Zambia College of Physicians Internal Medicine Podcast
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Zambia College of Physicians Internal Medicine Podcast
An Approach to Stroke — Recognition, Localization & Diagnostic Evaluation
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In this episode of the Zambia College of Physicians Podcast, Prof. Saylor discusses a practical clinical approach to stroke, focusing on hyperacute recognition, neurologic localization, stroke classification, stroke mimics, and diagnostic evaluation. Through case-based discussion, the episode explores how clinicians rapidly identify stroke syndromes, interpret neuroimaging, and establish etiologic diagnosis in acute cerebrovascular disease. Designed for clinicians, postgraduate trainees, medical students, nurses, and allied health professionals.
Guest: Prof. Deanor Saylor
Host: Teddy Kajimotu
Co Host: Kabaso Mwewa
Script Writer: Dr Kabaso Mwewa
Another episode of the Zambia College of Physicians Internal
Introduction of Guest and Hosts
SPEAKER_02Medicine Podcast. Today we'll be looking at a topic an approach to stroke from hyperacute recognition to long-term prevention. We are joined today by Professor Sayla. Professor Diana Sayla is an associate professor from the University of North Carolina, but she's been practicing neurology in Zambia for the last nine years. She's also led the development of the neurology training program in Zambia. Welcome.
SPEAKER_00Thank you so much for the invitation to be here today.
SPEAKER_02Thank you. We are also joined by our co-host, Dr. Kabasomwell.
SPEAKER_01Kabaso? ID.
SPEAKER_02Yeah, okay. Yeah, good. You're ready for another exciting episode?
SPEAKER_01Excited.
SPEAKER_02Okay, I thought you'd you'd stay away because it's stroke. I know your ID.
SPEAKER_01But there's also neural ID. That's true. That's true. That's true.
SPEAKER_00There's infectious causes of stroke too. Yeah, oh yeah, okay. That's it.
SPEAKER_02I guess we have two voice out. So so, Prof, before we open our section today, I think we have a lot of exciting things to look out for. Um, stroke is very common in our setup, and some people die for it. And if not managed well, a number of people will die from it. So I think that the audience should be very eager to listen to what has to be given today. Prof has a lot of experience and this is really going to be very useful. But before we get into it, perhaps Prof. You can tell us just a bit about what inspired you to go into neurology and what advice you can have for the trainees out there.
SPEAKER_00Yeah, great question. So I actually was late to deciding to go into medicine. Um I wanted to be a teacher growing up, but my mom actually had multiple sclerosis. And watching her kind of battle with MS and interacting with neurologists and the way they identified her condition and managed it inspired me to go into medicine. And so I went into medicine thinking that I was interested in
Early Career Life and Advice
SPEAKER_00neurology, but I still was open as I entered medical school. But I just found on every single rotation that I did that I was drawn to the neuropatients. You know, on surgery, I wanted to manage the patients who had the headaches. And on medicine, it was the patients who also had a diabetic neuropathy that needed to be managed. And I just was always drawn to those patients. And for me, um I loved the really complex cases in the hospital. And it seemed like the services that were always consulted on those cases were neurology and rheumatology. And if I hadn't done neurology, I think rheumatology would have been the thing that I did. But I loved that they and that neurology seemed like a mystery, but yet it was a puzzle that a really skilled diagnostician could put together. So someone who could take a really detailed history, do an exam, and put those two pieces of information together to really already have a good idea of what was wrong with the patient before a single investigation was done really inspired me. You know, I love the exam and the fact that you can localize a lesion really precisely if you know your exam and know your neuroanatomy. And I just think in modern medicine, there's not too many specialties still where those clinical skills really, really, really matter. Um, and I loved that about neurology. I think I also really like having longitudinal relationships with patients. And as a neurologist in the outpatient setting at least, you're almost like a primary care physician. You know, a lot of our disorders are chronic disorders, and so you can keep um managing the same patients, you know, as I've been here nine years, have been through marriages and divorces and deaths and births and all sorts of things with the patients that I see in clinic. And so I think it's a great opportunity to be able to establish these longitudinally meaningful patient-physician relationships as well.
SPEAKER_02Thank you. I I I had no idea that I did not know that that that that's what inspired you to go into it. Um Wow, that's that's very that's very hard for that. I I was thinking of you when when Prof mentioned that there are very few specialties in medicine where you can actually like make a diagnosis just from your physical exam. Because ID is always when you consult them, they always ask you what did you culture? True? Yeah. You didn't culture anything, they had coming, so so I think it is true that there are very few specialties. And and and what advice would you give prof for for the residents that are out there listening to the medical students about how they can choose their career paths, what things they need to look out for, and um and how they can actually just structure a good um career that will lead them somewhere.
SPEAKER_00Yeah, great question. Um, I think in choosing your specialty, you just have to know yourself and pay attention to yourself as you go through your rotations. You know, there are going to be rotations where it's hard to wake up in the morning and go to the hospital because you sort of dread them, and there will be rotations where you're excited and you can't believe the day is past when you're finishing. And so I think really paying attention to what excites you and what motivates you and what you enjoy learning about. Um, you don't want to choose a field where learning is a chore because you're gonna be learning the rest of your life. Um, and so I think that would be the number one advice on choosing a specialty is just find what motivates you and what you're excited to do, what doesn't feel like work and choose that. Um and then as far as a career is concerned, again, I think it's uh similar to thinking about what you're excited to do. You know, if if you love getting in the clinic and being with patients and that's what energizes you and you come home after a long clinic day feeling fulfilled and energized, then it sounds like a clinician is the right way to go. You know, if you are more excited about thinking about how to prevent the next Ebola outbreak in Zambia and what public health interventions are needed, then maybe public health is the way to go. You know, if you were really into your biostatistics and epidemiology courses and couldn't wait to get into Stata or SAS and code and find out what data your six-year undergraduate project showed, um, then research might be the way to go. But I think again, thinking about what really, really motivates and excites you to go to work the next day and and keep going because it's a hard profession that we've chosen. Um and you want your career to be to align with your passions and not feel forced. Um, you know, a career's a long time to dread what you do every day. And so I think really thinking about what you're excited about and then working to design your career to match that interest.
SPEAKER_02Yeah, thank you. I I I think that's that's the biggest gap I can speak for myself as well. I think sometimes as as young trainees, we we tend to choose careers based on people we envy and not based on our strengths. So someone can look at someone they really admire and say, I wanna do this, I wanna go into this specialty because this person is doing so great in it. Without actually sitting down to retrospect what you actually like and what your strengths like. And we have a lot of frustrated people as a result because they start something and it doesn't work out the way they thought it would. So they easily give up because there's no drive, like you said. You can't keep waking up for something you don't enjoy.
SPEAKER_01Exposure is also another factor. Yeah, if someone who's never been exposed maybe to other fields, the super subspecialty, try that they don't get to think about those things besides thinking of the four major disciplines surgery, obstetric and gynecology, pediatrics, and as well as uh internal medicine. Yeah, so that maybe maybe that's very true.
SPEAKER_02To start our case, uh I think to our discussion, prof, we'll now get into the meat of our discussion today. Um we'll just start with a prompt, which is a clinical case. Uh it won't be it won't flow like the usual clinical cases, just so you know. So he's a 64-year-old man with hypertension diabetes who suddenly develops right-sided weakness and a slurred speech while at home. So he arrives in the emergency department and gets a CT done, and um the radiologist tells us that this person has an ischemic stroke. So, regarding classification of strokes themselves, could you just quickly run us through the major classifications of these strokes in the context of ischemic um hemorrhagic and the subtypes that may exist?
SPEAKER_00Yeah, great question. So, in terms of stroke, the first big classification is going to be an ischemic stroke versus a hemorrhagic stroke. Um, and if we start with hemorrhagic strokes, so these are strokes where a blood vessel has ruptured. Um, and they really fall into just a few categories. You know, in Zambia, 90% of hemorrhagic strokes or more probably are hypertensive hemorrhages. And so these are going to be from your small vessels that over time from having chronic hypertension lose flexibility, and then when they have increased blood pressure, usually acutely increased blood pressure, very high, the vessel itself will rupture. So when we're thinking about classifying hemorrhagic strokes, we think about hypertensive hemorrhages as primarily happening in five major locations. So you have your deep structures, so basal ganglia, thalamus, and internal capsule, and then you have your posterior fossa structures, so your cerebellum and then brainstem. And in particular, in the brainstem, the pons is the most common location. And so in general, if somebody comes in and they're very hypertensive, and by very hypertensive, systolic at least over 180, often well over 200, diastolic over 110 usually, and they have a hemorrhage in one of those five locations, you really don't need to do further investigations. These are hypertensive hemorrhages. Outside of those locations, when you start having hemorrhages not in the deep structures, so out in the lobes of the brain, we call those low bar hemorrhages. Now these are harder to classify and have a greater range of etiologies. So low bar hemorrhages in older people, we think about cerebral amyloid angiopathy as a major cause in people over 60. Then we also think about things like vascular malformations. So you can have a dural AV fistula, arteriovenous malformation, you can have an aneurysm. Any sort of abnormal vasculature can lead to low bar hemorrhages. And then we think about underlying masses that bleed. And so that's another possibility for low bar hemorrhages. And then just to make it confusing, hypertension also can cause low bar hemorrhages. And so that's still a possibility if you're seeing a patient with a low bar hemorrhage. But those patients require more investigation than the patients who come in hypertensive with hemorrhages in those classic locations. When we go to ischemic strokes, primarily we're thinking about whether this is a large vessel occlusion or whether it's a small vessel or lacunar infarct. So large vessel occlusions being strokes in the vascular distribution of the named blood vessels in the brain, your middle cerebral artery, your posterior inferior cerebellar artery, these are large vessel occlusions versus your lacunar infarcts, which are tend to be smaller, deeper, and again, those same structures where we tend to get hypertensive hemorrhages. And then finally, if we have multifocal strokes, we often think about a cardioembolic or some sort of athroembolic or some sort of embolic phenomenon. And so those are sort of the three classifications we think of in ischemic stroke. So again, a patient comes in, your first question is, is this an ischemic or a hemorrhagic stroke? If it's hemorrhagic, you're thinking, is it in one of those five locations? It's typical for hypertensive hemorrhages. And the patient is hypertensive, then you're done. If it's a low bar hemorrhage, more in the lobes of the brain, that has a bigger differential and requires more workup. If you're going down the ischemic stroke path, you're thinking, is this a large vessel occlusion? Is it a small vessel occlusion? Or when we get the scan, do we see multifocal infarcts? And those again have their own differentials as well.
SPEAKER_02Thank you so much, Prof. Um, one thing I've noticed is there's a bit of confusion in nomenclature. Where does a subarachnoid bleed count as a hemorrhagic stroke?
SPEAKER_00It's a good question, and the answer is it depends. Um, so some people do include any bleeding in the brain as a hemorrhagic stroke. Um some people, when they say hemorrhagic stroke, they really mean intraperenchal hemorrhage. Um so I tend to use it more to mean intraperenchymal hemorrhage. So we're only talking about strokes in the parenchyma of the brain itself. Um, but technically, um, hemorrhagic strokes can include subarachnoid hemorrhage, epidural hematomas, subdural hematomas, basically any intracranial bleed. Um but usually people mostly mean um intraperenchomal hemorrhages.
SPEAKER_02Okay. It's a trick I learned in the exam. Like if they ask you types of, if they ask you about hemorrhagic things, you can just say subarachnoid hemorrhage. And so no, that's not a stream, like no, but it is according to this book. Just choose which book, so yeah, no, that's I think that's very clear, bro. Uh when it comes to when it comes to uh the pathophysiology of stroke, I think mostly on the ischemic aspect, um, there is the concept of the ischemical uh as well as the penumbra and riperfusion, which also has an impact on management, as as we'll touch at a later time. How could you explain this uh these three to in a way that would make it very easy for our audience to understand?
SPEAKER_00Sure. So when we're thinking about ischemic stroke, so these are going to be caused by a thrombus um blocking a blood vessel. And so immediately after you get that blockage, within two or three minutes, you get an infarct core beginning. So these are going to be the neurons closest to the blocked vessel that immediately lose all blood flow. And so within a couple of minutes of not getting blood flow, these neurons are going to be completely infarcted, meaning they're completely dead. There's no restoring them. But outside of that core, which is very near the thrombus itself, there's going to be a much larger area that is hypoperfused. And it's hypoperfused because it's not getting its main blood supply, but there's still some collaterals from other blood vessels that are open that are able to provide some blood flow in that region. And so that penumbra, that hypoperfused but not yet dead tissue, represents potentially salvageable brain. Usually the penumbra is symptomatic. So patients are going to have symptoms of a stroke that include the area of the penumbra. But if you can restore blood flow to the penumbra, you can actually improve or at least prevent worsening of the symptoms. And then reperfusion occurs when we are able to get rid of that clot. So that could be through drugs like tissue plasminogen activator, tinectoplase, the thrombolytic drugs. It could be through mechanical thrombectomy. It could be from luck, right? A TIA is actually a stroke that tried to happen, but the clot moved, right? And so anything that dislodges that clot in some way allows blood flow to be restored. And then you get reperfusion of the core, the infarct core, as well as the penumbra. It's great to get reperfusion of the penumbra because you're salvaging tissue. Reperfusion of that infarct core can actually make things worse because you can imagine that if you suddenly restore blood flow to a dead tissue, it doesn't regulate the blood flow well. And sometimes you can actually get symptomatic hemorrhage when you get reperfusion. And so reperfusion is sort of a double-edged sort. Okay.
SPEAKER_02Is there a time frame to um when the penumbra, the area around the point of necrosis or the point of death, is there a time frame to when that will also become completely reversible? Because you mentioned you can reverse it. Is there a time frame for that?
SPEAKER_00It's a good question. Um we don't know the answer exactly. Um, so you know, we'll talk more about treatment, but in our acute therapies for stroke, like thrombolysis or thrombectomy, we have very defined timeframes. Um, you know, thrombolysis is within four and a half hour. Thrombectomy, depending on the vessel involved, can go up to 24 hours. So we know that in some strokes, there is viable penumbra for at least 24 hours after a stroke. But those time frames for those interventions are really based more on when the risk of complications outweighs potential benefit. And so for some people who do not have a lot of collateral uh vasculature to supply a penumbra, you can get a complete infarct very, very quickly. Some people who happen to have good collateral supplies can have a penumbra that can be viable for more than 24 hours. And you'll even see in some patients that as you start to say lower their blood pressure, they become more symptomatic. And if you increase their blood pressure again, they become less symptomatic. And that's because there's a penumbra that's getting supply when the blood pressure is higher and that loses that supply when we drop the blood pressure. And you can see in some patients that happen for even two, three, four days after an infarct. And so there's no defined time period. In some patients, it happened, the penumbra is gone really quickly. In some patients, it can last for several days. Um, there are imaging techniques we can use, particularly with MRI imaging, MRI perfusion studies, or even CT perfusion studies, that can give us an idea for this patient what is the volume of the infarct core, what is the volume of the penumbra, and give us an idea of how worthwhile an intervention is to try to um uh gain reperfusion to save the penumbra.
SPEAKER_02Okay, all right, I think that's very clear.
SPEAKER_01Yeah, so so can we say it's actually or biological time is going.
SPEAKER_00Absolutely. So with every minute that passes, um you lose millions of neurons after a stroke. And so um treatment, recognition, and treatment of stroke um is an emergency. And literally we're losing neurons with every minute that passes. So it's really, really important for people to seek care early, but it's also really important for them not to sit in our emergency room for four hours waiting to be seen as well.
SPEAKER_01Okay, I don't make it that point is very important because a patient may seek help like a time, but then they they sit in the emergency room for four hours.
SPEAKER_02Yeah. Absolutely. Waiting for the doctor to see them. Okay, no, I think I think that's very clear. Um another thing that comes up when we're seeing stroke patients, like in this case that we gave this male 64 who presented with weakness on right side on one side of the body, um, is localization. And and you mentioned that it's one of the things that you actually loved about neurology that you can actually come up with a clinical diagnosis just based on physical examination of the patient. So we wanted to just have a brief discussion about these syndromes, uh the clinical syndrome of strokes in the context of MCS strokes, ACS strokes, PCS strokes. We'll start with those three. And then maybe, depending on we can we can we can look at brain stem strokes and how at least the the general physician should approach them in terms of clinical assessment and lacuna strokes. So maybe you can run us through those, prof. I think this is this is what most of us have been waiting for.
SPEAKER_00Sure. Well, maybe I can start with just my general approach to um, you know, is this a large vessel stroke? Is this more of a lacuna stroke? Um, and and how I think about localizing those. Um and it and it does become important both in terms of workup and management, whether we're dealing with a large vessel occlusion or lacuner infarct. And if you're not working in a center that has neuroimaging, you just have to use your exam, right, to make that decision. And even if you are at a center with neuroimaging, it may take three days to get. And so you still have to use your exam to make that decision. So I think the first question that I like to ask when I'm seeing a patient is are there cortical signs, right? And so cortical signs are neurologic functions that are located predominantly in the cortex. And so those are things like your language, when it's affected, you get aphasia neglect, so a parietal lobe function where you start to neglect half of the world. You also can get field cuts from occipital cortex involvement. So you get a homonymous hemionopia. You can get a gaze deviation from involvement of the frontal eye fields. And so that's the first thing I'm looking for on my exam is are there signs of cortical involvement? Because if there is a sign of cortical involvement, we are likely dealing with a large vessel occlusion. Um, if there's no signs of cortical involvement, Then I know that we're kind of out of the big stroke territory and going more into the small vessel strokes, the lacuna strokes. And I think what I hope you noticed is that I didn't say I look at how weak they are or how numb they are, because actually you can get worse weakness with small vessel strokes than with bigger MCA strokes, for example. And so the presence or degree of weakness or numbness isn't going to really help you in deciding what kind of stroke you have. It's these other signs. So if there's no cortical signs, I know we're dealing with a smaller stroke. And so then I'm thinking, is this one of those deep structures, the thalamus, basal ganglia, internal capsule, or is this more in the brainstem? And so things that can point you to a brainstem stroke are going to be crossed findings. So you can get weakness on one side of the face and then the other side of the body. You can get numbness on one side of the face, the other side of the body, you can get numbness and weakness on different sides of the body. Those would be crossed findings or significant cranial neuropathies. So if you have a third nerve palsy, for example, with what you think is an ischemic stroke, that would probably be a nuclear third nerve palsy from a midbrain stroke. If you get a lower motor neuron facial pattern weakness plus a sixth nerve palsy, that's probably a ponteen stroke. And so you start thinking about do I see signs of cranial neuropathies that may not be true cranial neuropathies, but actually involvement of the cranial nerve nuclei in the brainstem. And so if I see either crossfindings or cranial neuropathies, I'm thinking brainstem stroke. If I see a stroke that doesn't have cortical signs and doesn't have brainstem, then we're dealing with those subcortical kind of deep strokes. So that's kind of my general approach to localization. And then from there we go and go into specific syndromes. So I think the the most famous syndrome is your MCA or middle cerebral artery stroke. And so for here it depends on which side of the brain we're on. So if you think about the left MCA vascular distribution, that is going to cover the majority of the frontal lobe as well as the temporal lobe and part of the parietal lobe. And in a left MCA stroke, you're going to the cortical finding you're going to see is an aphasia. So sometimes you get a Broca's aphasia, which is a non-fluent aphasia where patients are having difficulty producing words. Their comprehension is relatively spared, although still not completely spared, but they have this non-fluent, effortful, hard speech production. You can also get a Wernicke's aphasia where patients are talking, talking, talking, talking, but saying made up things, stringing together words that don't make any sense at all, and their comprehension is completely gone as well. Or you can get a global aphasia where there's just no understanding and no verbal output as well. So you're looking for aphasia. You can also get visual field cuts due to involvement of the optic tracts going back to the occipital lobe. And then you often get a gaze deviation where the patient will look towards the side of their stroke. So a left MCA, they'll be looking to the left and really not paying attention or looking with their eyes to the right very much. So those are the signs that I look for in addition to the contralateral hemiparasis, hemisensory loss that help me know that this is a left MCA stroke. I think an important note is that we're always taught that in an MCA stroke you have face and arm more than leg weakness. And that is true, but it's rarely true in the acute setting. So when you're seeing someone on the first day or first couple of days after their stroke, they often present with a very dense hemiplegia. But then as you watch them recover, you'll see that their leg recovers more than their face and their arm do. So I think don't be thrown off by the fact that patients come in with a dense hemiplegia and they still have an MCA stroke. If we then go to the right MCA stroke, you're still going to have the hemisensory loss and the hemiparasis. You're still going to have a visual field cut. You can have a gaze deviation this time to the right, but the cortical sign that you're looking for is neglect. So is the patient aware of the left half of the world? You can assess that by asking them to point at the people around the bed, and you'll find that they point at everybody on the right. And once they get to the midline, they stop. Sometimes people have hemibody neglect where if you show them their left hand and ask whose hand it is, they'll say it's your hand. So there are different types of neglect you can assess. But if you're seeing somebody coming in with a left hemiparasis and neglect, we're really thinking this is likely a right MCA stroke. When you go to anterior cerebral artery strokes, poemoprop.
SPEAKER_02Sorry, it's very dense. We need to break it down. We need to go step by step. So I'll I'll take you back to the left MCS stroke. And you uh you mentioned that if there's cortical involvement in this case, you can have um voice abnormality, specifically aphasia. And I think aphasia is one thing that most people look for when they're assessing someone's voice stroke. Um how how do we just go about to classify aphasia from a left MCS stroke? And this is this is in the context that this patient is left brain dominant. Yeah.
SPEAKER_00Great question. So um so I think you're asking, like, if you have a left-handed patient, for example, right? Um so it is true that some people who are left-handed will have language on the right side of the brain. Um, but actually 90% of left-handed people still have their language in the left hemisphere. So they're still, even the majority of left-handed people will still present with aphasia with a left MCA stroke. If you're seeing someone come in with a left hemiparasis indicating a right-sided weakness or right-sided infarct and aphasia, then they could, if they're left-handed, that makes sense. Okay. Um, but I think one of the things I see that people often confuse is aphasia and dysarthria, right? Um so dysarthria is a motor problem of speech. It's a problem of articulation. So the patient can understand language, they know what they want to express, they can express themselves, except that you can't understand their speech. And in really severe forms, you can actually get anarthria where they have so much difficulty with the motor production of speech that they don't produce speech at all. And that can be hard to distinguish from someone coming in with global aphasia, where there's no speech production, but there's also no comprehension. And so that that's the really important difference there is that patients who are aphasic have a really hard time with comprehension, with following commands. Patients who are dysarthric or anarthric should still be able to follow commands. Another important thing is that language we automatically equate to speaking, but language is not just spoken language. So written language, reading, is also a form of language that localizes to those same language centers. And so patients who have dysarthria should still be able to read and follow what they've read. They should still be able to write their thoughts out without a problem. Whereas an aphasic person, all of those different types of language should be um should be involved. And I think the other thing that I see many times is patients who have a Wernicke's aphasia are classified as having altered mental status rather than having a localizable neurologic problem. And I think part of that comes to this tendency to just say when people are confused that they have irrelevant talking. And some of you who've rounded with me know that that's a soapbox I often get on and say we should strike this from our medical lexicon, right? Um, because there's a difference. You know, if if a patient comes in and they're seeing their dead grandmother and talking to her, or they're telling you that there's birds flying around the clinic room, that's altered mental status, right? What they're saying doesn't make sense because it's out of context. But if you just wrote down a sentence that they're saying, it makes sense, right? Whereas Wernicke's aphasia, patients are stringing together words that do not make sense at all. You know, it might be tree, green, TV, road, you know, something that's not a sentence in any context. And so it's really important to classify these patients who come in as altered and figure out are they really just confused or are they having a language problem that's the barrier to communication?
SPEAKER_02Okay, another very basic one. Aphasia and dysphasia.
SPEAKER_00Are they the same? I think I think dysphasia is a British term and aphasia is the American term. Okay, so you can we can use them. We can use them interchangeably, yeah. All right.
SPEAKER_02Then what about uh transcortical aphasia?
SPEAKER_00Good question. So these are um they're good to know about. I expect my neurology registrars to know about. Um I don't I wouldn't I wouldn't include this on your exam. But transcortical aphasia is basically there are several different kinds, but there are particular functions of speech that are maintained. So oftentimes repetition is maintained, even though naming and comprehension are not. Um so there's transcortical motor, sensory different phase um different kinds, but they're essentially they don't fit neatly into brokas or Wernicke's, often because repetition is still maintained.
SPEAKER_02Okay, I think I need to stop asking my interns what transcortical aphasia is. I think I've lost it a couple of times. Yeah, but I I think this is very high yield to know because I think aphasia and dysphasia, and like Prof. Sometimes there's a bit of confusion between aphasia and altered mental status. And I've I've had challenges with this, and and this is something you probably agree with me, Kabaso. Like how many times have you seen patients writing patients, writing notes for stroke patients, and they start by saying GCS. And their GCS is called mortar, whatever it is, I, whatever it is. Then on Vable, this patient has confused speech in inverted comas because of probably a wenekaze aphasia, so it's called less. I don't know what your comments are on the use of the Glasgow coma scale to stroke patients to this center.
SPEAKER_00Yeah. Um, I mean the GCS is really a trauma score, right? Um, it's not a a neuroscore, and so it's not a score that I would typically go to for any neuropatient unless they were coming in as a trauma. Um, you know, the NIH stroke scale is much more detailed. There's free training available online, and it gives a much more accurate um idea of how severe the stroke is for a patient.
SPEAKER_02Yeah, so we need to stop scoring GCS for our stroke patients, guys. Yeah, it's it's a common thing, I see. Yeah, every stroke patient GCS, GCS.
SPEAKER_00Every neuropatient.
SPEAKER_02Every neuropatient, GCS. So it's it's yeah.
SPEAKER_01So I think and and and then it also brings a lot of confusion when it's hemorrhagic and they need to involve neurosurgeons. They'll make a decision based on the GCS, GCS. And then now it's difficult at times to convince them to actually intervene.
SPEAKER_00Yeah. Yeah, no, I think it is definitely much more of a surgical and trauma scale that um those specialties use a lot more. Neurologists really don't use it for them for the vast majority of patients.
SPEAKER_02No, thank you so much, this is very helpful. Um the ACA syndrome, please.
SPEAKER_00Yeah, so ACA syndrome um is primarily going to involve your leg fibers, so you'll get unilateral weakness of your leg. Um, the other thing that people often underappreciate is that the ACA um also supplies the micturitician center. So patients will often come in with very prominent, usually urinary retention, but sometimes incontinence as well. So that's your ACA syndrome. Your PCA um syndrome, the posterior cerebral artery, can actually look a bit like an MCA stroke, um, except that you don't have the aphasia or the neglect. And instead you have a very, very dense homonymous hemionopia. Um, you know, you can get field cuts with MCA strokes, as I mentioned. They tend to be quadrantinopias. Sometimes they can be hemionopias, depending on how much of the MCA territory is taken out. But with a PCA stroke, you're going to get a very, very, very dense hemionopia. Um, but you also get hemiparasis, hemi-sensory loss as well. Um and maybe just a small clinical pearl here as well. One of the things that's very common in a PCA stroke is for patients to start having visual hallucinations in the side that they have the field cut on. So essentially the brain acutely can't see anything and it starts just making things up because it's used to having input. And it's often very scary for patients because they're aware that they're hallucinations, but they're also aware that they're seeing them and they don't know why they're seeing them. And so if you do have a patient with a PCA stroke, sort of asking them and normalizing it and letting them know that that's a normal phenomenon can be really helpful.
SPEAKER_02That's that's very that's very informative for me. I I read an article. Um I may not remember the action so properly, but I think maybe a uh vertebra artery stroke or vascular artery stroke. But it was in the context of saying you can have a stroke when you're when you're at the saloon or you're seeing your baba, uh, where they if if they extend your neck rapidly, you can actually have a stroke. I I I don't know if that's a thing.
SPEAKER_00It is actually. So um you're probably talking about a vertebral artery dissection. Yes. Um, so you know, vertebral artery and carotid artery dissections are a cause of stroke. It's one of the things we think about, particularly in young people or people without any other stroke risk factors. Um, and you know, some of it is just bad luck. You know, we've all been to you know the beautician and had our necks moved around and not had dissections, but there may be a genetic predisposition or an anatomical predisposition in some people to have a dissection. Um, and then once you get a vessel well dissection, you can have a clot forming there at the area of the dissection, and then that clot can dislodge and go on to form a stroke. Um, so that's the risk factor. Um, chiropractors can sometimes cause dissections with manipulating the neck. You can see it when people, we don't have oceans in Zambia, but people get hit by a wave in the ocean and they can get it after, certainly after a car accident or some sort of neck trauma, whiplash. Um, that's a risk factor for dissections as well.
SPEAKER_02Yeah, so so for someone like me, um, if I have if I don't have it by now, it probably won't happen, right?
SPEAKER_00We we all hope so, Teddy.
SPEAKER_02We all hope so. I think I think I need to reduce the number of times I go to the mama. This is very scary. At least cowers of keeps an approval, so I think you go less often though, right? Yeah, yeah, so the risk is low, statistically speaking, right?
SPEAKER_03Yeah, yeah.
SPEAKER_02So I think I think prof you've you've highlighted a couple of things. I don't know what your comment would be on. Maybe it's it's a bit too detailed for for our audience. Um targeting. We mentioned brainstem strokes, um, but would you want to add a thing or two about brainstem syndromes themselves?
SPEAKER_00Yeah, um, I mean, there's you can read in the textbook, there's lots of different brainstem syndromes. Um, I think probably the most well known is the lateral medullary syndrome or the Wallenberg syndrome. Um, some classic things here that these patients present with really, really severe hiccups. Um, so that is quite common. You can also get a tosis with uh Wallenberg syndrome as well. Um, but I think for our purposes, you know, where in the brainstem the um the stroke happens doesn't really change our management or even our diagnostics for the patient. And so I think just recognizing it as being in the brainstem is is sufficient.
SPEAKER_02Okay. Thank you so much. Another thing that usually happens um sometimes we can have patients being tagged as stroke. And on further evaluation, they actually don't have a stroke, and then you can have people getting stuck. Well, if it's not a stroke, then what what is it? So that happens every once in a while, especially in places where where, like you said, people rush to diagnose this patient. You mentioned that even where we are, we need to take the time to take a good history, examine the patient, and probably localize something that makes sense, but sometimes we just rush to do a CT. CT comes out normal, MRI comes out normal. So what things um can mimic a stroke?
SPEAKER_00Great question. So I think these stroke misdiagnoses are can fall broadly into two categories. So one is that this really was an acute neurologic event, um, and it just wasn't a stroke. And so what kind of things can cause acute focal deficits? There's really only four. Um, so stroke being one of them, and then a transient ischemic attack or TIA being another, um, a post-dictyl Tods paralysis. So sometimes patients will have a seizure, maybe they're alone in the room and nobody sees the seizure, and then they're discovered and they're not moving their left side, and so it's assumed that they've had a stroke, but then later on they recover and we realize that they had a seizure that led to a postdictal Tods. And then the final one is hemiplegic migraines, which are quite uncommon but can happen. And these patients develop weakness or focal deficits like a stroke, almost always in the context of a severe migraine as well. So the presence of a headache when that happens can be helpful in differentiating those. So that's I think the category of misdiagnoses, but otherwise appropriate history. But I think the biggest cause is just not taking a careful history. So it's getting better now than when I arrived nine years ago. Um, but when I arrived nine years ago, anyone who had a hemiparasis was just told they had a stroke. It didn't matter whether it developed over two seconds or two months. Yeah. It was just labeled a stroke. And so I think the key here is that a stroke develops acutely, not just acutely, hyperacutely, right? If you see a stroke happen, you know exactly when it happens. And if somebody's coming in with worsening weakness, even over 24 hours, that's generally not a stroke, that's something else. And so I think history is important and then um time uh trajectory is important. So if you're seeing someone an hour after their symptom onset, you won't know that it's maybe a TIA or that it's a postdictal TODS. But over the next couple of days, as their symptoms improve, now you start to go back to your differential and think, okay, if this wasn't a stroke, was it a TIA? Was it a TODS paralysis? Was it a hemiplegic migraine?
SPEAKER_02Yeah, I I I always thought as as a resident that um hemiplegic migraine was just a neurologist way of making the exam harder. Yeah, because like it is quite rare.
SPEAKER_00I think I in nine years I've seen one in Sambia, so it is quite rare.
SPEAKER_02Yeah, that's right. Because 'cause they'll keep asking me, what else? And then when you're like, I don't know, like hemiplegic migraine, you're like, okay, I I didn't think of that. Um regarding TIA approach, there's there's there's actually confusion around TIA from from what I've gathered. I'm saying that because I was confused once. Is it actually 24 hours or 30 minutes or one hour? I hear it was 24 hours and then the terminology changed. So so what's the exact time frame in a practical setting? We can actually say this is a TIA.
SPEAKER_00Yeah, that's a great question. So um the WHO definition of a TIA remains a focal neurologic deficit that completely resolves within 24 hours without any better explanation. Okay. That being said, um, in higher resource settings, the definition is a focal neurologic deficit that resolves without any evidence of infarction on an MRI. So um, you know, and and so it's in reality, there are people who have a minor stroke, say young people who have a minor stroke that may pretty much fully recover from their stroke in 24 hours. Um, so when you just use the clinical definition, you are probably classifying some people who actually had strokes as TIA. Um, and what we've realized in higher income settings where MRIs are more accessible, especially acutely, is that somebody comes in, they had a hemiparasis for two hours, it resolved. We put them in the MRI scanner at Hour 4, and we see that there actually are still some infarcted areas. And maybe they're small, maybe it was an embolic stroke, and that embolism just broke up and became smaller, but they're still infarcted areas. And so even if they meet the WHO clinical definition for TIA, they have evidence of infarction on their MRI and so they're classified as stroke.
SPEAKER_02Okay. So I'm even more confused now. Was there at any point in I know guidelines change every year and definitions are refined every year. Was there at any point where part of the criteria for TIA included not having anything on your imaging suggestible with stroke?
SPEAKER_00So that is the definition that's usually used in higher income settings. Okay. It's the WHO definition, the clinical definition that we tend to use in our setting. Okay. Because usually these patients who have a stroke but fully recover within 24 hours, their strokes are small enough that we're not going to see them on a CT anyway. So you really need to have access to MRI imaging, ideally within 24 to 48 hours, to say whether or not someone's had an infarct in association with their clinical TIA syndrome. So it's not super practical in our setting. The reality is that TIA is an ischemic stroke that tried to happen, right? And so we're going to manage them essentially like a stroke anyway. So whether or not we classify some strokes as TIAs using a WHO clinical definition doesn't matter too much to the patient because we're going to do the same things for them either way.
SPEAKER_02Okay. So if if I'm answering this from the context of the student, I'm a resident, I'm having my exam, and the question says define what a TIA is. Yeah. What's a safe way to write it?
SPEAKER_00I think you're very justified to use the WHO definition. Okay. Yeah. So a focal neurologic deficit that resolves within 24 hours. Okay. And I also want to point out a common thing I see registrars and students mistake is that a patient develops stroke symptoms, they improve, but they don't resolve. Okay. And people call them a TIA because they improved. But remember the definition of a TIA is that they resolve. So if they have a dense hemi parasit or hemiplegia, and then six or eight hours later they're less weak, but they're still weak. That's still a stroke, right? A TIA has to have complete resolution to meet that definition.
SPEAKER_02All right. That's that's that sounds clear. I'm sure Akabasa, you thought TIA was straightforward, right?
SPEAKER_01Especially the differences in definitions.
SPEAKER_02I I think for me the turning point was at some point during my training, I I think yeah, actually. I think one of the consultants was a Henriquali. I think I made a consultation and they asked me to do an MRI. Wait, why am I doing an MRI? Like where are we so I I I actually read a bit more about it and I realized that okay. Because like like like profile clarified, really there's no mention of an MRI when you look at the actual definition by WHO. But you know, WHO generally makes its recommendations based on what is feasible for most countries. Yeah, so so it's it's good to have that context too. Yeah. Um having answered that prof now, I think what would be your recommended um approach to diagnostic uh for stroke patients? What investigation uh should we do?
SPEAKER_00Yeah, great question. So ideally, all stroke patients should get at minimum a C a CT scan. A non-contrast CT should be sufficient. I know that that is not practical in a lot of our facilities, but ideally that would be done. And then from there, there's a core set of blood investigations that I like to see. So in somebody who's had a stroke, I want to get a hemoglobin A1C, I want to get a lipid profile, and then I want to check their RPR as well as their HIV status. So both um neuro syphilis and HIV increase your risk of stroke. And in our setting, the um the population prevalence of both infections is high enough that it's warranted to check that in all patients. So um lipids, A1C, RPR, HIV in everyone. Then everyone needs a cardiac workup as well. So ideally, if possible, um getting at least an ECG and ideally an echocardiogram as well. And then from there, it's always great if we can get vessel imaging, meaning either a carotid ultrasound or a CT angiogram or MR angiogram, both of the head and the neck, to look for large vessel atherosclerosis and the carotids or even intracranial atherosclerosis as well. That tends to not be practical for the majority of our patients. So we tend not to do it all that often, but that is that would be part of the ideal workup as well. The other thing that is hard to do in our setting is that ideally stroke patients are put on telemetry for at least 48 to 72 hours to look primarily for paroxysmal atrial fibrillation. Again, that's really, really challenging in our setting. So I think at minimum everybody gets those four blood tests and hopefully an ECG, ideally an echo, ideally neuroimaging of some kind as well.
SPEAKER_02Okay. On the lipid profile, what which ones are you particularly interested in from the context of stroke?
SPEAKER_00It's a great question. I mean, all of them have all of every dyslipidemia increases your risk of stroke, right? So having a low HDL is a poor prognostic sign for stroke. Um, having a high LDL or high triglycerides or just a high total cholesterol increases your risk of stroke. LDL tends to be the one we think about the most. That's where we have our LDL goals for secondary prevention. Um, but you know, if you saw somebody with significant hypertriglyceremia, ideally you'd manage that as well because that's still a stroke risk factor.
SPEAKER_02Yeah. The cardiology world has been a buzz with the discovery of a polyprofotent B. The LP smaller. I uh because of its tendency to predispose people to um acute coronary syndrome. I I reckon the pathophysiology should be should be the same, right?
SPEAKER_00Yeah, those are those are two hot biomarkers in stroke right now as well. Um and I think the hard part is is I don't know what to do about them when I identify them, right? I like to do things that are clinically meaningful and I'm not sure what I'm doing with those when I get them, but they do seem to explain some stroke risk um that we hadn't been able to explain before.
SPEAKER_02Okay. Um regarding other causes, other rare causes of stroke, um, what is your recommendation on when to look for them? For example, autoimmune disease, um coagulation abnormalities and postpolipid syndrome. In which age groups, in which kinds of patients would you ask for an extended panel of test?
SPEAKER_00Yeah, great question. So um it's all about you know the phenotype of the patient in front of you. So if you have an older patient, certainly over 60, but probably over 50, who has you know known stroke risk factors, hypertension, hyperlipidemia, diabetes, um, obesity, you know, metabolic syndrome, then you really don't need to do investigations beyond what I've already mentioned. But if you have a young patient, so less than 50 is generally the definition of stroke in the young, sometimes less than 55, those more standard risk factors are usually not the explanation for their stroke. And so it's in those patients, those young patients, that we need to do the additional investigation. So as you mentioned, we talked about dissections earlier. So thinking about vascular abnormalities, whether they be acquired like dissections or some other predisposition, um, you have hypercoagulable syndromes, you have autoimmune causes, um, you have hypercoagulability from underlying malignancy, right? And so any young person with stroke needs an additional workup. These, again, I think everyone with stroke should be tested for HIV, but the most common cause for stroke in the young in our setting is HIV. And so for sure, those patients need to be evaluated for HIV. Another common cause in our setting is rheumatic heart disease. And so these patients ideally definitely listening for a murmur, but ideally getting an echo to see if there's evidence of rheumatic heart disease is important. Um, syphilis, you know, again, in our neuro syphilis, um, the form that causes strokes tends to be in the acute setting of syphilis. So somebody with a more recent syphilis infection is actually at greater risk for meningovascular syphilis than somebody with a more longer-term chronic infection. And so in young people, that again should be evaluated carefully. So I think patients who are young, and then the other group is patients who keep having strokes, right? Especially if you feel confident that they're taking their aspirin or their secondary prevention. Um, if somebody is coming in with multiple strokes in a few months, even within a year, then you want to start thinking about do they have an underlying malignancy? Do they have a vasculitis, which doesn't just happen in young people, right? And so um start thinking more broadly about patients who have maybe typical risk factors but are having an atypical course with lots of strokes close together.
SPEAKER_02Thank you so much. That's very that's very helpful.
SPEAKER_01Prof, you mean you talk about neuroimaging and then um just mentioned that in Catholic now of the city. So if um before he's consulted and decided to do a CT scan and definitely suspected as well. What are some of the how can they differentiate uh ischemic from uh immunologic and the electric scan?
SPEAKER_00Great question. So I think the assuming we're in in an ideal situation where someone is getting their CT within a few hours of onset of symptoms, um it's important to remember that we're doing that CT primarily to look for hemorrhage because ischemia can take up to 24 hours to appear on a CT scan. And small infarcs, particularly lacuner infarcs, particularly brainstem infarcks, may never appear on a CT scan. You may only see those on an MRI. And so getting a normal CT scan in a patient who clinically has a stroke tells you for sure this is not a hemorrhagic stroke, but it could still be an ischemic stroke, right? And it likely is still an ischemic stroke, even with a normal CT, assuming you've taken a good history and done a good exam. So I think that's the first clinical pearl is that a normal CT does not exclude stroke. I think another common thing for us is that we are often getting neuroimaging on day seven, eight, nine, ten after a stroke. And the primary way of differentiating ischemic and hemorrhagic strokes is based on density, right? Ischemic strokes are hypodens, hemorrhagic strokes are hyperdense or bright on a CT scan. You have to remember that the natural imaging features of blood is that by day seven to 10 they become isodense, and then after that, it also becomes hypodense. And um lacuner infarcts and hypertensive hemorrhages have a predilection for the same parts of the brain. And so if I get a CT scan on day 12, day 13 after a stroke, and I see a hypodensity in the basal ganglia, I don't really know whether that patient had a hemorrhagic stroke or whether they had an ischemic stroke based on the CT alone. Again, if we can get an MRI, we can now use our heme sequences like GRE or SWI to say for sure whether there was blood in that area. But beyond seven to ten days, you're not going to see blood anymore on a CT scan. So you can also err on the other side of calling a hemorrhagic stroke ischemic because of the timing of the imaging.
SPEAKER_02It's a very useful question. One of the things I I came across during my training that kept popping up for ischemic stroke was the hyperdense MCS sign. It's it's very commonly spoken about, but I I never saw the few times I looked at neural imaging. I I say the few times I did because prof has looked at thousands of them. So like I I I I I know my rap kit, but I haven't said few of them. I don't know what your comment on that. How often do we get that? In which phase of doing the stroke do we get it? And then there's also been debates about not really debates. I think there are some authors that recommend that if somebody comes in with a stroke that happened today and I do a plain CT within the next 30 to one hour, I may not see anything at all. So, like, when also should when is the right timing to do a CT for stroke?
SPEAKER_00Good question. So taking the first one, the hyperdense MCA. Um it's it's not uncommon in MCA strokes, right? So you're because it's an MCA sign, you're automatically limiting it to the fact that it can only be there in patients who are having MCA strokes. Um and then it's often overlooked if you're not specifically looking for it. So oftentimes we'll see CTs that are read as normal, but when we go look at them, you can see that there's a hyperdense MCA sign. So I do think it's useful, but in a really selected subset of stroke patients. Um, regarding your second question, I mean, I think there's the textbook answer and there's the practical answer, right? Um so a textbook answer is if you only have access to a CT and the initial CT is normal, that you should repeat it 24 to 48 hours later. My question is if you already know the patient has had a stroke, right? You've taken the history, after 24 hours, they're not better, right? So their deficits have persisted. What difference does that CT make for you, right? And so I tend, if I see a normal CT in the first 24 hours and that patient still looks like they've had a stroke on day two or day three, I actually don't repeat the imaging because I I don't think it's going to change my management of the patient in any way. And in a setting where our patients pay for every single investigation, right? Um, I want everything they pay for to have the potential to change what I do for them.
SPEAKER_02Okay. That that's very clear. I hope oh, so yeah, clear on that too. Yeah. So um this brings us to the end of the first segment of our discussion on structure. Um we are going to look at an approach to management in the second segment. Um it will be very practical. So we hope people that we hope that people will be eating, would have had their lunch by the time they listen to the second meeting. So you have to time it properly. You want to listen to it? Yeah. So from today's discussion, what would be the take-home method from what we discussed?
SPEAKER_00Oh, great question. So I think the first take home is to take a careful history and do a good exam, right? And make sure that we are in fact dealing with a stroke. Um the second take-home, I guess we talked about if you get the CT and it's normal, what's the right time to do it? But I would also argue that there, if you have the opportunity to get neuroimaging, you should get it as soon as possible, even though it may be normal initially. Um, because as we'll talk about in the next session, whether you're managing an ischemic or hemorrhagic stroke matters, and it matters particularly early on. And so obtaining early neuroimaging whenever possible can really guide the rest of your management as well. Um, and then, you know, I think the third thing is just to remember HIV is a really big risk factor for stroke care. You know, in our stroke cohorts, 20 to 25 percent of patients have HIV, and in about 40% of them, HIV is their only risk factor. And so I think particularly we see a lot of young stroke care, and really, really, really making sure we're investigating those patients for HIV is important.
SPEAKER_02Sorry, for a bucket talk. I hope we won't scare anyone with the answer. I don't know what the answer will be either. Um I think in an infectious disease world, you is a good thing, I think. You guys love it. Yeah, yeah. So, Prof. When these patients with HIV come in stroke, does it What does it literally just show? Does the viral load matter? Or the risk is the same?
SPEAKER_00No, so it's that's a complicated question. Um the viral load definitely matters. Um I will say that our understanding of HIV stroke is really evolving and is pretty incomplete right now. So we know that HIV at least doubles your risk of stroke, both ischemic and hemorrhagic stroke, actually. There's very little research at all into the mechanisms of hemorrhagic stroke in people with HIV. In um people with HIV, in ischemic stroke, there seem to be different categories. So an advanced HIV disease, HIV stroke is often related to a CNS opportunistic infection that has an infectious vasculitis. So cryptococcal meningitis, TB meningitis, those are the big culprits there. Um in people who have well-controlled long-standing HIV disease, it tends to be the metabolic syndrome, right? We know that they're at higher risk of developing dyslipidemias and all of these metabolic syndrome risk factors. And then there's this group in the middle who are the recently initiated on ART group. And so there's been great work out of Malawi that's recently been replicated in South Africa, and we've seen it in our study as well, that actually the six-month period after ART initiation seems to be the highest risk period for stroke. Um, and we think that that is because there's some sort of iris phenomenon, the immune reconstitution inflammatory syndrome, potentially to HIV itself. Um, maybe that that's where HIV vasculopathy comes in. Um, but it also seems that the degree of immunosuppression at the time of ART really um influences that, just like any iris, right? The lower your CD4 count is, the higher your viral load is, the higher your risk of iris is. And so we think that that's the case in um this risk period of six months after ART initiation, that if somebody has a relatively low viral load, high CD4 count, their risk seems to be lower. Whereas if somebody with a greater degree of immunosuppression at the time of ART initiation seems to have this particularly high risk of stroke.
SPEAKER_02Thank you so much. Uh this segment, I think only people that listen to completion will benefit from it. Because I closed it. So they dropped off, they won't know the answer to this one. Well, it's been a pleasure having you, Prof. I I have learned a lot today. I don't know about Kawaso. You have?
SPEAKER_01Yeah, and a lot of um things have been put in place. Yeah, yeah, it's very educative. Yeah, very educated.
SPEAKER_02People tend to think that the podcasts are mostly for the audience, but the people that benefit the most are actually the costs. So thank you so much, bro, for giving us this chance for making time for this.
SPEAKER_00Of course, thanks for the opportunity.
SPEAKER_02You can say bye to our audience, please.
SPEAKER_00Bye, everybody. Have a great day.
SPEAKER_02Bye bye. Thank you.