What's up Ninja Nerds? In this video today we're going to be talking about stroke syndromes. Before we get started though, please The most amazing way that you can continue to support us to make these awesome videos for you guys is to hit that like button, comment down in the comment section, and please subscribe. Also, if you guys want to follow along with this comprehensive lecture on stroke syndromes, we'll have a link.
Go click on that. Check out the notes and the illustrations that we have available to you guys. All right, Nidgenerds, let's get into it. All right, so let's talk about stroke syndromes.
Why do we need to know stroke syndromes? Well, the basic thing is that when someone comes in with an ischemic stroke or a hemorrhagic stroke, they're going to present with particular neuro deficits dependent upon that vascular territory that gets hit. And so we need to know what vessel supplies pretty much what area of the brain or brain stem.
And if that is affected, what types of clinical manifestations will be evident. I think that's pretty much it. So let's start off talking about the MCA syndrome or middle cerebral artery syndrome. So briefly, we need to say middle cerebral artery, what parts of the brain does it supply? That'd be a nice little.
kind of get you know thing to start off with. I think the best way to look at it is this tiny little diagram here in green. The green is representative of the MCA division.
So the MCA division you have supplying the frontal lobe here, you have it supplying part of the parietal lobe, and you even have it supplying part of the temporal lobe. Okay so that's a really important thing to remember. It supplies a good chunk of the brain. Frontal lobe, parietal lobe, temporal lobe. Now, the big thing to remember is it supplies more of the lateral side of the parietal lobe and the frontal lobe, okay?
Big thing to remember. So, let's talk about, first, some of the frontal lobe things. So if we take a slice of the brain in a coronal section and we take that slice just in front of the central sulcus, okay just in front of it, we're going to be looking at the frontal lobe now in a coronal section.
So imagine there's our coronal section. On one side I'm representing kind of the vascular territory. So here's going to be the frontal lobe, here this little bump there is a part of the temporal lobe. The frontal lobe in the medial portion is supplied by the anterior cerebral artery.
This whole chunk here of the lateral portion of the frontal lobe is the MCA and even a little bit of the temporal lobe is MCA and just that bottom portion there is the PCA in blue. When someone develops a middle cerebral artery stroke and they knock out a particular area in that frontal lobe, if you guys look here on this side view here, here this in black is the central sulcus. In front of it here is your primary motor cortex. That's where the voluntary movement of skeletal muscles occur. knock out the MCA and you don't supply blood flow to that primary motor cortex what happens?
You can't move the opposite the contralateral side of the body. So for example, let's take for example here, here's your right MCA division and let's say that you knock out this portion here where these little red neurons are. So if we follow these red neurons from the right primary motor cortex they'll come down, coronar radiata, internal capsule, through the crust cerebra, through the pons, dacusate of the pyramids. go down to the spinal cord, and supply the muscles on the left side. You knock these out, you develop weakness on the left side.
But here's where we've got to be really specific. You guys really need to remember your frontal lobe anatomy and function. What we take the slice, they like to put that little man there called the homunculus, right?
Little motor homunculus. It tells you what parts of the body this portion of the brain supplies. If we take a look here, I want it really basic. Face upper extremity.
lateral portion of that motor cortex, lower extremities, medial portion of that motor cortex. So when you knock out the MCA, kind of match it up there, I'm getting face and upper extremities way more than I'm gonna get any lower extremity involvement. Boom, contralateral hemipalasia, so paralysis of the face, upper extremity, way more than the lower extremity. Boom, roasted, move on to the next thing.
Let's take a slice, let's take it, imagine, it's gonna be the same drawing. Take a slice, a little bit farther back. Now we're gonna go behind the central sulcus.
We go behind the central sulcus, here's that black line, there's our central sulcus. We have a blue strip here, that's our sensory strip. That's our primary somatosensory cortex.
Imagine you knock that bad boy out. What's gonna happen? Well, it's gonna lead to sensory loss on the contralateral side.
What kind of sensations? All of them. It could be touch, pain, temperature, proprioception, vibration, all of them.
You lose those. on the contralateral side. Let's make sense of it.
Imagine here's some skin and that's where there's some touching occurring. No, no, don't be weird about it. This information comes up via either the dorsal column, if it's kind of like your fine discriminative touch, or if it's like your crude touch, maybe via the spinothalamic system, it'll come up, cross over, and go.
If it's coming from the left, skin of the left side of the body, it'll go. to the brain on the right side, okay? Now you develop an infarct within the MCA or some type of lesion of the MCA, knocks out that portion, you lose sensation to the contralateral side of the body. Again, same thing, sensory homunculus. Lower extremities supplied more particularly medially by the ACA, and then laterally is going to be the MCA, that's your face and upper extremities.
So you get contralateral sensory loss involving what? Face upper extremities more than lower extremities. Really quickly here, I mentioned that there's two divisions, the superior division and there's an inferior division of the MCA. Really, really briefly, if you kind of imagined here, let's do it in a super bright color here, pink. When the MCA kind of tucks underneath this lateral sulcus, it kind of comes out from the lateral sulcus and gives a branch off here and gives a branch off there.
This branch here is called the inferior division. This branch here is called your superior division. The superior division.
division of the MCA is what supplies that primary motor cortex and primary somatosensory cortex. So if you injure that vessel, that superior division, it affects these territories. It wouldn't be affected if you hit the inferior division of the MCA.
Okay, so remember that. All right, let's move on to the next thing. Contralateral, weakness, sensory loss, boom, face, upper extremity, more than lowers. Next thing is the frontal eye fields.
Okay, same thing, take a side view of the brain. Here you have that black strip. What is that called? That's your central sulcus. In front of it, you have the motor strip, primary motor.
We already talked about that one. Behind it, you got the primary somatosensory. Already talked about that one. Then a little bit more interior.
What do you have? A little pink dot there is called your frontal eye fields. Your frontal eye fields still fall within that green, the territory of the MCA. If we want to be specific, though, what division?
It'd be the superior division, right, of the MCA that's getting hit, particularly. leading to this lesion in the frontal eye fields. All right, so we have an idea that the frontal eye fields is still supplied by the superior division of the MCA. We know that it's in the frontal lobe. What happens, though, if it gets knocked out?
Well, we have to briefly, and I mean briefly, talk about what the heck it does. Frontal eye fields, let's say that we take a coronal section, where the frontal eye fields would be, and here we have that kind of view. Frontal eye fields, let's say that we have the right side. So let's say here's your right frontal eye field.
It'll send these axons down to a structure here, and you're... pons. Here in orange, the left one, called the PPRF, the left paramedian pontine reticular formation, stimulates that guy.
That guy, when he's stimulated, he then tells this blue neuron called your sixth nerve nucleus, hey buddy, go ahead and fire and tell that lateral rectus muscle to contract. And when it contracts, it's going to abduct the eye outwards. Okay? Oh, cool. I'll do that for you.
Also, why don't you tell the third nerve, because you're connected, it to the other third nerve via what's called the medial longitudinal fasciculus. So tell that right third nerve, hey buddy, go ahead and fire for me. And when you fire, tell that medial rectus to go ahead and pull your eyes that way as well.
So generally what should happen is when the right frontal eye field fires, your eyes deviate to the left. What do you think would happen though if you knock out that right frontal eye field? Do you think your eyes will be able to deviate to that left side or gaze to that left side? No. What happens is if this left side is working, fine and properly and it's doing everything it needs to do, the left side is going to tell the eyes to be to the right normally.
There's nothing that's interfering with that. So it'll be unopposed now by this damaged right frontal eye field and guess where the eyes will start to preferentially deviate naturally at rest? To the right side, the same side as where the lesion is.
So we call that ipsilateral gaze deviation. Okay sometimes they even call it a gaze preference. So it's because you're knocking out that frontal eye field if it's on the right your eyes will deviate to the right. Boom roasted on to the next one. The next area here is called your Wernicke's area.
Wernicke's area is a really cool area. So it helps us to comprehend, understand language, if you will. So language can be written, it can be spoken, it can be nonverbal.
And so a lot of that stuff can be picked up from two particular sensations. If I'm speaking to you and you guys are hearing my voice that's hitting your auditory cortex, when it hits your auditory cortex, it sends that information to Wernicke's area, right, from your primary auditory cortex. You also see me writing. things down, you see me drawing arrows and referring to things and giving you nonverbal cues. right?
So that information from the occipital lobe from your visual cortex will also get sent to the Wernicke's area. The Wernicke's area will then take that information about language, analyze it, recognize it, and help us to comprehend what is being spoken or written. If you develop a lesion within the MCA, but we got to be very very particular, think about that that kind of blood flow again, we'll do it in green since that was kind of what we were trying to indicate with the MCA. It sneaks up under the lateral sulcus or the sylveon fissure, gives off this division, and then gives off this one.
What division do you think it's going to get hit? The inferior division. So inferior division of the MCA, if it gets hit, can lead to the Wernicke's area becoming affected.
If it's affected, can you comprehend language? No. So comprehension of language is gone.
The other thing that happens is that Wernicke's area loves to communicate with this blue area in the frontal lobe. lobe called Broca's area. Tells Broca's area, hey buddy, I understand language. Can you tell them what you actually understand?
So then you would tell Broca's area. Broca's area controls the muscles of the speech, which allows for the production of language, expression of language. So in someone who has Wernicke's aphasia, they can express language properly and fluently, but because they can't comprehend language, it literally makes no sense. It's nonsensical. And so that is important to remember with Wernicke's.
area leading to, if there is an MCA lesion, Wernicke's aphasia. What we particularly like to call it, though, is receptive aphasia. Okay, boom, roasted. We'll move on to the next one.
Broca's area. You guys are probably already picking this up because you guys are so darn smart. But again, same thing, MCA kind of sneaks under, right?
So you have that kind of like that M1, M2 segment that sneaks over here, particularly M2 segment. And then branches there, there, and then there. If we have Broca's area, which is going to be this little blue little dude right here. If we knock that out, that falls within what division? The superior division of the MCA.
So if we hit the superior division of the MCA, that could lead to the damage to Broca's area. What does Broca's area do? We already kind of introduced that already. Receives information... from the Wernicke's area as well as other areas, other motor areas, and helps for the production of speech.
Enables particular types of cranial nerves. Cranial nerves 5, cranial nerves 7, cranial nerves 10 and 9 and all of these. 12. It helps for the production of speech in a particular way.
If Broca's area is affected, speech will no longer be fluent and it won't be able to be expressed properly. Even though you can comprehend language and understand what everybody's saying or what you're reading, you just can't express it properly. And so that's what happens with Broca's area being damaged, leading to what's called Broca's aphasia. Next thing is the optic radiations.
Okay, so another little diagram here, if you will. So imagine here we have a little baby. diagram and again you have that MCA sneaking underneath the sylvan fissure and it gives off this one and then it gives off this one right well you have these things called optic radiations optic radiations kind of like to move through the parietal lobe and the temporal lobe okay and so what happens is when someone develops a MCA lesion if you will that's knocking what part the inferior division of the MCA, it can affect the optic radiations that are moving through the temporal lobe and even a little bit through the parietal lobe. So if that happens, you can lead to a particular visual dysfunction because optic radiations... you can already get from the word optic radiations.
It has something to do with the visual pathway. We'll briefly explain this. But if you knock out the inferior part of the MCA, it can lead to some visual pathway dysfunction. Let's briefly explain what the heck I mean.
So let's say here we have a portion of that, like here's your optic radiations, right here after the thalamus going back to the occipital lobe, right here, that's all optic radiations. If someone develops an MCA infarct or an MCA lesion that leads to an infarct of this territory here, where the optic radii... are running through, whether that be through the temporal lobe, whether that be through the parietal lobe, whatever that inferior MCA division is getting hit, that knocks out these optic radiations. Let's follow the optic radiations backwards to the eyeball and see what type of visual information they're picking up. So, for example, if we follow this blue one back here, boom, you hit on this part of the retina.
Remember that this part of the retina picks up visual information from this visual field. Then if we follow the maroon one back, the maroon one, da-da-da-da-da-da. Boom.
This is going to be this part of the retina, kind of towards the nasal part of the retina. Again, remember, this picks up visual information from this part of the visual field. Okay. So if we kind of recap here, this is, if we look at this, let's say that.
This is the right side of the brain and this is the left half of the brain. Okay? If you develop a lesion within the inferior division of the MCA, you knock out the optic radiations on the left side.
What happens to your visual field loss? you lose the visual fields on the contralateral side, the right visual fields. And so if I knock out my right visual fields, that's the contralateral side of where the lesion is, but they're kind of similar.
So we call that contralateral homonymous hemianopia. So if you have a left-sided MCA infarct on that inferior division, you knock out those left optic radiations, you won't be able to see the visual fields on your right side. Let's move on to the last part here. which is the MCA division particularly on the right side.
So I didn't preface this before. So Broca's area, Wernicke's area, they're primarily on the dominant side, okay? And the dominant side of your brain is usually the left side since most people are right-hand dominant. So the left side of their brain is where the Broca's area and Wernicke's area reside. So if I knock out the left MCA, I'm going to potentially see these two symptoms.
If I knock out the right MCA, it's unlikely that I'll see these two symptoms. I'll actually see... these particular symptoms present.
So what could I see if I knocked out that right MCA for the non-dominant hemisphere primarily? You see two particular things that I want you to remember. Apraxia and hemi-neglect. Apraxia is very interesting. It's where your motor system is intact.
So your muscles are fine. There's no issue there. You have the willingness to want to perform a motor movement, but you just can't figure out how to do it. So there's a difficulty in being able to actually...
act out that movement even though you are and willing to do it. Examples of these is idiomotor apraxia. For example, hey can you lift up your right arm? Instead of them lifting up their right arm they'll do something weird and maybe they'll just give like two fingers or if you tell them give me a thumbs up they'll give you two fingers. They start mixing up their movements and kind of don't really know how to really perform the movements properly.
Eyelid apraxia is very common where you ask them hey open up your eyes. They're There's nothing wrong with the levator palpebra superioris. It's working fine. It can contract and elevate the eyelid, and they want to do it.
They just don't know how to do it. And then ideational apraxia. Give them a marker and say, hey, draw me something.
They'll look at this, and they'll be like, dang, I know this is a marker, and I want to draw something, but I don't know how to use this dang thing. And that's ideational apraxia. So, again, recapping it, motor function's intact. Willingness to do the function is okay, but they just don't know how to do it or kind of really go about performing that activity.
Neglect is also very interesting. So again, you knock out that right MCA, which is usually the non-dominant side, you neglect the sensations on the contralateral side of the body, just like you would if you knocked out your primary motor, primary sensory cortex, whatever. The same concept. For example, knock out my right MCA. If I have hemi-neglect, let's say that you have a patient.
You're going into the room. You have three people in the room, one here in front of them, one here on the right of them, and then one over here to the left of them. And let's say that you ask the patient, hey, how many people are in the room? They will see the person in front of them. They will see.
see the person to the right of them, but they will not be able to see the person in their left visual field because they're neglecting their left visual field. So that's an example of one. The other thing here is sensory.
If you take and have the patient close their eyes, and then you say, okay, I want you to tell me which side of your body I'm touching, and you touch both of the sides simultaneously, they'll say, oh, you're only touching my right side. You want to know why? Because they're neglecting all of the sensations on the left side of their body and so that's what can happen with right MCA infarcts usually they're referring to it as the non-dominant hemisphere. Okay that tells us what we need to know about MCA syndrome which is the most important one let's now talk about ACA syndrome. Alright so let's talk about ACA syndrome so ACA syndrome anterior cerebral artery syndrome you knock out one of those ACA's.
So ACA is gonna supply pretty much what part of the brain so it supplies primarily the medial frontal lobe and the medial parietal lobe It even hits a little bit of the basal ganglia as well, parts of it. So what I really want us to focus on is, it's kind of similar to what we talked about with the MCA in the beginning, the primary motor and primary somatosensory cortex. This should actually be a very quick recap, we shouldn't have to spend tons of time, is that if we take a look here at the side view of the brain.
Here's going to be our central sulcus right here and then in front of it is the primary motor cortex, right? If we draw here in pink what portion is actually ACA, it's kind of kind of be like this if you really want to think about it. That's all going to be the ACA. And then if we had here before just to kind of like in a dash line here, what was this part here? That one.
was the MCA, right? So when we're talking about the kind of the different territories here, the ACA is hitting more of that medial strip of the primary motor and primary somatosensory cortex, whereas that MCA is hitting more of the lateral portion. So what do you guys think? Do we really... need to go too hard here let's briefly blow through it here if we take a coronal section in front of the central sulcus where the primary motor cortex would be upper motor neurons are going to come down be the coronal radiata internal capsule crust the rebrae through the pons, decassate at the pyramids, come down to lower motor neurons, and go to the muscles on the contralateral side.
You develop a lesion in the ACA, particularly the medial territory. You knock this out. You develop weakness on the contralateral side.
But what does the motor homunculus tell you? For MCA, it was face upper extremities, as represented here in green. For ACA, it's pink here, which is lower extremities. You're knocking out lowers more than the the uppers and the face. Boom, roasted.
What about the blue stuff here? Go back, take another section. Imagine that this is another section and we're taking it behind the central sulcus where the primary somatosensory cortex is, where sensations are basically involved.
We take these sensations coming from the skin, coming up, maybe dorsal column, maybe spinothalamic tract, and eventually going from the left side of the body to the right cerebral hemisphere. If you develop a lesion in the ACA, you knock out the sensations coming from this portion, contralateral sensory loss. Again, remember your sensory homunculus.
For the face and upper extremities, that was the MCA territory, but for lower extremities, that was primarily ACA territory represented in pink. So you get contralateral sensory loss involving what? Lowers, more than uppers, and the face.
Boom, roast, we just did it, right? We blasted through that pretty quickly. Now.
Move on to the next one. So the next part is the paracentral lobule. The paracentral lobule is a very interesting little thing.
Imagine here for a second, we were taking a look at the brain from the side, right? Imagine I cut it in a sagittal section and I remove that right piece. So now you're just looking at the left half of my brain from the medial side.
So here's that view. Here you see like your corpus callosum here. And then above it in this pink kind of structure there is what's called the paracentral lobule.
The paracentral lobule is interesting because it kind of picks up sensory and motor information. So there's kind of going to be like some sensory information here that comes to the paracentral lobule. And there's also motor information that is involved and connected from the paracentral lobule to the urinary bladder and some parts of the bowels.
But a big one to remember is the urinary bladder. If you knock out the paracentral lobule. out the paracentral lobule from an ACA infarct, because again, you're falling within that kind of like medial strip of the ACA. This is all ACA right here. So if I were to kind of highlight here, this is all ACA.
If you knock out that paracentral lobule, you no longer have proper sensory and motor function of the urinary bladder, and maybe somewhat of the bowels too, so there is what's happening of urinary incontinence and fecal incontinence. So you accidentally go pee-pee or poo-poo. So that is the basic concept of the paracentral lobule.
So we got contralateral weakness, contralateral sensory loss, more particularly lowers than uppers, and we got urinary fecal incontinence if you hit that paracentral lobule. The other thing that we should remember here is again, take another medial view of that cerebral hemisphere, and we're looking at that left cerebral hemisphere. It also can hit another portion here.
So if we kind of again, and pink here, all of this would get hit from A. ACA lesion. Okay, what are these two areas that I want you guys to think about? These are particularly more for behavior. Okay, behavior, decision-making, things like that.
So we have here in green the prefrontal cortex. You guys know that prefrontal cortex is involved in tons of things. Emotions, memories, decision-making, personality, behavior, executive. function, all that stuff. The anterior cingulate cortex is kind of involved with also aspects of memory, but a part of our limbic system.
So whenever you knock out these two structures, it leads to particular behavioral and decision-making abnormalities. kind of classify these as a boolean and a kinetic mutism so a boolean is basically they have a significant decrease in motivation willingness any desire to want to do anything purposeful like verbally or our motor example you come into the room you say hey miss Jones can you please lift up your left arm there'll be a very significant delay and kind of a very decreased desire to want to lift up her arm if she even does hey, can you tell me where you are? What's your name?
There'll be a significant delay if even if she does respond to what's your name or where you are. So because there's this decreased willingness, desire, and motivation to want to interact or. Perform verbal or motor activities.
That's a boolean if you knock out these two structures If you knock out both of them because you get a bilateral ACA lesion you get even worse You get to the point where you don't talk and you don't move because you have no No desire, no willingness, no willpower to want to interact verbally or motor via a kinetic, no movement, mutism, no verbal communication. All right. So the next part here of the ACA syndrome is if you hit like a and again, we're adding this in just real quick.
quick little thing, is that there's this little red area. Remember I told you that the Broca's area can receive information from Wernicke's, and it can receive it from another motor area, particularly within the frontal lobe. And so this little red area within the anterior superior frontal lobe communicates with the Broca's area, and it's involved in speech, okay?
If you develop an ACA lesion, particularly in that dominant hemisphere, that left side, primarily, usually, right? You're going to knock out this structure here, and it's connection to the the Broca's area. And so what happens is, is you develop, again, some difficulty with speech production.
So because it's responsible for communicating with Broca's area, there is going to be some difficulty in telling the Broca's area to be able to engage in speech, engage in expression of speech. So there will be some non-fluent or decreased speech ability, but comprehension will be intact. Same like Broca's area, because why?
Why should comprehension be intact? for both this red and this blue thing. Are you touching Wernicke's area? No.
So since Wernicke's area isn't getting involved, comprehension should be intact. So asking them, hey, what's this called? Oh, it's a marker. Oh, if I pull out my phone, what's this called?
Oh, it's a phone. Now, here's where it can be a little bit different between Broca's and blue and red for this transcortical motor aphasia. If you say, hey, can you repeat after me? No ifs, ands, or buts, or today is a bright and sunny day.
And they can do that. That isn't. indicative of transcortical motor aphasia.
If they can't do that, it's indicative of Broca's aphasia. So you can still get aphasia from ACA syndrome, but remember that if it's transcortical motor aphasia, you can differentiate it from Broca's by asking them to repeat phrases. If they can, it's transcortical motor, unlikely for it to be Broca's. Okay, that covers our ACA syndrome. What do I really want to do next before we go on to the next thing called the ICA, I want to talk about this thing called watershed zones.
We talk about this in acute ischemic strokes called watershed infarcts that can happen from global hypoperfusion. You remember kind of like if you take a top look at the brain, right? Take a top look at it. And here we have the frontal lobe. And you can represent that it's frontal lobe because here's anterior, here's posterior, here's your central sulcus.
Okay. In front of the central sulcus is going to be the frontal lobe. Behind the central sulcus is parietal lobe here.
Remember what I told you, the lateral portion of the frontal and parietal lobe is supplied by green, which one? MCA, right? So this is all MCA.
And then the medial portion of the frontal and parietal lobe is supplied by the ACA. Where they meet here in red is called that watershed zone. And those zones are really kind of susceptible to very low perfusion.
So if you drop their perfusion to these particular areas, they're very susceptible. And the neurons and brain tissue in that zone can become... damaged.
What happens then is you start to kind of fall within that category. Remember here we have like lower extremities and then over here we have like face and upper extremities and then somewhere here in between is kind of like your trunk and like the proximal extremities of the lower proximal lower extremities proximal upper extremities. You're kind of going to be falling right within that part of the trunk at the proximal extremities upper and proximal lower extremities and so because of that that when someone gets a infarct of that watershed zone in the MCAACA territory, you knock out that proximal upper extremities and proximal lower extremities. But again, think about this. If you get frontal lobe where that primary motor strip is, what would happen?
You develop weakness, right? And it could cause contralateral weakness or contralateral hemiplegia. If you knock out the parietal part where the primary somatosensory cortex is, what do you get?
You get sensory loss of the contralateral side as well. So again... Big thing to think about with watershed zone, particularly MCA, ACA, if you knock that out, you develop proximal upper extremity weakness and sensory loss, proximal lower extremity weakness and sensory loss, and we also call this man-in-a-barrel syndrome. So that covers MCA, ACA watershed zone as well as the MCA, ACA syndromes. Let's move on to ICA syndrome.
All right, so we talked about ACA, we talked about MCA, we talked about the MCA, ACA watershed zone. Let's talk about the ICA, and actually, nicely, this would be a good... quick recap of the MCA. and ACA because the ICA is a very large vessel and what happens if you guys remember your your circle of willis blood flow it comes up and branches into the ACA and MCA and also there's another little vessel that I'll talk about really quickly called the ophthalmic heart So if we kind of take a look here again, coronal section, looking at the brain here and again you got your let's just say here you have the frontal lobe and then here you have your temporal lobe. Here in that circle there, this circle is is representing the ICA.
This is coming up and feeding the circle of wills, the anterior circulation of the circle of wills. And what happens is it gives off this one that's moving towards this actual portion here, towards the medial portion, and will supply the medial portion of the frontal prilob. This is called your ACA. And then you're giving off this other portion here, which is gonna feed laterally through that lateral sulcus, sylvanian fissure, come out and give off the superior and inferior divisions that'll supply.
the lateral portion of the frontal lobe, parietal lobe, and the temporal lobe. What is that? That's your MCA. If you develop an occlusion or injury or damage of the ICA, you could potentially lead to a decreased or no blood flow via the ACA or decreased no blood flow via the MCA.
So what could happen is you could present with an MCA syndrome. Let's test your knowledge. Contralateral hemiplegia, contralateral sensory loss, where?
Face uppers more than lowers. frontal eye fields what happens you get ipsilateral gaze deviation you hit Wernicke's you get Wernicke's aphasia you get Broca's you get Broca's aphasia you hit the right non-dominant side you get apraxia hemine neglect and if you hit those optic radiations you get contralateral homonymous hemianopia ACA you get contralateral hemiplegia contralateral sensory loss of what lowers more than the face and the uppers if you also have the paracentral lob you get urinary fecal incontinence if you also untie of that hit the prefrontal cortex and the anterior cingulate gyro. So you get a boolean achinetic mutism and if you hit that motor connection between the Broca's you get transcortical motor aphasia. We just recap those now. That's ICA if you get a severe enough damage to it.
Now one other thing the PCA is primarily a posterior circulation vessel comes off that vertebra basilar system and 5% of patients they may have what's called a fetal PCA variant. So be aware of that. Sometimes you can actually have an orange here, that PCA come off of the internal carotid artery rather than it come off the vertebrobasilar system. So if someone also develops posterior circulation stroke, like PCA division, which we'll talk about here, and you think that they have a problem with their ICA, think about that fetal PCA variant. The last thing I want to talk about with ICA is the ICA also affects this vessel.
So here's your ICA, and it gives off a vessel called the ophthalmic. artery which will help to feed the central retinal artery some of the ciliary arteries that supplies the retina if you have a decreased blood flow to the ICA okay and then into the the ophthalmic artery central retinal arteries you can develop this transient type of monocular vision loss so for example right ICA right transient monocular vision loss and that's called amaurosis fugax if it is not reversed or treated then what can happen this can become complete damage to the retina and complete monocular vision loss. So that's another thing to think about with ICA. If they develop MCA syndrome, ACA syndrome, plus or minus PCA syndrome, if they have that fetal PCA variant and transient ipsilateral monocular vision loss, think about ICA syndrome.
All right. So we talked about the MCA. We talked about the ACA.
We talked about the ICA. We even talked a little bit about the MCA, ACA watershed zone. So we haven't talked just yet about the PCA we've kind of introduced it the posterior cerebral artery but there's another watershed zone that I want to talk about before we start going into the posterior circulation so stroke syndromes so this is called your MCA PCA watershed zone just like the ACA MCA I think about if you take a an actual axial cut okay so you're taking an axial cut of the brain and we're gonna take it to where we get part of the like frontal lobe here maybe parietal lobe and then you get back here your occipital lobe. Well where we get to the point of where the MCA and ACA territory start to come together and kind of meet one another, we'll represent that here in this red color, that is going to be the MCA PCA watershed zone.
Just as an example here, right here would be your MCA ACA watershed zone where we get that man-at-a-barrel syndrome. If you knock out the MCA PCA watershed zone, which you see with global hypoperfusion because of this section where they meet is very Very, very sensitive to low blood flow or low oxygen carrying capacities, you can get these watershed infarcts. And it leads to visual dysfunctions.
Two of the types that you probably want to remember, the most important one is prosopagnosia. So prosopagnosia is actually relatively sad. What happens is the person can visual... see. So the primary visual cortex is intact but when you start involving kind of the association areas which you get closer to that MCA, PCA, watershed zone it starts affecting the ability to analyze, recognize, and identify what those objects you're seeing are.
seeing are or people you're seeing are. For example, Rob is filming me right now. I know that there's an object there. I analyzed him.
I know he's there and I know that it's Rob. For someone who has potentially this MCA, PCA, watershed zone infarct, they'll know that there's an object there, but they won't be able to make out who that person is. It was relatively sad. The other one that can happen here is balance syndrome.
Relatively rare, but balance syndrome is kind of a triad, if you will, of simultanous. So, you know those little things called the Ishihara color plates where they have like, you know, red and green and blue and whatever, and it's used to like form a number within that, maybe like the number four is in there. The individual will be able to see the different colors, but won't be able to see how the colors make a image such as the number four.
So that's called simultagnosia. The other thing they can get is what's called optic ataxia, which is very different from cerebellar ataxia. If we do like the finger to nose test, they'll have. have difficulty bringing their finger from their nose to the patients I'm to the to the clinicians finger but they won't have a problem bringing it back to their nose so it could be something like this and back here something like this back here perfectly The last part of the triad is oculomotor apraxia, where they just have, again, all the extraocular muscles are moving.
Functionally, they're intact. They have the willingness to move their eyes, but they just can't execute the movement, or they don't know how to be able to move their eyes in kind of a horizontal fashion. So it's called oculomotor apraxia.
I think that gives us a good idea pretty much of kind of talking about our anterior circulation strokes as we start to transition into our posterior circulation stroke syndromes. So let's briefly talk about these. Recapping anterior circulation strokes. syndromes.
We talked about anterior cerebral, middle cerebral, internal carotid, and we also talked about that MCA-ACA watershed zone, and we briefly started to get into that MCA-PCA watershed zone. Anterior circulation strokes are by far the most common, 70% of strokes. Posterior circulation, which we're going to talk about now, is getting towards like the occipital and brainstem area. This is covered by the posterior cerebral artery, the basilar artery, and the vertebral artery, and these account for...
for the 30% of stroke syndromes that we're gonna talk about now. So let's go ahead and now focus on posterior circulation strokes, starting with the PCA territory. All right, so let's talk about the posterior circulation stroke syndrome.
So now we're getting into the PCA, the posterior cerebral artery. So posterior cerebral artery, really interesting one, supplies a pretty decent chunk of the brain stem, particularly the midbrain. So we'll talk about some of the midbrain syndromes. It also supplies the occipital lobe, we already know that. So we're gonna talk about some visual defense.
and then it also supplies another structure called the thalamus, which is very important as well. Alright, so let's talk about particularly the posterior cerebral artery. So again, a nice little view here, I like to look at that side view, just to give us a good idea here. So when we look at the side view here, we can see here in green is the MCA territory hitting that lateral frontal parietal upper part of the temporal. For the ACA, we're getting the medial frontal and parietal.
And then the PCA, you're getting that occipital lobe, and then you're getting down here into the temporal lobe, right? So we know that. So, Here's where we got to talk a little bit about this first one, which is if we start involving this kind of visual cortex area. So you know you have what's called the primary visual cortex and the association cortex. And these are responsible for taking in visual information from the optic.
radiations, from the optic tracks, all of that good stuff. So if we take, for example, let's say here is going to be right, here is going to be left. This is going to be a nice quick recap of the MCA. Here, let's say that we have a a infarct or a lesion of the PCA that knocks out this left visual field area, particularly the left visual cortex.
So because of that, if you kind of track all of that stuff back like we did before from that side, you're going to lose the visual field here on the opposite side, and you're going to lose this visual field if you track all of these back. So this is the left, particularly like occipital lobe lesion. So what's going to happen is you're going to lose your visual fields on the right side contralateral side. So we call that contralateral homonymous hemianopia.
Okay, so that's what you would see with a lesion, particularly involving the kind of your visual cortex and the Association cortex. Alright ninjas let's move on to the next part here which is the midbrain part of the PCA territory right so we talked about the PCA supplied the cortical part of the occipital lobe a little bit of the temporal lobe we talked about the thalamic involvement now let's talk about its extension into the brainstem particularly the midbrain. There's three midbrain syndromes that I really want you to know there's actually another one too but this is the these are the three main ones I want you to take away from this if you knock out the PCA.
So here the midbrain you got the ventral part of the midbrain so this is the part here if I were to kind of denote this this is anterior part of the midbrain posterior part of the membrane okay if you knock out the midbrain there's different syndromes that can develop the first one that can happen here is if you knock out the third nerve as well as the corticospinal tract. So if you knock out the third nerve in the corticospinal tract, that leads to what's called Weber syndrome. Knock out the third nerve, you get ipsilateral third nerve palsy because the third nerve doesn't cross. The other thing is you get contralateral hemiplegia. This may be somewhat confusing.
You're hitting your left corticospinal tract, which is in the left crust cerebri. You guys know what happens, right? Whenever we have the corticospinal tracts, it starts from the cortex, comes down to the coronaradiata, internal capsule. moves through the midbrain.
Imagine for a second here that we come down the pons, come down to the medulla. What does it do when it gets to the medulla at the pyramids? Crosses and goes to the muscles on the contralateral side.
So if you knock out that left crust cerebri, where again, the corticospinal tracts are running, you get weakness on that contralateral side. And then same thing, the third nerve is what supplies particularly a bunch of different muscles. But one of the big things to remember here is that it's going to lead to what's called a down and kind of of out movement of the eye and if you hit those parasympathetic fibers it may even cause some dilation as well.
Alright so we got Weber syndrome down. Third nerve palsy, ipsilateral, contralateral hemiplegia, Weber syndrome. Next one is Claude syndrome.
Claude syndrome as you're going at the level of the red nucleus now. So here we were at a particular level we want to go for Claude syndrome go to the level of where the red nucleus is in the midbrain. When you go to the level of the red nucleus you still have that third nerve there but Whenever someone has Claude's Syndrome due to a PCA lesion, you knock out two particular structures. One is the third nerve. Again, if you have third nerve that's injured in this Claude's Syndrome, it's going to cause a down and out movement of the eye.
It also could cause dilation if you hit the parasympathetic fibers. But you're also going to hit this thing called the red nucleus. What does the red nucleus do? The red nucleus is a part of your rubrospinal tract, so it involves kind of like distal flexion, but it also loves to communicate with the eye. with your cerebellum.
Loves to communicate with the contralateral cerebellum. So if you knock out the red nucleus, you knock out the communication with the contralateral cerebellum. So for example, if you knock out that left red nucleus, in this case, for example, this is gonna be right, this is gonna be left.
If you knock out that left red nucleus, you're altering the connection between that right cerebellum and the left red nucleus. That's gonna lead to ataxia on that side of where the cerebellum was communicating. with the red nucleus. So for example, if it's the right cerebellum communicating with the left red nucleus, you would develop ataxia on the contralateral side to the red nucleus, but the same side of the cerebellum.
So we call that contralateral ataxia. So again, brief recap for Claude, as you hit third nerve, so ipsilateral third nerve palsy, you hit the red nucleus, leading to contralateral ataxia because you communicate with the contralateral. contralateral cerebellum. Next one is Benedict Syndrome.
Benedict is basically Weber and Claude. That's all you need to remember. It's Weber and Claude. So you're knocking out the red nucleus, you're knocking out the third nerve, and you're knocking out those corticospinal tracts.
So what do you get? If you knock out third nerve, you get ipsilateral third nerve palsy, down-out movement, you hit the parasympathetic, dilation. You hit the corticospinal tracts, crosses again later at the pyramids, you get contralateral hemiplegia.
And if you hit the red nucleus, again that communicates. keeps with the contralateral cerebellum, you'll get contralateral ataxia. Boom, roasted, we just hit PCA syndromes. Let's move on to the next thing, which is your basilar artery syndrome. All right, let's move on to the next thing, which is the basilar artery syndromes.
So basilar artery is a beast, all right? So this supplies a good chunk of the brainstem, particularly the pons and the cerebellum, okay? So we're talking about the superior, anterior, and inferior part of the cerebellum. So again, if you want to recap it, what is the basilar artery supply?
It supplies the pons. It supplies the superior, interior, and inferior part of the cerebellum. And we're going to make sense of all this.
It's actually relatively easy. So let's take a look here at the quick little blood flow supply here. So we have particular numbers that I want you guys to know. We'll briefly recap, though, kind of the circulation, right? So here we're going to have your vertebra arteries, right?
Those come off of your what? So you remember how you have your brachiocephalic, and that goes in, for example, let's say brachiocephalic goes into the subclavian, and then it goes into the internal carotid, or the common carotid. So off of that kind of subclavian, you can have those vessels called the vertebrals that can pop off.
So you have the vertebral arteries that are going to be here. They'll give off a branch that we'll talk about later in the vertebral artery stroke syndromes, which is called your pica. Eventually, the vertebral arteries will come together, fuse, and make this big mama here.
This is number one. Number one. one that I want you to remember is the basilar artery. It's basically from this whole chunk right here to this whole part right here is going to be our basilar artery.
So basilar artery supplies a very good chunk of the pons but what I want you to really really remember is that the basilar artery gives off lots of branches. The basilar artery branches that actually are going to be little branches that penetrate into the pons the paramedian branches to supply primarily the medial pons. So when you guys think basilar artery artery, its branches, the immediate branches off of it is going to be the paramedium branches. Those supply the medial pons. Another thing that happens is as the basilar artery tracks, tracks, tracks, tracks up.
So we actually should say that the basilar artery comes up about here. It gives off a branch here called the PCA. That's number two.
So PCA is the number two branch off of the, in this case, the basilar artery. And that's the part that we already talked about, gives way to the midbrain, supplies the occipital lobes, temporal lobe, even hits that thalamus, right? The other one is we move our way down. So number one, number two, we got PCA. Number three off the basilar artery here is this guy called the superior cerebellar artery.
Superior cerebellar artery, what do you think this implies? The superior cerebellum. Move on to the next one.
So we got, again, vertebrals coming up, basilar. Basilar goes all the way up, gives off PCA. Then it gives off SCA. Then if we come down a little bit, the other branch that it gives off here, number four, is the anterior inferior cerebellar artery.
That supplies the. the lateral portion of the pons and it supplies the anterior and inferior portion of the cerebellum thus its name quick recap again vertebrals come up fuse make basilar basilar extends all the way from the pons upwards up here branch it gives up at the top is the pca the one that it gives off underneath that is the sca and the one that it gives off underneath that is the aica or the anterior inferior cerebellar artery got it now that we know that and we know that the basilar, its immediate branches give off medial pons. ICA gives off lateral pons, anterior inferior cerebellum.
SCA supplies the superior cerebellum. We know the big, big vessels that we need to know now for the basilar artery. Let's talk about these now.
So the first thing I want you guys to remember is the basilar artery gives off a little pair of medium branches that supply the medial pons. If you knock out the little pair of medium branches of the basilar artery, you don't give blood supply to the medial pons. You lead to nerve damage.
neuro deficits from the destruction of all the structures in the medial pond. So we need to know what in the heck is in the medial ponds. Let's do that.
Let's do it from dorsal to ventral. From the dorsal part here, kind of in the midline, you have a particular nucleus and this is the sixth nerve nucleus. Sixth nerve nucleus is also known as the abducens nerve.
So abducens nerve, if you hit this, so let's say here again, this is kind of this blue is marking the territory. You see all this blue here? This is all basilar artery, the paramedian branches of the basilar artery.
So that's all kind of encompassing this part here, if you guys can imagine that. If we knock out the paramedian branches, we don't give blood supply to the sixth nerve nucleus, what does the sixth nerve do? It abducts the eye, the same eye. So if it's the left abducens nerve, it's going to abduct the left eye.
If you knock that out, you develop ipsilateral sixth nerve palsy. Can't abduct that left eye. What's the next one? Go here to this little maroon colored one.
That maroon color. guys called the MLF medial longitudinal fasciculus what does it do connects it's a midline structure that connects the third nerve at the top fourth nerve and the sixth nerve all I want you to remember is it helps to conjugate eye movement so if you want to move your eyes to the right you have to have your left medial rectus contract and you also have to have your right lateral rectus contract so that MLF helps to coordinate and conjugate movements properly with those extra ocular muscles okay between what structures you're connecting connecting, three, four, and six. If you knock that out, it's going to lead to what's called internuclear ophthalmoplasia.
Your eye's going to be all wonky because you're not going to be able to coordinate the eye movements conjugately properly because you knocked that structure out. Move to the next thing. As we go a little bit more interior, we got this blue structure here called the PPRF, the paramedium pontine reticular formation. This also is involved in kind of conjugating eye movements as well. So if you knock out that, you develop a loss of gaze to that same side of where that paramedium pontine reticular formation is.
So you won't be able to gaze in this case to the left side and so because of that the actual preference or deviation will occur towards the contralateral side. this case the right side. Okay so again quickly recapping PPRF, you knock that out, your conjugate gaze is affected, you can't gaze properly to the same side, if you can't gaze to that left side now what happens is your eyes start to deviate to the contralateral side.
Next one, move again, medial here, but again going anterior as we're working from back to anterior here. We got this green structure called the medial liminiscus. If you knock out the medial liminiscus, what does it do? It takes sensory information.
What kind of sensory information? Fungus. mind, discriminative touch, proprioception, vibration, all of that stuff takes it up from the body up to the central nervous system.
If you knock that out, and in this case, it's on the left side, if you hit the left medial meniscus, you're gonna lose. sensations such as fine, discriminative touch, proprioception, vibration on what side? The right side in this case okay so we the contralateral side so that's where you get contralateral loss of sensations.
Move again anterior and you got this big old red thing here called the corticospinal tracts that are running through the pons. You even have corticobulbar tracts which control muscles of the head and neck as well but either way you knock that thing out it hasn't crossed yet right so if it's on the left side that you're knocking out that corticospinal tract. it hasn't crossed yet at the pyramids, but eventually it will, it'll come down to the pyramids and cross and go to the other side.
So you're going to get contralateral hemiplegia of what? The entire side of that body. In this case, if it's the left corticospinal tract, you'll develop right-sided weakness of the face, the upper extremity, lower extremity trunk. Boom, roasted, we just hit the medial pons. But what do I want you to remember?
What artery is primarily occluded? It's the paramedian branches of the basilar artery there that we're knocking out. come down to the next one what did i tell you comes off of the uh the basilar artery okay it was number four comes off of it and supplies the anterior inferior cerebellum and supplies the lateral pons that was the ica so look at this diagram here here we have the basilar which was supposed to be this territory right here kind of kind of like make it like that so it fits but that was our basilar artery territory is that getting hit right now from those paramedian branches no what structure structures would be getting hit if you're over here. Ooh baby, we hitting that ICA. We hitting that ICA.
So the ICA is going to involve more of that lateral pons, which we told you when we talked about that above, and it's also going to hit the anterior inferior cerebellum. So let's talk about what it does though. If the ICA is affected, you don't get blood supply to the structures in the lateral pons.
So let's know what's in the lateral pons, and if we damage that, what would happen? Let's work our way out. out from the most lateral part of the pons and let's kind of work our way laterally medially and anteriorly okay so we're going to work from here and we're going to go this way so first thing here is you got these structures here most laterally and maroon called the middle cerebellar peduncles so those are a communication system they're a highway system between the pons and the cerebellum allowing for a nice communication there between them now remember what it does is it takes sensory information from your spinal cerebellar pathways and takes that input puts that into the cerebellum so that the cerebellum can say, hey, I'm receiving all this proprioceptive information, all of this kinesthetic information, and I'm knowing where the position of the body is in three-dimensional space. If you knock out that middle cerebellar peduncle, on this case, the left side, All of that proprioceptive and kinesthetic information coming up via the spinal cerebellar pathways on the left side is going to get knocked out. And you're going to not be able to coordinate where your position of your body is in a three-dimensional space.
And so this can lead to ipsilateral ataxia. because you're hitting that middle cerebellar peduncle and everything for cerebellum is always ipsilateral okay so that's what happens there knock out the middle cerebellum peduncle ipsilateral ataxia because that's where the spinal cerebellar pathways are going into the pons. Move our way, again, we're going to go kind of medially and work our way anteriorly.
So we're going to hit this purple structure here. This purple structure is your vestibular nuclei and a little bit of the cochlear nuclei. So your vestibular nuclei are responsible for what? A lot of your equilibrium, right? So your dynamic equilibrium, your static equilibrium.
And so what happens is if you affect these things, you can lead to a loss of that equilibrium and that kind of presents sometimes as vertigo. And vertigo also is not too great because what happens is when Whenever someone's really, really dizzy and they have a lot of these abnormalities in their equilibrium, it loves to stimulate what's called the chemo trigger zone. And that chemo trigger zone will induce nausea and vomiting from that kind of like really...
significant vertigo. So they can develop vertigo, nausea, vomiting. Also the vestibular cochlear system also does have a communication with what's called your vestibulo-ocular reflexes.
And so because of that they can also develop these beating of movement. of the eye is called nystagmus. If you hit the cochlear nuclei, what does the cochlear nuclei do?
They're responsible for receiving information from that spinal organ of Corti, right? Literally, sound, amplitude, pitch, all of that stuff. stuff for hearing, for sound stimulus.
So if you lose that, you can obviously develop deafness and sometimes a very high-pitched sound called tinnitus. So we got ipsilateral ataxia, we got deafness, vertigo, nausea, vomiting, and nystagmus. Now we go to the green structure here.
The green structure here is called your descending sympathetic fibers. So those are coming from your hypothalamus. You remember hypothalamus has the descending sympathetic fibers that run down through the spinal cord. If we knock these out, you knock out the sympathetic fibers.
supply particularly to like the face and the eyelid and the eye the actual muscles of the eye particularly the the ciliaris muscles okay so what happens here so what happens is if you knock out the sympathetic tracts you develop what's called horner syndrome on that that same side so ipsy lateral so if you knock that left sympathetic tracts you develop left-sided horner syndrome so what does that consist of well you knock out the muscles uh the tarsal plate muscles and so what happens is you can develop ptosis of the upper eyelid You can cause anhydrous. So again sympathetic supply supplies sweat glands. So you'll have anhydrous of that side. And sympathetic supply also goes to the pupillary muscles. So normally your sympathetic wants to dilate the pupils.
But if you knock out the sympathetic system what happens? They'll actually constrict and that's called a meiosis of the pupils. Okay boom roasted move on.
Okay now we go again we're gonna move this way. We'll come back to this little bugger a little bit later. Okay we're gonna move on to this red one here. The red one there is called your spine. So this is actually part of your trigeminal nuclear system.
So you remember your trigeminal nucleus, you have the different parts in the midbrain, the mesencephalic part, you have the central pontine part or principal pontine, and then underneath that you have the spinal trigeminal nucleus. Well, you have that nucleus and then you have the tract. When you knock out the nucleus, particularly where the motor nuclei are, the motor nuclei of the fifth nerve, I'm sorry, the fifth cranial nerve, nerve, which is the trigeminal nerve, you affect the muscles that they supply, which is the mastication muscles. And so if you knock out that left side, you'll affect the muscles on the left side, leading to decreased effectiveness of the mastication muscles on that left side.
The other thing is all of the sensations of the face come from the trigeminal nerve and that all gets taken into that trigeminal system. So the trigeminal tracts also are going to get hit. And so you're going to get ipsilateral loss of... pain, temperature, some of the touch and proprioceptive sensations from the face.
That's where you get ipsilateral sensory loss, ipsilateral weakness of the mastication muscles. Boom, roasted. What's the next? Let's move on to this little blue dude.
The blue dude is actually going to be your spinothalamic tracts. So these are taking particularly pain, temperature, some of the crude touch, pressure sensations, not from the face, but from the body. So from your upper extremity, your trunk, and your lower extremities. So for example, if you knock out that spinothalamic tract on the left side, you're going to develop what? Remember what happens when you have sensations coming in via the spinothalamic tract?
They come into the spinal cord and they immediately cross at that level of the spinal cord usually. Depending upon that maybe one to two levels to tract of the sore, but again the whole point is it crosses the level of spinal cord and then ascends. So it's already crossed and we're at that point here at the pons, that means that if you knock out this structure, the spinothalamic tract, the sensations are going to be on the right side. so you'll develop contralateral loss of pain temperature maybe even some crude touch and pressure sensations okay so that's what you'll get there and then the last but not least is this dude here sitting in the middle is just their facial nerve nucleus so the facial nerve nucleus you actually know that it kind of wraps around the sixth nerve and then goes out right but if you hit the facial nerve okay what happens if you hit the left side it's ipsilateral so you can develop ipsilateral facial weakness usually though it's the it's the lower kind of like third part of the face, okay?
So it's the lower third part of the face, okay? But again, you're gonna develop ipsilateral facial weakness, usually the lower part of the face. That covers the lateral pons, which again is supplied by what part?
Ica, medial pons, the paramedian branches of the basilar. All right, let's finish off talking about, again, the other branches that we didn't really completely discuss. We really talked about the medial pons and lateral pons, but we didn't talk about the cerebellum.
Because remember, the basilar artery does supply not just the pons. but the superior anterior inferior part of the cerebellum through what vessels though? Well, the superior cerebellar artery supplies the superior cerebellum that comes off kind of the top part of that basilar and then a little bit underneath that is going to be the icica that supplies the anterior inferior part of the cerebellum either way You occlude these vessels you damage those vessels you don't get blood supply to the cerebellum. Cerebellum is involved in so many things like posture, tone, coordination, a lot of different things like that. So if you knock that out, you can develop things like ataxia.
So obviously kind of like loss of the coordination. You can develop dysmetria. Difficulty being able to kind of like track particular spaces, like when you're trying to move your finger to nose.
So finger to my nose, to the actual clinician's finger. They may overshoot it or they may undershoot it and they may have problems bringing it back to their nose as well. Dysdiatokinesis, they have difficulty with kind of like those rapid alternating movements. They might have like an irregularity in there and not be able to do it as quick. And so things like that can kind of come up as well.
So again, when we talk about basilar artery syndromes, think about all... of these things coming up, but think about what vessel supplies the medial pons, paramedia branches of the basilar, lateral pons is ICA, and then for the cerebellum we're talking about superior cerebellar and ICA. I think we nailed that home, let's move on to the last part which is the vertebral artery syndromes.
Alright Ninjineers, we are at the end, I promise I know that this has been tough but let's stick through it together, we got this Ninjineers, we can do this. So we're going to finish up with vertebral artery syndromes. Now, vertebral arteries, I want you to remember, supplies the last part of the brainstem.
So we know PCA hits the midbrain, right? We know the basilar hits our pons, superior cerebellum, anterior inferior cerebellum. Vertebral is going to hit the medulla and the posterior inferior part of the cerebellum, right? So let's talk about that.
Before we do that though, let's briefly talk about the blood supply, recapping it again. So again, what do we have these structures here coming up off of the subclavians? Your vertebrals. So that's number one, right?
So vertebrals, your right and left vertebral arteries. What do we say that they need to remember? What do these supply?
They give off their little branches. And particularly, they give off their branches through what's called the branch in the middle here, you see this thing right here number two, that's called the anterior spinal artery. So what happens vertebrals come up as they come up and approach one another to become the basilar, they give off this little branch here called the anterior spinal artery. So the anterior spinal artery is particularly the branch that supplies the medial medulla, but we can still say the vertebrals also supply the medial medulla.
So when I say what gives you the blood supply to the medial medulla, you should say your vertebrals and your anterior spinal artery. Okay, good. We got that. We come up.
As we come up, we recap this. As we come up, we fuse together and make the basilar. What comes off the top of the basilar? PCAs. What comes off underneath?
that superior cerebellar artery what comes off underneath that like the last thing I need to talk about is as we come up before the vertebrals fuse and form the basilar not only do they give off anterior spinal artery but they give off this thing here what's that bad boy number three number three is your pica which is the posterior inferior cerebellar artery what does that supply what do we have left remember I told you vertebrals should give off a bunch of branches at the end of it though you should supply medulla you should should supply what else? The posterior inferior cerebellum. Well we got vertebral getting the medial medulla, we got anterior spinal hitting the medial medulla, what's left?
Lateral medulla, pica, and posterior inferior cerebellum, pica. So that's what I want you to remember. Vertebral, anterior spinal give you medium medulla. Pica gives you lateral medulla, posterior inferior cerebellum. Boom, roasted.
Let's move on to that stuff then. Similar to the basilar. We take a look at the medulla. We take a cross-section through the medulla.
We have here in organization, posterior part of the medulla, anterior part of the medulla. When we look at this, we see our vascular territories here in that cross-section. And blue, as you see here through the midline, is what?
The vertebral arteries and the anterior spinal artery. That's supplying the structures in the medial strip of the medulla. Now we need to know what are the structures in the medial strip of the medulla. If we damage them, what are the clinical features? We're so good ninja nerds, aren't we?
We know this stuff. Boom, smack dab here in the middle. You have what's called the 12th cranial nerve, the hypoglossal nerve. The hypoglossal nerve is obviously responsible for a ton of things.
tongue movement, right? So protrusion of the tongue, moving it left, moving it right, moving it up, moving it down, curling it, all of that good stuff. So if you knock out, for example, in this case, the left 12th nerve, you won't be able to allow for it. There'll be weakness on that left side.
Okay. So there can be weakness on the left side of the tongue. What will happen is, is that the right half of the tongue from that normal right 12th nerve will overpower and deviate the tongue to the weak side which in this cases are left side because the left 12th nerves injured so because of that you injured the left 12th the weakness on that left side, right side overpowers and the tongue deviates to the same side as where the lesion is present, which is the left side.
So you get ipsilateral deviation of the tongue. Alright so we got the 12th nerve nucleus. The next thing is this green structure here in the middle and this may sound familiar to what we already talked about within the medial pons. Medial and meniscus is responsible for what?
Picking up fine touch, proprioceptive, discriminative touch, vibrations, all that stuff and bringing it up from one side of the body up through the brainstem into the other side of the brain. If you knock out that left medial lemuniscus, you're going to knock out sensations. to the contralateral side of the body. As long as it's after, because medial meniscus comes after the nucleus gracilis, the nucleus cuneatus, which is kind of the bottom part of the medulla. So if you knock out that medial meniscus, you knock out contralateral, proprioception, fine touch, discriminative touch, and all of those things to the contralateral side, so right side in this case.
So that's what you get here when you knock out that medial meniscus. Left corticospinal tract. Remember, we're at the pyramids, but we haven't gotten to the bottom.
As you go down the pyramids, the... The decussation of the corticospinal tracts occur at the bottom of the pyramid. So if we were at the decussation point, then yeah, we could potentially have ipsilateral weakness. But we're at the point where we haven't decussated yet within the medulla.
And so because of that, you get no crossing yet. Eventually it will cross, so you're going to get contralateral hemiplegia. So if it's on the left side of the medulla that you're hitting, you're going to develop right-sided weakness or right-sided hemiplegia. okay or paralysis that covers the medial medulla which is supplied by what strip here vertebral and anterior spinal artery so again to recap it ipsilateral third twelfth nerve palsy medial limoniscus so loss of contralateral sensations uh all the sensations we discussed and corticospinal tract contralateral hemiplegia so we talked about the medial medulla let's now talk about the lateral medulla so we know again medial medulla was supplied by the vertebral artery anterior spinal artery we can see that by that like territory that we colored here in blue Now imagine if we kind of go out laterally, do you see the vertebral arteries and anterior spinal arteries hitting that territory? No, that's within the realm of the pica, right?
So if we knock out the pica, we knock out the structures that are supplied within the lateral medulla. So what are the structures in the lateral medulla? And what happens if those things are damaged?
Let's start here laterally, work our way kind of like medially and then anteriorly. Because again, this is the same section as compared here. So this is still like the posterior portion. This is the anterior portion that's lateral, lateral, medial. So first thing here at the lateral part of this left part of the medulla here is going to be the inferior cerebro.
peduncles. It's the same thing that we talked about with pons. It's just instead of it being middle, it's inferior.
The spinal cerebellar pathways or any kind of proprioceptive pathways are coming up into the cerebellum and then it's going to be moving into the cerebellum from the medulla via these inferior cerebellar peduncles. If you knock out that connection, you knock out the ability to be coordinating our proprioceptive sensations which is involved in coordination. So if you knock out that left inferior cerebellar peduncle, you knock out the sensory proprioceptive information going to the to the left cerebellum, and so that's going to lead to ipsilateral ataxia. Because again, everything with the cerebellum produces ipsilateral symptoms, and compared to the cortex, which is contralateral. So again, knock out the inferior cerebellar peduncle, you knock out the communication of proprioceptive sensation to the left cerebellum, you need the ipsilateral ataxia.
Move immediately to this blue structure here called the nucleus ambiguus. This is the big, big, big, big, big one that I want you guys to remember. A lot of this stuff is pretty much the same what we talked about with lateral pontine involved. it's the same this is the really big difference here when you talk about lateral medulla involvement as you're involving the nucleus ambiguous the nucleus ambiguous is the nucleus that gives way to particular nerves motor nerves for cranial nerves 9 glossopharyngeal cranial nerves 10 Vegas and a little bit of this accessory nerve cranial nerve 11 these go and supply particular muscles involved in speech and swallowing Okay, and so what are some of those muscles? It's muscles of the soft palate, muscles of the uvula, muscles of the pharynx, muscles of the larynx.
All of those things are involved and particularly stimulated by the nerves coming from the nucleus ambiguous. If you develop a lesion in the pica and you knock out that nucleus ambiguous, you knock out motor supply to all of the larynx, pharynx, soft palate, and uvula. And this can produce what's called a bulbar palsy. Ipsilateral, so you're affecting the same side.
So what can that do? look like. One thing is you affect the ability to swallow because you're hitting those pharynx muscles that can cause dysphagia. You're affecting the speech production because you're hitting the larynx muscles that's causing dysphonia. You're affecting your reflexes.
You know whenever you take like a tongue depressor and tap on someone's pharynx or tonsillar walls it triggers a gag reflex or if you take an endotracheal tube and you go down and deeply suction or aspirate things from their carina or trachea that causes a cough reflex which is elicited by your vagus nerve. If you damage that, you then have a decrease or absent cough gag reflex. And the last thing is, again, remember that cranial nerve 10 supplies the uvula.
There's two halves of the uvula supplied by cranial nerve 10. If there's actually a decreased supplier injury to, in this case, the left vagus nerve, that left side of the uvula isn't going to be able to contract. And so what happens is it starts to deviate to the opposite side because the other side is working properly and yanking it to the other side. And so you have a kind of what's called a contralateral uvular deviation.
So big things to remember. This is the huge, huge, huge one to remember when there's lateral medulla involvement because of a pica lesion. You know what another name for the lateral medulla kind of lesion is or syndrome? We call it Wallenberg syndrome.
So remember that. Sometimes that can show up on your board exams. All right, so we got inferior cerebellar peduncle.
We got nucleus ambigus with the bulbar palsies. The next one that we have here is this purple one called the vestibular nuclei. Now, vestibular nuclei are involved with static equilibrium, dynamic equilibrium.
And so what happens is they help to... to be involved in a couple things. One in maintaining balance. The other one is they help to allow for the proper movement of our eyes whenever we're like shifting our head from side to side or up and down.
And whenever there is involvement of a lot of issues with the vestibular nuclei that can communicate with what's called our chemo trigger zone, which is involved in nausea and vomiting. If you injure the vestibular nuclei, you then alter your ability to maintain static and dynamic equilibrium, which leads to vertigo. You... alter the connection to the chemo trigger zone and now there's more stimulation of it that it causes nausea and vomiting and you alter the vestibuloocular reflex which is causing nystagmus.
Now move out a little bit here to this green structure called the sympathetic tracts, the descending sympathetic fibers that come from the hypothalamus. You hit those, you cause ipsilateral horner syndrome which we already talked about with the pons which leads to decreased sweating and hydrosis. You cause ptosis of that upper eyelid and then and then you cause the pupil to not be able to dilate.
Instead, it constricts, which is called meiosis. Next thing is this blue structure here called the trigeminal nucleus. Now, the trigeminal nucleus in the pons, there was the central pontine nucleus, but there was the motor component of it as well that controlled mastication muscles.
In this part here, in the medulla, the lateral medulla, it's called the spinal trigeminal nucleus, but there's no motor component of that trigeminal nerve there. It's just sensory involvement there. And the tract.
The trigeminal tract is also there as well. So you have the spinal trigeminal nucleus and the associated tract there, only picking up sensory information like pain, temperature, touch, proprioception, from that same side of the face. You whack that left spinal trigeminal nucleus and tract, you lose sensations such as pain, temperature, touch, proprioception, from that left side of the face. Thus, ipsilateral loss of sensations of the face.
Last thing here is that spinal thalamus. tract. Spinal thalamic tracts, you have the anterior and lateral, they carry crude touch, temperature, pressure, right?
If you knock this thing out on that left side, remember, spinal thalamic tracts cross at the level of the spinal cord whenever they're coming into the spinal cord. So if you knock that out, you're going to be affecting sensations on the contralateral side. So for example, you knock out that left spinal thalamic tract here in the lateral medulla, you cause loss of sensations on the right side, contralateral side, which is going to be, in this case, pain, tension. temperature, crude touch, and pressure. That would cover all of the things that could become present when there's lateral medullary involvement, Wallenberg syndrome, due to what kind of vessel damage?
The pica, okay? Whereas if it's medial medulla, that's going to be vertebral artery, more particularly the anterior spinal artery. Let's move on to the last part.
So we know that the vertebrals, again, we already kind of concluded this at the beginning. They supply medulla, and they supply... posterior inferior aspect of the cerebellum. So let's quickly recap that blood supply to the cerebellum. So again, we have vertebral artery here.
So we'll kind of mark this here as vertebral. We only see one half of it in the sagittal view. Here's your vertebral artery.
Gives off this branch here called the pica. Pica supplies the posterior inferior aspect of the cerebellum. Then you come up here to this part here called the basilar artery. And the basilar artery will give off respectively the icus, supplying the anterior anterior. inferior cerebellum and then it'll give off the superior cerebellar artery which will apply the superior cerebellum.
The one that we have to focus on with respect to the vertebral arteries is you knocking out the pica. If you knock out the pica you affect the blood supply to the posterior inferior aspect of the cerebellum. If there is a involvement of the cerebellum this is important because it leads to alter abnormalities within. coordination, posture, balance, things of that nature, which can present as ataxia.
If you injure the right cerebellum, you cause ataxia on the right side. If you injure the left cerebellum, you cause ataxia on the left side. So how will this present? In this case, they can have ipsilateral ataxia and this can also present with what's called dysmetria whenever they're trying to do the finger to nose test we already talked about that or this diatokinesis with rapid alternating movements and this would cover vertebral artery stroke syndromes as well as all of the stroke syndromes ninja nerds you guys got through it alright ninja nerds in this monster of a video we talk about stroke syndromes I really hope that it helped I truly hope that it makes sense and if you guys did enjoy it continue to support us Ninja Nerds we love you we thank you and as always until next time