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Virtual Didactic - Stroke Syndromes presented by M ...
Stroke Syndromes Led by Monica Verduzco-Gutierrez, ...
Stroke Syndromes Led by Monica Verduzco-Gutierrez, MD
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All right, let's go ahead and get started. Welcome to AAP virtual didactics. My name is Sterling Herring. I'm a PGY3 at Vanderbilt and we will talk a little bit more about the purpose of these didactics if this is your first time, but first we want to specifically recognize and appreciate those people who have been particularly affected by this pandemic. We recognize that for some of us, it's been a little bit more personal than for others. And so we certainly appreciate and support all of you who are being more affected by this than those of us who are a little further back from the front lines. So thank you. So again, the goals of this didactic session is to augment the didactic curricula that are currently existing in your locations and your programs, to offload overstretched faculty with some of the logistical difficulties that have been going on since this pandemic started, to provide additional learning opportunities for off-schedule residents. Again, with some of these shifts in scheduling that have occurred, we recognize that didactics have been difficult and sometimes filling that time with meaningful learning opportunities has been difficult. And then obviously to develop further learning opportunities and support physiatrists in general during the COVID-19 outbreak. Housekeeping issues. We just want to keep everybody video and audio muted. That'll be on us, but if we mute you, just know it's not personal. We're just trying to keep everything clean and bandwidth high. If you have any questions, please send them to me. You should be able to click in your, if you see a little thing that says participants, you should see Sterling Herring somewhere on that list, and you can send your questions over to me and I will ask them at appropriate times. If you have any general questions, suggestions, concerns, please send them to that email or you can track us down on Twitter. So without further ado, I'm really excited about today's presenter, Dr. Monica Verdusco-Gutierrez in San Antonio. She's the chair down there and we're excited to hear from her. So thank you for joining us. Yes, happy to be here even though my stuff on the bottom is wrong, so. Sorry about that. That's all right. Okay, so we're talking today about stroke syndromes. I will start sharing my screen. Can you also see video of me? Okay, great. So I'll just say hello to everyone first. Thanks for being here. So a couple of reasons why I give this talk. First, I do neuro rehab and stroke rehab. I really enjoy that. Secondly, it's usually one that I've given at Baylor's board review course every year for years and years and years. And it's really helpful. And not only for people who might be studying for tests, because we're not learning tests. We're doing this to learn how to treat our patients when we see patients with stroke to kind of figure out how we should be seeing them, observing them, testing them. Just kind of a trigger warning. It's a very sensitive topic. Of course, we're talking about stroke. And some of the stuff, the way I'm going to have you remember this stuff, might seem a little bit light, just because that's how I, in my brain, remember some of this stuff. Though, it is a very serious topic overall. All right, now we will get started. The other thing is, it's going to be interactive during part of it. So you are going to be using poll everywhere. So in a little while, let's show you how to get onto that, what websites are available, or how to text and answer your questions, because I want to see kind of how you are doing with the information. So we will start with this is the first question. So you can either text or respond on the internet. And this is your pre-test. So a patient's eye is turned down and outward and has ptosis. What cranial nerves affected? Right, seems like everyone's really smart this morning, great, or afternoon, depending on where you are. Okay, maybe I don't even need to give the lecture. Let's see, next one. Oh, stop, next. I moved on, you're probably still answering. So next question, locked-in syndromes, a lesion of what area? I'm not gonna give the answer yet, but just kind of pre-test knowledge of where you are. Good, good, smarty pants here. All right, a PCA stroke could cause what? Can't write, can't read, can't pee, can't climb a tree. Okay, can you, yes, all right. Great, so I'll start talking just briefly about the definition of stroke. So that's when blood supply to the brain isn't getting where it's supposed to, and you can have a focal or global neurologic deficit. And so it's both, it's kind of two oppositions. You can either have an ischemic stroke or hemorrhagic stroke and it's two different things. An ischemic, where blood's not getting to where you want it to be, and hemorrhagic, where there's blood that's in this limited waltz space and is causing compression, and that's where the damage is made. And before, we used to have, if the symptoms were greater than 24 hours, they'd call it a stroke, and if the symptoms were less than 24 hours, they would call it a TIA, but that is pretty old school now. And so now TIA is really a tissue-based diagnosis. And so I used to think, well, that person had a TIA, but they got an MRI and the MRI had a brain lesion. So how is that really a TIA? Because it wasn't transient because there was something still in the brain. Well, that's why it's changed. And so TIA is really when there's an absence of an infarction. They have symptoms, it gets better, but there's nothing on imaging. And so now, even if the symptoms go away quickly, but they have an infarct or a lesion, then it's gonna be considered a stroke. So most strokes, 80 to 85% are gonna be ischemic strokes and most are thrombotic. And so this is patients that they have a progressive deficit and it's not something that's really quick onset like you would expect an embolic one. And so for these strokes, the thrombosis, it's just a small in situ obstruction of an artery. And usually this is caused by atherosclerosis versus embolic. This is usually something, it's particles of debris that are breaking off usually from a heart chronic atrial fibrillation and causing a very quick deficit. So those are the strokes that, and they can have multiple just depending on how those little particle of debris break off. Lacunar, it's usually those are the small ones that's due to lipohyalinosis and hypertension basically. And those are subcortical and cause the pure syndromes. And then also you can have systemic hypoperfusion or kind of an anoxic injury. In hemorrhagic stroke, which is a smaller percentage, 15 to 20% of strokes, this is from weakened blood vessels that rupture and bleed and it's the blood there that makes the damage to the area. And then it's either the intracerebral hemorrhage or subarachnoid hemorrhage. And ICH, I would say the top three causes of that is hypertension, hypertension, and hypertension. So hypertension really needs to be controlled. So what about our brain anatomy? So this is what a brain, so now we're gonna go a little bit into the stroke syndromes and you have to know, okay, this is what our brain looks like. It weighs about three pounds. And I know you think three pounds may not be that much, but actually humans have a very high brain weight to body weight ratio. And that, so that makes us really special in our visible surface is the cortex and that gives us our higher level functions and intelligence. And so it's due to the neurons and into the folds. I don't know if any of y'all have ever had an MRI before, but when I had before, I'd always look and be like, okay, how are my folds? Do my folds look good? Oh, they do. Okay, I'm feeling good. And so there's actually other animals that have kind of more folded type brains and that's monkeys and dolphins. So you think those are kind of what we consider more intelligent animals versus mice, which just have smooth brains. And we have the subcortex part of the brain is gonna be below the cerebral cortex. That's our normal functioning, brainstem, midbrain, forebrain area. So just kind of think about your little walnut. It uses a lot of energy. Your brain takes up even though it only weighs three pounds but it takes a lot of our energy every day to have our brain work and do things, even though we're doing a lot of stuff subconsciously. So that's why it's affected so much, even when you have a very small period of hypoxic ischemic event, that you can get very poor outcomes from that. So the next part to know is the anatomy of the brain. And so we have two paired arteries that are bringing blood to the brain. So internal carotid arteries and vertebral arteries. And so the internal carotid arteries is gonna do our anterior circulation. The vertebral arteries are gonna do the posterior circulation. And so the internal carotid arteries, it's gonna be most of the cerebrum and the vertebral arteries is gonna be cerebellum, the brainstem, the underside of the cerebrum. And then circle of Willis. Usually when I give this lecture in real time, I like the residents to draw the circle of Willis. That's kind of a nice thing to draw, but knowing it's important when we think about stroke syndromes and what can be affected. If you have just the normal picturesque circle of Willis, then it gives you a little bit of backup. Meaning if something clogs off somewhere else, then you have a circle to kind of take over the circulation. And so that's good. I myself have had an angio and have seen that I don't have a, I have hypoplastic PCOM and it's just something that's genetic. I've been born like that. So I don't have a perfect circle, which when I found out was really upsetting, but I'll be okay. So we're gonna go into the anterior circulation first, again, coming off the internal carotid arteries. So that's gonna be anterior cerebral artery and middle cerebral artery. Posterior cerebral artery can be both either anterior or posterior circulation. And it's different for everyone. Again, there's just genetic variance. For the sake of this picture, I put it in the anterior circulation, but for a lot of people it's in the posterior circulation. So the color goes with what it covers. And then so anterior cerebral artery is the blue. It's gonna be the medial aspect of the hemispheres and the frontal lobes, basically. The middle cerebral arteries is basically the lateral aspects of the hemispheres, which is mostly parietal lobe and some temporal lobe. And the posterior cerebral artery is the posterior inferior surface of the temporal lobe in the visual cortex. And I'm going to stop sharing for a while just to show you. So when you think about this, inside, this is the ACA territory. These are the MCA territories. In the back here is your PCA territory. So again, I'm a very visual and kinetic learner, so I kind of like to see where it is on my head. So for you, that's our first part of knowing Stroke Syndrome is putting that together. Okay, back to sharing. Resume slideshow. So the next thing to look at is your cortical humunculus. And so this is where I think, okay, there is the little man that's hanging off the inside of my head, hanging on by his toes and falling down from there. So when you remember where I said, okay, in the middle was your ACA area, so that's the part of the lower motor strip, because I said that's the guy hanging on with his toes and his leg. And then when you go into the MCA part or where the parietal is, that's your upper limb motor strip is in the MCA distribution. So then that's when you start thinking MCA stroke, their arms affected more than their leg, ACA type stroke, their lower limb's going to be more affected. So kind of put the cortical humunculus together with where the vessels are going. So internal carotid artery. So we're going to start going into what the stroke syndromes actually are. So again, the internal carotid artery is a very variable syndrome. And that's the one that I call the good, the bad and the ugly, depending on what happens and what kind of circulation you have. So you may have, so for people who have ACA and MCA off the same internal carotid artery, then those are mostly the areas that are affected. So the good is no symptoms because, and that's 30 to 40% of people, and that's because they have good collateral circulation. That means they have a circle, the circle's all intact, and their circulation is great and they're not going to have any symptoms. The bad is the ocular infarction or transient monocular blindness, which is the amniorosis fugax. And that's when they just get one eye and the vision goes away. And that's because the internal carotid artery, the ends of it goes and supplies the retina. So that's when it's the central retinal artery occlusion. And a lot of, maybe 25% of patients who end up having ICA strokes will have that as their first symptom, getting that amniorosis fugax. And then the ugly is when you get a stroke there and you just infarct the whole MCA and ACA distribution, and you're going to get very severe stroke symptoms, contralateral motor and sensory symptoms. So just remember those type of, all three of those things could happen, just depends on the circulation and the presentation. So we're going to go into the MCA next. So you can see there's a picture, T2 weighted image. This is a complete area of the whole MCA distribution. And so again, MCA, we said that's the parietal area of the brain. That's the one where the arm more than the leg. So, and that's the motor strip and the sensory strip are in those areas. So that means you're going to have contralateral weakness and have hemisensory loss of the face, the arm more than the leg, and a homonymous hemianopsia. And that's because the projections of the eye fields go through there. The Pravot sign or the ipsilateral gaze preference. So we have our frontal eye fields, which are kind of in between the frontal and parietal lobes. And so your frontal eye fields is what controls your ability to move your eyes in both directions. But the one on one side helps control your contralateral movement to the opposite, looking to the opposite side. So let's say you'd have a right-sided stroke. Well, that means that that's supposed to control you looking to your left. So you're going to just not be able to look to the left. And these patients might present with a strong gaze preference to the right. So again, look at the patient, look at their gaze preference. I've seen someone on acute rehab have acute stroke. And one of the main things we noticed was this ipsilateral gaze preference. So take a look at that. If it's the dominant side of the MCA, which for most people is the left side of your brain, then you're going to get receptive and expressive aphasia. If it's on the non-dominant side, then those patients get the hemineglect as their main symptom, along with the weakness and the hemisensory loss. So now we're going to be talking about the superior division. So in this picture, you can say, okay, the superior division is mostly the parietal lobe versus the inferior division of the MCA is mostly going to be the temporal lobe. So in the parietal lobe, if the superior division's affected, then this is again, motor stripped, sensory stripped. So they're going to have weakness of the arm greater than the leg and the face, again, because of where it is. And they could have weakness of both, but the arm is usually the worst. And that's usually what you're going to see as they recover, that the arm doesn't recover as completely or as much as the leg does. And they also, then they have the contralateral hemisensory loss also. And the eye deviation that we talked about, they can get the hemianopsia as well. Then if it's the dominant hemisphere, their aphasia is going to be Broca's aphasia, just because of where the Broca's area is. And then the non-dominants where they get the hemineglect, visual spatial issues, and a prosody. So a prosody is when someone talks, their volume goes up, their volume goes down. And so patients that are aprosodic, they don't have those changes. So I have some patients that are with this type of non-dominant MCA stroke, and they'll seem very monotone or flat. Hey, Dr. Gutierrez, how am I doing with my recovery? And so it's just part of the area that was affected from their stroke. So it's something to notice when you see patients. And then usually these are embolic occlusions that cause superior division. So the inferior division, so you can kind of see the little bit difference of why in the superior division, Broca's affected, because it's kind of more on the parietal area, versus in the inferior division stroke, these patients who have dominant lesions, it's a little bit lower, it's closer to the temporal area. So they have more Wernicke's receptive aphasia if it's an inferior division dominant side stroke. These patients also have the vision loss. So it's either a homonymous hemianopsia or upper quadrant anopsia. And then the non-dominant side, they can get hemineglex, a big thing, and affective agnosia, which is inability to read people's affect. So they can't tell if someone's mad or happy, they have difficulty reading affects. And usually the motor and sensory is generally intact because that is in the superior division of the MCA. So neglect is something that I love seeing on exam. It is something that I want you to look for more when you're examining stroke patients. And there's a lot of ways to see it and it's also called unilateral neglect, hemispatial neglect, or spatial neglect. And so there's a lot of cortical areas that are implicated. So you can see there's a right side hemisphere and there's inferior parietal lobe that can be affected, a temporal parietal junction that's affected, inferior frontal gyrus, middle frontal gyrus. And so a lot of any of these areas, again, it can be, we said MCA division, even some of the frontal, so ACA divisions can be affected and can affect neglect as well. So this is usually non-dominant, but even 25% of people who have dominant lesions will have neglect. And neglect actually ends up being something that's very, a poor prognostic sign because if someone doesn't realize the left side is there, they're not gonna use it as well, they're not going to be able to wait there for walking and such. So there's so many different ways that neglect presents and different ways to test it. So it isn't always the traditional, like what you think is like the guy who just shaves on one side of his face because that's all he can see. Usually patients will try to shave both sides, but it'd be like on the left side, it's just everything's missing, you know, they didn't shave really well, and the other one might be shaved perfectly well. And a lot of times some other tests you can do, you know, you think of the clock drawing test, that's one thing to do, but you can draw a home and have them draw it, they might only draw half of it. The other one is a line bisection test. So there you have them, okay, I'm drawing the line now put a, you know, a line in the middle of it and they'll put it on the right side because they can't see the left line. And then the Albert test or the cancellation test, you put a lot of lines and ask them to put a line through the middle of the lines that they see and you can see on this one, they're neglecting all the ones on the left side. So that's some way to do it. Some patients I've seen, they eat all their food and they eat only the stuff on the right side of their plate. You can switch their plate around and then they'll start eating again because they just totally don't see what's on the left side. And then, you know, maybe it was before your time, Siegfried and Roy, they were the first Tiger Kings before the other Tiger Kings. And they were in Vegas and they'd do a show, unfortunately Roy had a tiger attack and had a big stroke and he had a non-dominant, I think it got his carotid, so ICA stroke. And one of the things that you can see from him and one thing you might see in some of your patients that have neglect is that their glasses, especially on their left side, don't go right behind their ear because they kind of can't feel, it's not feel but also know where it is and some of the spatial issues that they have. So their glasses will often be crooked because of not putting it at the right place. So just something to notice with your hemi-neglect patients. Gertzman syndrome, so this syndrome is one of the MCA syndromes. They have agraphia, so they have inability to write, acalcula, cannot calculate, finger agnosia, and left-right disorientation. So that is, you can grab their finger and say, you know, what, grab their thumb and what is this? And they don't know what a thumb is or you can grab their ring finger and they wouldn't be able to name what their fingers are. The calculation thing, we had a patient with this syndrome and we had seen him and he was an accountant. And so accountants, you expect to be able to count very simple math and these patients may not be able to add five plus six. And so you can start with, you know, just testing, asking those types of questions and you can ask them to write and they have issues with left-right disorientation as well. And so the way that I remember this one, Gertzman syndrome sounds a little bit like German or there's German spelled out in there. And so I said, when I'm in Germany, I wouldn't be able to count. I don't know German. I wouldn't know my right left because I've not ever been there before. I couldn't calculate anything. So that's kind of my way of remembering the Gertzman syndrome. So I think about being lost in Germany and I've actually now, before I gave this, I've been in Germany and I've been to Germany a couple of times. That was the last time I was in Frankfurt and you see, I don't even know up or down or left or right. So that's how I remember it. So ACA syndromes. And this one also is variable depending on where the stroke or the thrombosis is. So what's important about this picture. So number two is your ACA, which you can see coming this way off the ICA and going up into the middle to supply the inner parts of the cerebrum. And the three is the ACOM, the anterior communicating. So if you have an occlusion of one of the ACAs that's distal to the ACOM, then you're going to have a stroke on that area of the brain. Again, like we talked about the Mohawk area, the inner part of the brain. So you're going to have contralateral hemiplegia. It's going to be more of the leg than it is going to be of the hand and face. Not as much of that. You're going to get contralateral hemisensory loss, again, in that same area of more leg. Again, looking towards the lesion, we talked about the frontal eye fields being affected. Gaggen-Halton or peritonea. So that is, let me show you me again, is a peritoneal abnormal movement. And so with this, these are those patients where you try to move their arm and it seems like they're fighting you. And so you're trying to move it, they seem like they're fighting you, and that is called a peritoneal. In this case, Gaggen-Halton, which I think is German or something, to push against. And so these patients, because our frontal area of our brain is more premotor cortex, so you think about planning movements. So that's where movement's abnormal. So you'll have then movement and movement planning issues. Okay, how do I go back to where I was? They will also have grasp reflex or groping. So they sometimes go back to these frontal disinhibition signs. Gait apraxia, again, premotor cortex. So it's planning, so they have more apraxia where they might have movement, but they can't plan to do the movement, so they have difficulty with gait. They can have transcortical motor aphasia if it's on the dominant side, and urinary incontinence, because again, we have frontal control areas for urination, so they may have a lot of incontinence. So again, we said ACA, frontal lobe. So what comes with frontal lobe is some of our executive functioning, so they'll have a lot of executive dysfunctions and cognitive dysfunctions. So these are the neuropsychological features that they can have in ACA syndromes. And so one way that I like to think about ACA is, so you all recognize her? That's Brittany Spears, and at one point in her life, she just decided to shave her hair and go bald, and so she actually started in the area of her ACA, or in her, you know, right in the middle, which is part of the brain that she wasn't using oratically. So I decided she has some very famous songs you may or may not have heard that go with some of these ACA syndromes. So for ebulia, that's when patients just don't do anything. They don't want to talk. They don't have any energy to do anything. And it's almost like they're depressed, but you can't really get them to do anything. So that's her song that's called Make Me. For agitation, you know, that's pretty self-explanatory. A patient can get very agitated when they have frontal lobe lesions. That goes with her song, You Drive Me Crazy. Motor perseveration, so they will just want to either follow what you do or do things over and over again. There's a frontal assessment battery test you can do on patients, and there's a go, don't go test that they may just want to follow what you're doing. It has to do with claps, and so that one is her song, you know, Hit Me Baby One More Time. There's memory impairments. You need your higher executive functions to be able to remember things. And so that's the Oops, I Did It Again song. Emotional ability, again, is affected by our frontal lobes. And anosognosia is when you don't have insight that you have a problem. And so these are my patients that it's usually right side and right frontal, and they think they're completely fine, and that they're ready to go to work, and why can't they go to work? And this might be someone who's totally plegic, and so they're the ones who are begging to go back to work when they probably should not be going back to work, because they have just no insight into what's wrong with them. All right, if you have an occlusion at the stem of your ACA, and you have it, it's proximal to your ACOM, and your ACOM's good, then you can get collateral circulation to cover the other ACA, so that's well-tolerated, and you shouldn't have any effects. And some people have, again, they may not have an ACOM or an ACOM, it's just an ACA that's coming from the same stem, and so if you stroke out your ACA, then you're going to stroke out both of them. And so then that's like having bilateral ACAs being affected by the stroke, so you're going to have both legs be weak, so it's almost, they look like they're paraplegic, they can have the aphasia, incontinence, a lot of the frontal personality changes, the disinhibition signs and the personality dysfunction, so some of the disinhibition signs you might want to check for a glabellar tap, try, you know, look and see if they have utilization behaviors. I have some patients with a grasping, and those are ones that, you know, might get your hand and not let go. I have one that would just, like, grab onto my white coat, and if I ever had to do injections on him, we'd have to bring someone else into the room for asbestos injections, because I couldn't have him grabbing onto me while I was using a needle. So posterior circulation, we'll go into that now. So for posterior circulation, there's vertebrobasilar arteries and the posterior cerebral arteries. So these are the vertebral arteries that are going to supply the medulla, the basilar artery supplies the pons and the midbrain, and some of the longer arteries coming out are going to do the cerebellum. The posterior cerebral arteries, again, some come off the basilar, some come off the ICA, or you can have one or one, and that's going to do the underside of the brain and mostly the occipital lobe. So for PCA syndromes, again, you can see the PCA, the underside of the cerebrum, occipital lobe area, the deep branches come in here, kind of where the thalamus is and the internal capsule is as well. So again, hemisensory deficit, because it's going, again, into the thalamic area. Visual impairments, because it's occipital lobe, and so it's how you see things. Visual agnosias, so what, not being able to recognize things. Prosopagnosia, that is inability to recognize faces, which I always think is really interesting if you want to test someone for that. So sometimes this is a congenital thing. I used to have a trainee in the past and he had it congenitally. Some patients have it acquired because of a stroke. And so the way I test this is I will get, you know, we've had patients where we've showed them a picture and it could be a picture of, you know, their family member and they wouldn't be able to recognize them. Or a lot of times when I want to test this, I'll show them a picture of, you know, if it's an older person of John F. Kennedy, and most older people know who that is, but some are like, that's a nice young man. And you might think that they have this PCA syndrome that's caused issues with ability to recognize face. The other thing is this also affects their ability to recognize their own face. And so this can be an issue or, you know, when they're out in crowds or when they're looking. So the example I say is, you know, if they were to be going to a big sporting event and they would go to the restroom and there's a lot of people, you know, washing their hands with all those mirrors, they wouldn't be able to recognize which of their own faces in the mirror. And so sometimes they have to do something like when they go up to the mirror, close their eyes or make a funny face, and they know the one making the funny face or all the facial expressions is their own, and then they know, you know, they can look and see, you know, if they need to wipe anything off. Dyschromatosia has to do with inability to recognize colors. So again, you can just, if someone has a PCA stroke and you see someone that has a PCA stroke, these are things, tests you can do. So, you know, have them look at colors and say what color it is. Alexia without agraphia, so that's what it sounds like. They cannot read, but they can write. And that one's pretty striking. I might have a patient get a pen and I can write, or I'll write something, cat, and show them. And they cannot say, and they cannot read cat. And this could be an attorney or someone who's known to read really well. And then I can say spell cat, and they can just, they'll get the pen and they'll write out cat. So they can still write, but they can't read. And then memory deficits, again, it goes into this hippocampal area and fornix that affects their memory. So that's mostly the PCA syndromes. And so again, occipital lobe, think about the connection with the vision, which is why they get all these visual agnosias. And then the thalamus goes to perforating arteries, so that's where some of the sensory deficits happen. So again, they're going to get the contralateral homonymous hemianopsia. And this is a nice little picture. That is not what someone sees when they have a hemianopsia. Their brain fills in the little black side. And so they might think they see, you know, continuing of trees, but really we know when we test their, their eye fields that they can only see a little part. And sometimes that's all they have is a visual field defect. And then again, we talked Alexia with autographia, it's a very popular one, it's really interesting to see, so make sure you're testing for it. And then visual or color anemia, and that is one thing that I always think about, okay, if they have that, what does it go with? And when my daughter was three, when you're three, you should be able to know what, how many, your colors, right? So when my daughter turned three, I was trying to test her on her colors because, you know, everything has to happen on that day that they turn three or not, but, and she wasn't doing great with her colors and I was worried, oh my gosh, what if she has a tumor in her, you know, occipital lobe? She did not. She picked up colors. It just happened, you know, a few months later, it's fine. So these are some special PCA syndromes. Anton syndrome or the Anton Babinski syndrome. So this is the bilateral PCA stroke. And this is the one you can see in the picture there that causes cortical blindness. And so they get, it's both sides. They get bilateral vision loss. And the other thing is that they are, like I said, your brain fills it in. So they have denial that they're blind. They think that they can see, and a lot of times they'll confabulate to make up that they can see. And so that's a very interesting one to see. We'll get some sight back at a patient, a couple of these patients with very, very striking Anton syndrome and usually color is one of the first things they'll start seeing. And then eventually just, they never got full sight, but did get some sight back for sure. And the way I remember this, I don't know, this is kind of a Texas place called Anton's, Anton's and it makes sandwiches. And when I was an intern years ago, they used to, you know, feed us these sandwiches all the time. And so I got very sick of them and they weren't great. So I said, you wished you were cortically blind to eat at Anton's, just, you know, they have a bad connotation, but that'll remind me of the syndrome. Valence syndrome. So this one is also bilateral PCA, but it's more at the watershed area, a parietal occipital watershed. And so for this one, you get optic ataxia, optic apraxia, and simultaneosia. And so this, the optic ataxia is not really an ataxia. It just means that because of the issue, they look like it's a taxid movement because they have impairments of their hand movements that are visually guided. And then apraxia is they have the loss of the voluntary eye movement. So, you know, look to the left, look up, they can't do it. But if they were to hear something, they can turn their eyes to look in that direction. So they still have the reflex eye movements. And the simultagnosia is they can't see more than one object at a time. And so again, this sometimes again, goes with issues with them reading and, you know, a patient of mine that had this, you'd have to put the letters really big and she wouldn't even be able to read the whole word. She'd have to kind of just look at the letters each one at a time because she'd only see one thing at a time. And so the way I read Balance Syndrome is kind of like Ball, B-A-L-L, Ballance Syndrome. So when you are learning baseball, then you want to keep your eye on the ball. So that's my way of remembering simultagnosia, just trying to remember one thing at a time. And Alexia with Adigraphia, here you can see it left, usually a dominant PCA stroke, pure word blindness, and they can also have contralateral homonymous hemianopsia. So again, if you see this, the other thing, they're physically gonna be fine. They're not gonna be weak. They're gonna be strong. It's just gonna affect their ability to read, which can be very limiting for someone who has a job where they had to read all the time. We're gonna go into some of the brainstem syndromes now. So again, you have your midbrain, your pons and your medulla. And this is always like, oh my gosh, the brainstem, it's the hardest thing ever. The medial, major cranial nerves in the midbrains, three. In the pons, it's six. Seven is pretty big too. And then the medulla, it's 12 here. So there is something, the brainstem rule of four. So if you have time or on your own, you can look it up on YouTube. And it's by Peter Gates. And he came out with this in 2005. And it's gonna use rules of four and a simplified method for understanding brainstem anatomy for non-neurologists. So again, you have to understand the brainstem blood supply. So you have the paramedian branches. So these are these little branches that come off of the bacillar. And those are gonna be, if these are included, those are gonna be the medial brainstem syndromes. And then you have your long circumferential branches out here, the superior cerebellar artery, the ica, the pica. And these longer circumferential ones are gonna lead to the lateral brainstem syndromes. And so there are four rules. So there's four structures in the midline that begin with M, four structures to the side, or those are the lateral ones that begin with S. There is four cranial nerves in the medulla, four in the pons, and four above the pons. And it's actually one and two are not in the brainstem. Three and four are in the main, in the midbrain. Five, six, seven, eight are in the pons. Nine, 10, 11, 12 are in the medulla. So they're very nicely divided. And then the four motor nuclei that are in the midline are gonna be those that divide equally into 12, except for one and two, because remember we said one and two is not in the brainstem. So that's gonna be three, four, six, and 12. So once you know that, then you said, okay, what are the four medial structures? So to know if it's a medial brainstem syndrome. So the motor pathways medial, or the corticospinal tract, so that'll give you contralateral weakness of arm and leg. The medial lemniscus is there, so they'll get contralateral loss of vibration and proprioception. The MLF is there too, so that gives them the ipsilateral intranuclear ophthalmoplegia. And then the motor nucleus and nerve of the affected cranial nerve. So remember we said the one in the midline are the ones that are divisible by 12 that are not one and two. So three, four, six, and 12. And it just depends on what part of the brainstem you're in to know which cranial nerve is affected. And then usually it's gonna be crossed. So ipsilateral cranial nerve, contralateral strength. So the four side structures, you have the spinocerebellar pathway. And so that's gonna give you ipsilateral ataxia of the arm and leg, the spinothalamic pathway. So contralateral pain and temperature of the arm and leg. The sensory nucleus of the fifth cranial nerve is very long, and that'll give you ipsilateral alteration of pain and temperature on the face. So again, we're seeing cross-bindings. That's how you know it's brainstem. And then the sympathetic pathway, which is the ipsilateral Horner syndrome, with ptosis and meiosis. So then this gives you kind of a lot, so knowing those two, you can think longitude and latitude. So midbrain, pons, medulla. And if it's, you know, is it the medial stuff or the lateral stuff? And then what cranial nerves are affected in each of those brain areas? So, like I said before, the four cranial nerves in the medulla, nine through 12, in the pons, five through eight, and the cranial nerves that are in the midbrain are three and four, or above the pons, one through four. And I won't go through all the cranial nerves y'all tested before that really well with cranial nerve three and the effect. Again, it's gonna be ipsilateral to the side of the lesion. So again, take-home message, if it's a medial brainstem syndrome, consists of those four M's and their relevant cranial nerves. If it's a lateral brainstem, it's gonna be the four S's, plus the cranial nerves. It depends if it's in the pons, then it'll be five, seven, eight. If it's in the medulla, nine, 10, 11. And if it's both, then you have to think it's the whole basilar artery or occlusion of the basilar artery. So Weber syndrome. So this is gonna be penetrating branches to the midbrain. I know this brain is not a spectacular brain, but you can see light up the medial part of the midbrain here. And we said, okay, midbrain, that's cranial nerve three, and then they're gonna get weakness, contralateral hemiplegia, and their cranial nerve three is gonna be affected. So their eye is gonna be down and out. And so this is how I like to remember Weber syndrome. So this is W for Weber, but it's also one, two, three, because cranial nerve three is affected. And then if you flip it, it's in the midbrain. So you can kind of think about Weber, cranial nerve three in the midbrain. Okay. And we'll go back to slideshow. The Millard-Gubler syndrome. So this is one of the classical cross brainstem syndromes with a unilateral lesion of the bilateral portion of the caudal pons involving the fascicles of cranial nerve six and seven. So those are gonna be ipsilateral findings there, but you're gonna get contralateral hemiplegia and Algesian hypoesthesia because it affects the pyramidal tracts there. I don't have a great way of remembering that one, but you think pons, what cranial nerves in the pons, six and seven. So that's what's affected. And it's also called the facial abducens hemiplegia syndrome, which is kind of exactly what's affected. Facial nerve, abducens nerve, and their hemiplegic, again, crossed findings. The medial medullary syndrome. So I said, okay, in the medulla, the cranial nerve, it's in the middle. It's gonna be 12. We said that's nine, 10, 11, 12 are there, but the only one in the midline is 12. And so you're gonna get ipsilateral hypoglossal palsy, contralateral hemiparesis, and contralateral medial lemnisca and sensory loss. So I'm going to show y'all about the, where I say licking towards the lesion. So your tongue, you have muscles on both sides of your tongue like this. So if you have ipsilateral, let's say this side is affected, then the weakness, and when you try to stick out your tongue, since it's weak, it's gonna deviate towards the side of the lesion. So that's why I said that you're licking the lesion because that's the way the tongue goes in a medial medullary stroke. Okay, so the thalamic pain syndrome, this one is also called Desjardins-Rousseau syndrome. So we said deep penetrating branches of the PCA is going to go into the thalamic area and they have hemisensory loss and hemisensory body pain. So these patients, they almost seem like, that doesn't seem like it's gonna be real. They're making this up because I will have patients that say, I have a line right here in the middle of my face, in the middle of my body, and I can feel it numb or painful on one side. So this is the traditional post-stroke pain. And though it doesn't seem real, it is really a stroke syndrome. And so that's why I put this there, that these patients might be very angry and some doctors think that they have conversion, but again, give them, always teach, give people the, you know, see if they have the risk factors, see if they need a workup for a stroke, even with some symptoms that might see a little bit different. So Wallenberg's is the lateral, also called the lateral medullary syndrome. So he said, okay, he said, we're gonna think about the rules again, what goes on lateral. So this one is, they're not weak, but they're gonna have the Horner's, they're gonna have decrease in pain and temperature on their face on the ipsilateral side, but on their contralateral body, decreased pain and temperature. And then they can get cerebellar signs because of the ataxia and such on that side of the body. And so this is very interesting. Like I said, they don't have weakness, but they do have one side that seems to be, you know, less affected, their upper extremities. And the usual, one thing that really affects people with this, like their pain and temperature is affected is when they're taking a shower and they turn the water on, you might turn the water on with your dominant hand and your other hand, you feel, you know, to make sure the water's not too hot, but if they use their side that has a decreased temperature, then they still might be getting into a, you know, a bath or a shower that's way too hot or way too cold. So they have to really learn what side to use to check things regarding temperature or pain. So again, remembering what the lateral structures are, spinocerebellar pathway, so that's why they get ipsilateral ataxia. So right, they don't wanna check the water with their ataxic side, cause that's not the strong side. So then they end up checking it with the side where they don't have sensation. So maybe someone should check the water for them. Spinal thalamic pathway is affected. So that's the pain and temperature, the fifth cranial nerve and the Horner syndrome. So get no muscle weakness cause nothing was midline there. But remember we said cranial nerves, nine, 10, 11 are affected. So they have dysphagia, dysarthria, hoarseness. They can get hiccups, nystagmus, diplopia, vertigo, and it affects the lateral medulla, which is why it's also called lateral medullary syndrome, but it's usually a pica occlusion or a vertebral artery occlusion. And then my way of remembering this, so this is Marky Mark Wahlberg. I know his last name is not Wallenberg, but close enough how I remember Marky Mark. And so I think like, if I were to meet him in real life, and we're talking about like young, buff Marky Mark, then I wouldn't have muscle weakness, but I might have some dysarthria, some hoarseness, a little, the hiccups and diplopia and get a little ataxic. And so that's kind of my way of remembering the Marky Mark Wahlberg syndrome. So what about lacunar infarction? We talked about those being related to hypertension usually and caused by, I don't know, calcinosis. And these, because they're small and they're into small areas, then they're gonna cause more of the PURE syndrome. So it's not gonna be something crossed. It's not gonna be a lot of motor miss this with this, no. So the posterior limb of the internal capsule is what will give them a PURE motor hemiplegia. And so that one, I kind of try to remember by, okay, PURE motor, it starts with a P and then the P also starts with a P. So that's just my way of remembering it for test taking. Dysarthro Clemsie-Hann syndrome is if it's anterior limb of the internal capsule. And then hemibolismus is if you get a contralateral subthalamic nucleus that's affected. So those are just kind of ones to remember. Basilar artery occlusion syndrome, also what's called locked-in syndrome. So this is gonna be bilateral ventral pons. Again, as we talked about, if the basilar artery is affected, you're gonna kind of get everything, both the medial syndromes and the lateral syndromes, all the rules are gonna be affected. These patients are gonna be awake and aware because it spares the reticular activating system. They're going to be weak on both sides, so tetraparetic. And all they're gonna be able to do is move their eyes vertically or blink. And so this is something that's pretty, very, very serious when it happens. And I happened to have a patient who was amazing. He was the rocket man because he worked making special things for NASA and for astronauts. And he had done such high-level things that he wasn't even able to tell his wife what he would make for astronauts. And so one day he was away on a trip as part of his job and didn't go into the office with the person he was supposed to go to that day. And they thought it was kind of weird. And then they called his wife and she said, no, he's over there. And finally got someone to go into his hotel room and he had been down for several hours. They took him to the hospital. He ended up having a large bacillary artery stroke and was locked in. And of course they were like, oh, this looks bad. He's doing bad. He's not gonna live. They're like, no, he's smart. He's there. He seems like he's blinking. And they said, okay, well, he's supposed to be a rocket scientist. Let's see. And they asked him, what's the square root of 25? And he blinked five times. And that showed them that he was really in there because again, reticular activating system intact, cortex intact. And so they did everything to keep him alive. He was before, other than a rocket man, he was a marathon runner. He is a reason why I run marathons because I wanted to do it in honor of my patients who couldn't run anymore. So that's me running my first marathon, the same one as him, the Houston Marathon. We have been to the United States Capitol building to talk to our congressmen about important things related to patients who have disabilities and to have as much access as possible for them. And he uses a Tobii EyeGaze system. So he types notes up with his eyes and then he has a computer read him off to the congressman's office to talk about issues important to him. And unfortunately I did lose him a couple months ago, but he lived over 10 years with locked in syndrome, probably one of the patients to live the longest in the world with it. All right, so now we're gonna do our post-test if you want to see how you did. Everyone kind of got this one right the first time. So patient's eye is turned down outward and has ptosis. What cranial nerve is affected? Yes, the ocular motor is the right answer. You said locked in syndrome is a lesion of what area? So that one we learned bilateral ventral pons. Now we know that, all right. What's prosopragnosia and where's the lesion? And you can put comments, this is for comments. Can you get anything? What are people saying? I'm not, I'm not seeing anything. Oh, everyone forgot about inability to recognize faces. That was your little... Here it goes, here it goes. Colorblindness, whoop, the inability to recognize faces. Yeah. PCA, inability, yeah, we're getting a lot of that. Yeah, PCA, inability to recognize faces. Okay, good, good, good. All right. Okay, where's the lesion there? You can... Did I... Yeah, okay, where's the lesion there? Or what stroke did this person have? Everybody's saying right MCA. Yeah, right MCA. So then what would you expect to see? So you can kind of text in what you would... Yes, it's MCA, but now what, based on right MCA, what do you think the patient's going to have? Aphasia, remember I said it's right, so it's not usually the dominant side. Yes, upper limb's weaker than the lower. Yes, a big hemispatial neglect. Right, neglect patient. So she had very, you can see like her, she did, it was even some ACA was affected as well. She had ICA related stroke and she had very severe neglect. Arm was, is still very, very weak compared to her leg. She had a lot of visual issues as well. She is an aphrodisiac patient. Yeah, good. Lots of, but this is also, let's see if this works, her now, and she's someone, this is, she's probably eight years out from her stroke and she is, you know, still working on, on getting and improving and getting better. And she did not do this at the beginning. And this is something that just with a lot of practice and time, she is, you know, has hemiplegia on her left side and, but is still trying to get herself better. So PCA stroke could cause what? So y'all were right that, you know, remembering the alexia without agraphia, so they can't read. Where is the lesion for gaitapraxia? Not PCA. So it's kind of like the, the planning, the motor planning area. ACA, yes. Okay, good. Yeah. All right. And where's the lesion for Gagin-Halton? So we talked about that, that movement, abnormal movement disorder, ACA, ACA, yes. Good. All right, a couple. So if you go online, you can kind of click where you want, you know, click or just kind of get a feel for where people are right now. I'm sorry, if you're in another country, you can kind of put it out to the side. Sorry for not being inclusive of all other countries. Okay, so we have some, East Coast, West Coast, Texas, Midwest. Yay, it's my Texas peeps. Okay. No one's in Hawaii right now? No, no. Okay, good. Just kind of, thank you for those again, on the front lines right now, or not in the front lines, and just being supportive of each other. So that leads me to, I'm going to take a picture of this. I think it's pretty cool. Last question, and this is how I feel about AAP's virtual didactic. So poor, fair, excellent, somewhere in between. Okay, so I'm going to take a picture of this, because I think it's pretty cool. So I'm going to take a picture of this, because I think it's pretty cool. Okay. All right, awesome. So thanks a lot for listening today, hope you learned a lot about stroke, a very serious topic that I love that I kind of made it through med school making mnemonics and such, so that's how it helps me remember stuff, but again, it's important just to think about these syndromes when you see patients and to kind of test them out so you can see exactly what deficits they have so you know exactly how you need to rehab them and how these deficits can affect their life. So thank you, if you have any other questions. Perfect, thank you so much. Looking at the questions here, I'm seeing a lot of thanks. I did get a question about whether the slides will be available, the lecture itself will be available online on the AAP website, and I'll pull that up here in a second. The slides themselves will not be, and this will be available for viewing but not for downloading. We also got a lot of feedback from the where are you from piece in the chat box, so everything from Venezuela to Peru to Canada, Saudi, a lot of different places. So thank you all for joining us today. So thank you all for joining us, that is the website and it has the schedules for the rest of this week and into next and it also has links to the recordings of all of these lectures. So please go on, if you or your colleagues were unable to watch this complete lecture, feel free to go on there and watch it at a later time. Hit us up on Twitter, those are our handles and thank you all for joining and thank you Dr. Gutierrez.
Video Summary
In this video, Dr. Monica Verdusco-Gutierrez discusses various stroke syndromes. She starts by introducing the purpose of the session and acknowledges those who have been affected by the pandemic. The goals of the didactic session are to augment existing curricula, support overworked faculty, provide additional learning opportunities for off-schedule residents, and support physiatrists during the COVID-19 outbreak. Dr. Gutierrez provides housekeeping instructions and introduces the presenter for the day, Dr. Monica Verdusco-Gutierrez. Dr. Verdusco-Gutierrez discusses different stroke syndromes, including ocular infarction, thrombosis, embolism, lacunar infarctions, and more. She explains the anatomy of the brain and how strokes can affect different areas, leading to specific symptoms. She mentions different syndromes related to strokes, such as Weber syndrome, Gertzman syndrome, Millard-Gubler syndrome, and more. Dr. Verdusco-Gutierrez also discusses special syndromes related to posterior circulation and brainstem. She provides examples and memory aids to help remember different stroke syndromes. The lecture concludes with a post-test and audience feedback. Overall, the video provides a comprehensive overview of stroke syndromes and their corresponding symptoms.
Keywords
stroke syndromes
COVID-19 outbreak
ocular infarction
thrombosis
embolism
lacunar infarctions
anatomy of the brain
specific symptoms
Weber syndrome
Gertzman syndrome
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