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Uh everyone can hear me. So uh today's topic uh will be about uh ischemic stroke. So this is general overview of the whole process of from uh start of it to the treatment methods to prevention. So uh moving on, I hope everyone can hear me now. Uh let me know if you can't hear me. OK. OK. So moving on, uh let's start with the general definition of uh ischemic stroke. So as no ischemic stroke is a vascular event. So it most vascular events there, occlusion, it's a acute onset. So, ischemic stroke is an acute onset event when there's a loss of blood supply to a certain area of the brain. So this loss of blood su this area of the brain will lead to a loss of neurological function uh towards the body of the patient. Now, there's another thing which is called dia which is called transient ischemic attack. Now, the old definition of transient ischemic attack was uh there's loss of function that is uh loss of function of the body for less than 24 hours. That is after loss of function, they regain their function in within 24 hours. That is old definition. But the uh current definition is that uh that is there's a temporary cerebral ischemia that results in focal neurological deficits without infarction. Uh Now, can uh can anyone tell me the difference between infarction and ischemia? II, I put the question in. Uh Yes. Yes. Yes. Doctor Sara ischemia is inadequate blood supply. Uh an Yes, yes. Doctor Wager. Thank you. Thank you. Yes, these are uh now uh moving on now when we talk about uh before moving on to about stroke and anything, let's talk about the general blood supply of the brain. As you all know, I am sure all of you must have seen this uh blood sup in circular villus, uh which you must have seen during your anatomy sessions uh during 1st, 2nd year, first year. So generally we arty sees uh the internal carotid artery comes like this. It gives out the middle cerebral artery uh and the anterior cerebral artery that is here. And the from posteriorly, we have the posterior Basar artery which gives you the posterior cerebellar arteries. This post cerebral artery and this uh middle cereal connect by this posterior communicating artery and the anterior communicating arteries you can see here. So what you can see is it interning back up to the brain. So this helps uh it, it helps make sure that even though one artery in this area in this, even if one artery gets blocked, there's a blood supply in the surrounding way and can, can go suel that area. So that is uh what the c of vi is, how it's been made. Uh Moving on. Uh With this uh general idea about the blood structure of the brain, we shall look at the regions where the particular uh this main arteries is this uh anterior artery, middle cere artery and the posterior, but the main areas that is supplied to. So, as you can see in this diagram here, we see uh the anterior cerebral artery as as the Antero artery supplies this frontal cortex area, that is the anterior, superior and medial frontal frontal cortex areas. The middle cerebral artery or middle cerebral artery supplies the frontal par right lobe. So as you know, we have the lobes in the brain, the frontal lobe, parietal lobe, occipital lobe and the uh temporal lobe and inside there in lobe, this is not normally taken into account. So this uh an inter media supplies this frontal lobe, right lobe and superior part of the temporal lobe. Uh which uh um another clear diagram here also. And then you have the posterior given blue here. So it supplies the occipital cortex mostly and the inferior temp inferior temporal lobe and also the thalamus area. So this area this in thalamus area it supplies here and also just for just put the posterior in cerebral artery, which is a branch from this area. Uh here. What disease posterior A R this post infer cere artery. So that supplies the lateral medulla and the inferior cerebellum. So this is the overall blood supply of the brain. I hope uh this is a clear idea for you all about the blood cell brain because stroke is a vascular. So it all the all the symptoms and signs that develop in the patient. It all depends on the particular artery that becomes blocked and the symp and the area is supply in the brain and the function of the brain. So, moving on. Now, when you talk about the middle, but the symptoms, as I mentioned before, uh these are symptoms, uh symptoms depend on the particular area area that this artery supplies and the symptoms develop. So when we talk about a media artery block, so and as I mentioned earlier, the middle ceb artery supplies the frontal lobe, right lobe and superior temporal lobe. This leads to a contralateral uh paralysis of the body. So, contras what I mean by here. Now, as you can see in this image here, the lesion of the stroke there, the occlusion of the blood supply occurs in the left side of the brain. But the symptoms in all occur on the right side of the body, the right, right lower limb, right, uh upper limb, the right side of the face symptoms and all all occur right side of the face. So that's what you mean this contralateral lesion. And what do you mean by this upper motor neuron and low motor neuron. Can someone uh like uh tell us what uh the upper motor neuron lesion and a low motor neuron lesion. Uh Yes. Doctor bar, upper motor neuron lesion means the brain and the spinal cord is the main nervous system areas affected and low motor neuron means the peripheral nervous system is affected. Yeah, that is just the general idea. So the sy what you can see in these uh two upper motor neuron lesion and low perineural lesion. Can you give me the difference between what happens in those two? Ok. Uh someone else can also please do try. OK, so I will uh oh sorry, sorry, Doctor Sarah. The question was uh what are the features you can see in the upper motor neuron lesion and a lower motor neuron lesion. Uh I will, I will tell the answer. So what you see in upper motor neuron lesion is it's when the brain or spinal, the higher cor the high and the spinal cord and the brain they are being affected. So what you see here is you see a spastic paralysis, the spastic paralysis means there is a rigidity in these movements and all. And uh there is increased uh that the tone of the tone of that area is increased like the increased tone in that particular limb. An example of it. And there is no atrophy seen in this ural lesion. And we see there's increased reflexes increased tendon reflexes and a positive babinski sign that is the plantar uh planter. The pla the plantar reflex is positive that is plata but there is no uh fasciculations uh is seen in the upper lesion. Doctor sara fasciculations is a feature of low motor neuron lesion. So other features in low lesion, you as you can see flaccid paralysis, that is the decreased tone and the CV atrophy. But this uh plantar reflex that is the reflex is negative. So those are the features that differentiate the upper motor neuron lesion, low motor neuron lesion. I'm sure uh you all can go through it uh later. So, moving on with our topic here. So what we see in a in a stroke, in a stroke, what you see is we see an upper motor lesion. So we see increased uh reflexes and we see increased uh positive babinski sign spastic paralysis and there is no atrophy and there is no vascular and fibrillations. So those are things you see in ischemic in the contra side of the body. What else you see is? You can see uh you know, media cerebellar artery occlusion, we can see contralateral he which I will show you in the future like oil. But it is that is a uh eyesight defects, then the gaze, the eyes move, move towards the side of the infarction. So as the brain is affected, this reis affected this side. So eyesight will move our gaze and move towards the side of the lesion that is towards this left side. And also you can see there's dysphasia and there also dysphagia and there's apraxia also. So dysphasia is due to uh as you can see the middle artery supplies this particular area. So there can be dysphasia and also case aasa. So that is a uh dysphagia occurs there. Now, moving on, we talk about the anterior cerebri artis anti supplies the anterior sued frontal lobe. So uh the frontal lobe mostly uh mostly is about the motor cortex areas, that is the prefrontal cortex, the motor cortex area. So there will be hemiparesis. And what we see is we see uh the primity reflexes in pediatrics must have uh if you learn that in there primity reflexes, which we lose as we gain uh the control over them. So what we see in when the frontal lobe is affected, we see that these primity reflexes are being brought up again, such as example, here's grasp reflex and then uh moving on, we can see if the patient can present incontinence and there's this artery also. Now, uh I'm sorry. Uh I forgot to mention one question. So can you all tell me uh looking at the diagram, looking at this diagram here, can you tell me uh which limbs will be affected more uh compared to when uh example, if the middle cerebellar is affected, which limb do you think the upper limb or the lower limb will be affected more. I put the pressure down uh push down in the chat box. So it's easier for everyone to Yes, Doctor Sarah, I will. Uh OK. So as you can remember, I'm sure you all have seen the hormone color, the motor hormone color and the uh sensory hormone color. So with this diam, we can explain uh which area limb is affected most. So as you can see in this picture with this picture and this picture together you can uh you can see this area, the lateral area. So the brain, this area supply the mo uh supplied by the middle cerebral artery and the top part is supplied with an artery. So same image if you take here, these areas are supplied by the middle cerebral artery and these areas supplied by the Teri ceri art. So from this, what you can see is that in an artery occlusion, the lower limb is affected more than upper limb and in the middle cerebral artery occlusion, the upper limb is affected more uh more than the lower lips. So I'm sure you uh I guess I hope you understood these differences. So yeah. So when you see patients, you can identify these differences, I hope you don't got this out. Did they get it? Uh why or the difference between a middle se occlusion and um an occlusion? The difference in the how the limbs are affected? Ok. OK. Thank you doctor Sa OK. Now, moving on from that. Now, also we can see we uh there's a posterior cerebral artery which comes from the vertebral arteries behind giving the bacill artery, the posterior artery. Now, the posterior cerebral supplies occipital lobe and the inferior temporal lobe as well as the thalamus. So because uh occipital lobe is affected your, as I mentioned, I tell you what there is contralateral hous hemianopia with macular sparing. And also there is hemisensory loss because the thalamus is affected because also the spine, all the sensory pathway goes through the thalamus. So there is he loss, there can be memory deficits with vertigo, nausea. And also uh I'm sure you also heard the po pica that's posterior cerebral artery, which is a lateral med syndrome. It's called later Med syndrome syndrome. So uh I'm sure this is a topic form because uh it also has similar symptoms. Now, this way, I wanted to mention you all about this uh uh this contralateral he and the this is what happens in the occipital region. So what you can see in five, this is what happens when the posterior cerebral artery is affected. What you can see uh here what I see this. So as you can see in number five, the lesion is on the right side, my right side, I'm sure it's in your right side too. The right side of the patient is where the lesion is. But you can see here the defect, vision defects on the left side. So that is what it means. Contralateral and it's homonym, he same side is affected hous uh hemianopia, both side half of the vision is affected. And as I can see this, this is the macular area. So here there's macular spa. So what I can understand is in uh occipital lobe damage that's contra to hom he, these are uh is optic pathway. I'm sure you will learn in your ophthalmology or other new CRE ex cranial examination, screening classes, all these pathways and all. Uh I hope you, I hope you got this. Uh what I mean by con to home. You may OK. Here the same, the country so many in the military, the same. I hope you got it. Oh, sorry, doctor, sorry, sorry, sorry. Uh I hope everything. I hope. Uh it's clear now now. Good. Oh OK. So sorry, sorry, sorry. But uh yeah. Yes, doctor me. I will explain pika uh after the session. OK. Uh It's OK with you for me. Uh explain after the session. Oh OK. Ok. Uh Sorry, Doctor uh Pica Pica is not much. Uh nothing much. So it is when the uh the posterior inferior cerebral artery, which you can find here, this artery is are blocked. So this posterior ince artery, it supplies the we the lateral medulla and inferior cerebellum. So what you can see in the lateral medulla, uh we can find the cranial uh 9, 10, 11, 12 and also the inferior cerebellum uh signs. So what we can find the cerebellar signs as well as low low cranial signs. I hope you got it. OK. I will explain more uh at the end the session. Sorry. Uh sorry, doctor me. OK. So moving on, uh what are the causes for this uh ischemic stroke? So, a ischemic stroke can occur due to a thrombo uh thrombo uh thromboembolism that is an embry goes away from a particular location to another place to the brain or it can be to occlusion of the arteries supplying the brain. So a cardia em a cardia embry is uh when the colic Emla is when uh there is atrial fibrillation that is in this atrial fibrillation and thrombus can form, that's the atrial thrombus can form in the heart which can shoot up to the brain or it can be due to ventricle thrombi or it can be a rheumatic heart disease which forms thrombus in the vas areas. And also it can also go or it can be to ventricle aneurysms which uh allows a clot to form in the heart due to aneurysm in non contracting areas. So it can also cause. So it can be due to an arterial emb that is in the aosis cause. And a thrombus forms in the internal carri artery that also can shoot up or the internal carotid artery itself can become blocked. So as the major, the anterior middle cerebral artery are branches of the internal carotid artery. This can lead to stroke or attic cause uh o another cause can be this infectious emboli which is a bacterial endocarditis or it can be due to a paradoxical embolism. Paradoxical embolism can be due to after say AD VT which can go into the heart and cross and go. There's a uh say a SD or VST. The paradox embolism can occur which can cross the heart from the left uh right, left side and it can go directly to the brain. Now, other rare other causes, rarer causes. We have hypercoagulable states such as uh inhaled thrombophilia. These are an increased risk of uh coagulation. There is increased of thrombus formation or it can be due to polycythemia which increases the hemoconcentration or it can be due to hormonal contraceptive use hormone replacement therapy, sickle cell disease, vasculitis, uh uh arterial dissection. So, these are the causes but there are multiple causes uh for stroke. Now, moving on. Now, uh when we talk about stroke, the assessment and management of stroke both should occur simultaneously because stroke is an emergency. Active stroke is an emergency. So we should uh assess the patient stabilize the patient along with the stabilization, we should manage the patient. Uh along with the stabilization, we should assess the patient also. So as all emergencies, we should start off with uh ABC that is uh airway breathing circulation. If the patient has uh any uh airway uh that is if the patient has la low decreased level of consciousness because of the stroke, we should always uh make sure the airway is patent and open. Uh And if the patient is having oxygen uh level, that is hypoxia oxygen, less than 92 or 94 we should always provide them with oxygen and make sure the patients uh is stable and the c circulation I will come to BP management in uh uh the few slides. And after that, we should uh go for the vital parameters that is pulse, blood pressure, as I mentioned, respiratory temperature. And always, we should check for the blood sugar level because hypoglycemic can mimic stroke symptoms. So we should always check this hypoglycemic initially. If the patient is unconscious or if the patient is having this, we should always give uh a small amount of glucose to uh exclude stroke, exclude this hypoglycemia. After that, we go for a quick neurological examination, we check the Glasco comma score, uh pup examination. And if there's any lateralizing signs such as hemiparesis or the symptoms of stroke, the hemiparesis or less facial drooping or a pronated drift, we should go identify those signs. Uh I think, you know, pronate drift is when you keep both arms outside, in a prone prone side, both arms stretch the prone side and ask the patient to close their eyes uh slowly with time. If there is positive pronated drift, the arm will close uh rotate to the other side. I hope that's uh what 20 is now moving on all the things we should screen for any signs of cerebral herniation. Also, this can be done with the the diagnosis, imaging modalities. Also, then also we can attempt uh to localize sign in and stroke symptoms. As I mentioned earlier, we should, if we, if the patient can talk or the patient can talk with the bystander who was there, you can ask them to uh ask them what the signs and symptoms and take, try to take a quick history from them. And also we should perform the severity assessment that is NAHSAHSS score. So I'll show you what is this, this is HSHSS score. I'm I hope you all can see the diagram uh uh table properly. If you can just Google it, uh checking for NHS uh score, that is a severity uh assessment score, which you can uh fill in this and I severity of this. So this also it depends how you're gonna manage the patient, forget and moving on. After that, we should go on to uh I, I go on to do an imaging uh modality because uh this stroke, we asked, I forgot to mention stroke. It can be due to ischemic stroke as well as it can be due to hemorrhagic stroke. A hemorrhagic stroke is when there is bleeding outside into the cerebrum into the cerebrum into the brain that is hemorrhagic stroke. So, both the stroke means there's decreased blood supply at the in line that's decreased blood supply to the brain parenchyma. So that's why we should always go for an initial, that is NC CT or CT is done. If initial image modality, we don't do an MRI because uh if the MRI it's better, it is better to identify early stroke but is less commonly available and takes longer. So we, we do NC CT scan. This NC CT scan will help exclude uh hemorrhagic stroke. So we can exclude hemorrhage. So then it should be uh ischemic stroke. So this can be a NC CT scan can be used that is a non contrast CT of the head and also the NCC, they can identify any stroke mimics uh anything like uh say uh anything else meaning stroke such as uh any traumas or if you any brain tumors, uh even infection, I infection can be um uh excluded. And also, I'm sorry to mention the history. We should also exclude other causes of uh stroke like even such as uh any hemiplegic migraine that is a migraine or it can be after a seizure episode, the patient can become unconscious. That is post thought paras uh it can be due to metabolic encephalopathy. So for that only we should do go for additional studies that is we should do uh glucose studies. Uh we should go on, we should um says that we should do the lab studies that is glucose. As I mentioned, serum troponin is to check for any cardiac abnormality because cardiac abnormal, as I mentioned is a causative factor for uh stroke. And there you should do a coagulation panel to check for the thrombophilia and the basic metabolic profile to check for this metabolic encephalopathy and CBC to check if there's any infection. And uh ECG and for cardiac evaluation should be done to exclude atrial fibrillation or any other cardiac causes. Uh Yes, doctor me in cerebral herniation, we can uh identify using this uh this NC CT scan itself. You can uh choose that to find if there is any uh cerebral herniation. Uh I will check up on that and I will let you know about the standard protocols about screening for cerebral herniation. Yeah, I hope uh it was clear, Doctor Mimi I using the NC CT scan. It's a scan, the N CT scan will show the structure of the brain, right? So we can identify this uh cerebral edema and if there's pushing on the brain to herniation, oh, if there is more, I will uh uh research on that, then I will let you all know. Yeah. So moving on, we can do any other neurovascular studies such as AC T PE or am uh Mr A to ident any stenosis or dissection of arteries, arteries. Now, moving on, talking about BP management and BP management. If the, if the patient is uh not undergo reperfusion therapy, we should keep the BP at 2 21 20. Because after a stroke, the BP naturally rises up. This is because the BP rise up to push, the blood is trying to push through the clot. And then the stroke, there is a blockage and moving to the cereal tissues. So naturally, the BP rises and decreases in a few days. So we do, if the patient is not undergoing reperfusion therapy, we don't uh we keep the BP below about 2 21 20. But if the patient is undergoing reperfusion therapy, we should reduce the BP to less than 1 85 1 10 and keep the BP less than 1 81 05. You should keep the BP less than 1 81 05 for the 1st 24 hours after the treatment. So these are the agents that we use. Mostly we use labetalol, we can use clevidipine or niCARdipine. Now, when we talk about uh this is the main thing, specific treatment of acute ischemic stroke that is in any blockage. The agent used thromb is we use RT P A. So RT P A, we use his place or a place mostly. But the side effects of this drug is it can cause bleeding and that is it can cause in inter hemorrhage or the risk of angioedema. There is uh hypersensitive allergic reaction to it. Now, we should always give RT P if there's any indications and if there, if there is indication and there are no contraindications, only RT should be given. So the indications can be a indication like the child if the patient is more than 18 years old. And uh there's a diagnosis of ischemic stroke with the neural deficit and the patient comes to you within 4.5 hours. So if the patient has a stroke and comes to you within 4.5 hours, then we can give RT P the contraindications are if the patient is having resolving stroke symptoms, uh that I mentioned is a tia or if there is a patient that has he had trauma in the three months or the patient is having a known history of inventing hemorrhage or the BP, as I mentioned earlier, if you're giving an this uh so reperfusion therapy that you should make sure the BP is less than 1 85 1 10. So if it is more than that, you should not uh give this or there is uh symptoms of subarachnoid hemorrhage. That is uh the major symptom. Uh you can understand Subarus hemorrhages. The patient will complain to you about uh a headache that is the most severe headache in their life. That's the most severe headache in life. That will be the major complaint in subarachnoid hemorrhage or the patient is having any history of G I or ge hemorrhage within the past three weeks or the patient is having uh having arterial puncture and no compressible sight in the past seven days or a patient received heparin in the past 48 hours or has elevated APTT, it is a coagulation uh defect or is a platelet count is less than 100,000 per microliter. So even if uh if you give this pill count, if it takes some time, you start giving RT P and if the results come saying if the platelet count less than 100,000 point, then you stop. So we don't wait for this much during practice. Uh Moving on, uh moving on alternative to this uh reperfusion therapy is what we have the mechanical uh mechanical thrombectomy. So, mechanical thrombectomy is where we surgically go into the artery. Uh So we go into the artery that is we uh go through the femoral artery, radial artery, eating a via and we go and mechanically remove the uh clot. So this um me method is uh this method can be used if the patient is having fibri, a patient who under fibri and it is ineffective or it is contraindicated as the contraindication measure there. If the patient cannot do uh this uh thrombolysis therapy, we can go for this mechanical thrombectomy. A thrombectomy is eligible for patients if the patient is coming 6 to 16 to 24 hours after stroke. So, a recent study says 16 hours, but 24 hours are still some books say 24 hours. So 16, 16 to 24 hours after a stroke, you can go for the mechanical um mechanical thrombectomy. Now, this is the indications the inclusion indications if the patient is more than 18 years or if they're having a large occlusion, such is the proximal artery occlusion, uh occupations having, as I mentioned a score which is checking severity. It's around six, we can go for this or there's limited and ct. So if you uh if there's a particular area in the brain that's affected, if you remove the clock only, it's a simple procedure than giving the whole body. This uh thrombolysis or the patient is having a patient who previously independent in living activities. This uh living at the independent living activities can be measured by the ranking scale. So this is a ranking scale. It quantifies a degree of disability and dependence in uh daily activities before and after severe stroke. So we should always assess this in our history assessment also uh with the patient or by center, how the patient was before having a stroke that he can, he was doing everything by himself or he was uh taking care of someone else. So that also affects the way we treat the patient. And also I mentioned earlier, the symptom on is uh between 6 to 24 hours. Now, uh as I mentioned before, as the first slide, we uh talked about the transient ischemic attack when there is only a uh ischemia where there's, but there's no infarction, but this is a ischemic attack. This can further move on to cause stroke to the patient uh to assess the risk of stroke. After the tia we do. We have the AB B CD two score. So here it is a age more than 60 BP. See is the clinically whether this patient is having weakness or is having only isolated speech defect only. And then we check for the duration of these uh symptoms. If it's more than 60 minutes, less than 60 minutes or less than 10 minutes of the patient is having diabetes. So as we all know, diabetes is a major risk factor for multiple conditions in the body. So we should always be check all about diabetes. And also after 24 5, uh find the score, the score states how the score estimates the risk of stroke in two days. So the 67 is high risk, 45 is moderate risk. 0 to 2 is a low risk. Finally, now, finally, when talking about prevention, this is secondary prevention of stroke. If the patient is having a recurrence of stroke, if a patient already had stroke and we should prevent a stroke or the patient had tia to prevent a stroke happening. Uh First line, we can go for clopidogrel, this th this anti drugs uh aspirin clopidogrel. Now, here they have dual therapy, aspirin plus uh uh release of uh aspirin plus another drug dip or, and if patients having atrial fibrillation, we should go for anticoagulation. And uh if the patient is having high BP, they have a risk of developing atherosclerosis or even hemorrhagic stroke, we should maintain the low BP of AC with ace inhibitors and diuretics. A statin therapy can be used to stabilize the plaques are in plaques and finally, we can go for carotid end toy. When we surgically remove any plaques found in the carotid arteries. This has uh a benefit if the stenosis is more than 70%. So that is it.