Stroke Syndromes: MCA, ACA, ICA, PCA, Vertebrobasilar Artery Strokes | Pathophysiology

0:13What's up Ninjanerds? In this video

0:15today we're going to be talking about

0:16stroke syndromes. Before we get started

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0:30follow along with this comprehensive

0:32lecture on stroke syndromes, we'll have

0:34a link, go click on that, check out the

0:36notes and the illustrations that we have

0:38available to you guys. All right

0:40Ninjanerds, let's get into it. All

0:42right, so let's talk about stroke

0:43syndromes. Why do we need to know stroke

0:44syndromes? Well, the basic thing is that

0:46when someone comes in with an ischemic

0:47stroke or hemorrhagic stroke, they're

0:49going to present with particular neuro

0:51deficits depending upon that vascular

0:53territory that gets hit. And so we need

0:55to know what vessel supplies pretty much

0:58what area of the brain or brain stem,

1:00and if that is affected, what types of

1:02clinical manifestations will be evident.

1:04I think that's pretty much it. So, let's

1:06start off talking about the MCA syndrome

1:08or middle cerebral artery syndrome.

1:11So, briefly we need to say, middle

1:13cerebral artery, what parts of the brain

1:14does it supply? That'd be a nice little

1:16kind of get, you know, thing to start

1:17off with. I think the best way to look

1:19at it is this tiny little diagram here

1:21in green. The green is representative of

1:24the MCA division.

1:25So, the MCA division you have supplying

1:28the frontal lobe here. You have it

1:30supplying part of the parietal lobe, and

1:32you even have it supplying part of the

1:33temporal lobe. Okay, so that's a really

1:36important thing to remember. Supplies

1:37good chunk of the brain. Frontal lobe,

1:40parietal lobe, temporal lobe. Now, the

1:42big thing to remember is it supplies

1:43more of the lateral side of the parietal

1:46lobe and the frontal lobe, okay? Big

1:48thing to remember. So, let's talk about

1:50first some of the frontal lobe things.

1:53So, if we take a slice of the brain in a

1:55coronal section, and we take that slice

1:58just in front of the central sulcus,

2:00okay? Just in front of it. We're going

2:01to be looking at the frontal lobe now in

2:03a coronal section. So, imagine there's

2:04our coronal section.

2:06On one side I'm representing kind of the

2:08vascular territory. So, here's going to

2:10be the frontal lobe. Here this little

2:11bump there is a part of the temporal

2:13lobe.

2:14The frontal lobe in the medial portion

2:17is supplied by the anterior cerebral

2:18artery.

2:19This whole chunk here, the lateral

2:22portion of the frontal lobe, is the MCA.

2:25And even a little bit of the temporal

2:26lobe is MCA, and just that bottom

2:28portion there is the PCA in blue.

2:32When someone develops a middle cerebral

2:34artery stroke

2:35and they knock out a particular area in

2:38that frontal lobe, if you guys look here

2:40on this side view here, here this in

2:42black is the central sulcus. In front of

2:44it here is your primary motor cortex.

2:47That's where the voluntary movement of

2:49skeletal muscles occur.

2:50If you knock out the MCA and you don't

2:53supply blood flow to that primary motor

2:55cortex, what happens? You can't move the

2:58opposite, the contralateral side of the

2:59body. So, for example, let's take for

3:01example here.

3:03Here's your right MCA division. And

3:05let's say that you knock out this

3:07portion here where these little red

3:09neurons are. So, if we follow these red

3:11neurons from the right primary motor

3:14cortex, they'll come down corona

3:16radiata, internal capsule, through the

3:17crus cerebri, through the pons,

3:19decussate of the pyramids, go down to

3:21the spinal cord, and supply the muscles

3:23on the left side. You knock these out,

3:26you develop weakness on the left side.

3:29But, here's where we got to be really

3:29specific.

3:31You guys really need to remember your

3:32frontal lobe anatomy and function.

3:35What we take the slice, there's they

3:37they like to put that little man there

3:38called the homunculus, right? Little

3:40motor homunculus. It tells you what

3:42parts of the body this portion of the

3:45brain supplies. If we take a look here,

3:47I want it really basic.

3:50Face, upper extremities, lateral portion

3:52of that motor cortex. Lower extremities,

3:55medial portion of that motor cortex. So,

3:58when you knock out the MCA, kind of

4:00match it up there, I'm getting face and

4:03upper extremities way more than I'm

4:05going to get any lower extremity

4:06involvement. Boom, contralateral

4:08hemiplegia, so paralysis of the face,

4:10upper extremity way more than the lower

4:12extremity. Boom, roasted, move on to the

4:14next thing.

4:16Let's take a slice. Let's take it

4:17imagine. It's going to be the same

4:19drawing.

4:20Take a slice a little bit farther back.

4:22Now, we're going to go behind the

4:24central sulcus.

4:25If we go behind the central sulcus,

4:26here's that black line, there's our

4:28central sulcus. We have a blue strip

4:30here. That's our sensory strip. That's

4:32our primary somatosensory cortex.

4:35Imagine you knock that bad boy out.

4:37What's going to happen? Well, it's going

4:38to lead to sensory loss on the

4:40contralateral side. What kind of

4:42sensations? All of them. It could be

4:44touch, pain, temperature,

4:47proprioception, vibration, all of them.

4:49You lose those on the contralateral

4:51side. Let's make sense of it.

4:53Imagine here's some skin, and that's

4:55where there's some touching occurring.

4:58No, no, don't be weird about it. This

5:00information comes up via either the

5:02dorsal column, if it's kind of like your

5:04fine discriminative touch, or if it's

5:06like your crude touch, maybe via the

5:08spinothalamic system, it'll come up,

5:09cross over, and go. If it's coming from

5:12the left skin of the left side of the

5:13body, it'll go to the brain on the right

5:16side, okay?

5:18Now, you develop an infarct within the

5:20MCA or some type of lesion of the MCA,

5:23knocks out that portion, you lose

5:25sensation to the contralateral side of

5:27the body. Again, same thing, sensory

5:30homunculus.

5:32Lower extremities supplied more

5:33particularly medially by the ACA, and

5:36then laterally is going to be the MCA,

5:38that's your face and upper extremities.

5:40So, you get contralateral sensory loss

5:41involving what? Face, upper extremities

5:44more than lower extremities.

5:46Really quickly here, I mentioned that

5:48there's two divisions,

5:50uh the superior division and there's an

5:52inferior division of the MCA. Really,

5:54really briefly, if you kind of imagined

5:56here, let's do it in a super bright

5:57color here, pink.

5:59When the MCA kind of tucks underneath

6:01this lateral sulcus,

6:03it kind of comes out from the lateral

6:05sulcus and gives a branch off here, and

6:07gives a branch off there, okay? This

6:09branch here is called the inferior

6:11division. This branch here is called

6:14your superior division. The superior

6:16division of the MCA is what supplies

6:19that primary motor cortex and primary

6:22somatosensory cortex. So, if you injure

6:24that vessel, that superior division, it

6:27affects these territories. It wouldn't

6:29be affected if you hit the inferior

6:31division of the MCA, okay? So, remember

6:33that.

6:34All right. So, move on to the next

6:36thing. Contralateral weakness, sensory

6:38loss, boom, face, upper extremity more

6:40than lowers.

6:42Next thing is the frontal eye fields.

6:44Okay, same thing, take a side view of

6:45the brain. Here you have that black

6:47strip. What is that called? That's your

6:50central sulcus. In front of it you have

6:52the motor strip, primary motor, we

6:53already talked about that one. Behind

6:54you got the primary somatosensory,

6:56already talked about that one. Then a

6:58little bit more anterior, what do you

6:59have? A little uh pink uh dot there is

7:02called your frontal eye fields. Your

7:05frontal eye fields still fall within

7:06that green, the territory of the MCA. If

7:09you want to be specific though, what

7:10division?

7:12It'd be the superior division, right? Of

7:13the MCA that's getting hit uh

7:15particularly leading to this lesion in

7:17the frontal eye fields. All right, so we

7:19have an idea that the frontal eye fields

7:21is still supplied by the superior

7:22division of the MCA. We know that it's

7:24in the frontal lobe. What happens though

7:26if it gets knocked out? Well, we have to

7:27briefly, and I mean briefly, talk about

7:29what the heck it does.

7:31Frontal eye fields, let's say that we

7:32take a coronal section where the frontal

7:34eye fields would be,

7:35and here we have that kind of view.

7:38Frontal eye fields, let's say that we

7:39have the right side. So, let's say

7:40here's your right frontal eye field.

7:43It'll send these axons down to a

7:45structure here in your pons

7:47here in orange, the left one, called the

7:49PPRF, the left paramedian pontine

7:52reticular formation.

7:54Jeez.

7:54Stimulates that guy.

7:56And that guy, when he's stimulated, he

7:58then tells this blue neuron called your

8:00sixth nerve nucleus, "Hey buddy, go

8:02ahead and fire and tell that lateral

8:04rectus

8:05muscle to contract." And when it

8:07contracts, it's going to abduct the eye

8:09outwards, okay? "Oh, cool. I'll do that

8:11for you. Also, why don't you tell the

8:13third nerve, because you know, you're

8:15connected to the other third nerve

8:18via what's called the medial

8:19longitudinal fasciculus. So, tell that

8:20right third nerve, 'Hey buddy, go ahead

8:22and fire for me, and when you fire, tell

8:24that medial rectus to go ahead and pull

8:27your eyes that way as well.'

8:28So, generally what should happen is when

8:30the right frontal eye field fires, your

8:32eyes deviate to the left. What do you

8:34think would happen though

8:35if you knock out

8:37that right frontal eye field? Do you

8:38think your eyes will be able to deviate

8:40to that left side or gaze to that left

8:42side? No. What happens is if this left

8:45side is working fine and properly and

8:47it's doing everything it needs to do,

8:48it's going the left side is going to

8:50tell the eyes to be to the right

8:51normally. There's nothing that's

8:52interfering with that. So, it'll be

8:54unopposed now by this damaged right

8:58frontal eye field, and guess where the

8:59eyes will start to preferentially

9:01deviate naturally at rest? To the right

9:05side, the same side as where the lesion

9:08is. So, we call that ipsilateral gaze

9:11deviation, okay? Sometimes they even

9:13call it a gaze preference. So, it's

9:15because you're knocking out that frontal

9:17eye field. If it's on the right, your

9:19eyes will deviate to the right. Boom,

9:21roasted, on to the next one.

9:24The next area here is called your

9:26Wernicke's area.

9:28Wernicke's area is a really cool area.

9:29So, helps us to comprehend, understand

9:31language, if you will. So, language can

9:33be written, it can be spoken, it can be

9:35nonverbal. And so, a lot of that stuff

9:37can be picked up from two particular

9:38sensations.

9:40If I'm speaking to you and you guys are

9:42hearing my voice, that's hitting your

9:44auditory cortex. When it hits your

9:46auditory cortex, it sends that

9:48information to Wernicke's area, right?

9:50From your primary auditory cortex. You

9:52also see me

9:54writing things down.

9:55You see me drawing arrows and referring

9:58to things and giving you nonverbal cues,

10:00right?

10:00So that information from the occipital

10:03lobe from your visual cortex will also

10:05get sent to the Wernicke's area. The

10:06Wernicke's area will then take that

10:08information about language, analyze it,

10:10recognize it, and help us to comprehend

10:13what is being spoken or written.

10:16If you develop a lesion within the MCA,

10:20but we got to be very very particular.

10:23Think about that that kind of blood flow

10:24again. We'll do it in green since that

10:26was kind of what we were trying to

10:28indicate with the MCA.

10:29It sneaks up under the lateral sulcus or

10:32the Sylvian fissure, gives off this

10:34division, and then gives off this one.

10:37What division do you think it's going to

10:38get hit? The inferior division. So

10:41inferior division of the MCA, if it gets

10:43hit, can lead to the Wernicke's area

10:45becoming affected. If it's affected, can

10:48you comprehend language? No. So

10:51comprehension of language is gone.

10:54The other thing that happens is that

10:55Wernicke's area loves to communicate

10:57with this blue area in the frontal lobe

11:00called Broca's area. Tells Broca's area,

11:02"Hey buddy, I understand language. Can

11:04you tell them what you actually

11:05understand?" So then you would tell

11:07Broca's area. Broca's area controls the

11:09muscles of the speech, which allows for

11:10the production of language, expression

11:13of language. So in someone who has

11:15Wernicke's aphasia, they can express

11:17language properly and fluently,

11:20but because they can't comprehend

11:22language, it literally makes no sense.

11:24It's nonsensical.

11:26And so that is important to remember

11:28with Wernicke's area leading to if there

11:31is an MCA lesion, Wernicke's aphasia.

11:35What we particularly like to call it

11:37though is receptive aphasia, okay? Boom,

11:40roasted. Move on to the next one.

11:42Broca's area,

11:43you guys are probably already picking

11:44this up cuz you guys are so darn smart.

11:47But again, same thing. MCA kind of

11:48sneaks under, right? So you have that

11:50kind of like that M

11:511 M 2 segment that sneaks over here,

11:53particularly M 2 segment segment, and

11:55then branches there, there, and then

11:58there.

11:59If we have Broca's area, which is going

12:00to be this little blue little dude right

12:03here,

12:05if we knock that out, that falls within

12:07what division?

12:09The superior division of the MCA. So if

12:11we hit the superior division of the MCA,

12:14that could lead to the damage to Broca's

12:15area. What does Broca's area do? We

12:17already kind of introduced that already.

12:19Receives information from the Wernicke's

12:20area as well as other areas, other motor

12:22areas,

12:23and helps for the production of speech.

12:26Enables particular types of cranial

12:28nerves, cranial nerves five, cranial

12:30nerves seven, cranial nerves

12:3310 and nine and all of these and 12, and

12:35helps for the production of speech in a

12:37particular way.

12:38If Broca's area is affected, speech will

12:40no longer be fluent, and it won't be

12:43able to be expressed properly. Even

12:45though you can comprehend language and

12:47understand what everybody's saying or

12:48what you're reading, you just can't

12:50express it properly. And so that's what

12:52happens with Broca's area being damaged

12:54leading to what's called Broca's

12:56aphasia. Next thing is the optic

12:57radiations, okay? So

13:01another little diagram here, if you

13:02will. So imagine here we have a little

13:04baby diagram.

13:06And again,

13:08you have that MCA sneaking underneath

13:11the Sylvian fissure, and it gives off

13:13this one, and then it gives off this

13:14one, right?

13:16Well, you have these things called optic

13:18radiations. Optic radiations kind of

13:19like to move through the parietal lobe

13:21and the temporal lobe, okay? And so what

13:23happens then is

13:25when someone develops a MCA lesion, if

13:28you will, that's knocking what part?

13:31The inferior division of the MCA. It can

13:34affect the optic radiations that are

13:36moving through the temporal lobe and

13:37even a little bit through the parietal

13:39lobe.

13:40So,

13:42if that happens, you can lead to a

13:43particular visual dysfunction cuz optic

13:45radiations, you can already get from the

13:47word optic radiations, that has

13:48something to do with the visual pathway.

13:49We'll briefly explain this.

13:51But if you knock out the inferior part

13:53of the MCA, it can lead to some visual

13:55pathway dysfunctions. Let's briefly

13:57explain what the heck I mean. So let's

13:58say here

14:00we have a portion of that like here's

14:02your optic radiations right here after

14:04the thalamus going back to the occipital

14:06lobe right here. That's all optic

14:07radiations.

14:08If someone develops an MCA infarct or

14:11MCA lesion that leads to an infarct of

14:13this territory here where the optic

14:16radiations are running through, whether

14:17that be through the temporal lobe,

14:18whether that be through the parietal

14:19lobe, whatever that inferior MCA

14:21division is getting hit, that knocks out

14:23these optic radiations. Let's follow the

14:26optic radiations backwards to the

14:28eyeball and see what type of visual

14:30information they're picking up. So for

14:31example, if we follow this blue one back

14:33here, boom. You hit on this part of the

14:35retina. Remember that this part of the

14:36retina picks up visual information from

14:38this visual field, okay? Then if we

14:41follow the maroon one back,

14:44the maroon one,

14:46boom. This is going to be this part of

14:48the retina kind of towards the nasal

14:49part of the retina. Again, remember this

14:51picks up visual information from this

14:54part of the visual field. Okay. So if we

14:56kind of recap here, this is if we look

14:59at this, let's say that this is the

15:00right side of the brain, and this is the

15:02left half of the brain, okay?

15:04If you develop

15:06a lesion within the inferior division of

15:08the MCA, you knock out the optic

15:10radiations on the left side. What

15:12happens to your visual field loss? Well,

15:14you lose the visual fields on the

15:17contralateral side, the right visual

15:20fields. And so if I knock out my right

15:22visual fields, that's the contralateral

15:24side of where the lesion is, but they're

15:26kind of similar. So we call that

15:29contralateral homonymous hemianopia. So

15:32if you have a left-sided MCA infarct on

15:36that inferior division, you knock out

15:37those left optic radiations, you won't

15:39be able to see the visual fields on your

15:41right side. Let's move on to the last

15:43part here,

15:45which is the MCA division particularly

15:47on the right side. So I didn't preface

15:50this before. So

15:52Broca's area, Wernicke's area,

15:54they're primarily on the dominant side,

15:58okay? And the dominant side of your

15:59brain is usually the left side since

16:01most people are right-hand dominant. So

16:03the left side of their brain is where

16:05the Broca's area and Wernicke's area

16:08reside.

16:09So if I knock out the left MCA, I'm

16:12going to potentially see these two

16:14symptoms. If I knock out the right MCA,

16:17it's unlikely that I'll see these two

16:20symptoms. I'll actually see these

16:22particular symptoms present, okay?

16:25So what could I see if I knocked out

16:27that right MCA, okay, for the

16:29non-dominant hemisphere primarily? You

16:31see two particular things that I want

16:33you to remember, apraxia and

16:34hemineglect.

16:36Apraxia is very interesting. It's where

16:39you your motor system is intact. So your

16:41muscles are fine. There there's no issue

16:43there.

16:44You have the willingness to want to

16:45perform a motor movement, but you just

16:47can't figure out how to do it. So

16:49there's a difficulty in being able to

16:51actually act out that movement even

16:53though you are and willing to do it.

16:55Examples of these is ideomotor apraxia.

16:58Uh for example, "Hey, can you lift up

17:01your right arm?" Instead of them lifting

17:03up their right arm, they'll do something

17:04weird, and maybe they'll just give like

17:06two fingers. Or uh if you tell them give

17:08me a thumbs up, they'll give you two

17:10fingers. They start mixing up their

17:12movements and kind of don't really know

17:13how to really perform the movements

17:15properly.

17:17Eyelid apraxia is very common

17:19where you ask them, "Hey, open up your

17:20eyes." There's nothing wrong with the

17:22levator palpebrae superioris. It's

17:24working fine. They can contract and

17:25elevate the eyelid, and they want to do

17:26it. They just don't know how to do it.

17:28And then ideational apraxia. Give them a

17:30marker and say, "Hey, draw me

17:31something." They'll look at this and

17:33they'll be like, "Dang, I know this is a

17:34marker, and I want to draw something,

17:36but I I don't know how to use this dang

17:37thing." And that's ideational apraxia.

17:40So that's again recapping it, motor

17:42function's intact, willingness to do the

17:44function is is okay, but they just don't

17:46know how to do it or kind of really go

17:47about performing that activity. Neglect

17:50is also very interesting.

17:51So again, you knock out that right MCA,

17:53which is usually the non-dominant side.

17:55You neglect the sensations on the

17:57contralateral side of the body, just

17:58like you would if you knocked out your

17:59primary motor primary sensory cortex,

18:01whatever. The same concept. For example,

18:04knock out my right MCA.

18:05If I have hemineglect, you let's say

18:08that you have a patient. You're going

18:09into the room. You have three people in

18:11the room, one here in front of them, one

18:13here on the right of them, and then one

18:14over here to the left of them. And let's

18:16say that you ask you ask the patient,

18:18"Hey, how many people are in the room?"

18:19They will see the person in front of

18:21them. They will see the person to the

18:22right of them, but they will not be able

18:24to see the person in their left visual

18:25field because they're neglecting their

18:28left visual field. So that's an example

18:30of one.

18:32The other thing here is sensory. If you

18:34take and have the patient close their

18:36eyes, and then you say, "Okay, I want

18:38you to tell me which side of your body

18:39I'm touching." And you touch both of the

18:42sides simultaneously, they'll say, "Oh,

18:44you're only touching my right side." You

18:46want to know why? Because they're

18:47neglecting all of the sensations on the

18:50left side of their body. And so that's

18:53what can happen with right MCA infarcts,

18:55usually referring to it as the

18:57non-dominant hemisphere, okay? That

19:00tells us what we need to know about MCA

19:02syndrome, which is the most important

19:04one. Let's now talk about ACA syndrome.

19:06All right, ninjas. So let's talk about

19:07ACA syndrome. So ACA syndrome, anterior

19:09cerebral artery syndrome, you knock out

19:11one of those ACAs.

19:13So ACA is going to supply pretty much

19:15what part of the brain? So it supplies

19:16primarily the medial frontal lobe and

19:18the medial parietal lobe, okay? It even

19:20gets hits a little bit of the basal

19:21ganglia as well,

19:23parts of it. So what I really want us to

19:26focus on is

19:28it's kind of similar to what we talked

19:29about with the MCA in the beginning, the

19:30primary motor and primary somatosensory

19:32cortex. This should actually be a very

19:33quick recap. We shouldn't have to spend

19:34tons of time. Is that if we take a look

19:36here at the side view of the brain.

19:38Here's going to be our central sulcus

19:40right here, and then in front of it is

19:42the primary motor cortex, right? If we

19:44draw here in pink what portion

19:46is actually ACA, it's kind of going to

19:48be like this if you really want to think

19:49about it. That's all

19:51going to be the ACA.

19:53And then if we had here before just to

19:55kind of like in a dash line here, what

19:57was this part here?

19:59That was the MCA, right? So when we're

20:01talking about the kind of the different

20:03territories here, the ACA's hitting more

20:06of that medial strip of the primary

20:07motor and primary somatosensory cortex,

20:10whereas that MCA is hitting more of the

20:11lateral portion. So what do you guys

20:13think? Do we really even need to go too

20:15hard here? Let's briefly blow through it

20:17here.

20:18If we take a coronal section in front of

20:21the central sulcus where the primary

20:23motor cortex would be,

20:25upper motor neurons are going to come

20:26down via the corona radiata, internal

20:28capsule, crus cerebri, through the pons,

20:31decussate at the pyramids, come down to

20:33lower motor neurons, and go to the

20:35muscles on the contralateral side. You

20:37develop a lesion in the ACA,

20:40particularly the medial territory, you

20:42knock this out, you develop weakness on

20:45the contralateral side. But what does

20:47the homotor homunculus tell you? For

20:49MCA, it was face upper extremities, as

20:52represented here in green. For ACA, it's

20:55pink here, which is lower extremities.

20:57You're knocking out lowers more than the

20:59uppers and the face. Boom, roasted. What

21:02about the blue stuff here?

21:04Go back, take another section. Imagine

21:06that this is another section, and we're

21:08taking it behind the central sulcus

21:10where the primary somatosensory cortex

21:12is, where sensations are basically

21:14involved. We take these sensations

21:16coming from the skin,

21:18coming up, maybe dorsal column, maybe

21:20spinothalamic tract, and eventually

21:22going from the left side of the body to

21:25the right cerebral hemisphere.

21:27If you develop a lesion in the ACA, you

21:30knock out the sensations coming from

21:32this portion, contralateral sensory

21:34loss. Again, remember your sensory

21:36homunculus.

21:38For the face and upper extremities, that

21:40was the MCA territory, but for lower

21:42extremities, that was primarily ACA

21:44territory represented in pink. So you

21:47get contralateral sensory loss involving

21:49what? Lowers more than uppers and the

21:52face. Boom, roasted. We just did it,

21:54right? We blasted through that pretty

21:55quickly. Now,

21:57move on to the next one. So the next

21:59part is the paracentral lobule. The

22:00paracentral lobule is a very interesting

22:02little thing. Imagine here for a second

22:03we were taking a look at the brain from

22:05the side, right? Imagine I cut it in a

22:07sagittal section and remove that right

22:08piece. So now you're just looking at the

22:10left half of my brain from the medial

22:12side. So here's that view.

22:15Here you see like your corpus callosum

22:16here, and then above it in this pink

22:19kind of structure there is what's called

22:20the paracentral lobule. The paracentral

22:22lobule is interesting because it kind of

22:24picks up sensory and motor information.

22:26So there's kind of going to be like some

22:27sensory information here

22:29that comes to the paracentral lobule,

22:31and there's also motor information that

22:33is involved and connected from the

22:36paracentral lobule to the urinary

22:39bladder and some parts of the bowels,

22:40but big one to remember is the urinary

22:42bladder.

22:43If you knock out the paracentral lobule

22:46from an ACA infarct, because again,

22:48you're falling within that kind of like

22:49medial strip of the ACA. This is all ACA

22:52right here. So if I were to kind of

22:53highlight here,

22:55this is all ACA.

22:59If you knock out that paracentral

23:00lobule, you no longer have proper

23:02sensory and motor function of the

23:04urinary bladder, and but maybe somewhat

23:06of the bowels, too. So there is what's

23:08happening of urinary incontinence and

23:10fecal incontinence. So you actively go

23:11pee pee, go poo poo.

23:13So that is the basic concept of the

23:14paracentral lobule. So we got

23:16contralateral weakness, contralateral

23:18sensory loss, more particularly lowers

23:20than uppers, and we got urinary fecal

23:22incontinence if you hit that paracentral

23:23lobule. The other thing that we should

23:25remember here

23:26is again, take another medial view of

23:29that cerebral hemisphere, and we're

23:30looking at that left cerebral

23:31hemisphere. It also can hit another

23:33portion here. So if we kind of again, in

23:35pink here, all of this

23:38would get hit

23:41from a

23:44ACA lesion.

23:46Okay? What are these two areas that I

23:48want you guys to think about? These are

23:49particularly more for behavior. Okay,

23:51behavior, decision-making, things like

23:52that.

23:53So we have here in green the prefrontal

23:55cortex. You guys know that prefrontal

23:56cortex is involved in tons of things,

23:58emotions, memories, decision-making,

23:59personality, behavior, executive

24:01function, all that stuff.

24:03The anterior cingulate cortex is kind of

24:04involved with also aspects of memory,

24:06but a part of our limbic system. So

24:08whenever you knock out these two

24:10structures, it leads to particular

24:12behavioral and decision-making

24:14abnormalities. And we kind of classify

24:17these with as abulia and akinetic

24:19mutism. So abulia

24:21is basically they have a significant

24:25decrease in motivation, willingness,

24:28any desire to want to do anything

24:31purposeful like verbally or or motor.

24:34Example, you come into the room, you

24:35say, "Hey,

24:36Miss Jones, can you please lift up your

24:39left arm?" There'll be a very

24:40significant delay in and kind of like

24:43very decreased desire to want to lift up

24:44her arm if she even does. "Hey, can you

24:46tell me where you are? What's your

24:48name?" There'll be a significant delay

24:50if even if she does respond to what's

24:52your name or where you are. So because

24:55there's this decreased willingness,

24:56desire, and motivation to want to

24:59interact or perform verbal or motor

25:01activities. That's abulia if you knock

25:03out these two structures.

25:05If you knock out both of them, cuz you

25:07get a bilateral ACA lesion, you get even

25:10worse. You get to the point where you

25:11don't talk and you don't move cuz you

25:14have no desire, no willingness, no

25:17willpower to want to interact verbally

25:19or motor via akinetic, no movement,

25:22mutism, no verbal communication. All

25:25right, so the next part here of the ACA

25:26syndrome is if you hit like a and again,

25:28we're adding this in just real quick

25:29little thing, is that there's this

25:31little red area. Remember I told you

25:32that the Broca's area can receive

25:33information from Wernicke's, and it can

25:35receive it from another motor area,

25:37uh particularly within the frontal lobe.

25:40And so this little red area within the

25:43anterior superior frontal lobe

25:45communicates with the Broca's area, and

25:47it's involved in speech. Okay? If you

25:49develop an ACA lesion, particularly in

25:51that dominant hemisphere, that left

25:53side, primarily, usually, right? You're

25:56going to knock out this structure here

25:58and its connection to the Broca's area.

26:00And so what happens is is you develop

26:03again

26:04uh some difficulty with speech

26:06production.

26:07So because it's responsible for

26:08communicating with Broca's area, there

26:11is going to be some difficulty in

26:13telling the Broca's area to be able to

26:14engage in speech, engage in expression

26:17of speech. So there will be some

26:19non-fluent or decreased speech ability,

26:23but comprehension will be intact. Same

26:25like uh Broca's area because why? Why

26:28should comprehension be intact for both

26:29of this red and this blue thing? Are you

26:32touching Wernicke's area? No. So since

26:34Wernicke's area isn't getting involved,

26:35comprehension should be intact. So

26:37asking them, "Hey, what's this called?"

26:38Oh, it's a marker. Oh, "What's If I pull

26:41out my phone, what's this called?" Oh,

26:42it's a phone.

26:43Now, here's where it can be a little bit

26:45different between Broca's in blue and

26:47red for this transcortical motor

26:50aphasia.

26:51If you say, "Hey, can you repeat after

26:52me, 'No ifs, ands, or buts, or today is

26:55a bright and sunny day'?" And they can

26:57do that, that is indicative of

26:59transcortical motor aphasia. If they

27:01can't do that, it's indicative of

27:04Broca's aphasia. So you can still get

27:06aphasia from ACA syndrome, but remember

27:12that if it's transcortical motor

27:13aphasia, you can differentiate it from

27:15Broca's by asking them to repeat

27:18phrases. If they can, it's transcortical

27:20motor, unlikely for it to be Broca's.

27:22Okay?

27:23That covers our ACA syndrome. What do I

27:26really want to do next before we go on

27:27to the next thing called the ICA?

27:30I want to talk about this thing called

27:31watershed zones. We talk about this in

27:33acute ischemic strokes called watershed

27:35infarcts. They can happen from global

27:36hypoperfusion.

27:38You remember uh kind of like if you take

27:40a top look at the brain, right? Take a

27:42top look at it, and here we have the

27:45frontal lobe, and you can represent that

27:47that's frontal lobe because here is

27:48anterior, here's posterior. Here's your

27:51central sulcus. Okay?

27:54In front of the central sulcus is going

27:55to be the frontal lobe. Behind the

27:57central sulcus is parietal lobe here.

27:59Remember what I told you? The lateral

28:01portion of the frontal and parietal lobe

28:03is supplied by green, which one?

28:05MCA, right? So this is all MCA.

28:08And then the medial portion of the

28:10frontal and parietal lobe is supplied by

28:12the ACA. Where they meet here in red is

28:15called that watershed zone. And those

28:17zones are really kind of susceptible to

28:20uh to very low perfusion. So if you drop

28:22their perfusion to these particular

28:23areas, they're very susceptible, and the

28:25neurons and brain tissue in that zone

28:28can become damaged.

28:30What happens then is you start to kind

28:32of fall within that category. Remember

28:34here we have like lower extremities, and

28:36then over here we have like face um and

28:39upper extremities, and then somewhere

28:41here in between is kind of like your

28:43trunk and like the proximal extremities

28:45of the lower

28:47proximal lower extremities, proximal

28:48upper extremities.

28:49You're kind of going to be falling right

28:51within that part of the trunk at the

28:53proximal extremities,

28:55upper and proximal lower extremities.

28:57And so because of that, when someone

28:59gets an infarct of that watershed zone

29:01in the MCA ACA territory, you knock out

29:05that proximal upper extremities and

29:07proximal lower extremities. But again,

29:09think about this. If you hit frontal

29:11lobe where that primary motor strip is,

29:14what would happen? You develop weakness,

29:15right? And it can cause contralateral

29:18weakness or contralateral hemiplegia. If

29:20you knock out the parietal part where

29:22the primary somatosensory cortex is,

29:23what do you get? You get sensory loss of

29:25the contralateral side as well. So

29:28again, big to think to think about with

29:29watershed zone, particularly MCA ACA,

29:33if you knock that out, you develop

29:34proximal upper extremity weakness and

29:36sensory loss, proximal lower extremity

29:39weakness and sensory loss, and we also

29:40call this man in a barrel syndrome.

29:43Okay? So that covers MCA ACA watershed

29:46zone as well as the MCA ACA syndromes.

29:49Let's move on to ICA syndrome. All

29:51right, so we talked about ACA, we talked

29:52about MCA, we talked about the MCA ACA

29:54watershed zone. Let's talk about the

29:56ICA. And actually nicely, this would be

29:58a good quick recap of the MCA and ACA

30:00because the ICA is a very large vessel.

30:03And what happens, if you guys remember

30:04your your circle of Willis blood flow,

30:06it comes up and branches into the ACA

30:10and MCA. And it also there's another

30:11little vessel that I'll talk about

30:12really quickly called the ophthalmic

30:14artery. So, if we kind of take a look

30:16here, again,

30:18coronal section,

30:19looking at the brain here. And again,

30:21you got your let's just say here you

30:23have the the frontal lobe and then here

30:25you have your your temporal lobe. Here

30:27that in that circle there, this circle

30:29is representing the ICA. This is coming

30:32up and feeding the circle of Willis, the

30:34anterior circulation of the circle of

30:36Willis.

30:37And what happens is it gives off this

30:38one that's moving towards this actual

30:41portion here, towards the medial

30:42portion, and will supply the medial

30:44portion of the frontal and parietal

30:45lobe. This is called your ACA. And then

30:48you're giving off this other portion

30:49here,

30:50which is going to feed laterally through

30:52that lateral sulcus Sylvian fissure,

30:54come out, and give off the superior and

30:56inferior divisions that will supply the

31:00lateral portion of the frontal lobe,

31:01parietal lobe, and the temporal lobe.

31:03What is that? That's your MCA.

31:05If you develop an occlusion or injury or

31:08damage of the ICA,

31:11you could potentially lead to a

31:14decreased or no blood flow via the ACA

31:17or decreased no blood flow via the MCA.

31:19So, what could happen is you could

31:22present with an MCA syndrome. Let's test

31:23your knowledge. Contralateral

31:25hemiplegia, contralateral sensory loss

31:27where?

31:28Face uppers more than lowers. Frontal

31:30eye fields, what happens? You get

31:32ipsilateral gaze deviation. You hit

31:34Wernicke's, you get Wernicke's aphasia.

31:35You hit Broca's, you get Broca's

31:37aphasia. You hit the right non-dominant

31:39side, you get apraxia hemi-neglect. And

31:42if you hit those optic radiations, you

31:43get contralateral homonymous hemianopia.

31:46ACA, you get contralateral hemiplegia,

31:48contralateral sensory loss of what?

31:51Lowers more than the face and the

31:52uppers. If you also hit the paracentral

31:55lobule, you'd get urinary fecal

31:56incontinence. If you also on top of that

32:00hit the prefrontal cortex and the

32:01anterior cingulate gyrus, you get abulia

32:03akinetic mutism. And if you hit that

32:05motor connection between the Broca's,

32:07you get transcortical motor aphasia. We

32:10just recap those now.

32:12That's ICA if you get a severe enough

32:15damage to it. Now, one other thing, the

32:18PCA is primarily a posterior circulation

32:21vessel. Comes off that vertebra basilar

32:23system. In 5% of patients, they may have

32:26what's called a fetal PCA variant. So,

32:29be aware of that. Sometimes, you can

32:32actually have an orange here that PCA

32:34come off of the internal carotid artery

32:37rather than it come off the vertebra

32:38basilar system. So, if someone also

32:40develops posterior circulation stroke

32:42like PCA division, which we'll talk

32:43about here,

32:45and you think that they have a problem

32:46with their ICA, think about that fetal

32:48PCA variant.

32:50The last thing I want to talk about with

32:51ICA

32:53is the ICA also affects this vessel. So,

32:55here's your ICA.

32:57And it gives off a vessel called the

32:58ophthalmic artery, which will help to

32:59feed the central retinal artery, some of

33:01the ciliary arteries that supplies the

33:03retina.

33:04If you have

33:06a decreased blood flow

33:08to the ICA, okay, and then into the the

33:10ophthalmic artery, central retinal

33:11arteries, you can develop this transient

33:14type of monocular vision loss. So, for

33:16example, right ICA, right transient

33:18monocular vision loss. And that's called

33:20amaurosis fugax.

33:22If it is not reversed or treated, then

33:26what can happen? This can become

33:27complete

33:29damage to the retina and complete

33:31monocular vision loss. So, that's

33:33another thing to think about with ICA

33:36if they develop MCA syndrome, ACA

33:38syndrome, plus or minus PCA syndrome if

33:40they have that fetal PCA variant, and

33:43transient ipsilateral monocular vision

33:45loss, think about ICA syndrome. All

33:48right, so we talked about the MCA, we

33:50talked about the ACA, we talked about

33:51the ICA. We even talked a little bit

33:53about the MCA ACA watershed zone. So,

33:58we haven't talked just yet about the

34:00PCA. We've kind of introduced it, the

34:01posterior cerebral artery. But there's

34:03another watershed zone that I want to

34:05talk about before we start going into

34:07the posterior circulation stroke

34:09syndromes.

34:10So, this is called your MCA PCA

34:11watershed zone. Just like the ACA MCA,

34:15I think about if you take a an actual

34:18axial cut, okay? So, you're taking an

34:20axial cut of the brain.

34:23Um and we're going to take it to where

34:24we get part of the like frontal lobe

34:27here, maybe parietal lobe, and then you

34:28get back here your occipital lobe.

34:31Well, where we get to the point of where

34:33the MCA and ACA territory start to come

34:35together and kind of meet one another,

34:37we'll represent that here in this red

34:39color, that is going to be the MCA PCA

34:42watershed zone. Just as an example here,

34:45right here would be your MCA

34:47ACA watershed zone where we get that man

34:49in a barrel syndrome.

34:51If you knock out the MCA PCA watershed

34:54zone, what you see with global

34:56hypoperfusion because of this section

34:58where they meet is very very sensitive

35:00to low blood flow or low oxygen carrying

35:03capacities, you can get these watershed

35:05infarcts.

35:06And it leads to visual dysfunctions.

35:09Two of the types that you probably want

35:11to remember, most important one is

35:13prosopagnosia. So, prosopagnosia is

35:15actually relatively sad.

35:17What happens is the person can visually

35:19see. So, the primary visual cortex is

35:21intact. But when you start involving

35:23kind of the association areas, which you

35:25get closer to that MCA PCA watershed

35:28zone, it starts affecting the ability to

35:30analyze, recognize, and identify what

35:33those objects you're seeing are or

35:35people you're seeing are. For example,

35:38Rob is filming me right now. I know that

35:40there's an object there. I analyzed him.

35:42I know he's there and I know that it's

35:43Rob. For someone who has the potentially

35:46this MCA PCA watershed zone infarct,

35:48they'll know that there's an object

35:50there, but they won't be able to make

35:51out who that person is. That's

35:53relatively sad.

35:55The other one that can happen here

35:57is Balint's syndrome. Relatively rare,

36:00uh but Balint's syndrome is kind of a a

36:01triad, if you will, of simultagnosia.

36:04So, um you know those little things

36:06called the Ishihara color plates where

36:07they have like, you know, red and green

36:09and blue and whatever, and it's used to

36:11like form a a number within that, maybe

36:14like the the number four is in there.

36:16The individual will be able to see the

36:18different colors, but won't be able to

36:20see how the colors make an image such as

36:23the number four. So, that's called

36:25simultagnosia.

36:27The other thing they can get is what's

36:28called optic ataxia, which is very

36:29different from cerebellar ataxia. So,

36:31when you do like the finger-to-nose

36:32test, they'll have difficulty bringing

36:34their finger from their nose to the

36:36patient's um to the to the clinician's

36:38finger, but they won't have a problem

36:40bringing it back to their nose. So, it

36:41could be something like this and back

36:43here. Something like this,

36:45back here perfectly.

36:47The last part of the triad is ocular

36:49motor apraxia, where they just have,

36:51again, motor the all the ocular

36:53extraocular muscles are moving and

36:54functionally they're intact. They have

36:56the willingness to move their eyes, but

36:57they just can't execute the movement or

36:59the they don't know how to be able to

37:00move their eyes in kind of a horizontal

37:02fashion. So, it's called ocular motor

37:04apraxia.

37:06I think that gives us a good idea pretty

37:07much of kind of talking about our

37:09anterior circulation strokes as we start

37:10to transition to our posterior

37:12circulation stroke syndromes. So, let's

37:14briefly talk about these. Recapping

37:16anterior circulation stroke syndromes,

37:18we talked about anterior cerebral,

37:20middle cerebral, internal carotid, and

37:22we also talked about that MCA ACA

37:24watershed zone, and we briefly started

37:27to get into that MCA PCA watershed zone.

37:30Anterior circulation strokes are by far

37:32the most common, 70% of strokes.

37:35Posterior circulation, which we're going

37:36to talk about now, is getting towards

37:38like the occipital and brainstem area.

37:41This is covered by the posterior

37:43cerebral artery, the basilar artery, and

37:46the vertebral artery. These account for

37:47the 30% of stroke syndromes that we're

37:49going to talk about now.

37:51So, let's go ahead and now focus on

37:52posterior large circulation

37:56All right, so let's talk about the

37:58posterior circulation stroke syndrome.

38:00So, now we're getting into the PCA, the

38:01posterior cerebral artery. So, posterior

38:03cerebral artery, really interesting one.

38:05Supplies a pretty decent chunk of the

38:07brainstem, particularly the midbrain.

38:09So, we'll talk about some of the

38:10midbrain syndromes. It also supplies the

38:13occipital lobe, we already know that.

38:15So, we're going to talk about some

38:16visual defects. And then it also

38:18supplies another structure called the

38:19thalamus, which is very important as

38:21well.

38:22All right, so let's talk about the

38:25particularly the posterior cerebral

38:26artery. So, again, a nice little view

38:27here. I like to look at that side view

38:29just to give us a good idea here. So,

38:30when we look at the side view here, we

38:32can see here in green is the MCA

38:34territory hitting that lateral frontal,

38:35parietal, upper part of the temporal.

38:37For the ACA, we're getting the medial

38:39frontal and parietal. And then the PCA,

38:41you're getting that occipital lobe, and

38:43then you're getting down here into the

38:44temporal lobe. All right, so we know

38:45that.

38:47Here's where we got to talk a little bit

38:48about this first one, which is if we

38:50start involving this kind of visual

38:52cortex area. So, you know you have

38:54what's called the primary visual cortex

38:56and the association cortex. And these

38:58are responsible for taking in visual

39:00information from the optic radiations,

39:02from the optic tracts, all of that good

39:04stuff. So, if we take, for example,

39:07let's say here is going to be right,

39:10here is going to be left. This is going

39:11to be a nice quick recap of the MCA.

39:14Here, let's say that we have a infarct

39:18or a lesion of the PCA that knocks out

39:21this left visual field area,

39:24particularly the left visual cortex. So,

39:27because of that, if you kind of track

39:28all of that stuff back like we did

39:30before from that side, you're going to

39:32lose the visual field here on the

39:33opposite side, and you're going to lose

39:36this visual field if you track all of

39:37these back. So, this is the left uh

39:40particularly like occipital lobe lesion.

39:42So, what's going to happen is you're

39:44going to lose your visual fields on the

39:45right side of the contralateral side.

39:48So, we call that contralateral

39:49homonymous hemianopia.

39:52Okay? So, that's what you would see with

39:54a lesion particularly involving the kind

39:58of your visual cortex and association

40:00cortex. All right, ninjas, let's move on

40:02to the next part here, which is the

40:03midbrain part of the PCA territory,

40:05right? So, we talked about that the PCA

40:06supplied the cortical part of the

40:08occipital lobe, a little bit of the

40:09temporal lobe. We talked about the

40:10thalamic involvement. Now, let's talk

40:12about its extension into the brainstem,

40:14particularly the midbrain. There's three

40:15midbrain syndromes that I really want

40:17you to know. There's actually another

40:18one, too, but this is the These are the

40:19three main ones I want you to take away

40:21from this if you knock out the PCA. So,

40:23here the midbrain, you have the ventral

40:25part of the midbrain. So, this is the

40:26anterior part here. If I were to kind of

40:28denote this, this is anterior part of

40:30the midbrain, posterior part of the

40:31midbrain. Okay?

40:33If you knock out the midbrain, there's

40:35different syndromes that can develop.

40:38The first one that can happen here is if

40:40you knock out the third nerve as well as

40:45the corticospinal tract. Okay? So, if

40:47you knock out the third nerve and the

40:48corticospinal tract, that leads to

40:49what's called Weber's syndrome. Knock

40:51out the third nerve, you get ipsilateral

40:52third nerve palsy because it the third

40:54nerve doesn't cross.

40:56The other things you get contralateral

40:57hemiplegia. This may be somewhat

40:59confusing. You're hitting your left

41:01corticospinal tract, which is in the

41:02left crus cerebri. You guys know what

41:04happens, right?

41:06Uh whenever we have the corticospinal

41:08tracts, starts from the cortex, comes

41:09down through the corona radiata,

41:11internal capsule, moves through the

41:12midbrain. Imagine for a second here that

41:14we come down the pons, come down to the

41:16medulla. What does it do when it gets to

41:17the medulla at the pyramids? Crosses and

41:20goes to the muscles on the contralateral

41:21side. So, if you knock out that left

41:24crus cerebri where again the

41:26corticospinal tracts are running, you

41:28get weakness on that contralateral side.

41:31And then same thing, the third nerve is

41:32what supplies particularly uh a bunch of

41:35different muscles, but one of the big

41:36things to remember here is that it it's

41:39going to lead to what's called a down

41:41and kind of out movement of the eye. And

41:43if you hit those parasympathetic fibers,

41:45it may even cause some dilation as well.

41:48All right. So, we got Weber's syndrome

41:49down. Third nerve palsy, ipsilateral

41:51contralateral hemiplegia, Weber's

41:53syndrome. Next one is Claude's syndrome.

41:56Claude's syndrome

41:57is you're going at the level of the red

41:58nucleus now. So, here we were at a

42:01particular level. We want to go to for

42:02Claude's syndrome, go to the level of

42:04where the red nucleus is in the

42:06midbrain.

42:07When you go to the level of the red

42:08nucleus, you still have that third nerve

42:10there. But whenever someone has Claude's

42:12syndrome due to a PCA lesion, you knock

42:14out two particular structures. One is

42:17the third nerve. Again, if you have

42:19third nerve that's injured in this

42:22Claude's syndrome, it's going to cause a

42:23down and out movement of the eye, right?

42:26It also could cause dilation if you hit

42:27the parasympathetic fibers.

42:29But you're also going to hit this thing

42:30called the red nucleus. What does the

42:32red nucleus do? The red nucleus is a

42:35part of your rubrospinal tract, right?

42:37So, it involves kind of like distal

42:38flexion, but it also loves to

42:40communicate with your cerebellum. Loves

42:43to communicate with the contralateral

42:45cerebellum. So, if you knock out the red

42:48nucleus, you knock out the communication

42:50with the contralateral cerebellum. So,

42:52for example, if you knock out that left

42:54red nucleus

42:55uh in this case, uh for example, this is

42:57going to be right, this is going to be

42:58left. If you knock out that left red

43:00nucleus, you're altering the connection

43:03between that right cerebellum and left

43:04red nucleus. That's going to lead to

43:06ataxia on that side of where the

43:09cerebellum was communicating with the

43:11red nucleus. So, for example,

43:14if it's the right cerebellum

43:15communicating with the left uh red

43:18nucleus, you would develop ataxia on the

43:21contralateral side to the red nucleus,

43:23but the same side of the cerebellum.

43:26Okay? So, we call that contralateral

43:28ataxia. So, again, brief recap brief

43:31recap for Claude's is you hit third

43:33nerve, so ipsilateral third nerve palsy,

43:36you hit the red nucleus leading to

43:37contralateral ataxia because you

43:39communicate with the contralateral

43:41cerebellum. Okay?

43:44Next one is Benedict's syndrome.

43:46Benedict's is basically Weber's and

43:47Claude's. That's all you need to

43:49remember. It's Weber's and Claude's. So,

43:51you're knocking out the red nucleus,

43:53you're knocking out the third nerve, and

43:55you're knocking out those corticospinal

43:56tracts. So, what do you get? If you

43:58knock out third nerve, you get

43:59ipsilateral third nerve palsy, down out

44:01movement, you hit the parasympathetic,

44:02dilation. You hit the corticospinal

44:04tracts, crosses again later at the

44:06pyramids, you get contralateral

44:07hemiplegia. And if you hit the red

44:09nucleus, again that communicates with

44:10the contralateral cerebellum, you'll get

44:12contralateral ataxia. Boom, roasted. We

44:15just hit PCA syndromes. Let's move on to

44:18the next thing, which is your basilar

44:20artery syndrome. All right, ninjas,

44:22let's move on to the next thing, which

44:23is the basilar artery syndromes. So,

44:25basilar artery is a beast, all right?

44:28So, this supplies a good chunk of the

44:30brainstem, particularly the pons and the

44:33cerebellum. Okay? So, we're talking

44:34about the superior, anterior, and

44:36inferior part of the cerebellum. So,

44:37again, if you want to recap it, what

44:39does the basilar artery supply? It

44:40supplies the pons. It supplies the

44:42superior, anterior, and inferior part of

44:44the cerebellum. And we're going to make

44:45sense of all this. It's actually

44:46relatively easy. So,

44:49let's take a look here at the quick

44:50little blood flow supply here. So, we

44:52have particular numbers that I want you

44:54guys to know. We'll briefly recap though

44:56kind of the circulation, right? So, here

44:58we're going to have your vertebral

44:59arteries, right? Those come off of your

45:01what?

45:02So, you remember how you have your your

45:04brachiocephalic and that goes into For

45:05example, let's say brachiocephalic goes

45:07into

45:10carotid or so the common carotid. So,

45:12off of that kind of subclavian, you can

45:14have those vessels called the vertebrals

45:16that can pop off. So, you have the

45:17vertebral arteries that are going to be

45:19here. They'll give off a branch that

45:21we'll talk about a later in the

45:22vertebral artery stroke syndromes, which

45:24is called your PICA. Eventually, the

45:26vertebral arteries will come together,

45:27fuse, and make this big mama here. This

45:30is number one. Number one that I want

45:32you to remember is the basilar artery.

45:35It's basically from this whole chunk

45:37right here

45:39to this whole part right here is going

45:41to be our basilar artery. So, basilar

45:43artery supplies a very good chunk of the

45:44pons, but what I want you to really,

45:46really remember is that the basilar

45:48artery

45:49gives off lots of branches.

45:51The basilar artery branches that

45:53actually are going to be little branches

45:54that penetrate into the pons, the

45:56paramedian branches, supply primarily

45:59the medial pons. So, when you guys think

46:01basilar artery, its branches, the

46:03immediate branches off of it, is going

46:05to be the paramedian branches. Those

46:07supply the medial pons.

46:09Another thing that happens is as the

46:11basilar artery tracks tracks tracks

46:12tracks up, so we actually should say

46:14that the basilar artery comes up to

46:15about here, it gives off a branch here

46:17called the PCA. That's number two. So,

46:20PCA is the number two branch off of the

46:23in this case the basilar artery, and

46:25that's the part that we already talked

46:26about gives way to the midbrain,

46:27supplies the occipital lobes, temporal

46:29lobe, even hits that thalamus, right?

46:32The other one is we move our way down.

46:33So, number one, number two, we got PCA.

46:35Number three off the basilar artery here

46:38is this guy called the superior

46:40cerebellar artery. Superior cerebellar

46:42artery, what do you think it supplies?

46:44The superior cerebellum. Move on to the

46:46next one. So, we got it again.

46:47Vertebrals coming up, basilar, basilar

46:49goes all the way up, gives off PCA, then

46:51it gives off SCA, then if we come down a

46:53little bit, the other branch that it

46:55gives off here, number four,

46:57is the anterior inferior cerebellar

46:59artery.

47:00That supplies the lateral portion of the

47:02pons and it supplies the anterior and

47:05inferior portion of the cerebellum, thus

47:07its name. Quick recap again. Vertebrals

47:10come up, fuse, make basilar. Basilar

47:13extends all the way from the pons

47:14upwards up here.

47:16Branch it gives up at the top is the

47:17PCA.

47:19The one that it gives off underneath

47:20that is the SCA. And the one that it

47:22gives off underneath that is the AICA or

47:25the anterior inferior cerebellar artery.

47:27Got it?

47:28Now that we know that and we know that

47:31the basilar, its immediate branches give

47:33off medial pons, AICA gives off lateral

47:36pons, anterior inferior cerebellum.

47:38SCA supplies the superior cerebellum. We

47:41know the big, big vessels that we need

47:43to know now for the basilar artery.

47:45Let's talk about these now. So, the

47:47first thing I want you guys to remember

47:49is the basilar artery gives off little

47:51paramedian branches that supply the

47:52medial pons. If you knock out the little

47:55paramedian branches of the basilar

47:57artery, you don't give blood supply to

47:59the medial pons, you lead to

48:01neurodeficits

48:02from the destruction of all the

48:03structures in the medial pons. So, we

48:05need to know what in the heck is in the

48:07medial pons. Let's do that. Let's do it

48:10from dorsal to ventral.

48:12From the dorsal part here, kind of in

48:14the midline, you have a particular

48:16nucleus and this is the sixth nerve

48:18nucleus. Sixth nerve nucleus is also

48:20known as the abducens nerve. So,

48:23abducens nerve, if you hit this, so

48:26let's say here again, this is kind of

48:28this blue is marking the territory. You

48:29see all this blue here? This is all

48:31basilar artery, the paramedian branches

48:33of the basilar artery. So, that's all

48:34kind of encompassing

48:37this part here, if you guys can imagine

48:38that.

48:40If we knock out the paramedian branches,

48:41we don't give blood supply to the sixth

48:43nerve nucleus. What does the sixth nerve

48:45do? It abducts the eye, the same eye.

48:47So, if it's the left abducens nerve,

48:48it's going to abduct the left eye. If

48:51you knock that out, you develop

48:53ipsilateral sixth nerve palsy. Can't

48:55abduct that left eye.

48:57What's the next one? Go here to this

48:58little maroon colored one. That maroon

49:00colored guy is called the MLF, medial

49:03longitudinal fasciculus. What does it

49:05do?

49:06Connects. It's a midline structure

49:08that connects the third nerve at the

49:10top, fourth nerve, and the sixth nerve.

49:13All I want you to remember is it helps

49:14to conjugate eye movement. So, if you

49:16want to move your eyes to the right, you

49:18have to have your left medial rectus

49:19contract, and you also have to have your

49:21right lateral rectus contract. So, that

49:23MLF helps to coordinate and conjugate

49:25movements properly with those

49:27extraocular muscles, okay? Between what

49:30structures you're connecting? Three,

49:32four, and six.

49:33If you knock that out, it's going to

49:35lead to what's called internuclear

49:37ophthalmoplegia. Your eyes are going to

49:38be all wonky because you're not going to

49:40be able to coordinate the eye movements

49:42conjugately properly because you knocked

49:44that structure out.

49:46Move to the next thing. As we go a

49:48little bit more interior, we got this

49:49blue structure here called the PPRF, the

49:50paramedian pontine reticular formation.

49:53This also is involved in kind of

49:54conjugating eye movements as well. So,

49:57if you knock out that, you develop a

50:00loss of gaze to that same side of where

50:02that paramedian pontine reticular

50:04formation is. So, you won't be able to

50:06gaze in the this case to the left side.

50:09And so, because of that, the actual

50:11preference or deviation will occur

50:12towards the contralateral side, in this

50:15case, the right side. Okay? So, again,

50:17quickly recapping PPRF, you knock that

50:20out, your conjugate gaze is affected,

50:22you can't gaze properly to the same

50:24side. If you can't gaze to that left

50:26side now, what happens is your eyes

50:28start to deviate to the contralateral

50:31side.

50:32Next one. Move again. Medial here, but

50:35again going anterior as we're working

50:36from back to anterior here. We got this

50:39green structure called the medial

50:40lemniscus.

50:42If you knock out the medial lemniscus,

50:43what does it do? It takes sensory

50:45information. What kind of sensory

50:46information? Fine discriminative touch,

50:48proprioception, vibration. All of that

50:51stuff takes it up from the body up to

50:53the central nervous system. If you knock

50:55that out,

50:56and in this case, it's on the left side.

50:59If you hit the left medial lemniscus,

51:02you're going to lose sensation such as

51:03fine discriminative touch,

51:05proprioception, vibration on what side?

51:07The right side in this case, okay? So,

51:09we the contralateral side. So, that's

51:11where you get contralateral loss of

51:13sensations.

51:15Move again anterior and you got this big

51:17old red thing here called the

51:19corticospinal tracts that are running

51:20through the pons. You even have

51:21corticobulbar tracts which control

51:23muscles of the head and the neck as

51:24well.

51:25But either way, you knock that thing

51:27out, it hasn't crossed yet, right? So,

51:29if it's on the left side that you're

51:31knocking out that corticospinal tract,

51:32it hasn't crossed yet at the pyramids.

51:34But eventually it will, it'll come down

51:35to the pyramids and cross and go to the

51:37other side. So, you're going to get

51:38contralateral hemiplegia of what?

51:41The entire side of that body. In this

51:43case, if it's the left corticospinal

51:45tract, you'll develop right-sided

51:46weakness of the face, the upper

51:49extremity, lower extremity, trunk.

51:51Boom, roasted. We just hit the medial

51:53pons. But what do I want you to

51:54remember?

51:55What artery is primarily occluded? It's

51:57the paramedian branches of the basilar

52:00artery there that we're knocking out.

52:03Come down to the next one.

52:05What did I tell you comes off of the

52:08uh the basilar artery? Okay? It was

52:10number four. Comes off of it and

52:12supplies the anterior inferior

52:13cerebellum and supplies the lateral

52:15pons.

52:16That was the AICA. So, look at this

52:19diagram here. Here we have the basilar

52:21which was supposed to be this territory

52:22right here.

52:24I'm going to kind of like make it like

52:25that so it fits, but that was our

52:26basilar artery territory. Is that

52:28getting hit right now from those

52:29paramedian branches? No. What structures

52:32would be getting hit if you're over

52:33here? Ooh, baby, we hitting that AICA.

52:37We hitting that AICA. So, the AICA is

52:39going to involve more of that lateral

52:40pons which we told you when we talked

52:42about that above, and it's also going to

52:44hit the

52:45anterior inferior cerebellum. So,

52:49let's talk about what it does though.

52:51If the AICA is affected, you don't get

52:53blood supply to the structures in the

52:55lateral pons. So, let's know what's in

52:57the lateral pons, and if we damage that,

52:59what would happen?

53:01Let's work our way out from the most

53:03lateral part of the pons, and let's work

53:05our way laterally, medially, and

53:07anteriorly. Okay? So, we're going to

53:09work from here and we're going to go

53:10this way.

53:12So, first thing here is you got this

53:14structure here most laterally in maroon

53:16called the middle cerebellar peduncles.

53:18So, those are a communication system.

53:19They're a highway system between the

53:20pons and the cerebellum. Allowing for a

53:23nice communication there between them.

53:25Now, remember what it does is it takes

53:27sensory information from your

53:28spinocerebellar pathways and takes that

53:31and puts that into the cerebellum so

53:32that the cerebellum can say, "Hey, I'm

53:34receiving all this proprioceptive

53:36information, all of this kinesthetic

53:38information. I'm knowing where the

53:39position of the body is in

53:40three-dimensional space." If you knock

53:42out that middle cerebellar peduncle on

53:45this case, the left side, all of that

53:48proprioceptive and kinesthetic

53:50information coming up via the

53:52spinocerebellar pathways on the left

53:53side is going to get knocked out. And

53:55you're going to not be able to

53:56coordinate where your position of your

53:58body is in a three-dimensional space.

54:00And so, this can lead to ipsilateral

54:02ataxia cuz you're hitting that middle

54:04cerebellar peduncle, and everything for

54:06cerebellum is always ipsilateral. Okay?

54:09So, that's what happens there. Knock out

54:11the middle cerebellar peduncle,

54:13ipsilateral ataxia because that's where

54:14the spinocerebellar pathways are going

54:16into the pons.

54:19Move our way again. We're going to go

54:20kind of medially and work our way

54:21anteriorly. So, we're going to hit this

54:22purple structure here.

54:24This purple structure here is your

54:25vestibular nuclei and a little bit of

54:27the cochlear nuclei. So, your vestibular

54:29nuclei are responsible for what? A lot

54:31of your your equilibrium, right? So,

54:34your dynamic equilibrium, your static

54:36equilibrium. And so, what happens is if

54:38you affect these things, you can lead to

54:40a loss of that equilibrium. And that

54:41kind of presents sometimes as vertigo.

54:44And vertigo also is not too great

54:46because what happens is whenever

54:47someone's really, really dizzy and they

54:49have a lot of these abnormalities in

54:50their equilibrium, it loves to stimulate

54:52what's called the chemo trigger zone.

54:54And that chemo trigger zone will induce

54:56nausea and vomiting from that kind of

54:59like really significant vertigo. So,

55:02they can develop vertigo, nausea,

55:03vomiting. Also, the vestibulocochlear

55:06system also does have a communication

55:08with what's called your vestibulo-ocular

55:10reflexes. And so, because of that, they

55:12can also develop these beating of

55:14movements of the eyes called nystagmus.

55:18If you hit the cochlear nuclei, what

55:20does the cochlear nuclei do? They're

55:22responsible for receiving information

55:23from that spinal organ of Corti, right?

55:25Literally, sound amplitude, uh pitch,

55:29all of that stuff for hearing, for sound

55:31stimulus. So, if you lose that, you can

55:34obviously develop deafness and sometimes

55:36very high-pitched sounds called

55:38tinnitus.

55:39So, we got ipsilateral ataxia, we got

55:41deafness, vertigo, nausea, vomiting, and

55:44nystagmus. Now, we go to the green

55:45structure here.

55:46The green structure here is called your

55:48descending sympathetic fibers. So, those

55:50are coming from your hypothalamus. You

55:51remember hypothalamus has the descending

55:53sympathetic fibers that run down through

55:54the spinal cord? If we knock these out,

55:57you knock out the sympathetic fiber

55:59supply particularly to like the face and

56:02the eyelid and the eye the actual

56:04muscles of the eye. Uh particularly the

56:07the ciliaris muscles, okay? So, what

56:09happens here?

56:11So, what happens is if you knock out the

56:13sympathetic tracts, you can develop

56:15what's called Horner's syndrome on that

56:17that same side. So, ipsilateral. So, if

56:18you knock out that left sympathetic

56:20tracts, you develop left-sided Horner's

56:22syndrome. So, what does that consist of?

56:23Well, you knock out the muscles

56:25uh the the tarsal plate muscles. And so,

56:27what happens is you can develop ptosis

56:28of the upper eyelid.

56:30You can cause anhidrosis. So, again,

56:32sympathetic supply supplies uh sweat

56:34glands. Uh so, you'll have anhidrosis of

56:36that side.

56:37And sympathetic supply also goes to the

56:40pupillary muscles. So, normally, your

56:42sympathetic wants to dilate the pupils.

56:44But if you knock out the sympathetic

56:45system, what happens? They'll actually

56:47constrict. And that's called miosis of

56:49the pupils, okay?

56:52Boom, roasted. Move on. Okay, now we go

56:54again. We're going to move this way.

56:55We'll come back to this little bugger a

56:56little bit later, okay? We're going to

56:58move on to this red one here. The red

57:00one there

57:02uh is called your spinal So, this is

57:03actually part of your your trigeminal's

57:05nuclear system. So, you remember your

57:07your trigeminal nucleus? You have the

57:09different parts in the midbrain, the

57:11mesencephalic part, you have the central

57:12pontine part or principal pontine, and

57:15then underneath that you have the spinal

57:17trigeminal nucleus. Well, you have that

57:18nucleus and then you have the tract.

57:20When you knock out the nucleus,

57:22particularly where the motor nuclei are,

57:25the motor nuclei of the fifth nerve I'm

57:27sorry, the yeah, the fifth cranial nerve

57:29which is the trigeminal nerve, you

57:31affect the muscles that they supply

57:34which is the mastication muscles. And

57:36so, if you knock out that left side,

57:37you'll affect the muscles on the left

57:39side leading to decreased effectiveness

57:41of the mastication muscles on that left

57:44side. The other thing is

57:46all of the sensations of the face come

57:49from the trigeminal nerve. And that all

57:51gets taken into that trigeminal system.

57:54So, the trigeminal tracts also are going

57:56to get hit. And so, you're going to get

57:57ipsilateral loss of pain, temperature,

57:59some of the touch and proprioceptive

58:01sensations from the face. That's where

58:04you get ipsilateral sensory loss,

58:06ipsilateral weakness of the mastication

58:08muscles. Boom, roasted. What's the next?

58:11Let's move on to this little blue dude.

58:13The blue dude is actually going to be

58:15your spinothalamic tracts. So, these are

58:17taking particularly pain, temperature,

58:20some of the crude touch, pressure

58:22sensations not from the face, but from

58:24the body. So, from your upper extremity,

58:26your trunk, and your lower extremities.

58:28So, for example, if you knock out that

58:29spinothalamic tract on the left side,

58:32you're going to develop what?

58:33Remember what happens when you have

58:34sensations coming in via the

58:35spinothalamic tract? They come into the

58:37spinal cord and they immediately cross

58:38at that level of the spinal cord

58:40usually. Maybe depending upon that,

58:41maybe one to two levels the tract will

58:43be sore. But again, the whole point is

58:45it crosses the level of spinal cord and

58:46then ascends.

58:48So, if it's already crossed and we're at

58:50that point here at the the pons, that

58:52means that if you knock out this

58:53structure, the spinothalamic tract, the

58:55sensations are going to be on the right

58:58side. So, you'll develop contralateral

59:00loss of pain, temperature, maybe even

59:02some crude touch and pressure

59:03sensations. Okay? So, that's what you'll

59:05get there.

59:06And then the last but not least is this

59:08dude here sitting in the middle.

59:10It's just their facial nerve nucleus.

59:12So, the facial nerve nucleus, you

59:13actually know that it kind of wraps

59:14around the sixth nerve and then goes

59:16out, right? But if you hit the the

59:18facial nerve, okay? What happens if you

59:20hit the left side? It's ipsilateral. So,

59:23you can develop ipsilateral facial

59:25weakness. Usually though, it's the it's

59:27the lower kind of like third part of the

59:29face, okay? So, it's the lower third

59:30part of the third part of the face.

59:33Okay? But again, you're going to develop

59:35ipsilateral facial weakness usually the

59:37lower part of the face.

59:39That covers the lateral pons, which

59:41again is supplied by what part?

59:43AICA. Medial pons?

59:45The paramedian branches of the basilar.

59:47All right, let's finish off talking

59:48about again the other branches that we

59:49didn't really completely discuss. We

59:51really talked about the medial pons and

59:52the lateral pons, but we didn't talk

59:54about the cerebellum cuz remember the

59:55basilar artery does supply not just the

59:57pons, but the superior anterior inferior

1:00:00part of the cerebellum through what

1:00:01vessels though?

1:00:03Well, the superior cerebellar artery

1:00:04supplies the superior cerebellum. That

1:00:06comes off kind of the top part of that

1:00:07basilar.

1:00:08And then a little bit underneath that is

1:00:10going to be the AICA that supplies the

1:00:12anterior inferior part of the

1:00:13cerebellum.

1:00:14Either way,

1:00:16you occlude these vessels, you damage

1:00:17those vessels, you don't get blood

1:00:18supply to the cerebellum. Cerebellum's

1:00:20involved in so many things like posture,

1:00:22tone, coordination, uh a lot of

1:00:24different things like that. So, if you

1:00:25knock that out, you can develop things

1:00:26like ataxia.

1:00:28Uh so, obviously kind of like loss of

1:00:30the coordination. You can develop

1:00:32dysmetria, so difficulty being able to

1:00:34kind of like track uh particular spaces

1:00:36like for when you're trying to move your

1:00:37finger to nose. So, so finger to my nose

1:00:40to the to the actual clinician's finger,

1:00:42they may overshoot it

1:00:44or they may undershoot it and they may

1:00:45have problems bringing it back to their

1:00:46nose as well. Dysdiadochokinesia, they

1:00:49have difficulty with kind of like those

1:00:50rapid alternating movements. They might

1:00:52have like an irregularity in there and

1:00:54not be able to do it as quick.

1:00:56And so, things like that can kind of

1:00:57come up as well. So again, when we talk

1:01:00about basilar artery syndromes, think

1:01:02about all of these things coming up,

1:01:05but think about what vessel supplies the

1:01:07medial pons? Paramedian branches of the

1:01:09basilar. Lateral pons is AICA. And then

1:01:13for the cerebellum, we're talking about

1:01:14superior cerebellar and AICA. I think we

1:01:17nailed that home. Let's move on to the

1:01:19last part, which is the vertebral artery

1:01:20syndromes. All right, ninjaneers, we are

1:01:22at the end. I promise. I know that this

1:01:24has been tough, but let's stick through

1:01:26it together. We got this, ninjaneers. We

1:01:28can do this. So, we're going to finish

1:01:30up with vertebral artery syndromes. Now,

1:01:32vertebral arteries is I want you to

1:01:33remember supplies the last part of the

1:01:35brainstem. So, we know PCA hits the

1:01:37midbrain, right? We know the basilar

1:01:40hits our pons, superior cerebellum,

1:01:42anterior inferior cerebellum. Vertebral

1:01:44is going to hit the medulla

1:01:46and the posterior inferior part of the

1:01:49cerebellum, right? So, let's talk about

1:01:51that. Before we do that though,

1:01:54let's briefly talk about the blood

1:01:56supply recapping it again. So again,

1:01:58what do we have these structures here

1:01:59coming up off of the subclavians?

1:02:01Your vertebrals. So, that's number one,

1:02:03right? So, vertebrals, your right and

1:02:04left vertebral arteries. What do we say

1:02:06that they need to remember? What do

1:02:08these supply? They give off their little

1:02:09branches.

1:02:11And particularly, they give off their

1:02:12branches through what's called uh the

1:02:14branch in the middle here. You see this

1:02:16thing right here, number two?

1:02:17That's called the anterior spinal

1:02:19artery. So, what happens? Vertebrals

1:02:21come up. As they come up and approach

1:02:22one another, they become the basilar.

1:02:24They give off this little branch here

1:02:26called the anterior spinal artery.

1:02:28So, the anterior spinal artery is

1:02:30particularly

1:02:31the branch that supplies the medial

1:02:33medulla, but we can still say the

1:02:34vertebrals also supply the medial

1:02:37medulla. So, when I say, "What gives you

1:02:39the blood supply to the medial medulla?"

1:02:40you should say your vertebrals and your

1:02:43anterior spinal artery.

1:02:45Okay, good. We got that. We come up. As

1:02:48we come up, we recap this. As we come

1:02:51up, we fuse together and make the

1:02:53basilar. What comes off the top of the

1:02:54basilar? PCAs. What comes off underneath

1:02:57that? Superior cerebellar artery. What

1:02:59comes off underneath that? AICA.

1:03:02The last thing I need to talk about is

1:03:03as we come up before the vertebrals fuse

1:03:06and form the basilar, not only do they

1:03:08give off anterior spinal artery, but

1:03:10they give off this thing here. What's

1:03:12that bad boy, number three?

1:03:14Number three is your PICA, which is the

1:03:16posterior inferior cerebellar artery.

1:03:19What does that supply? What do we have

1:03:20left? Remember I told you vertebrals

1:03:22should give off a bunch of branches at

1:03:23the end of it though, you should supply

1:03:25medulla,

1:03:27you should supply what else?

1:03:28The posterior inferior cerebellum.

1:03:31Well, we got vertebrals getting the

1:03:33medial medulla. We got anterior spinal

1:03:35hitting the medial medulla. What's left?

1:03:37Lateral medulla?

1:03:39PICA and posterior inferior cerebellum,

1:03:42PICA. So, that's what I want you to

1:03:44remember. Vertebrals, anterior spinal

1:03:45give you medial medulla. PICA gives you

1:03:48lateral medulla, posterior inferior

1:03:49cerebellum. Boom, roasted. Let's move on

1:03:52to that stuff then. Similar to the

1:03:54basilar,

1:03:55we take a look at the medulla. We take a

1:03:57cross section through the medulla. We

1:03:59have here in organization, posterior

1:04:02part of the medulla, anterior part of

1:04:04the medulla.

1:04:05When we look at this, we see our

1:04:07vascular territories here in that cross

1:04:08section. In blue, as you see here

1:04:10through the midline,

1:04:12is what? The vertebral arteries and the

1:04:15anterior spinal artery.

1:04:17That's supplying the structures in the

1:04:18medial strip of the medulla. Now, we

1:04:20need to know what are the structures in

1:04:22the medial strip of the medulla. If we

1:04:23damage them, what are the clinical

1:04:25features?

1:04:26We're so good, ninjaneers, aren't we? We

1:04:28know this stuff.

1:04:29Boom, smack dab here in the middle,

1:04:32you have what's called the 12th cranial

1:04:34nerve, the hypoglossal nerve. The

1:04:37hypoglossal nerve is obviously

1:04:38responsible for tongue movement, right?

1:04:39So, protrusion of the tongue, moving it

1:04:40left, moving it right, moving it up,

1:04:42moving it down, curling it, all of that

1:04:43good stuff.

1:04:45So, if you knock out, for example, in

1:04:47this case, the left 12th nerve, you

1:04:51won't be able to allow for it there'll

1:04:53be weakness on that left side. Okay, so

1:04:55there's going to be weakness on the left

1:04:55side of the tongue.

1:04:57What will happen is is that the right

1:04:59half of the tongue from that normal

1:05:01right 12th nerve will overpower and

1:05:04deviate the tongue to the weak side,

1:05:07which in this case is our left side

1:05:10because the left 12th nerve's injured.

1:05:12So, because of that, you injure the left

1:05:1412th nerve, the weakness on that left

1:05:16side, right side overpowers, and the

1:05:19tongue deviates to the same side as

1:05:22where the lesion is present, which is

1:05:24the left side. So, you get ipsilateral

1:05:25deviation of the tongue. All right, so

1:05:27we got the 12th nerve nucleus. The next

1:05:28thing is this green structure here in

1:05:30the middle. And this may sound familiar

1:05:31to what we already talked about within

1:05:32the medial pons. Medial lemniscus is

1:05:36responsible for what?

1:05:37Picking up fine touch, proprioceptive,

1:05:40discriminative touch, vibrations, all of

1:05:41that stuff and bringing it up from one

1:05:43side of the body up through the

1:05:44brainstem into the other side of the

1:05:46brain.

1:05:47If you knock out that left medial

1:05:49lemniscus, you're going to knock out

1:05:51sensations to the contralateral side of

1:05:54the body as long as it's after cuz

1:05:56medial lemniscus comes after the nucleus

1:05:58gracilis, the nucleus cuneatus. It's

1:06:00just kind of at the bottom part of the

1:06:01medulla. So, if you knock out that

1:06:03medial lemniscus, you knock out

1:06:05contralateral proprioception, fine

1:06:06touch, discriminative touch, and all of

1:06:08those things to the contralateral side,

1:06:10so right side in this case.

1:06:12So, that's what you get here when you

1:06:14knock out that medial lemniscus.

1:06:16Left corticospinal tract. Remember,

1:06:18we're at the pyramids, but we haven't

1:06:20gotten to the bottom as you go down the

1:06:21pyramids, the decussation of the

1:06:24corticospinal tracts occur at the bottom

1:06:26of the pyramid. So, if we were at the

1:06:27decussation point, then yeah, we could

1:06:30potentially have ipsilateral weakness,

1:06:33but we're at the point where we haven't

1:06:35decussated yet within the medulla. And

1:06:37so, because of that, you get no crossing

1:06:40yet. Eventually, it will cross, so

1:06:41you're going to get contralateral

1:06:43hemiplegia. So, if it's on the left side

1:06:45of the medulla that you're hitting,

1:06:47you're going to develop right-sided

1:06:49weakness or right-sided hemiplegia.

1:06:52Okay, or paralysis.

1:06:55That covers the medial medulla, which is

1:06:56supplied by what strip here? Vertebral

1:06:58and anterior spinal artery. So again, to

1:07:00recap it, ipsilateral third 12th nerve

1:07:02palsy, medial lemniscus, so loss of

1:07:05contralateral sensations,

1:07:07all the sensations we discussed, and

1:07:09corticospinal tract contralateral

1:07:10hemiplegia. So, we talked about the

1:07:12medial medulla. Let's now talk about the

1:07:14lateral medulla. So, we know again,

1:07:15medial medulla was supplied by the

1:07:16vertebral artery, anterior spinal

1:07:18artery. We can see that by that like

1:07:20territory that we colored here in blue.

1:07:22Now, imagine if we kind of go out

1:07:24laterally, do you see the vertebral

1:07:26arteries and anterior spinal arteries

1:07:27hitting that territory? No, that's

1:07:30within the realm of the PICA, right? So,

1:07:32if we knock out the PICA, we knock out

1:07:33the structures that are supplied within

1:07:35the lateral medulla. So, what are the

1:07:37structures in the lateral medulla and

1:07:39what happens if those things are

1:07:40damaged? Let's start here laterally,

1:07:42work our way kind of like uh medially

1:07:44and then anteriorly.

1:07:46Cuz again, this is the same section as

1:07:48compared here. So, this is still like

1:07:50the posterior portion. This is the

1:07:51anterior portion. That's lateral,

1:07:53lateral, medial.

1:07:55So, first thing here at the lateral part

1:07:57of this left part of the medulla here

1:07:59is going to be the inferior cerebellar

1:08:01peduncles. It's the same thing that we

1:08:03talked about with pons.

1:08:05It's just instead of it being middle,

1:08:06it's inferior. The spinocerebellar

1:08:08pathways or any kind of proprioceptive

1:08:09pathways are coming up into the

1:08:11cerebellum and then it's going to be

1:08:13moving into the cerebellum from the

1:08:15medulla via these inferior cerebellar

1:08:16peduncles. If you knock out that

1:08:18connection,

1:08:20you knock out the ability to be

1:08:21coordinating our our proprioceptive

1:08:23sensations, which is involved in

1:08:24coordination. So, if you knock out that

1:08:26left inferior cerebellar peduncle, you

1:08:28knock out the sensory proprioceptive

1:08:30information going to the left

1:08:32cerebellum. And so, that's going to lead

1:08:33to ipsilateral ataxia because again,

1:08:36everything with the cerebellum produces

1:08:37ipsilateral symptoms as compared to the

1:08:39cortex, which is contralateral. So

1:08:41again, knock out the inferior cerebellar

1:08:43peduncle, you knock out the

1:08:44communication of proprioceptive

1:08:46sensation to the left cerebellum, you

1:08:48lead to ipsilateral ataxia.

1:08:50Move medially to this blue structure

1:08:52here called the nucleus ambiguus. This

1:08:54is the big big big big big one that I

1:08:55want you guys to remember. A lot of this

1:08:57stuff is pretty much the same what we

1:08:58talked about with lateral pontine

1:09:00pontine involvement. It's the same. This

1:09:02is the really big difference here when

1:09:04you talk about lateral medulla

1:09:05involvement is you're involving the

1:09:07nucleus ambiguus. The nucleus ambiguus

1:09:11is the nucleus that gives way to

1:09:12particular nerves, motor nerves for

1:09:15cranial nerves nine, glossopharyngeal,

1:09:17cranial nerves 10, vagus, and a teensy

1:09:20little bit of this accessory nerve,

1:09:22cranial nerve 11. These go and supply

1:09:24particular muscles involved in speech

1:09:27and in swallowing, okay? And so, what

1:09:29are some of those muscles? It's muscles

1:09:31of the soft palate, muscles of the

1:09:32uvula, muscles of the pharynx, muscles

1:09:35of the larynx. All of those things are

1:09:37involved and particularly

1:09:39stimulated by the nerves coming from the

1:09:42nucleus ambiguus. If you develop a

1:09:44lesion in the PICA and you knock out

1:09:46that nucleus ambiguus, you knock out

1:09:49motor supply to all of the larynx,

1:09:51pharynx, soft palate, and uvula. And

1:09:53this can produce what's called a bulbar

1:09:56ipsilateral, so you're affecting the

1:09:57same side.

1:09:59So, what can that look like? One thing

1:10:01is you affect the ability to swallow

1:10:03because you're hitting those pharynx

1:10:04muscles. That can cause dysphagia.

1:10:06You're affecting the speech production

1:10:08because you're hitting the larynx

1:10:09muscles. That's causing dysphonia.

1:10:11You're affecting your reflexes. You

1:10:12know, whenever you take like a tongue

1:10:14depressor and tap on someone's pharynx

1:10:15or tonsillar walls, it triggers a gag

1:10:18reflex. Or if you take an endotracheal

1:10:20tube and you go down and deeply suction

1:10:22or aspirate things from their carina or

1:10:24trachea, that causes a cough reflex,

1:10:26which is elicited by your vagus nerve.

1:10:29If you damage that, you then have a

1:10:31decreased or absent cough gag reflex.

1:10:35And the last thing is again, remember

1:10:36that cranial nerve 10 supplies the

1:10:38uvula. There's two halves of the uvula

1:10:40supplied by cranial nerve 10. If you so

1:10:42if there's actually a decreased supply

1:10:44or injury to in this case the left vagus

1:10:47nerve,

1:10:48that left side of the uvula isn't going

1:10:51to be able to contract. And so, what

1:10:52happens is it starts to deviate to the

1:10:55opposite side because the other side is

1:10:56working properly and yanking it to the

1:10:58other side. And so, you'd have a kind of

1:11:00what's called a contralateral uvular

1:11:01deviation. So, big things to remember,

1:11:03this is the huge huge huge one to

1:11:05remember when there's lateral medulla

1:11:07involvement because of a PICA lesion.

1:11:09You know what another name for the

1:11:10lateral medulla kind of lesion is or

1:11:13syndrome? We call it Wallenberg

1:11:15syndrome. So, remember that. Sometimes

1:11:16that can show up on your board exams.

1:11:18All right. So, we got inferior

1:11:19cerebellar peduncle. We got nucleus

1:11:20ambiguus with the bulbar palsies. The

1:11:23next one that we have here is this

1:11:24purple one called the vestibular nuclei.

1:11:25Now, the vestibular nuclei are involved

1:11:27with static equilibrium, dynamic

1:11:29equilibrium.

1:11:30And so, what happens is they could they

1:11:31help to be involved in a couple things.

1:11:33One in maintaining balance.

1:11:35The other one is they help to allow for

1:11:37the proper movement of our eyes whenever

1:11:39we're like shifting our head from side

1:11:41to side or up and down.

1:11:43And whenever there is involvement of a

1:11:45lot of issues with the vestibular

1:11:48nuclei, that can communicate with what's

1:11:49called our chemo trigger zone, which is

1:11:51involved in nausea and vomiting.

1:11:53If you injure the vestibular nuclei, you

1:11:55then alter your ability to maintain

1:11:57static and dynamic equilibrium, which

1:12:00leads to vertigo. You alter the the

1:12:02connection to the chemo trigger zone,

1:12:04and now there's more stimulation of it

1:12:06that it causes nausea and vomiting. And

1:12:08you alter the vestibulo-ocular reflex,

1:12:10which is causing nystagmus.

1:12:14Now, move out a little bit here to this

1:12:15green structure called the sympathetic

1:12:17tracts, the descending sympathetic

1:12:19fibers that come from the hypothalamus.

1:12:21You hit those, you cause ipsilateral

1:12:22Horner's syndrome, which we already

1:12:24talked about with the pons, which leads

1:12:25to decreased sweating, anhidrosis.

1:12:29You cause ptosis of that upper eyelid,

1:12:31and then you cause the pupil to not be

1:12:33able to dilate, instead it constricts,

1:12:35which is called miosis.

1:12:37Next thing is this blue structure here

1:12:39called the trigeminal nucleus. Now, the

1:12:41trigeminal nucleus in the pons, there

1:12:42was the

1:12:43uh central pontine nucleus, but there

1:12:46was the motor component of it as well

1:12:48that controlled mastication muscles.

1:12:50In this part here in the medulla, the

1:12:53lateral medulla, it's called the spinal

1:12:55trigeminal nucleus, but there's no motor

1:12:56component of that trigeminal nerve

1:12:58there. It's just sensory involvement

1:13:00there. And the tract, the the

1:13:02the spinothalamic, sorry, the trigeminal

1:13:04tract is also there as well. So, you

1:13:06have the spinal trigeminal nucleus and

1:13:08the associated tract there only picking

1:13:10up sensory information like pain,

1:13:12temperature, touch, proprioception from

1:13:15that same side of the face. You whack

1:13:17that left spinal trigeminal nucleus and

1:13:19tract, you lose sensation such as pain,

1:13:22temperature, touch, proprioception from

1:13:24that left side of the face. Thus,

1:13:26ipsilateral loss of sensations

1:13:29of the face.

1:13:30Last thing here is that spinothalamic

1:13:31tract. Spinothalamic tracts, you have

1:13:33the anterior and lateral. They carry

1:13:35crude touch, temperature, pressure,

1:13:37right? If you knock this thing out on

1:13:39that left side, remember, spinothalamic

1:13:41tracts cross at the level of the spinal

1:13:43cord whenever they're coming into the

1:13:45spinal cord. So, if you knock that out,

1:13:47you're going to be affecting sensations

1:13:49on the contralateral side. So, for

1:13:50example, you knock out that left

1:13:52spinothalamic tract here in the lateral

1:13:54medulla, you cause loss of sensations on

1:13:56the right side, contralateral side,

1:13:59which is going to be in this case pain,

1:14:01temperature, crude touch, and pressure.

1:14:03And that would cover all of the things

1:14:06that could become present when there's

1:14:08lateral medullary involvement,

1:14:09Wallenberg syndrome, due to what kind of

1:14:11vessel

1:14:13damage? The PICA, okay? Whereas if it's

1:14:16medial medulla, that's going to be

1:14:19vertebral artery and more particularly

1:14:20the anterior spinal artery.

1:14:23So, we'll move on to the last part. So,

1:14:24we we know that the vertebrals, again,

1:14:26we already kind of concluded this at the

1:14:27beginning, they supply medulla and they

1:14:30supply posterior inferior aspect of the

1:14:33cerebellum. So, let's quickly recap that

1:14:36blood supply to the cerebellum. So,

1:14:37again, we have vertebral artery here.

1:14:39So, we'll kind of mark this here

1:14:41as vertebral. We only see one half of it

1:14:43in the sagittal view. Here's your

1:14:45vertebral artery. Gives off this branch

1:14:47here called the PICA.

1:14:49PICA supplies the posterior inferior

1:14:51aspect of the cerebellum.

1:14:52Then you come up here to this part here

1:14:54called the basilar artery. And the

1:14:56basilar artery will give off

1:14:57respectively the AICA supplying the

1:14:59anterior inferior cerebellum.

1:15:01And then it'll give off the superior

1:15:03cerebellar artery, which will apply to

1:15:04the superior cerebellum. The one that we

1:15:06have to focus on with respect to the

1:15:08vertebral arteries is you knocking out

1:15:10the PICA. If you knock out the PICA, you

1:15:13affect the blood supply to the posterior

1:15:15inferior aspect of the cerebellum. If

1:15:17there is a

1:15:18involvement of the cerebellum, this is

1:15:20important because it leads to altered

1:15:23abnormalities within coordination,

1:15:25posture, balance, things of that nature,

1:15:28which can present as ataxia. If you

1:15:31injure the right cerebellum, you cause

1:15:33ataxia on the right side. If you injure

1:15:34the left cerebellum, you cause ataxia on

1:15:36the left side. So, how will this

1:15:38present?

1:15:39In this case, they can have ipsilateral

1:15:42ataxia.

1:15:43And this can also present with what's

1:15:45called dysmetria whenever they're trying

1:15:46to do the finger-to-nose test. We

1:15:47already talked about that. Or

1:15:49dysdiadochokinesia with rapid

1:15:51alternating movements.

1:15:52And this would cover vertebral artery

1:15:55stroke syndromes as well as all of the

1:15:57stroke syndromes. Ninja Nerds, you guys

1:16:00got through it. All right, Ninja Nerds.

1:16:02In this monster of a video, we talked

1:16:04about stroke syndromes. I really hope

1:16:06that it helped. I truly hope that it

1:16:08makes sense. And if you guys did enjoy

1:16:10it, continue to support us, Ninja Nerds.

1:16:11We love you. We thank you. And as

1:16:13always, until next time.