which can because my affections, psychiatry disorders see the fullest there, one that is probably very common. Differential. Any D is Bell's palsy. You see that quite a lot. Where straight cool is put out for a Bell's palsy These have you on a second year are doing here today? We'll know, um, how to differentiate between the bells and a stroke by the lifting off the eyebrows. Okay, so if you do think it is a stroke, the clinical assessment and management should occur simultaneously with the goals of stabilizing the patient and keeping the door to neuroimaging. Time to minimum because you want the and identify this candidates for re profusion their past. You know it's possible because those are times sensitive. Importantly, only glucose a noncontrast neuroimaging are required prior to thrombi ambulate stick from thrombolytic therapy. Sorry, so the glucose test rules out certain stroke mimics on the neuroimaging rules out hemorrhagic stroke because the last thing you want to do is to send someone with a hammer addict stroke for thrombolytic therapy. So on the no circumstance you delay treatment to complete the remainder of the diagnostic diagnostic evaluation. A classic clinical presentation without evidence of a stroke clinic or intracranial bleeding on initial neuroimaging is typically enough to diagnose acute ischemic stroke in time limited settings. In terms off the clinical assessment, we want to secure their way. If the airway is protective, reflexes are impaired. Um, due to depressed level of consciousness or Bowlby dysfunction, you want a respiratory support. So you want to provide oxygen therapy to keep the saturations above 94%. That's the usual same planet and clinical settings. 100 to 94% is considered usual normal. Sorry. Um, if this isn't achieved, you want to consider them for mechanical ventilation, then you wanna hemodynamically support the patient as well. You want to ensure that the BP is kept within a normal range and you you would like to do a rapid focus neurological assessment. This includes a good history determining the type the time off symptom onset, or this unknown the time the patient was last seen well or a neurological baseline. You want to indentify any risk factors for a scheming stroke and also to rule out differential risk factors that a magic straight you want? The basic minimum neurological examination they expect you to do soon as possible is a GCS school. Um, people very examination to see if they're equal and and reacting on identifying any lateralizing science such as heavy priest spatial droop A to drift on. Do you want to screen for size of cerebral herniation? Some focus neurological examinations can be attempted to localize a lesion, but again, this should not, um, come before trying to get them for neuroimaging to rule out a magic stroke on to delay treatment. Otherwise so now we've gone over The critical management steps is important to understand the diagnostics on the screen. You can see the flow chart for if you suspect a stroke in a particular patient. What you should do is usually these flow charts available for most acute presentations. And they're really helpful in making sure that you don't know anything any important differentials on telling you what to do on how quickly so you. As I said, you prioritize neuroimaging for a scheme of strokes as soon as possible. You'd like to obtain initial noncontrast imaging without delay. CT Head is usually the initial imaging modality, but MRI brain is more sensitive for any stroke detection on CT, but it's less commonly available and takes a little bit longer. So on a noncontrast CT had this may be normal or show evolving ischemic changes over time. If it's under two hours after the event is usually no signs of infection in a large artery occlusion, there may be high predict hyperdense occluded vessels if it's within six hours after the event. In some cases, there are girly signs or cytotoxic a Dema, which means as hyperdense part. Try more of infarcted regions. Loss of cortical material Definitely a shin expensive, especially in the basal ganglia. An insider on a face man off the soul card 12 to 24 hours after the event. That's hypodense parent. Try um A on 3 to 5 days off. The event is maximum maximum extent of a demand mass effect by 2 to 3 weeks. After that infarcted regions appear. I so dance and in chronic in Fox they all appear hypodense onda well demarcated with negative mass effect. So the picture on the left is a noncontrast ct head on the picture. On the right is an MRI on an M I in the earlier cute stage. So six hours after the event, arterial and horsemen in Heisman or a hyperdense media sign may be visible, Um, and then late to keep, which is 6 24 hours after the event. In a T one but weighted image, you have a scheme occlusion appears hypo intense on a t two weighted um, image is chemically vision appears hyper intense and chronic in Forks. These can show very well signal intensity on MRI. Typical signal participation suggesting underlying etiology. For example, cardioembolic multiple lesions in different vascular territories, whereas large or three arthrosclerosis. You have scattered lesions in one basket of territory, so you don't want to order additional studies within the 1st 40 hours of symptom onset to determine the underlying etiology. These include lab studies, ECD s and further cardiac evaluation toe. Identify possible causing factors such as a shoe afibrillation, and you'd like to do more neurovascular studies being able to treatment. So you want to treat or eligible patients reproduce in therapy for acute ischemic stroke within the recommended time frames. Inclusion exclusion criteria from boluses on North Street and treatment decisions should be made in consultation with the neurologist taken into account multiple individual patient factors. So the age and that is used is intraventricular recombinant tissue plasminogen activator. For sure, they sometimes you see a little T capital P and capital A T P A. Um, and use either out of place or 10 IQ teleplays for the inclusion criteria is that there's no evidence or on there's acute disabling neurological symptoms. There are relative contraindication Z, but as I said, the inclusion exclusion criteria on North strict so some relative contraindication. However, there was a major surgery within 14 days. Whether unwrapped had intracranial aneurysm is present history of ischemic stroke within three months with witness seizure on self stroke. Major trauma within 14 days. My word stroke, which is non disabling or rapidly improving symptoms. Then, when we talk about the time frame from the onset of symptoms or last seen normal, which means that that baseline So, for example, for the elderly that baseline could be confused could be a lower gi CS. So you want to take a history from the people that they live with, or the people that care for them in order to understand where they're baseline waas. So the reproduce usual therapy is within three hours for patients over the age of 18 years old, with any disabling stroke in between 3 to 4.5 hours for select patients where you consult neurology, where you have unclear symptoms onset from the last known Baseline ST um, you can go up to nine hours again. This is when there's unclear symptoms of once it's there. But this really needs to be in discussion with neurology on only for very select few patients. So whether they are for Rebif, you didn't therapy. Will not you continue supportive? Care for a scheming stroke, including neuro protective measures, and you initiate secondary prevention over a current ischemic stroke, which we'll talk about the next side. You monitor and treat their complications and you provide early we have on mobilization. In terms of prevention, we have primary and secondary prevention. So the primary prevention is obviously the pool Anyone's hard stroke, in which you manage the modifiable risk factors really to decrease the likelihood over first stroke. So you manage the cardiovascular risks factors. Use cream patients with risk factors for obstructive sleep apnea and ensure adequate treatment, and you managed disease that can lead to stroke, such as atrial fibrilation, prosthetic heart valve and other risk factors. For stroke, including cardiac, carotid, artery stenosis, sickle cell disease, stop since use and hyper coagulation states here for secondary prevention. That's after a patient has had a stroke on after whether they had reperfusion therapy or not, if they were diagnosed with an ischemic stroke. You want to start antiplatelet treatment with aspirin or a pigeon girl? I'm sure you've had a little bout those in within 24 to 40 hours after symptom answer. And you want to treat underlying conditions if they do have any, such as atrial fibrilation, carotid artery stenosis again. And like primary prevention, you need to reduce these modifiable risk factors. Smoking, hypertension, hyperlipidemia and diabetes, which were all count towards the prevention off a secondary stroke. Sorry, that was fast. An extensive, um, you will get the slot, I say. Sorry, my wife. I just dipped