Understanding Brainstem Lesions and Syndromes

Hello ladies and gentlemen. I want to share with you a mnemonic for brainstem lesions. And this I found, I had a student with me who was studying for step one, and I saw that he had this little diagram, and I had never seen it before, and as it turns out it was a mnemonic for studying brainstem lesions. And brainstem lesions are not very common. Typically, if you see strokes, you're going to see MCA, ACA strokes, maybe occasionally PCA strokes. And those you'll really know because they're the bread and butter of stroke neurology. Brain stem lesions are a little bit less common and consequently you're not going to get a whole lot of exposure to them in day-to-day practice, especially if you're not a neurologist. So if you are, for instance, an international student or graduate who is studying for Step 1 and you're A lot of your knowledge from medical school is kind of pruned away and most of your knowledge is clinical practice. You're probably going to have to spend a lot of time with the brainstem lesions but luckily we have this mnemonic that will be really helpful for you if you know instead of memorizing all of the individual brainstem lesions to put together this chart you'll want to know how to do it. from there you should be able to get to all the brainstem lesions that you'll encounter on the step. So I go over the brainstem lesions in a different lecture more in detail. So this we're going to primarily focus on the mnemonic and how you can use it for answering test questions. If you haven't already please consider subscribing to my Patreon at www.patreon.com forward slash pwbmt If you can consider chipping in a dollar a month, a little bit goes a long way to help offset the cost of these videos. I have some premium features on there as well. So thank you in advance for your consideration. So this is what I'm talking about here, right? You've got the brainstem, and, you know, when you're doing the neuroanatomy, it's really complicated because there's three parts of the brainstem. They all look very different. So you have your midbrain, pons, and medulla. And... You can see they don't really look very similar. So they are all supplied by different vessels, all coming off of the posterior circulation of the circle of Willis. And you'll want to make sure that you know that cold, because if you don't know that, you're going to get into a lot of trouble on not only step one, but also two and three. So when you first approach the neuroanatomy of the brainstem, It's helpful to look at these illustrations, these little cartoon diagrams, because they really show you where everything is at. And primarily what you want to focus on are where the ascending and descending tracts are, as well as where the cranial nerve nuclei are, and then the basal ganglia. If you know that, you're pretty much good to go. Now, the step will probably give you a question where they tell you... here's a patient with a certain constellation of symptoms, let's say contralateral paralysis on one side, contralateral proprioception, and then on the opposite side, maybe they've got some tongue weakness. And from there, you will either need to tell them what artery is infarcted, or they may give you a diagram like this, a histologic specimen, and ask you to point to where the lesion is. is. So they may highlight different areas, label them 1, 2, 3, 4, and 5, and then you'll have to select which area is the lesion. That's two different ways that they could give it to you. Okay, you may also get a question showing you either this cartoon diagram or an actual brain stem, and you'll have to know where the different nerves are. So... for instance, if they tell you that the patient's got hearing loss on the left side and they've got vertigo, nausea, vomiting, you'll need to know that that's cranial nerve 8 and they won't have them labeled. They'll just have like A, B, C, D, or E and you'll have to be able to point to where it is. Those questions are a little less common, but you'll want to know where each of the cranial nerves originate from. So midbrain is three and four, pons is five through eight, and upper medulla is nine through twelve. Note that eleven is missing from there because it's kind of a black sheep as far as the cranial nerves go. So you must know these. You need to know your circle of willis. You need to know it cold. Remember there's anterior circulation arising from the internal carotid artery and there's posterior circulation arising from the vertebral arteries. As far as brain stem, we're mostly concerned about the posterior circulation. Remember that we have two vertebral arteries, one on each side. They give off picas on both sides and then they come together and go back down in this single. anterior spinal artery. When the vertebral arteries come together, first they give off AICA, anterior inferior cerebellar, and then there's a basilar artery that runs up the pons and gives off pontine arteries that supplies the medial pons. Then they split off, give off superior cerebellar, and then additionally they give off posterior cerebral arteries, which supplies the midbrain and also the occipital lobe. You'll see posterior cerebral artery infarctions come up occasionally and the big thing that they lead to is a visual field deficit and then the last branch is posterior communicating which as its name implies is the posterior communication with the anterior circulation the other thing you need to know is your ascending and descending tracts so I'm going to assume that you know these for our purposes here but that's corticospinal which is our motor tract and then also of DCML and spinothalamic. Okay, so let's get to the mnemonic. So we've got these nine boxes here, and each row corresponds to a different part of the brainstem. So we have our midbrain, pons, and medulla. And then we have lateral and medial. You just need to focus on one of the lateral sides, okay? Now, what are our medial cranial nerves? They are three, four, six, and 12. And the way you can remember this is all of these numbers are divisible by 12. So 3, 4, 6, and 12. 1 and 2 are missing, and that's because they don't have anything to do with the brainstem. 1 is olfactory, which isn't even really a discrete nerve. 2 is optic, and those come off the eyes and project to the occipital lobe. So 3, 4, 6, and 12. And please note that there are... these are paired nerves even though I only wrote them once. There's a cranial nerve three on the left and right, cranial nerve four on the left and right, and so forth. What are our lateral cranial nerves? So they are everything else five, seven, eight, nine, and ten. And notice that the numbers get higher as you go down and that's just because the way the cranial nerves are numbered just you're going from superior to inferior. The only big exception is five, but that's because you have multiple trigeminal nuclei extending from the midbrain all the way down to the medulla. So we're going to place it here for the purpose of our mnemonic right at the pontomedullary junction. What else do we have? We've got our tracts. So corticospinal tract and DCML run medially. I didn't put the decussation here. The decussation is in the lower medulla. So just bear in mind that in the midbrain the corticospinal tract and DCML are carrying fibers either to or from the contralateral side. So when you have lesions to the left brainstem it's going to affect the right side. On the lateral brainstem we have the spinothalamic tract pain temperature fibers that tract decussates in the spinal cord so we wouldn't see a decussation here anyway. And then we have sympathetic. fibers. And it's important to remember there that whenever you have a knockout of sympathetic fibers in the brainstem, you can get a Horner's syndrome. And remember that's meiosis, ptosis, and anhydrosis. Furthermore, we have cerebellar peduncles. You don't really need to know what those do individually, but just know that if they get knocked out, you're going to have ataxia. And Sarah Beller signs on the ipsilateral side. And then I put the substantia nigra here. Remember the substantia nigra is part of the basal ganglia. It projects dopaminergic neurons to the striatum and those dopaminergic neurons, when they fire to the striatum, have a disinhibitory effect on the thalamus which then allows you to initiate movement or fine-tune your movement. So there if there's a depletion or a degeneration of the substantia nigra. You're going to have difficulty initiating movement. We call that bradykinesia. That's what you see in Parkinson's. But you can have a knockout of your substantia nigra by having a midbrain stroke, and that's going to lead to ipsilateral substantia nigra knockout, which will wind up causing bradykinesia on the contralateral side, because this is going to motor cortex and then motor... motor cortex is going to the opposite side via the corticospinal tract. Okay now our circulation. So if you look at your diagram of the circle of Willis you'll see this all makes sense. The anterior spinal artery supplies the medial medulla, gives off two pica branches. Those go to the lateral medulla. And remember our vertebral branches come together from the basilar artery that supplies the medial pons and that's through those pontine arteries. And then it gives off aica. and AICA supplies the lateral pons. And then our posterior cerebral artery supplies the midbrain, the whole midbrain, as well as the occipital lobe. Now in particular, the midbrain is supplied by paramedian branches of the PCA, whereas the PCA proper supplies the occipital lobe. So if you have a stroke of your PCA, that's going to cause an occipital lobe stroke, which is going to cause visual field deficits. But if you just have a stroke of the paramedian branches of the PCA, then you're going to have a midbrain stroke, and we call that Weber's syndrome. Okay, so our first thing that we're going to talk about is medial medullary syndrome. So we knock out the medial medulla. Now, if you are able to draw this entire diagram, which you need to memorize in order to use this mnemonic. Well, you just circle the medial medulla and you know everything that's going to get knocked out. You know that this is going to be an anterior spinal artery stroke, and you know the main things that are going to get knocked out are corticospinal tract, your DCML, and cranial nerve 12. So what do we see? Well, the corticospinal tract knockout is going to give you contralateral hemiparalysis. The DCML knockout is going to give you contralateral loss of fine touch and vibratory sensation and then cranial nerve 12 remember that all the cranial nerves innervate the ipsilateral side so that is going to cause you to lose your muscles of your tongue on the ipsilateral side remember that's hypoglossal nerve and so that's going to cause a deviation towards the side of the lesion because you have unopposed motor control on the contralateral side that's going to push the tongue over to the side of the lesion so if you have the patient stick their tongue out like you're supposed to do when you're testing cranial nerve 12 you'll see a deviation towards the side of the lesion all right uh next we have lateral medullary syndrome and this is also known as wallenberg syndrome so what do we knock out here we knock out five eight nine and ten uh so we have a pica stroke and so the first thing we see with cranial nerves 9 and 10, that's going to be manifested primarily in a loss of gag reflex. Remember, the gag reflex is mediated by 9 sensory and 10 motor, so you will not have a gag reflex. Cranial nerve 8 is going to cause vertigo, vomiting, nystagmus, possibly some hearing loss. And then knocking out cranial nerve 5, this is a lower motor neuron of the lower motor. lesion of the trigeminal nerve. So this is going to cause some numbness along the face and possibly some difficulty chewing. All right. Now, in addition to this, you're knocking out sympathetic tract. So you're going to get a Horner syndrome and you're also knocking out spinothalamic tract. So you're going to get a contralateral loss of pain and temperature sensation. Okay so that is Wallenberg syndrome. What about lateral pontine syndrome? So lateral pontine syndrome is going to have two very important features. One is you're knocking out the medial cerebellar peduncle, so you're going to have ataxia, and you're also knocking out cranial nerve 7, so you're going to have an ipsilateral facial droop. All right, ipsilateral facial droop. droop and that's going to be because it's the lower motor neuron it's going to be the entire left side contralateral or ipsilateral face rather so facial droop and ataxia characterizes the lateral pontine syndrome you'll also have a loss of cranial nerve 8 that's why we drew it here and it's at the pontomedullary junction so You'll also have some vertigo, vomiting, nystagmus, and maybe some sensory neural hearing deficit as well. And then cranial nerve 5, remember, runs through the entire midbrain, well, through the pons and the medulla at least. So you'll also have some facial paralysis and some difficulty chewing. Okay, next we've got Weber's syndrome. Weber syndrome is a stroke of the paramedian branches of the PCA. So this is also known as superior alternating hemiplegia. But Weber syndrome works just as good. The test should give you both names. So what do we have up here? We have three and four, and we have the substantia nigra. So a loss of three is going to cause an oculomotor nerve palsy. And remember that oculomotor supplies pretty much... everything, all of the extraocular muscles except for the lateral rectus and the obliques. So what you're going to wind up with is you're going to have an eye that's down and out. So down and out eye. You're also knocking out the corticospinal tract. So you're going to end up with a hemiplegia. on the contralateral side and remember that when you knock out the corticospinal tract above the synapse with the lower motor neuron you have upper motor neuron signs and so upper motor neuron paralysis is different from lower motor neuron paralysis upper motor neuron paralysis is a spastic paralysis so you're going to have tense muscles you're going to have deep tendon reflexes that are exaggerated positive Babinski sign and so forth. So a spastic paralysis on the contralateral side. This is also going to knock out your cortical bulbar tract. So you're going to have a contralateral lower facial muscle weakness. Remember that your upper facial muscles get bilateral innervation. So the bilateral facial muscles will still work, but the sorry, the upper facial muscles will still work because they get bilateral innervation. The lower facial muscles only get contralateral innervation and so when you have an upper motor neuron stroke your upper facial muscles will be fine but your lower facial muscles on the contralateral side will be knocked out and that's in contrast to when you have a stroke of the of the facial nerve or the facial nucleus, that's lower motor neurons. So in that case, it's going to be the entire contralateral face. You're also knocking out substantia nigra, and that's going to lead to a contralateral Parkinsonism. Now remember, the substantia nigra is projecting to ipsilateral, it's projecting to the ipsilateral basal ganglia, caudate, putamen, and so forth. which is going ultimately to the ipsilateral motor cortex. But then the motor cortex is innervating the opposite side through the corticospinal tract. So you knock out the left substantia nigra, you wind up with right-sided hemiparkinsonism. And so you're going to have difficulty initiating movement on the opposite side. So that is Weber syndrome, and that is paramedian branches of the PCA. And then the last one I want to talk about is Cerebellopontine angle syndrome. This is not a stroke. So Cerebellopontine angle syndrome is caused by a compression of the... roughly at the pontomedullary junction. And this is typically due to an acoustic neuroma or a meningioma that compresses on that angle area. So the big ones that are going to get knocked out here are five and eight. Now, if you have an acoustic neuroma, you're already going to have signs of cranial nerve eight dysfunction, things like tinnitus and hearing loss. But if it's from a meningioma or something, you'll get those signs as well. You'll also have a knockout of cranial nerve 5, so you'll have ipsilateral jaw muscle weakness, difficulty chewing. You can also have a speech impediment because you're not able to move your jaw properly. And so forth. You can get also, because cranial nerve 5, division 1, ophthalmic, is responsible for your corneal reflex, you should have a loss of your corneal reflex as well. Now, because this is at the cerebellopontine angle, you'll have cerebellar signs on the ipsilateral side. So look for ataxia and stuff like that. And then finally, because you are obstructing the cerebellopontine angle, another sign you'll see in CPA syndrome is the is a non-communicating hydrocephalus because of an obstruction of the fourth ventricle. All right, so here you have five different syndromes that if you are able to draw this diagram, which shouldn't be difficult to do knowing your cranial nerves, knowing which ones are medial, which ones are lateral, knowing the circulation, knowing where the tracts are. If you can draw this diagram, you are good to go for these five. these five syndromes and you will be able to tell which artery is affected, which which structures are affected and of course you need to know all of the cranial nerves and what they do but if you know that then you should be able to piece things together and this shouldn't be difficult for you. All right so that is all I have if you have any questions. Write a note below. We'll see you later.

And those you'll really know because they're the bread and butter of stroke neurology. Brain stem lesions are a little bit less common and consequently you're not going to get a whole lot of exposure to them in day-to-day practice, especially if you're not a neurologist. So if you are, for instance, an international student or graduate who is studying for Step 1 and you're A lot of your knowledge from medical school is kind of pruned away and most of your knowledge is clinical practice. You're probably going to have to spend a lot of time with the brainstem lesions but luckily we have this mnemonic that will be really helpful for you if you know instead of memorizing all of the individual brainstem lesions to put together this chart you'll want to know how to do it. from there you should be able to get to all the brainstem lesions that you'll encounter on the step.

So I go over the brainstem lesions in a different lecture more in detail. So this we're going to primarily focus on the mnemonic and how you can use it for answering test questions. If you haven't already please consider subscribing to my Patreon at www.patreon.com forward slash pwbmt If you can consider chipping in a dollar a month, a little bit goes a long way to help offset the cost of these videos.

I have some premium features on there as well. So thank you in advance for your consideration. So this is what I'm talking about here, right?

You've got the brainstem, and, you know, when you're doing the neuroanatomy, it's really complicated because there's three parts of the brainstem. They all look very different. So you have your midbrain, pons, and medulla.

And... You can see they don't really look very similar. So they are all supplied by different vessels, all coming off of the posterior circulation of the circle of Willis.

And you'll want to make sure that you know that cold, because if you don't know that, you're going to get into a lot of trouble on not only step one, but also two and three. So when you first approach the neuroanatomy of the brainstem, It's helpful to look at these illustrations, these little cartoon diagrams, because they really show you where everything is at. And primarily what you want to focus on are where the ascending and descending tracts are, as well as where the cranial nerve nuclei are, and then the basal ganglia. If you know that, you're pretty much good to go. Now, the step will probably give you a question where they tell you...

here's a patient with a certain constellation of symptoms, let's say contralateral paralysis on one side, contralateral proprioception, and then on the opposite side, maybe they've got some tongue weakness. And from there, you will either need to tell them what artery is infarcted, or they may give you a diagram like this, a histologic specimen, and ask you to point to where the lesion is. is. So they may highlight different areas, label them 1, 2, 3, 4, and 5, and then you'll have to select which area is the lesion.

That's two different ways that they could give it to you. Okay, you may also get a question showing you either this cartoon diagram or an actual brain stem, and you'll have to know where the different nerves are. So... for instance, if they tell you that the patient's got hearing loss on the left side and they've got vertigo, nausea, vomiting, you'll need to know that that's cranial nerve 8 and they won't have them labeled.

They'll just have like A, B, C, D, or E and you'll have to be able to point to where it is. Those questions are a little less common, but you'll want to know where each of the cranial nerves originate from. So midbrain is three and four, pons is five through eight, and upper medulla is nine through twelve. Note that eleven is missing from there because it's kind of a black sheep as far as the cranial nerves go.

So you must know these. You need to know your circle of willis. You need to know it cold. Remember there's anterior circulation arising from the internal carotid artery and there's posterior circulation arising from the vertebral arteries.

As far as brain stem, we're mostly concerned about the posterior circulation. Remember that we have two vertebral arteries, one on each side. They give off picas on both sides and then they come together and go back down in this single. anterior spinal artery.

When the vertebral arteries come together, first they give off AICA, anterior inferior cerebellar, and then there's a basilar artery that runs up the pons and gives off pontine arteries that supplies the medial pons. Then they split off, give off superior cerebellar, and then additionally they give off posterior cerebral arteries, which supplies the midbrain and also the occipital lobe. You'll see posterior cerebral artery infarctions come up occasionally and the big thing that they lead to is a visual field deficit and then the last branch is posterior communicating which as its name implies is the posterior communication with the anterior circulation the other thing you need to know is your ascending and descending tracts so I'm going to assume that you know these for our purposes here but that's corticospinal which is our motor tract and then also of DCML and spinothalamic. Okay, so let's get to the mnemonic.

So we've got these nine boxes here, and each row corresponds to a different part of the brainstem. So we have our midbrain, pons, and medulla. And then we have lateral and medial.

You just need to focus on one of the lateral sides, okay? Now, what are our medial cranial nerves? They are three, four, six, and 12. And the way you can remember this is all of these numbers are divisible by 12. So 3, 4, 6, and 12. 1 and 2 are missing, and that's because they don't have anything to do with the brainstem. 1 is olfactory, which isn't even really a discrete nerve. 2 is optic, and those come off the eyes and project to the occipital lobe.

So 3, 4, 6, and 12. And please note that there are... these are paired nerves even though I only wrote them once. There's a cranial nerve three on the left and right, cranial nerve four on the left and right, and so forth.

What are our lateral cranial nerves? So they are everything else five, seven, eight, nine, and ten. And notice that the numbers get higher as you go down and that's just because the way the cranial nerves are numbered just you're going from superior to inferior.

The only big exception is five, but that's because you have multiple trigeminal nuclei extending from the midbrain all the way down to the medulla. So we're going to place it here for the purpose of our mnemonic right at the pontomedullary junction. What else do we have? We've got our tracts. So corticospinal tract and DCML run medially.

I didn't put the decussation here. The decussation is in the lower medulla. So just bear in mind that in the midbrain the corticospinal tract and DCML are carrying fibers either to or from the contralateral side. So when you have lesions to the left brainstem it's going to affect the right side.

On the lateral brainstem we have the spinothalamic tract pain temperature fibers that tract decussates in the spinal cord so we wouldn't see a decussation here anyway. And then we have sympathetic. fibers.

And it's important to remember there that whenever you have a knockout of sympathetic fibers in the brainstem, you can get a Horner's syndrome. And remember that's meiosis, ptosis, and anhydrosis. Furthermore, we have cerebellar peduncles. You don't really need to know what those do individually, but just know that if they get knocked out, you're going to have ataxia.

And Sarah Beller signs on the ipsilateral side. And then I put the substantia nigra here. Remember the substantia nigra is part of the basal ganglia. It projects dopaminergic neurons to the striatum and those dopaminergic neurons, when they fire to the striatum, have a disinhibitory effect on the thalamus which then allows you to initiate movement or fine-tune your movement.

So there if there's a depletion or a degeneration of the substantia nigra. You're going to have difficulty initiating movement. We call that bradykinesia.

That's what you see in Parkinson's. But you can have a knockout of your substantia nigra by having a midbrain stroke, and that's going to lead to ipsilateral substantia nigra knockout, which will wind up causing bradykinesia on the contralateral side, because this is going to motor cortex and then motor... motor cortex is going to the opposite side via the corticospinal tract.

Okay now our circulation. So if you look at your diagram of the circle of Willis you'll see this all makes sense. The anterior spinal artery supplies the medial medulla, gives off two pica branches. Those go to the lateral medulla.

And remember our vertebral branches come together from the basilar artery that supplies the medial pons and that's through those pontine arteries. And then it gives off aica. and AICA supplies the lateral pons.

And then our posterior cerebral artery supplies the midbrain, the whole midbrain, as well as the occipital lobe. Now in particular, the midbrain is supplied by paramedian branches of the PCA, whereas the PCA proper supplies the occipital lobe. So if you have a stroke of your PCA, that's going to cause an occipital lobe stroke, which is going to cause visual field deficits.

But if you just have a stroke of the paramedian branches of the PCA, then you're going to have a midbrain stroke, and we call that Weber's syndrome. Okay, so our first thing that we're going to talk about is medial medullary syndrome. So we knock out the medial medulla. Now, if you are able to draw this entire diagram, which you need to memorize in order to use this mnemonic. Well, you just circle the medial medulla and you know everything that's going to get knocked out.

You know that this is going to be an anterior spinal artery stroke, and you know the main things that are going to get knocked out are corticospinal tract, your DCML, and cranial nerve 12. So what do we see? Well, the corticospinal tract knockout is going to give you contralateral hemiparalysis. The DCML knockout is going to give you contralateral loss of fine touch and vibratory sensation and then cranial nerve 12 remember that all the cranial nerves innervate the ipsilateral side so that is going to cause you to lose your muscles of your tongue on the ipsilateral side remember that's hypoglossal nerve and so that's going to cause a deviation towards the side of the lesion because you have unopposed motor control on the contralateral side that's going to push the tongue over to the side of the lesion so if you have the patient stick their tongue out like you're supposed to do when you're testing cranial nerve 12 you'll see a deviation towards the side of the lesion all right uh next we have lateral medullary syndrome and this is also known as wallenberg syndrome so what do we knock out here we knock out five eight nine and ten uh so we have a pica stroke and so the first thing we see with cranial nerves 9 and 10, that's going to be manifested primarily in a loss of gag reflex.

Remember, the gag reflex is mediated by 9 sensory and 10 motor, so you will not have a gag reflex. Cranial nerve 8 is going to cause vertigo, vomiting, nystagmus, possibly some hearing loss. And then knocking out cranial nerve 5, this is a lower motor neuron of the lower motor.

lesion of the trigeminal nerve. So this is going to cause some numbness along the face and possibly some difficulty chewing. All right.

Now, in addition to this, you're knocking out sympathetic tract. So you're going to get a Horner syndrome and you're also knocking out spinothalamic tract. So you're going to get a contralateral loss of pain and temperature sensation.

Okay so that is Wallenberg syndrome. What about lateral pontine syndrome? So lateral pontine syndrome is going to have two very important features. One is you're knocking out the medial cerebellar peduncle, so you're going to have ataxia, and you're also knocking out cranial nerve 7, so you're going to have an ipsilateral facial droop. All right, ipsilateral facial droop.

droop and that's going to be because it's the lower motor neuron it's going to be the entire left side contralateral or ipsilateral face rather so facial droop and ataxia characterizes the lateral pontine syndrome you'll also have a loss of cranial nerve 8 that's why we drew it here and it's at the pontomedullary junction so You'll also have some vertigo, vomiting, nystagmus, and maybe some sensory neural hearing deficit as well. And then cranial nerve 5, remember, runs through the entire midbrain, well, through the pons and the medulla at least. So you'll also have some facial paralysis and some difficulty chewing. Okay, next we've got Weber's syndrome. Weber syndrome is a stroke of the paramedian branches of the PCA.

So this is also known as superior alternating hemiplegia. But Weber syndrome works just as good. The test should give you both names.

So what do we have up here? We have three and four, and we have the substantia nigra. So a loss of three is going to cause an oculomotor nerve palsy. And remember that oculomotor supplies pretty much... everything, all of the extraocular muscles except for the lateral rectus and the obliques.

So what you're going to wind up with is you're going to have an eye that's down and out. So down and out eye. You're also knocking out the corticospinal tract.

So you're going to end up with a hemiplegia. on the contralateral side and remember that when you knock out the corticospinal tract above the synapse with the lower motor neuron you have upper motor neuron signs and so upper motor neuron paralysis is different from lower motor neuron paralysis upper motor neuron paralysis is a spastic paralysis so you're going to have tense muscles you're going to have deep tendon reflexes that are exaggerated positive Babinski sign and so forth. So a spastic paralysis on the contralateral side.

This is also going to knock out your cortical bulbar tract. So you're going to have a contralateral lower facial muscle weakness. Remember that your upper facial muscles get bilateral innervation. So the bilateral facial muscles will still work, but the sorry, the upper facial muscles will still work because they get bilateral innervation. The lower facial muscles only get contralateral innervation and so when you have an upper motor neuron stroke your upper facial muscles will be fine but your lower facial muscles on the contralateral side will be knocked out and that's in contrast to when you have a stroke of the of the facial nerve or the facial nucleus, that's lower motor neurons.

So in that case, it's going to be the entire contralateral face. You're also knocking out substantia nigra, and that's going to lead to a contralateral Parkinsonism. Now remember, the substantia nigra is projecting to ipsilateral, it's projecting to the ipsilateral basal ganglia, caudate, putamen, and so forth. which is going ultimately to the ipsilateral motor cortex. But then the motor cortex is innervating the opposite side through the corticospinal tract.

So you knock out the left substantia nigra, you wind up with right-sided hemiparkinsonism. And so you're going to have difficulty initiating movement on the opposite side. So that is Weber syndrome, and that is paramedian branches of the PCA.

And then the last one I want to talk about is Cerebellopontine angle syndrome. This is not a stroke. So Cerebellopontine angle syndrome is caused by a compression of the...

roughly at the pontomedullary junction. And this is typically due to an acoustic neuroma or a meningioma that compresses on that angle area. So the big ones that are going to get knocked out here are five and eight.

Now, if you have an acoustic neuroma, you're already going to have signs of cranial nerve eight dysfunction, things like tinnitus and hearing loss. But if it's from a meningioma or something, you'll get those signs as well. You'll also have a knockout of cranial nerve 5, so you'll have ipsilateral jaw muscle weakness, difficulty chewing.

You can also have a speech impediment because you're not able to move your jaw properly. And so forth. You can get also, because cranial nerve 5, division 1, ophthalmic, is responsible for your corneal reflex, you should have a loss of your corneal reflex as well. Now, because this is at the cerebellopontine angle, you'll have cerebellar signs on the ipsilateral side.

So look for ataxia and stuff like that. And then finally, because you are obstructing the cerebellopontine angle, another sign you'll see in CPA syndrome is the is a non-communicating hydrocephalus because of an obstruction of the fourth ventricle. All right, so here you have five different syndromes that if you are able to draw this diagram, which shouldn't be difficult to do knowing your cranial nerves, knowing which ones are medial, which ones are lateral, knowing the circulation, knowing where the tracts are. If you can draw this diagram, you are good to go for these five.

these five syndromes and you will be able to tell which artery is affected, which which structures are affected and of course you need to know all of the cranial nerves and what they do but if you know that then you should be able to piece things together and this shouldn't be difficult for you. All right so that is all I have if you have any questions. Write a note below. We'll see you later.

Transcript for:Understanding Brainstem Lesions and Syndromes

Transcript for:
Understanding Brainstem Lesions and Syndromes