All right, so this podcast is going to be on stroke. I have a few pnemonics 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 a schemic 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 this resolved, 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. Clot dissolve 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 twenty four hours.
You may still hear about that in clinical as your preceptor. It's something that we used to use a while ago before we had MRI neuroimaging. The d emphasis 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, They're symptoms resolved in less than twenty four hours, so time based definition of a TIA, But then when they actually had an MRI done, they showed stroke on their MRI and in FARCT, so just be aware of that kind of try to get that time based definition out of your head. Focus on the tissue you based definition of a TIA, which is lack of tissue and farction. Visualize on neuroimaging m R, 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, an hour or so, and 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 amaurosis few gas and corodi brewy so amurosis few gas. 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 TIA's. 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
crodd artery circulation. This leads to hypoperfusion of the ocular arterial circulation. So basically your crodids are clogged, your eyes aren't get perfuse, and this temporarily shuts off the lights. That's am rosis, feu gacks, and the vignette. The way you'll see it described is as a curtain coming down in front of their eyes that generalize darkening or shadow in one eye. It can last a few seconds up to around thirty minutes. If you see it on a
vignette right away, be thinking of a tia. The other thing karadd brewing. So on physical exam you oscill tate the karateds. You hear this turbulent flow through the karads and this is due to after asclerotic plaque in the charatic arteries causing stenosis, and it can be a major cause of not only just a tia, but also in a schemic stroke. All right, now, let's talk about diagnosis. I'm going to briefly run through the diagnostic tests because
the thing is the workup. It's very much the same as in stroke, which I'm gonna go over next to more detail. The idea is though with the TIA is you start with your neuroimaging 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 time consuming, it's expensive, there's contraindications, so
t 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 MRA CCA crodi ultrasound. It's really important in patients with a TIA to rule out in 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 afterosclerotic disease? Do you have crodo stenosis? Because once you find your source, you can direct your secondary prevention at that afterrosclerotic disease, or you can intervene even with like a crowded and art directomy for instance. So that's really the cornerstone of your diagnostic workup for TIA. That's what i'd memorize. Your neuroimaging with CTR MRI and your neurovascular imaging MRA ct e CE. You also have your ancillary test. These aren't as important, but
I'm going to talk about them. Just you have an idea, so ec ECG to roull out, say a fib eco cardio gram where you're looking for your cardio embolic source for the TIA. Lab tests to 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 and rule out low blood sugar in those types of things. Now, treatment, there's a few things that you need
to know. So anti platelet treatment this one's really important. So aspirin or a combination of aspirin and clopidogril. This is probably the most important intervention to remember for TIA. So for almost all patients with the TIA who do not have a known cardio embolic source, so this isn't from like a fib throwing a clot. We start with anti platelet therapy, so this can be aspirin
is monotherapy or dual anti platelet therapy asprein and clopiedigril. You decide that depending on the on the risk score, which we'll talk about in a little bit. So remember that anti platelet treatment for almost all TIA patients. Now, if they have a cardio embolic source, you're going to use anti coagulation. So if they have I said before they have a FIB, you're going to start them on oral anti coagulation with warfarin or a direct oral anti coagulant to
prevent future emboli. So if it's a cardiomobolic source, your treatments a little bit different. And then you have your a little bit more invasive treatment, so crowded end artirectomy or crowded artery stentting. So if you see a neurovascular imaging the patient has significant crowded artery stenosis. Specifically, what we're looking for
is internal crowded artery stenosis fifty to ninety nine percent. You're going to intervene with revascularization of the crowd is, which can be done via an end ardirectomy. Or credit artery stentting, so you're looking for stenosis fifteen to ninety nine percent. And then also in the guidelines it says patients should have a life expectancy of over five years. All an end ardirectomy is is you basically cut open that crowded artery that has the stenosis in it, you pull out the
plaque, you suit, youre a backup. That's what an end ardirectomy is, or you have the options with stenting as well. Then finally for treatment this is important too. So you're intense 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 glycimic 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 generally 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 a sprinklopedograp that's going to be most of your patients with the TIA. And then remember reduce those
modifiable risk factors. That's the cornerstone of TIA long term management. Let's talk about one last thing for TIA. So there's something for your stroke risk called your ABCD square and I'm quoting up to date here, but up to Date calls the ABCD square AT 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 square IT score helps you determine a few things. So a patient that has a TIA 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 a type platelet therapy with aspirin and clop pedigreal, all depending on their score. And then finally helps you determine is the patient that's present in your office to day and the er going to get the full million dollar TIA work up or do they maybe just have complicated migraine and maybe we
don't need to do every diagnostic test in the book. So how high is their risk? So this calculator helps guide you with these types of things. So again, the assessment tool is known as the abc D square tool. Do not memorize it. Just be aware that it exists for stroke risk ratification. 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 square it stands for age sixty or over. That gives you one point blood pressure one forty systolic or a ninety or higher diastolic. That's another point. Clinical features, depending on what their features are, unilateral weaknesses two
points, isolated speech disturbances 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 if 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 a schemia without acute infarction. Remember Amurosi's few backs. That's probably the most important clinical manifestation. And then for treatment, I'd say the one thing you should definitely remember is your anti play lit treatment with aspirin. All right, So that's your tia. Let's move on to a stroke, all right. So for stroke, there's two
types of stroke. There's a schemic and hemorrhagic. So a schemic that's going to be your most common type, around seventy five to eighty percent of all strokes. And that's the one that will 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 schemic stroke, let's start with the schemic strokes. This is the one you need to
focus on. An aeschemic stroke is a sudden loss of blood circulation to an area of the brain, leading to death of tissue and loss of neurologic function. A schemic stroke is a compromised blood vessel leading to decreased profusion resulting in death of brain tissue. So remember in a tia, the clot dissolve 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 schemic stroke. There's thrombodic and there's embolic. So thrombodic is going to be by far, you're 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 athrosclerosis 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 in to plug it up and a thrombus forms around the plaque. This leads to inclusion of the blood flow distal to this area, which leads to the stroke. Second type is embolic, So embolic means the clock came from somewhere else in the body. It travels from a distal site, got lodged in the vessel of the brain and included the vessel.
Common cause of embolic stroke as a fib patient, as a fib throws, a clot from the heart clock gets lodged in the vessels of the brain, leaving you to stroke. If you ever forget which is which, like is a rombiotic or embolic the one where the clout traveling from somewhere else. The way that I remember that is embolic starts with an EE stands for elsewhere, aka, the clout 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 aclusion, 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 Anosky question and 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, et cetera. I do have a couple of 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 in a vignette. 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 contralateral involvement of the feet and legs. This is the most common area to be involved contralateral 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 continence, as possible to have weakness in the upper extremities, but the most common what's going to be on the vignette where you need to focus on is some kind of deficit in the lower extremities, so paralysis and sensory loss and the contralateral leg and foot. So how do you remember that antior cerebral artery stroke. As soon as you see antiior 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. Anterior cerebral artery stroke most commonly affects the contralateral leg and foot. So when you see ant tior cerebral artery stroke, think of an ANT on the floor, lifting your legs, stepping it on with your foot. Most commonly affects the contralateral leg and foot.
That's how you remember the most common presentation of anterior cerebral artery stroke. Think of an ant stepping up with lifting up your leg, stepping in up 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 eschemic 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 most common artery to be involved in an eschemic stroke. While you're looking for in the vignette is contralateral face in arm involvement as well as a phasia, So paralysis and sensory loss is going to be createst on the contralateral side of the face and the arm verse the lower extremities, and you also may see a phasia and middle cerebral artery stroke. A phasia, remember, is difficulty producing or understanding speech.
The way that I always remember this was instead of remembering middle cerebral artery MD D L E instead of middle cerebral artery. I remembered mattle 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 mad maddele cerebral artery. And think of somebody that's very mad. Think of like that cartoon image. Whenever 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 like shake it and then they like scream. They're like, ah, So that's what I want you to think of middle cerebral artery. Think of mad dule cerebral artery. I think of that cartoon character. His face is red and his face is red because remembering and commonly involves the face, the controlatero side of the face. That helps you 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 contralateral 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 you remember not necessarily that the patient with middle cerebral artery stroke is gonna be yelling, but it helps you remember, okay, the voice is involved, and then helps you remember a pass remember middle cerebral artery stroke. Think of madle cerebral ar restroke. Somebody's very mad. Arms
are up in the air, shaking them up in the air. That helps you remember the contralateral arm involvement. Their face is all red because they're angry. That helps remember the contra lateral side of the face. And then they're yelling, they're screaming. That helps you remember the aphasia the voice involvement. All right, So let's move on to our post serial circulation, specifically the post sious cerebral artery and the vertebra basler artery in general. If they mentioned
any kind of visual changes, you should be thinking posterior circulation. I wanted to break it down a little bit further though each individual 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 pc A 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 pc A stroke. So it's a visual defect involving the contralateral 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
contralateral side. That is homonymous, I mean enopia. 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 it back to you. And the way that I used to 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 posterious cerebral artery stroke, I 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, it makes much
easier. But if you think of two peas on their sides, they basically look like glasses, and that always helps for me. Remember, I just have this visual of two peas on their sides like glasses that it involves the eyes, the homonymous hemianopia that helps me remember two pieces glasses. Posterior starts with the P post serious cerebra auttery. 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 personal computer assistant, because Alexia sounds like Alexa, like Amazon Alexa and Amazon Alexa as a person 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 pneumonics, but that's the way that I used to remember it. Let's move on to the last thing,
which is going to be our vertebral basil or artery stroke. Now, the good thing about vertebro basel or attery stroke is most of the things you'll see in a vignette, most of the clinical manifestations all start with the V, and vertebro based lare auttery stroke also starts with the VS. So as soon as you see fortebro based law auttery stroke, think of all of your
V clinical manifestations. That's going to be vertigo, visual changes like diplopia, vomiting, and then the last one I kind of made this up on my own, but vibrating eyes because nice stagmus is another possible presentation of vertebral based law auttery stroke. And if you ever look at nice stagmus, 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, vertebro based lore
attery stroke. Remember they all start with VS. Those are clinical manifestations. If you remember that, you'll likely be able to pick it out on a vignette. Let's talk about diagnosis. So this is obviously going to 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 going to 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 want to make sure the presentation isn't due to hypoglycemia. Hypoglycemia can cause focal neurologic deficits that mimic a stroke so much. You must roll that out right away because 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 their 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 reperfusion therapy with intravenous thrombolysis like TPA, it's off the table. So again CT initial test of choice use 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 schemic stroke, but really the best way to look for a cute schemic stroke is going to be with an MRI,
like I talked about before, when you're 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's time consuming. CT just takes a few minutes. MRI is not available at every institution, MRI has a bunch of contraindications. So basically, again like over before, TIA MRI is a better test, but it's not used as often. Most of the time, non contrast CT it's
going to be your answer. That's why 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 isn't due to see your hypoglycemia. You have some additional tests as part of your work up. So 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 a fib A flutter which may have been the cause of an embolic stroke, and is this patient going to be are it 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 if 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 vegetations on the hart valves? From endocardiis, etc. So echo cardiogram is another important test, and then neurovascular imaging like we talked about before, its CTA MRA. Main thing is you
want to rule out a large artery oclusion. Make sure this patient isn't a candidate for something called a mechanical thromback to me, which we'll go over in a minute. So those are your ancillary tests or echo, your KG, 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 treatment que treatment. There's two things that you need to know TPA that's the really
big one, and then mechanical thrown back to me. All right, let's start with our thrombolytics. All to place aka TPA. So out of place is a thrombolytic drug. It's a clopbuster and its first line therapy for acute eschemic stroke patients. If it's initiated within four point five hours of symptom onset, and after four point five hours, there's really no point 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 four point five 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. And there's a whole laundry list. I wouldn't recommend memorizing them, but if you want to remember a few of the important ones,
they do have a little mnemonic. So instead of remembering TPA, I want you to add on a couple letters and make it t pain AKA the rapper may buy you a drink. So remember T pain instead of TPA. And remember T pain is forty five. That's how you used to remember some of the main contradications for TPA. So T pain is forty five. 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 contradication of TPA. The P stands for plately count less than one hundred thousand. A stands for active internal bleeding. The I stands for intracranial hemorrhage. Ever in their lives, the end stands for neurosurgery in the last three months, so any kind of intracranial or intraspinal surgery. The I N T pain IS stands for intestinal malignancy or intestinal hemorrhage in the last twenty one days. The S stands for stroke specifically, we're talking about
an aschemic stroke in the last three months. And then the forty five T pain IS forty five stands for then four point five hours. Let's talking about the four point five hours for a minute. So there's a few warnings, not absolute contradications to the four point five hour window, where you have to weigh the benefit verse risk. So in certain patients this four point five hour, it's cautioned that maybe it shouldn't be four point five, but maybe three
in certain patient populations. So these patients saw patients that are over eighty, patients that have a severe stroke classified by the nih SS score, patients that are on oral anti coagulants, or patients that have a combination of both previous ischemic stroke and diabetes molitis. Then generally it's safer to be within three hours, but not an absolute contraindication. You kind of have to weigh the benefit first risk, So that's just something to consider. Most patients will be within
that four point five hours. Those other patients you just want to kind of weigh the benefit verse risk, see maybe should they be within maybe a three hour window. Second treatment that I wanted to talk about is a mechanical thromback to me. So a mechanical thromback to me you have in interventional radiologists or another type of surgeon that goes in and literally just pulls the clot out works great, can be done in up to twenty four hours compared to four point
five hours. That you know the restriction with TPA, But the problem is not every hospital's equipped to perform the type of procedure, and it can only be used in patients that have a large arteryclusion the anterior circulation, so other patients aren't going to be eligible. It is a great alternative to TPA because obviously there's way less risk with this to mind only evass 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, because blood pressure is interesting.
So in patients within a schemic stroke, you don't touch their blood pressure unless their blood pressure is two O two twenty over one twenty, so either a systolic over two twenty or a diastolic over one twenty, or if you're giving them TPA, then you have to make sure you manage their blood pressure once it reaches a point of one eighty five or higher or one ten or
higher. So I'll talk about that again. So blood pressure and patients with a schemic stroke, if they're getting TPA, you want their blood pressure less than or equal to one eighty five, and diastolic blood pressure should be less than or equal to one ten. That wasn't in dedemonic, 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 two twenty over one twenty before you have to intervene. So why is that, Well, let's think
about that. When you have this clogged up cerebral artery, there's not much blood getting past the secluded area, and profusion pressure distal to that obstructed vessels actually really low. So this elevation and blood pressure, it's actually helping to maintain brain profusion past this point in those of schemic areas. So most of the time you actually don't want to turn down the pressure in an a schemic stroke. Some of your adjunct and your long term management treatment options, let's
talk about that too. So in addition to TPA, you're thrown back to me, there's a lot of interventions for schemic stroke that reduces the complications and it reduces stroke recurrence. So one, just like in our TIA, we have our anti platelet therapy asprinklopiedigrop. If they didn't get TPA, they need anti platelets. General it's going to be three hundred and twenty five milligrams of aspirin. If they had TPA, you have to wait at least twenty four
hours before you give them anti platelets. Also, statin therapy, this one's really important. There's clear evidence and study is that long term invasive statin therapy is associated with a reduced risk of recurrent eschemic stroke. And then of course lifestyle changes smoking cessation, exercise, weight reduction, crolling blood pressure, controlling diabetes is set to produce to reduce the risk of a future stroke. All Right, So that was our eschemic stroke. So let's talk a little bit
about our intracranial hemorrhages, our hemorrhagic strokes. I wanted to briefly touch on some of these intracranial hemorrhages, including some of the causes of our hemorrhagic strokes. I'm just going to focus on the basics. I'm gonna give you some demonics. Diagnosis is pretty similar across the board for these with the ctmmost cases, treatment is generally not going to be tested on. 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 duram matter. So it's a collection of blood that forms between your skull and the dura matter middle mini indual artery. So bleeding typically arises from the middle minigual 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, and 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 lookout for the evenend the 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 gonna have this bleeding that the outline or the surface is kind of 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 minigual artery tear. You have to remember the convex bleeding on the CT and be able to recognize that on a 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 in epidural hematoma, so EPI. If you rearrange those letters, you have the word pie. You can also the second two letters PI is spelled pie like pi like the mathematical term pie. So however you get there. As soon as you see epidural hematoma, I want you to think of a pie, and I want you to think of the sentence m A Lulu lemon pie, A Lulu lemon pie. So what does that stands for? So m A. So mm A stands for middle meningual arteries,
so m A. And then Lulu lemon pie. 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 Lulu, as soon as you see Lulu, think of lucid interval that's associated with your epidural hematoma. And then lemon is actually because and 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 and 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 pie. So as soon as you see epidural hematoma right away, be thinking of pie epi epi rearranged pie pie epideral hematoma, A lulu, lemon pie, a middleman, and you'll 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 dora and the arachnoid membranes overlying the brain bridging veins tear. So an acute subdural hematoma is usually caused by tearing of the bridging veins located between the arachnoid membranes and the dura,
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, a 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. Cerebral 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. On CT, you're gonna have a crescent shaped hematoma, so crescent shaped appearance because the bleeding follows the contour of the overlying dura 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 CT. So the way that you remember the things that you need to know for your subdural hematoma is instead of subdural as in you are so subdural hematoma, I remember subdural hematoma,
So sub d O O r all, so subdor all hematoma. And then door stands for drunk old overpass because it overpasses another way of saying bridge, and that helps you remember your bridging veins. And then the R endoor and indoor 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 indor 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 suboracnoin hemorrhage. So a few things you need to know about suberacto and hemorrhage. So this is going to be an extravasation of blood into the suborachnoid space between the pia and the arachnoid membrane, so you're bleeding within the Meninji's into the ventricles. Very aneurism rupture is going to be your most
common cause. So a rupture of a very aneurism, which is also known as a sac or aneurysm, it's going to be your most common cause of a suboractoine hemorrhage presentation. This is important severe headache aka worst headache of my life. So suboracto and hemorrhates has a very specific clinical presentation. I'm sure most of you have heard of this before, probably even before PA school. So patient with the suberacto and hemorrhage will often describe having the worst headache of
their life. It's also known as a thunderclap 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 ten out of ten 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 thunderclap headache.
Meningual symptoms so this is really important as well, because these patients may have symptoms of meningeal irritation, which is also known as meningismus. So you look for nucual rigidity, photophobia, lower back pain. It can occurs in as many as eighty percent of patients and it's from the breakdown of blood product in the CSF which leads to this aseptic meningitis. And then finally the diagnosis is a little bit different with a subarachnoid because we always talked about the CT.
I talked about that earlier. But with a patient with a subarachnoid hemorrhage, you want to consider a lumbar puncture. Now you're gonna 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 from the lumbar puncture is something known as xanthochromia, and it's this yellow tinged CSF which is from Billy Rubin and the CSF indicating old blood. So if both the CT and the LP are negative, you've essentially rolled out of suberachnoid. But you need both to say, definitively in patience with a high clinical suspicion because this can be fatal, so you don't want to miss it. Into
cerebral hemorrhage is the last one I'll go 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 to not test it on. But an interestcrebral hemorrhage. It's bleeding into the brain perencuma. It's the second most common cause of stroke after a schemic stroke. And then what you need to be looking for is a patient, an older patient, older age, and hypertensive,
so the risk for interest cerebral hemorrhage increases with advancing age. In addition, the most common eteology 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 and geopathy, ruptured vascular malformation, But focus on hypertension. That's the most common eteology. All right,
So that is stroke. Let's do five quick questions. See what you've retain. So question one. Sixty seven 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 pup out his
cheeks and you know prominent drooping on the right side of the face. This patient likely has a stroke of which cerebral artery, so that is going to be your middle cerebral artery, so left sided specifically, as we see contralateral involvement of the right upper extremities, we see contralateral involvement the right side of the face, and then aphasia. Remember your middle screbral artery. You're mad, your mattle cerebral artery. You're raising your arms up in the air.
It's patient has right arm involvement. Your faces read this patient has drooping on the right side of the face, and then you're yelling. Remember your phasia. This patient has trouble speaking. So middle cerebral artery left sided specifically in this patient question two. Sixty three year old Mail presents today to the emergency department complaining of next stiffness and a sudden onset severe headache. Unlike any other
he has had before. His path 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 enter 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. A suspicion has a history of a severe headache
which he describes came on suddenly. That's our thunderclap headache. In addition, he has meningial symptoms, so photophobia, remember he's asking the doctor to turn on the lights. Nucle rigidity, that 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 would be looking for again xanto chromia, which is from the breakdown of the red blood cells. In the CSF question three, seventy six year old male company by his daughter has been diagnosed with an acute schemic stroke. His blood pressure is one sixty eight over ninety two,
oxygen saturation ninety six percent pulse eighty eight temperature ninety eight point three. 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 two diabetes and Celiac disease. She's very worried about him, as stating, this is his second schemic stroke in the last three months. With his patient 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 thrombolycens TPA. It's 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 forty five, and you can remember the important ones. Question four, Which artery is the most common to be involved in an ischemic
stroke? So that is going to be your middle cerebral artery member, middle cerebral artery MCA, most common artery, and that's going to be in around seventy percent of the cases. It's going to be your MCA that's going to be involved in an a schemic 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 nicartapine into his IV to start lowering his blood pressure. Is
unable to receive TPA due to a gastro intestinal malignancy. The blood pressure in this patient has likely exceeded what systolic and or diastolic level level, so that is going to be systolic over two twenty and a diastolic over one twenty. So patients with a schemic stroke, we are not going to be treated with thrombolytic therapy. We stated this patient is not it's not a candidate due to
the GI malignacy. 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 two twenty and or diastolic blood pressure over one twenty. So remember these patients with a schemic stroke, the perfusion pressure distal 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 two twenty and or diastolic over one twenty 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, and good luck in PA school, your pants, your panory, and your ears