S1E42 Stroke

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And if you're like me, you're trying to figure out how artificial intelligence is changing the business world and our lives. So each week on Big Technology, I bring on key actors from companies building AI tech and outsiders trying to influence it. Asking where this is all going, they come from places like Nvidia, Microsoft, Amazon, and plenty more. So if you want to be smart with your wallet, your career choices, and meetings with your colleagues and at dinner parties, listen to Big Technology podcast wherever you get your podcasts. All right, so this podcast is going to be on stroke. I have a few mnemonics in there to help you remember the things you need to know for your exam. And of course, I'll try to keep it as brief as I can just to focus on the things you really need to know for your exam questions. As always, thank you so much for all of the really nice comments. I truly do appreciate that. So thank you for that. Let's go ahead and get started with stroke. We'll start with our TIA, our transient ischemic attack. Keep this part brief. There's not a lot of high yield stuff from TIA. Just a few things that you need to know of. So first, what is a TIA? So TIA is a transient episode of neurologic dysfunction caused by focal brain spinal cord or retinal schemia without acute infarction. That's the official definition from the American heart association and the American Stroke Association. So a TIA, it's a clinical diagnosis. It's often not the easiest diagnosis to make because the presentation can be highly variable. There's many differentials to consider. And often by the time the patient presents to you, their symptoms are already gone, but essentially a TIA looks exactly like a stroke and presentation, but the symptoms resolve they get better. That's the key. There's no tissue infarction. There's no tissue injury. So to put it really simply, TIA, there's a clot in a vessel, causes some transient symptoms, but it dissolved fast enough. The clot dissolved fast enough that it didn't lead to the death of brain tissue. I wanted to talk a little bit about the time-based TIA. So you may have heard that a TIA is described as a focal neurologic signs or symptoms lasting less than 24 hours. You may still hear about that in clinicals, your preceptor. It's something that we used to use a while ago before we had MRI neuroimaging. The deemphasis really came after multiple studies showed that up to half of classically defined time-based TIAs showed brain injury on MRI. So you had these patients, their symptoms resolved in less than 24 hours. So time-based definition of a TIA, but then when they actually had an MRI done, they showed stroke on their MRI and infarct. So just be aware of that. Kind of try to get that time-based definition out of your head. Focus on the tissue-based definition of a TIA, which is lack of tissue infarction, visualize a neuroimaging, MRI, etc. Now history and exam with the TIA, usually the symptoms are really brief. They're only going to last a few minutes, maybe up to a half hour or an hour or so. Often by the time these patients get to your office or the year to see you, the symptoms are already gone. So a lot of the actual exam is getting a good history. We'll talk more about the specific symptoms when we talk about stroke in a minute, but for TIA, there's really two things you should be familiar with that always seem to come up on exam questions and that's MROSFUGACs and keratin brulee. So MROSFUGACs, it's a transient, monocular vision loss. This one's really big. It always seems to come up on exam questions when we're talking about TIAs. Now there's obviously other causes, but if you see an exam question right away be thinking of a TIA. So what happens is you have an occlusion or stenosis of the internal carotid artery circulation. This leads to hypoprefusion of the ocular arterial circulation. So basically your carotids are clogged, your eyes aren't getting perfused and this temporarily shuts off the lights. That's MROSFUGACs. And the vignette, the way you'll see it described is as a curtain coming down in front of their eyes, a generalized darkening or shadow in one eye. It can last a few seconds up to around 30 minutes. If you see none of them yet, right away be thinking of a TIA. The other thing, keratin brulee. So on physical exam you osculate the keratids. You hear this turbulent flow through the keratids. And this is due to atherosclerotic plaque in the keratoc arteries causing stenosis. And it can be major cause of not only just a TIA, but also an ischemic stroke. All right, now let's talk about diagnosis. I'm going to briefly run through the diagnostic test because the thing is the workup, it's very much the same as in stroke, which I'm going to go over next in more detail. The idea is though, with the TIA, is you start with your neural imaging and suspect the TIA patients. So MRI CT. So early brain imaging with MRI or CT is indicated for all patients with suspected TIA. MRI does have greater sensitivity than CT, but the problem with MRI is it's time consuming, it's expensive, there's contraindications. So CT is often used more often than MRI, but if MRI is available, it is the better test of the two. So that's your that's your brain imaging. Then we talk about neurovascular imaging. So MRI, CTA, keratin ultrasound, it's really important in patients with a TIA to rule out an obstructive lesion in a large artery supplying the affected territory. So you image the vessels of the brain, the neck, you're looking for your source essentially. Do you have an intracranial atherosclerotic disease? Do you have keratid stenosis? Because once you find your source, you can direct your secondary prevention at that atherosclerotic disease or you can intervene even with like a keratin and our erectomy for instance. So that's really the cornerstone of your diagnostic workup for TIA. That's what I'd memorize. Your neural imaging with CT or MRI and your neural vascular imaging, MRI, CTA, etc. You also have your ancillary test. These aren't as important, but I'm going to talk about them just to have an idea. So ECG to rule out, say A5, echocardiogram, or you're looking for your cardio-embellic source for the TIA lab test, rule out metabolic and hematologic causes. But the main workup is going to be your brain imaging, your neurovascular imaging. So focus on those. But be aware of the EKG, the echo, the lab testing, your low blood sugar and those types of things. Now treatment, there's a few things that you need to know. So anti-plaitly treatment. This one's really important. So aspirin or a combination of aspirin and clopidogryl. This is probably the most important intervention to remember for TIA. So for almost all patients with a TIA who do not have a known cardio-embellic source. So this isn't from like A5 throwing a clot. We start with anti-plaitly therapy. So this can be aspirin as monotherapy or dual anti-plaitly therapy, aspirin and clopidogryl. You decide that depending on their, on their risk score, which we'll talk about in a little bit. So remember that anti-plaitly treatment for almost all TIA patients. Now if they have a cardio-embellic source, you're going to use anti-coagulation. So if they have like I said before, they have A5. You're going to start them on oral anti-coagulation with warfarin or a direct oral anti-coagulant to prevent future embelly. So if it's a cardio-embellic source, your treatment's a little bit different. And then you have your a little bit more invasive treatment. So crudid and argyrectomy or crudid artery stenting. So if you see a neurovascular imaging, the patient has significant crudid artery stenosis. Specifically what we're looking for is internal crudid artery stenosis. 50 to 99%. You're going to intervene with re-vascularization of the crudid, which can be done via an endar-directomy or crudid artery stenting. So you're looking for stenosis 50 to 99%. And then also in the guidelines, it says the patient should have a life expectancy of over five years. All in endar-directomy is, is you basically cut open that crudid artery that has the stenosis in it. You pull out the plaque, you suture it back up. That's what an endar-directomy is. Or you have the option is with stenting as well. Then finally for treatment, this is important too. So your intensive risk factor management, hyperlipidemia, hypertension, diabetes, smoking cessation. So the big thing with the TIA is the patient got a warning sign. Not everybody's going to get that lucky. So these patients need to make some significant lifestyle changes to prevent recurrence. So effectively treating their hypertension, getting started on high intensity statin therapy to lower their LDL, smoking cessation, limiting alcohol consumption, if they're diabetic, improving their glycemic control, reducing their modifiable risk factors to help reduce their future stroke risk. I don't necessarily think that'll be an exam question because it's kind of hard to ask that. But in general, you need to be aware of that because that's really important for treating these patients. So for treatment overall, the two most important things to remember is your anti-platelet treatment. So that's aspirin Clip Hit a Grub. That's going to be it. be most of your patients with the TAA and then remember reduce those modifiable risk factors. That's the cornerstone of TAA long-term management. Let's talk about one last thing for TAA. So there's something for your stroke risk called your ABCD squared and I'm quoting up to date here but up to date calls the ABCD squared score a simple but suboptimal assessment tool. So the test is far from perfect but it's still being used. You'll likely hear about it. So let's go over what it is what it's designed to be used for. So the ABCD squared score helps you determine a few things. So a patient that has a TAA is at a much higher risk for stroke in the future. So this calculator helps you to determine one how high the risk is for stroke in the near future. This test also helps determine how aggressive the treatment needs to be in these patients. So for instance it helps determine whether or not we're going to use just monotherapy with just aspirin or dual antiplatelet therapy with aspirin and clopidogrel depending on their score. And then finally it helps you determine is the patient that's present in your office today in the ER going to get the full million dollar TIA workup or do they maybe just have a complicated migraine and maybe we don't need to do every diagnostic test in the book. So how high is the risk? So this calculator helps guide you with these types of things. So again the assessment tool is known as the ABCD squared tool. Do not memorize it. Just be aware that it exists for stroke risk stratification and then I'm going to briefly go over it. But again I repeat don't memorize this just be aware of it. So if it comes up your preceptor mentions this you kind of have an idea of what it is like oh yeah that's the stroke risk assessment tool. So just be aware of it. I'm going to briefly go over it. So ABCD squared stands for age 60 or over that gives you one point blood pressure 140 systolic or a 90 or higher diastolic. That's another point clinical features depending on what their features are. Unilateral weaknesses two points isolated speech disturbance is one point. The duration of your TIA symptoms all gives you more or less points and then if they have diabetes that also gives you another point. How high their score is the higher risk of their two day stroke risk you know and you can look all those things up if you want the specifics again I don't think you need to memorize that but just be aware of it. What do you need to know for your TIA? There's three things I would say to take away if you're going to forget everything else. Remember what it's TIA is it's a transient episode of neurologic dysfunction caused by ischemia without acute infarction. Remember amyrosis few gaxes it's probably the most important clinical manifestation and then for treatment I'd say the one thing you should definitely remember is your anti-played treatment with aspirin. Alright so that's your TIA let's move on to stroke. Alright so for stroke there's two types of stroke there's a schematic and hemorrhagic so a schematic that's going to be your most common type around 75 to 80% of all strokes and that's the one that we'll really focus on as most of your questions are going to come from this hemorrhagic like I said it's much less common we'll touch on that at the end. So a schematic stroke let's start with a schematic stroke this is the one you need to focus on and a schematic stroke is a sudden loss of blood circulation to an area of the brain leading to death of tissue and loss of neurologic function. So a schematic stroke is a compromised blood vessel leading to decreased perfusion resulting in death of brain tissue. So remember in a TIA the clot is all fast enough so there was no brain death and stroke that's not the case we have death of brain tissue that's the key. Now there's two types of a schematic stroke there's thrombotic and there's embolic. So thrombotic is going to be bifar your most common so most common type and what happens is you have a thrombus that forms in the artery walls and this generally happens when you have atherosclerosis in the vessel so you have a plaque in the vessel something causes the fibrous cap of the plaque to shear off. So it opens up and then once this happens platelets come in to plug up that little fibrous cap that popped off and when that happens all the platelets come into plug it up and a thrombus forms around the plaque this leads to occlusion of the blood flow distal to this area which leads to the stroke. Second type is embolic so embolic means the clot came from somewhere else in the body. It traveled from a distal site got lodged in the vessel of the brain and occluded the vessel. Common cause of embolic stroke is a fib patient as a fib throws a clot from the heart. Clocates lodged in the vessels of the brain leading the stroke. If you ever forget which is which like is a thrombotic or embolic the one where the clot traveling from somewhere else the way that I remember that is embolic starts with an E E stands for elsewhere aka the clot came from elsewhere in the body just a little tip to remember which is which. Clinical manifestations all right so different arteries supply blood to different parts of the brain different parts of the brain as we know control different parts of the body. So you need to have a very basic understanding of occlusion of which vessel is going to lead to a deficit in which part of the body. This is important because it's likely going to come up I had this on an osc key question I had an exam question they're going to give you the patient presentation maybe they'll give you a left lower leg weakness and then they're going to ask you which type of stroke is this middle cerebral anterior cerebral etc. I do have a couple tricks for you to remember this. I'm not going to list every single symptom or deficit for each different artery I'm going to stick to just the very basics enough for you to pick it out and have been yet. So let's talk about first our anterior cerebral artery stroke. All right with an anterior cerebral artery stroke there's one thing you need to be looking for and that's control lateral involvement of the feet and legs. This is the most common area to be involved. Controlateral meaning if it's the left anterior cerebral artery involved the right leg or right foot will be affected. There's obviously other possible presentations urinary condens as possible to have weakness in the upper extremities but the most common what's going to be on the vignette when you need to focus on is some kind of deficit in the lower extremities. So paralysis and sensory loss in the control lateral leg and foot. So how do you remember that anterior cerebral artery stroke as soon as you see anterior cerebral artery stroke I want you to think of the first three letters which is ant and I want you to think of an ant. What do you do when you see an ant on the floor? You lift your leg and you step on it with your foot. Interior cerebral artery stroke most commonly affects the control lateral leg and foot. So when you see ant, anterior cerebral artery stroke think of an ant on the floor lifting your legs stepping in on with your foot most commonly affects the control lateral leg and foot. That's how you remember the most common presentation of anterior cerebral artery stroke. Think of an ant stepping on it with the lifting up your leg stepping in with your foot. That's anterior cerebral artery stroke. Let's move on to middle cerebral artery stroke. Now middle cerebral artery stroke is the most common artery to be involved in an ischemic stroke. The way that you remember that is middle cerebral artery MCA also stands for most common artery. So that's how you remember the MCA the middle cerebral artery is the most common artery to be involved in an ischemic stroke. What you're looking for in the vignette is control lateral face and arm involvement as well as aphasia. So paralysis and sensory loss is going to be greatest on the control lateral side of the face and the arm versus the lower extremities. And you also may see aphasia in middle cerebral artery stroke. Aphasia remember is difficulty producing or understanding speech. The way that I always remembered this was instead of remembering middle cerebral artery, M-I-D-L-E instead of middle cerebral artery I remembered Maddles cerebral artery, AKA M-A-D-D-D-L. I'm sorry M-A-D-D-L-E cerebral artery strokes. Instead of middle cerebral artery think of Maddles cerebral artery and think of somebody that's very mad. Think of like that cartoon image. Whatever you think of like a cartoon character being mad. What do they do? Their face gets all red. They raise their arms up in the air and shake it and then they scream. They're like, "Ah!" That's what I want you to think of. Middle cerebral artery think of Maddles cerebral artery. Think of that cartoon character. His face is red and his face is red because remembering commonly involves the face, the control lateral side of the face, it helps remember that. And then remember the arms are up in the air. They're shaking their arms up in the air. Remember most commonly affects the control lateral arm. That's their arms and their face being red. And then they're yelling. They're screaming because they're so mad. And that helps remember not necessarily that the patient with middle cerebral artery stroke is going to be yelling. But it helps remember, okay, the voice is involved and helps remember aphasia. So remember middle cerebral artery stroke think of Maddles cerebral artery strokes. Somebody's very mad. Arms are up in the air, shaking them up in the air. That helps remember the control lateral arm involvement. Their face is all red because they're angry. That helps remember the control lateral side of the face. They're screaming. That helps remember the aphasia, the voice involvement. All right, so let's move on to our posterior circulation. Specifically the posterior cerebral artery and the vertebral basal artery. In general, if they mention any kind of visual changes, you should be thinking posterior circulation. I wanted to break it down a little bit further though. Each individual will vessel and we'll discuss the unique presentation scene with each. So let's start with our posterior cerebral artery stroke. So two common things in a PCA stroke that you should be aware for the exam. First one is homonymous hemianopia. So that normally spares the macula because the macula is perfused from collateral flow from the middle cerebral artery. So again, homonymous hemianopia. So what this is, you can also see this in an MCA stroke, just an FYI, but it's much more common in a PCA stroke. So it's a visual defect involving the control lateral side. So either the two right or the two left halves of the visual fields of the eye. So basically half of the visual field is not being processed. You can just think of like half of the vision on one eye is just completely blacked out. So the visual field is blacked out on the control lateral side. That is homonymous hemianopia. And remember that for your PCA stroke, they may mention that it spares the macula again because remember that's perfused from the middle cerebral artery. The second thing that you need to know for your PCA stroke is something known as Alexia without a graphia, which means they cannot read, but they can write. So they cannot read, but they can write. So they can write out a whole story, but they can't read a back to you. And the way that I'm going to I just remember these two, let's talk about that. So the first thing is, this works much better with a visual like I have on YouTube, but I'll try to explain it. So basically when you think of your posterior cerebral artery stroke, when you think of like a P on its side, and if you think of a P on its side, it kind of looks like glasses, and I have a picture of this, it obviously works and makes it much easier, but if you think of two P's on their sides, they basically look like glasses, and that always helps for me to remember, I just have this visual of two P's on their sides like glasses that involves the eyes, the homonymous hemianopia that helps me remember, two P's as glasses, posterior, starts with the P posterior cerebral artery, and then the second thing is, Alexia without a graphia. The way that I used to remember that, is posterior cerebral artery, PCA. Alexia is your personal computer assistant, 'cause Alexia sounds like Alexa, like Amazon Alexa, and Amazon Alexa is a personal computer assistant, so Alexia is your personal computer assistant that helps me remember Alexia without a graphia. All right, so I know those aren't the best mnemonics, but that's the way that I used to remember it. Let's move on to the last thing, which is gonna be our vertebral basilar artery stroke. Now, the good thing about vertebral basilar artery stroke is most of the things you'll see in a vignette, most of the clinical manifestations all start with a V, and vertebral basilar artery stroke also starts with a V. So as soon as you see vertebral basilar artery stroke, think of all of your V clinical manifestations, that's gonna be vertigo, visual changes like diplopia, vomiting, and then the last one, I kinda made this up on my own, but vibrating eyes, because nice stagmas is another possible presentation of vertebral basilar artery stroke, and if you ever look at nice stagmas, basically the eyes are like shaking and vibrating off to the side. So that's how I remember that. Vertigo visual changes vomiting, vibrating eyes, vertebral basilar artery stroke, remember they all start with Vs. Those are your clinical manifestations. If you remember that, you'll likely be able to pick it out on a vignette. Let's talk about diagnosis. This is obviously gonna be pretty similar to the TIA workup, going a little bit more depth though. So when making the diagnosis in a patient with suspected stroke, the initial test, like right when they come in the door, that's gonna include a finger stick blood glucose, oxygen saturation, and a non-contrast CT. Those are the main diagnostic tests to guide acute therapy. The finger stick, it's important because you wanna make sure the presentation isn't due to hypoglycemia. Hypoglycemia can cause focal neurologic deficits that mimic a stroke. So you must rule that out right away 'cause that's really important to make sure this patient you think has a stroke, doesn't just have low blood sugar. So that's important as well. All right, let's talk about your CT head non-contrast. So CT of the head non-contrast. You're gonna do a CT of the head in any patient you suspect a stroke. This is your initial test of choice. Now, is a CT of the head used to make the diagnosis of an ischemic stroke? It's actually not, and that's a common misconception. The main purpose of a non-contrast CT is basically to tell us one thing. Is there blood? Is there no blood? Is this a hemorrhagic stroke or is it not? Because if there's blood present, and this is a hemorrhagic stroke, we know that reprefusion therapy with intravenous thrombolysis, like TPA, it's off the table. So again, CT initial test of choice used basically to guide treatment in regards to TPA and let us know whether or not this is a hemorrhagic stroke. It can pick up some early signs of acute ischemic stroke, but really the best way to look for acute ischemic stroke is going to be with an MRI. Like I talked about before when we were talking about our TIA. So MRI is a better test than a CT. It does a much better job at determining acute infarction. But the reason why we use CT compared to MRI more commonly is because MRI is time consuming. CT just takes a few minutes. MRI is not available at every institution. MRI has a much contraindications. So basically, again, like I went over before TIA, MRI is a better test, but it's not used as often. Most of the time, non-contrast CT is going to be your answer. It's what you'll probably use in real life. All right, so once you've done your neuroimaging, you've done a finger stick. Make sure this patient's presentation is in due to severe hypoglycemia. You have some additional tests as part of your workup. Let's first talk about your EKG. So you get an EKG because you want to know, does this patient have an arrhythmia? Do they have AFib, a flutter, which may have been the cause of an embolic stroke? And is this patient going to be started on anti-coagulation to prevent future strokes from this cardio-embolic source? Another thing you're going to use as your ancillary testing is an echo. So echo cardiogram. So with your echo, you're looking to detect cardiogenic and aortic sources of cerebral embolism. So basically, you're looking-- is there another bullet left in the chamber? Does this patient have another clot in the heart that could potentially lead to another stroke? Is there vegetation on the heart valves, from endocarditis, et cetera? So echo cardiogram is another important test. And then neurovascular imaging, like we talked about before, CTA, MRI. Main thing is you want to rule out a large artery occlusion. Make sure this patient isn't a candidate for something called a mechanical thrombectomy, which will go over in a minute. So those are your ancillary tests, your echo, your EKG, your neurovascular imaging. The main diagnostic test they'll focus on your non-contrast CT. That's going to be the one you get when they first come in. I'm the host of Big Technology podcast, a longtime reporter and an on-air contributor to CNBC. So each week on Big Technology, I bring on key actors from companies building AI tech and outsiders trying to influence it, asking where this is all going. They come from places like Nvidia, Microsoft, Amazon, and plenty more. 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The risks are actually going to outweigh the benefit of using TPA. There are some exceptions to the time that I'm going to go over in a minute, but most patients are going to be within that 4.5 hours of onset. Then the other thing is that you want to make sure is that this patient doesn't have any contraindications to TPA. There's a whole laundry list. I wouldn't recommend memorizing them. But if you want to remember a few of the important ones, I do have a little mnemonic. So instead of remembering TPA, I want you to add on a couple of letters and make it T-Pain, aka the wrapper, Mabayo drink. So remember T-Pain, instead of TPA, and remember T-Pain is 45. That's how you're used to remember some of the main contraindications for TPA. So T-Pain is 45. What that stands for? The T stands for trauma to the head in the last three months. So any kind of severe head trauma in the last three months is going to be a contraindication of TPA. The P stands for platelet count less than 100,000. A stands for active internal bleeding. The I stands for intracranial hemorrhage ever in their lives. The N stands for neurosurgery in the last three months. So any kind of intracranial or intracinous surgery, the I and T-Pain is stands for intestinal malignancy or intestinal hemorrhage in the last 21 days. The S stands for stroke. Specifically, we're talking about an ischemic stroke in the last three months. And then the 45, T-Pain is 45, stands for then 4.5 hours. So let's talk about the 4.5 hours for a minute. So there's a few warnings, not absolute contraindications to the 4.5 hour window, where you have to weigh the benefit of a risk. So in certain patients, this 4.5 hour, it's caution that maybe it shouldn't be 4.5, but maybe three in certain patient populations. So these patients are patients that are over 80. Patients that have a severe stroke classified by the NIH SS score. Patients that are on oral antidequagulants or patients that have a combination of both previous ischemic stroke and diabetes malitis. Then generally, it's safer to be within three hours, but not an absolute contraindication. You kind of have to weigh the benefit for a risk. So that's just something to consider. Most patients will be within that 4.5 hour. So as other patients, you just want to kind of weigh the benefit for a risk. See, maybe it should be within maybe a three hour window. Second treatment that I wanted to talk about is a mechanical thrombectomy. So a mechanical thrombectomy, you have an interventional radiologist or another type of surgeon that goes in and literally just pulls the clot out. Works great, can be done in up to 24 hours compared to 4.5 hours that there's a section with TPA, but the problem is not every hospital is equipped to perform the type of procedure, and it can only be used in patients that have a large artery occlusion in the anterior circulation. So other patients aren't going to be eligible. It is a great alternative to TPA 'cause obviously there's way less risk with this. It's a minimally invasive procedure, but the problem is it's not going to work with every patient. You have those exclusions that I talked about there. Okay, so those are your main treatment options. Let's talk about blood pressure for a minute 'cause blood pressure is interesting. So in patients with an ischemic stroke, you don't touch their blood pressure unless their blood pressure is too over 220 over 120. So either a systolic over 220 or a diastolic over 120. or if you're gay. giving them TPA, then you have to make sure you manage their blood pressure once it reaches a point of 185 or higher or 110 or higher. So let's talk about that again. So blood pressure in patients with a schemic stroke, if they're getting TPA, you want their blood pressure less than or equal to 185 and diastolic blood pressure should be less than or equal to 110. That wasn't in the mnemonics, so just be aware of that as well. If they're not getting TPA, you can actually let their blood pressure ride all the way up to 220 over 120 before you have to intervene. So why is that? Well, let's think about that. Well, you have this clogged up cerebral artery. There's not much blood getting past this occluded area and perfusion pressure distal to that obstructed vessels actually really low. So this elevation and blood pressure, it's actually helping to maintain brain perfusion past this point in those schemic areas. So most of the time, you actually don't want to turn down the pressure in a schemic stroke. Some of your adjunct and your long-term management treatment options, let's talk about that too. In addition to TPA, you're throwing back to me. There's a lot of interventions for a schemic stroke that reduces the complications and reduces stroke recurrence. So one, just like in our TIA, we have our antiplatelet therapy, aspirin, clopidogrel. If they didn't get TPA, the knee-toe antiplatelets generally, it's going to be 325 milligrams of aspirin. If they had TPA, you have to wait at least 24 hours before you give them antiplatelets. Also statin therapy, this one's really important. There's clear evidence and studies that long-term invasive statin therapy is associated with a reduced risk of recurrent ischemic stroke. And then of course, lifestyle changes, smoking cessation, exercise, weight reduction, controlling blood pressure, controlling diabetes, et cetera, to produce, to reduce the risk of a future stroke. So that was our ischemic stroke. So let's talk a little bit about our intracranial hemorrhagic strokes. I wanted to briefly touch on some of these intracranial hemorrhagic including some of the causes of our hemorrhagic strokes. I'm just going to focus on the basics. I'm going to give you some mnemonics. Diagnosis is pretty similar across the board for these with the CT and most cases. Treatment is generally not going to be tested on. It can range from supportive measures, clips and coils all the way up to craniotomy and severe cases. Okay, so let's start with epidural hematoma. So an epidural hematoma is bleeding between the skull and dura matter. So it's a collection of blood that forms between your skull and the dura matter. Fatal meninjial artery. So bleeding typically arises from the middle meninjial artery and a lot of times it's associated with a temporal skull fracture, particularly seen in children more common. Lucid interval. In the vignette, an epidural hematoma, they're always going to mention the patient had this loss of consciousness. Then it was followed by this lucid interval where they had this transient recovery. So this lucid interval where they got a bit better for a period of time. That's the key to look out for the end of vignette. If you see lucid interval, right away, be thinking of an epidural hematoma on your CT. You're going to have a convex shaped bleed. So you're going to have this bleeding that the outline or the surface is curved like the exterior of a circle or a sphere. It's hard to describe these things without visuals. So really there's three things that you have to know. You need to remember your middle meninjial artery tear. You have to remember the convex bleeding on the CT and be able to recognize that on the CT image. And then you need to remember that lucid interval. The way that you remember that is when you think of epidural hematoma. I want you to think about those first three letters and epidural hematoma. So EPI, if you rearrange those letters, you have the word pi. You can also, the second two letters, PI is spelled pi like, PI like the mathematical term pi. So however you get there, as soon as you see epidural hematoma, I want you to think of a pi. And I want you to think of the sentence, a lulu lemon pi, a lulu lemon pi. So what is that stance for? So M a. So M m a stands for middle meninjial artery. So a and then lulu lemon pi. I'm sure you've all heard of lulu lemon. That's like the athletic company that makes the leggings and stuff. So lulu lemon lulu stands for lucid interval. So L U L U. As soon as you see lulu, think of lucid interval. It's associated with the epidural hematoma. And then lemon is actually because in this makes sense when you look at the CT image. But if you look at a CT image, you have a convex shaped bleed. It looks exactly like the side of a lemon. And I have a picture on my YouTube channel. You can see it, but the bleed as soon as you see a CT image and it looks like there's like half a lemon on the CT sticking out, you'll be thinking of an epidural hematoma. So that's why I have lemon pi. So as soon as you see epidural hematoma right away, be thinking of pi, epi, epi, rearranged pi, epidural hematoma, mm, a lulu lemon pi, mm, a middle meninjial artery lucid. That's going to be your lulu and then lemon. Think of your lemon or convex shaped bleed on the CT. All right. So that is your epidural hematoma. Let's move on to our subdural hematoma. So this is bleeding that forms between the doora and the arachnoid membranes, overline the brain. Bidling veins tear. So an acute subdural hematoma is usually caused by tearing of the bridging veins located between the arachnoid membranes and the doora. So bridging veins remember that that's really important for subdural hematoma that will likely come up. Now as far as the patients are going to see this in, elderly alcoholics. So in a vignette, the patient will likely be elderly or an alcoholic who had some kind of trauma, a fall motor vehicle accident. The reason that we see this more commonly in this patient population is because cerebral atrophy is common in both older adults and those with the history of chronic alcohol abuse. Srebral atrophy results in this larger space between the dural membrane and the cortical surface of the brain and that increases tension on these bridging veins. So in these patients fall, they have a traumatic brain injury like in an MVA, these bridging veins. They're more susceptible to tearing because they're stretched and pulled across this greater distance. So in a C-T, you're going to have a crescent shaped hematoma. So crescent shaped appearance because the bleeding follows the contour of the overlying doora and it looks, I'm sure we've all seen a crescent moon, just that little sliver of moon. That's what it looks like on a C-T. So the way that you remember the things that you need to know for your subdural hematoma is instead of subdural as in du-ur. So subdural hematoma. I remember subdural hematoma. So SUV, D-O-O-R, all. So subdural hematoma and then doora stands for drunk old overpass because an overpass is another way of saying bridge and that helps you remember your bridging veins. And then the R-endore is the second letter in crescent. So subdural hematoma, drunk old, that's your patients that you'll see it in, overpass, that's your bridging veins. And then crescent, the R-endore is the second letter in crescent because you have a crescent shaped hematoma on CT. So that is your subdural hematomas. Let's move on to our subarachno and hemorrhage. So a few things you need to know about subarachno and hemorrhage. So this is going to be an extravization of blood into the subarachnoid space between the Pia and the arachnoid membranes. You're bleeding within the meninges into the ventricles. Berry aneurysm rupture is going to be your most common cause. So rupture of a berry aneurysm, which is also known as a sacular aneurysm, it's going to be your most common cause of a subarachno and hemorrhage. So this is a very important subarachnoid. So this is a very important subarachnoid embankment. This is important severe headache, aka worst headache of my life. So subarachno and hemorrhage has a very specific clinical presentation. I'm sure most of you have heard of this before, probably even before Pia school. So patient with a subarachnoid embankment will often describe having the worst headache of their life. So also known as a thunder clap headache because all of a sudden when they have this headache, the severe headache, it's not an insidious onset. It's this patient is feeling completely normal. And then all of a sudden they have this 10 out of 10 headache in a matter of minutes. So the same way like thunder all of a sudden just hits out of nowhere. That's the severe headache. It's also known as a thunder clap headache. Mininjial symptoms. So this is really important as well because these patients may have symptoms of meningial irritation, which is also known as meningism. So you look for a nuical rigidity, photophobia, lower back pain. It can occur as and as many as 80% of patients. And it's from the breakdown of blood products in this ESF, which leads to this aseptic meningitis. And then finally the diagnosis is a little bit different with the subarachnoid because we always talked about the CT. I talked about that earlier. But with the patient with a subarachnoid hemorrhage, you want to consider a lumbar puncture. Now you're going to get your CT like you did in all of your other types we went over. But in a patient with a negative CT that you really suspect may have a subarachnoid hemorrhage, you have to go a little bit further. You have to get a lumbar puncture. And this is going to be on your vignette where you look for on the lumbar puncture is something known as xanthochromia. And it's this yellow tingeed CSF, which is from Billy Rubin in the CSF indicating old blood. So if both the CT and the LPR negative, you've essentially rolled out a subarachnoid, but you need both to say definitively in patients with a high clinical suspicion because this can be fatal. So you don't want to miss it. Interest cerebral hemorrhages is the last one over. There's very little to know for this. There's not really much unique about it. And most things that don't have a lot unique about them are often not tested on. But an interest cerebral hemorrhage, it's bleeding into the brain perencoma. It's the second most common cause of stroke after a schemic stroke. And then what you need to be looking for is an patient, an older patient, older age and hypertensive. So the risk for interest cerebral hemorrhage increases with advancing age. In addition, the most common etiology of a spontaneous interest cerebral hemorrhage is hypertension. So look out for that. So elderly patients hypertension, those are the main ones you need to know of and then be aware of some of the other causes that are also common as well. So amyloid angiopathy. empathy, ruptured vascular malformation, but focus on hypertension that's the most comedy theology. Alright, so that is stroke. Let's do five quick questions to see what you've retained. So question one, 67 year old male with history of hypertension and hyperlipidemia arrives to the emergency department accompanied by his wife and daughter. His family members state he is unable to speak and he has not been able to lift his right arm. When you ask the patient to pop out his cheeks and smile, you know, a prominent drooping on the right side of the face. His patient likely has a stroke of which cerebral artery. So that is going to be your middle cerebral artery. So left side it's specifically as we see control lateral involvement of the right upper extremities. We see control lateral involvement the right side of the face and then aphasia. Remember your middle cerebral artery, your mad, your middle cerebral artery, your raising your arms up in the air. It's patient has right arm involvement. Your face is red. This patient has drooping on the right side of the face and then you're yelling. Remember your aphasia. This patient has trouble speaking. So middle cerebral artery left side it's specifically in this patient. Question two, 63 year old male presents today to the emergency department complaining of next stiffness and a sudden onset severe headache unlike any other he has had before. His past medical history includes only hypertension. While speaking to him, you notice he is squinting his eyes and asks if you can dim the lights. You order a CT of the head, which is negative, which additional test should be performed for the suspected diagnosis. So that is going to be a lumbar puncture. This patient has a history of a severe headache, which he describes came on suddenly. That's our thunder clappetic. In addition, he has meninjial symptoms. So photophobia. Remember he's asking the doctor to turn on the lights. Nucleurogenicity. That's stiffness of the pain of the neck. No history of migraines. So we should be suspecting a subarachnoid hemorrhage in this patient. And you start with your non-contrast CT. If that's negative, you have a high degree of suspicion for subarachnoid. You need to also order your lumbar puncture, which you'll be looking for again, Sanctocromia, which is from the breakdown of the red blood cells in the CSF. Question three, 76-year-old male company by his daughter has been diagnosed with an acute ischemic stroke. His blood pressure is 168/92, oxygen saturation 96%, pulse 88, temperature 98.3. He was known to be well two hours ago when his daughter spoke to him by phone. She states he has a history of hypertension, type 2 diabetes, and celiac disease. She's very worried about him as stating this is his second ischemic stroke in the last three months. And this patient be an ideal candidate for TPA, if not why. So that's going to be no, because he has a history of a schemic stroke in the last three months. Schemic stroke in the last three months is part of the exclusion criteria for IV thrombolysis TPA. So one of the many, again, I don't expect to remember all of them, but this is one of the important ones. And just remember, T pain is 45. You can remember the important ones. Question four, which artery is the most common to be involved in an ischemic stroke? Remember middle cerebral artery, MCA, most common artery. And that's going to be in around 70% of the cases. It's going to be your MCA that's going to be involved in an ischemic stroke. Question five, patient being treated for a schemic stroke is greeted by the treating physician who informs him they're going to administer a medication called Nicarter Peme into his IV to start lowering his blood pressure. He is unable to receive TPA due to gastrointestinal malignancy. The blood pressure in this patient has likely exceeded what systolic and/or diastolic level. So that is going to be systolic over 220 and a diastolic over 120. So patients with a schemic stroke were not going to be treated with thrombolytic therapy. We stated this patient is not a candidate due to the GI malignancy. We don't need to worry about those BP guidelines, but this patient that's not going to be treated with TPA should not have their blood pressure treated acutely unless the hypertension is extreme. That's going to be a systolic blood pressure over 220 or and/or diastolic blood pressure over 120. So remember, these patients with a schemic stroke, the perfusion pressure distilled to the obstructed vessel is low. So we need to keep that pressure high enough to maintain brain perfusion only if it's systolic over 220 and/or diastolic over 120. Do we treat like in this patient? All right. So that was your stroke. Hopefully that was helpful. Thank you so much for listening. And thank you as always for all of the really nice comments. I do appreciate it. You could look in PA school, your pants, your pen, and your EORs. Every day the world gets a little weirder and a lot more awesome. As for cool stuff daily as we take a quick look at science, tech, and the wait what stories that make you sound way smarter at dinner. Subscribe to cool stuff daily now because the future is happening fast and it's way too fun to miss.