Chapters
Posterior Circulation Clinical Signs and Symtoms | Clinical Presentation of Stroke - Part 2
Posterior Circulation Clinical Signs and Symtoms | Clinical Presentation of Stroke - Part 2
2012anteriorcirculationcontralateralcranialcrossedposteriorUHN
Posterior Circulation Vertebral Arteries and Occlusion | Clinical Presentation of Stroke - Part 2
Posterior Circulation Vertebral Arteries and Occlusion | Clinical Presentation of Stroke - Part 2
2012cerebellumdissectiondistalessentiallyinfarctlateralmedullamedullarypicaposteriorsyndromesUHNvertvertebral
Lateral Medullary Syndrome and Cerebellar Arteries | Clinical Presentation of Stroke - Part 2
Lateral Medullary Syndrome and Cerebellar Arteries | Clinical Presentation of Stroke - Part 2
2012aicabasicallybasilarbodybraincerebellarcerebellumcontralateralfeedfossahemiipsilateralmedialoccipitalpcaspicapontineposteriorsuperiorUHN
Cerebellar Stroke | Clinical Presentation of Stroke - Part 2
Cerebellar Stroke | Clinical Presentation of Stroke - Part 2
2012basilarcerebellumneurosurgerystrokeUHN
Posterior Cerebral Artery - Signs and Symptoms | Clinical Presentation of Stroke - Part 2
Posterior Cerebral Artery - Signs and Symptoms | Clinical Presentation of Stroke - Part 2
2012axialbasicallybasilarbifurcatescontralateralhemispherichomonymouslobeoccipitaloccipital lobeparietalpcapcasposteriortemporalthalamusUHNvision
Basilar Artery | Clinical Presentation of Stroke - Part 2
Basilar Artery | Clinical Presentation of Stroke - Part 2
2012anteriorbrainstemcranialessentiallyfibershemiparesishemisensorypenetratorpenetratorssyndromesUHNvariety
Brainstem Ischemia | Clinical Presentation of Stroke - Part 2
Brainstem Ischemia | Clinical Presentation of Stroke - Part 2
2012bodybrainbrain stemcontralateralcranialcranial nervecrossdysfunctionessentiallyipsilateralnerveponsresponsiblestemstrokeUHN
Presentation Based on Region Affected and Brainstem Localization | Clinical Presentation of Stroke - Part 2
Presentation Based on Region Affected and Brainstem Localization | Clinical Presentation of Stroke - Part 2
2012brainbrain stemcontralateralcranialcranial nervefacialinnervateipsilaterallocalizemidbrainmotornerveponsposteriorsensorystemstrokeUHN
Stroke - The Big Three | Clinical Presentation of Stroke - Part 2
Stroke - The Big Three | Clinical Presentation of Stroke - Part 2
2012arthrobasalcardioemboliccollateralizationcorticaldistallyembolicendotheliumetiologiesganglialacunarlenticulostriatestrokesubtypesthrombusUHNvesselvessels
Arteria Cerebri Media and Penetrating Arteries | Clinical Presentation of Stroke - Part 2
Arteria Cerebri Media and Penetrating Arteries | Clinical Presentation of Stroke - Part 2
2012cortexcorticalfibersinternallacunarmotorpenetratorpenetratorsposteriorsensorimotorsensorystructuresthalamusthoraxUHNvessels
Lacunar Occlusion and Classic Lacunar Infarct Syndromes | Clinical Presentation of Stroke - Part 2
Lacunar Occlusion and Classic Lacunar Infarct Syndromes | Clinical Presentation of Stroke - Part 2
2012basalbrainstemcerebellumdysarthriaganglialacunarmotorpenetratorspuresyndromesUHN
Transcript

[SOUND] [BLANK_AUDIO] Switching gears here now, talk a little bit about the posterior circulation. These present somewhat differently than anterior circulation. What these folks might present is anywhere from asymptomatic to comatose. And I really emphasize and try to make it simple, these are the signs to watch out for. Somebody comes in complaining

of dizziness, or double vision, or their speech is off, or they're having a hard time swallowing, or their coordination is off. These really should clue you in that you're dealing with a posterior circulation stroke. The clinical hallmarks of this, typically on exam you might see crossed findings. Now what do I mean by that? That means that you have cranial nerve deficits on one side, and the other side you

might have a contralateral problem. And I'll get into some examples in why that occurs exactly. This is a hallmark of the posterior circulation stroke, is crossed findings. Here's a nice example of this with some pictorial. But, again, emphasizing these five Ds. Sort of reviewing the vascular anatomy of the posterior circulation. We already went over this a little bit, but the bottom

line is it starts off with the verts which then travel through the bony framing of the cervical spine, they're very prone to trauma. And then basically come together forming the basilar. But do remember that the posterior inferior cerebral artery, that is, the PICA, comes off at the distal vert and feeds the lower portion of the cerebellum on each side. What happens if you have a PICA occlusion,

one of the most common syndromes at least from a vertebral dissection standpoint is what we would call a Lateral Medullary syndrome. And what this essentially means is that you've taken out the lateral medulla and essentially this is a very textbook posterior circulation syndrome. Sort of going through that is I emphasized when you have a brain stem infarct

typically if it's isolated to a hemi brain stem, you're going to get contralateral cranial nerve involvement and then contralateral body involvement. Here on this lateral medullary, you can see you've involved the spinal thalamic tract and I'll show you why but they end up having basically decreased pain and temperature on the contralateral body. And then all these other findings are

all ipsilateral and that's because they're involving the brain stem nucleus. And I'll go into that further into the talk here. Then the basilar is formed after the combination of verts coming together. They then travel up, the basilar's riding on the surface of the pons, sending in pontine perforators. It then gets to the base of the brain and then basically splits into the PCAs.

There's also several other arteries that feed the cerebellum coming off there. The AICA and superior cerebellar. And then basically the PCAs then feed the occipital lobe. Looking at the posterior circulation with respect to the cerebellar arteries, we've already talked a little bit about the PICA, which basically comes off of the verts before they come together to form the basilar. The AICA

and the superior cerebellar actually come off of the basilar artery and then these feed different portions of the cerebellum as you can see on the slide here. The superior does what it's described, the superior cerebellum. PICA we know gets the inferior portion, and then the medial portion of the cerebellum is supplied by AICA. Remember, strokes in the cerebellum present ipsilaterally, and

that's because of a double cross, so to speak, of the various tracts. So if somebody has a right cerebellar stroke, they are going to have right body control problems. If somebody has a left cerebellar stroke, they have left body control problems. That's an important message to take away. Now cerebellar strokes, because of the location of the cerebellum and the fact that it's in the posterior fossa

stroke there, or you're aware of a patient having a stroke there, the bottom line is you need to let neurosurgery know about this right away, okay? So the bottom line is if the cerebellum starts swelling up, there's very little room to give there and you can develop acute hydrocephalus. So I always emphasize that even if

it's a relatively small stroke, you just let neurosurgery be aware of this. There's nothing to do at that point. But if for some reason it bled, where the stroke enlarged, you might not have as much time to deal with things just based on the anatomy there. Continuing on. Now we've talked about about the verts, we've talked a little bit about the basilar and

we've talked about the cerebellum, and now we're at the distal end of the basilar. It then, as I told you, it bifurcates into the PCAs or posterior cerebral arteries. These then course around the brain stem. At the pons, mid-brain level, and then basically flow back and end up feeding the occipital lobe and part of the temporal lobe medially. And that's what you see here on these various diagrams.

You can see occipital lobe here and then a good portion of the temporal lobe is also supplied by those blood vessels. And what does that look like on our little picture that we'll keep going back forth. We're talking about the PCA territory back here and here it is on the axial cuts. What kind of signs and symptoms do you see with a PCA occlusion? You'll have vision loss. It will be on

the opposite side. It's just like any other hemispheric syndrome, that the division is basically your vision to whatever you've seen over on, say, the left side for example, is responsible for interpretation in the right occipital lobe. So right occipital lobe stroke, you can't see to the left. If you've got a left occipital lobe stroke, you can't see to the right. And

then as you're aware, this gives you a contralateral homonymous hemianopsia. Because the PCAs do feed part of the thalamus on their way back to the occipital lobe, you can also have contralateral face and limb sensory loss, and you can have a variety of cognitive deficits based on which parts of the temporal or parietal lobes in relation to the occipital lobe is involved. And so there's a

variety of different syndromes that one can experience. The only other thing we haven't talked about specifically is the basilar artery, we've described it a little bit. But basically

it rides on the anterior surface of the brainstem, predominantly the pons. And then it basically sends off all these variety of arteries we've already

talked about to the cerebellum. But it also supplies a variety of penetrators that can come in a variety of different patterns. And it gives you a variety of different symptoms. So the brainstem is essentially not only be the upper part of the spinal cord, so it can essentially induce all sorts of hemiparesis and hemisensory loss, because all the cranial nerves are located there. Having

strokes there, individuals can have problems with facial functions, swallow, and vision, in the sense of visual control. And there's numerous different syndromes out there, and we're not going to go through all of these, that just basically talk about, if this nucleus was lost in the setting of this specific track, then we can call this a certain syndrome. But at this point I think it is important

to be aware that there's a variety of brainstem symptoms and syndromes out there just based on which penetrator is involved. So i've emphasized that you can have cross findings between the face and body. The reason for that is because all the fibers

have to cross somewhere, and they actually have to get down to the body to actually move the arm and the leg as well as the sensation

from the arm and the leg. Essentially the way this works is you have these long tracks coming down from the brian or up to the brain, running up the spinal cord. They then tend to cross over, because remember the contralateral brain is responsible for the opposite side of the body. Your right brain is responsible for left body function. Your left brain is responsible for right

body function. This runs through the brain stem which is packed with these paired cranial nerve nuclei and then essentially if you end up having a stroke in the brain stem, the reason you get these get these crossed findings is, let's say you have stroke here, these are tracts that are running from the brain down to the body. I told you they tend to cross in a variety of different ways, but

many of them cross right before they enter the brain stem at the lower medulla. And essentially if you have a stroke say in the pons here, then this will take out those cranial nerve nuclei, it takes out those tracts. So you'll have ipsilateral cranial nerve dysfunction but you have contralateral body dysfunction. And that's just a really good pictorial of that. And the presentations can

be numerous, it just depends on where in the brain stem the

the midbrain upper pons is responsible for eye movement, the middle of the brain stem is basically facial control, and facial function, facial sensory, and then down low is basically control of our swallow etc.

Even some shoulder and head turning is involved with this. But the bottom line is if you've got a stroke and you've got cranial nerve deficits, you can sort of localize where in the brain stem it is based on what the deficits might be. I think summarizing in brain stem localization, each brain stem structure, cranial nerve nuclei innervate the ipsilateral structures. Since

the long tracks i.e. from the motor coming down from the brain, sensory coming up from the body are crossed, lesions can find on one side of the brains stem will present with ipsilateral cranial nerve findings, contralateral body motor and sensory findings. And if you see something with crossed findings know you're dealing with a posterior circulation stroke. We've talked about this a

little bit before, the varying different types of stroke and the

a lot of different etiologies that can cause stroke, and you just need to be cognizant. And whenever you're seeing a stroke patient it's really good to ask yourself exactly why is this patient having the stroke now?

Again there are three major types of stroke that I think you need to focus on. One of this would be cardioembolic sources or the aortic arch forming a thrombus and then it becomes embolic and travels distally up the vasculature. You can also have the plaque form in the neck from atherosclerosis, and then you can actually have small vessel disease. These are my sort of big three stroke

subtypes to be aware of. We really haven't talked much about lacunar stroke. These are the small penetrator vessels. I did describe to you that these basically come off of large vessels i.e. and these are located in the basal ganglia so you can have your lenticulostriate coming off say your MCA, feeding into these deeper structures as well as also the brain

stem after the basilar. And I showed you a pictorial of that if you slide back. But basically what these are is it's a small vessel, a penetrator, and then these give certain symptoms. You are not going to see cortical signs on somebody who is having a small vessel stroke. They can be devastating because they tend to hit very high real estate, very important centers, but they don't

affect the cortex. So in theory if somebody is having a lacunar stroke, clinically they can have quite devastating symptoms but they are going to be cognitively intact. Small vessel disease, this is typically related to hypertension and a variety of risk factors. Over time these small vessels, they don't have any smooth muscle in them so they essentially over time become very susceptible

to these risk factors. And essentially the internal wall structure changes and the lumen shrinks, the endothelium becomes irregular and they can be prone to micro clots and potentially even small arthro lesions. One key thing to note about this is because they are small vessels and they are end vessels they have no collateral supply. So if you

really take out one of these with a little clot, there is really not a whole lot you can do from collateralization to help that individual patient. Where are these located? I mentioned it to you a little bit here lenticulostriate. You can see they are end

to present based on which structures these

vessels are responsible for. Lacunar stroke would be you take out one of these vessels. It's not a whole group where if you have a large vessel stroke, you're basically covering up a group of these, maybe all of them even. And you can see not only are you taking these smaller vessels out, you're actually taking out this larger territory behind this. In a lacunar

syndrome, you've got one of these occluded, the MCA, for example, is still open. So there's still good blood flow out to the cortex hence there's not going to be any cortical signs associated with that. Again all these deeper structures are laid out in a specific pattern. And you can be aware of this pattern when you're looking at somebody clinically. But the posterior limb in the internal capsule is where

all the motor fibers end up and sensory fibers here end up running. The GNU has the face and then it works back on the thorax and leg. And you can see it's right next to the thalamus. A little penetrator that comes up into this area can take out part of the thalamus, take out the motor, and so you have the sensorimotor syndrome here. If it's a small penetrator that just sits in the thalamus

you get a sensory deficit. If it's just a small penetrator that maybe only goes to part of the posterior limit of the internal capsule, you'll just get a pure motor deficit out of that. These lacunar occlusions, because they are small penetrators and

these are all deep brain structures. The putamen, the thalamus,

the pons, the caudate, internal capsule. And there are some small penetrators in the cerebellum but predominantly, these are basal ganglia as well as brainstem stroke syndromes. There's numerous lacunar syndromes as I described to you particularly in the brainstem but I think the key ones are these five I've got listed here. Which is pure motor or pure sensory motor combo, clumsy hand dysarthria

and attacks of hemiparesis. I'm not going to go into extensive detail with these but I have given you a list of where the specific location can be and exactly how they how they present. I think in the end here the take home from this is the clinical presentation of any stroke, if you understand

the layout of the arteries, and you know what those arteries

part of the brain they are feeding, and what that part of the brain is responsible for doing. You can look at a patient and say okay, he can't do this, this and this, that correlates with this part of the brain, therefore this part of the brain is fed by this particular artery, and so before you've even done your imaging, you already know what you are dealing with. And I think that's

sort of my goal, is to help you feel more comfortable with that. I thank you, and good day. [BLANK_AUDIO]

Disclaimer: Content and materials on Medlantis are provided for educational purposes only, and are intended for use by medical professionals, not to be used self-diagnosis or self-treatment. It is not intended as, nor should it be, a substitute for independent professional medical care. Medical practitioners must make their own independent assessment before suggesting a diagnosis or recommending or instituting a course of treatment. The content and materials on Medlantis should not in any way be seen as a replacement for consultation with colleagues or other sources, or as a substitute for conventional training and study.

×
Create a free account to watch 3 clips every day. Upgrade for unlimited access.