DIP Episode 546 - Super HY USMLE Neurology Integrations (Step 1-3)

Welcome to episode 546 of the Divine Intervention Podcast. Into this podcast we'll be addressing a topic that I titled High-Eld Neurology Integrations for the USMLE exams. High-Eld Neurology Integrations for the USMLE exams. My goal with this podcast was to focus on certain things that are more structural in nature with neurology that people typically get wrong on exams. I personally feel that you'll find this podcast to be really helpful if you're taking step one or step two CK or step three. Because if I'm being completely honest, neurology on the USML Es, especially at the step two, step three level, they make it pretty easy because most people just kind of give up on it. And this may be something where if you just invest maybe like an hour or two, you could easily get like 10, 15 questions right easily on your exams. So let's go ahead and get right into it. So, and again, I'm going to try to start a little broad and then I'm going to go a little deep. And again, as we go, I'm just going to keep picking up structures. I'm just basically going to try to start from like the top of the head and kind of walk my way downwards in no specific order but try to make integrations as I go. So first thing, if you're thinking about the nervous system, I know many of you are thinking of the cerebral cortex, right? And we know that the cerebral cortex has different lobes, has the frontal lobe, has the parietal lobe, has the temporal lobe, has the occipital lobe.

That's the big stuff to know with the cerebral cortex. And the thing is it's pretty high yield to know what these different lobes are kind of notable for. So like for example, you exams, if you're thinking in terms of the frontal lobe, they can give you a question about a person having a calcified frontal lobe mass. And then they'll give you like histology. You notice that that mass has a friday appearance. I would hope when you see something like that, you're saying, oh, divine. This sounds an awful lot like an oligodendro glioma. Remember, oligodendro gliomas come from oligodendro sites. Oligodendro sites are the cells that mildly need things within the central nervous system. Remember, the analogous cell within the peripheral nervous system is the schwan cell. So if you think of a frontal lobe, think of a person having an oligodendro glioma. It's going to be an imaging. You're going to see a mass that is calcified. And then one thing to keep in mind with the frontal lobe on your test is they could give you a question about a person that the person seems to have understanding of what you're saying, but what they're saying, like they have fluent, actually, sorry, they seem to have understanding, but their speech is not fluent. They have a lot of trouble bringing the words out. Well, I would hope you're saying that, ooh, divine. This sounds an awful lot like a Broca's ephesia. Broca's ephesia is a Mudo ephesia.

And many times you're going to get it from having a stroke in your dominant, the dominant side of your brain. Broca's area is on the left side of the brain for purposes of the US Emily exams. So what artery supplies Broca's area? Well, I would hope you're saying divine is the middle cerebral artery. It's going to be the left middle cerebral artery. So if a person has a left MC stroke, they're going to have a Broca's ephesia. Again, remember Broca's area is not part of the parietal lobe. It's part of the inferior frontal lobe, part of the inferior frontal lobe. That's pretty high, you'll know, for purposes of your exams. And then, if we're looking at the other lobes, right, the parietal lobe, a big chunk of the parietal lobe is supplied by the middle cerebral artery. The parietal lobe has many things going through it. And I'm going to dig a little deeper into that as we go along. And in the temporal lobe, we know that the temporal lobe, that's where you have wernikis area. That's a thing that's very, very important to keep at the back of your mind, for example. Wernikis, wernikis, wernikis, wernikis area. Wernikis area, if you infarct that part of the brain again, you can get that from a left MC stroke. You have more of a sensory ephesia. So you have fluent speech. What you're saying makes absolutely no sense. What you're saying makes absolutely no sense.

And another thing that's pretty high, you'll know, the temporal lobe, for purposes of the USML Es, is that the temporal lobe is the site of origin of most seizures in the body. It's the site of origin of most seizures in the body. In fact, our friend at the MDM Es, I kid you not, they love to test that association at all. One other thing that you miss you, you exams with a temporal lobe, is, let me give you an image of the temporal lobe. You see a lot of white in it. And this, let's say, is like an MRI. And the person has been having headaches for the last two days, very high fever, no co-rigidity. And then they give you like a CSF sample. What should you expect in that person's CSF sample? I hope you're saying that men, you expect to see a lot of red blood cells. You expect to see a lot of lymphocytes. That person has HSV meningitis. That person has HSV in cephalitis. Remember, HSV meningitis, HSV in cephalitis has a pretty election for the temporal lobe. And the temporal lobe, again, that's why many times when people have HSV meningitis or in cephalitis, they're going to have seizures. Because again, I literally just said that a temporal lobe is a very critical region of the brain, where many seizures originate from. And again, remember, her piece, HSV has this weird thing, where it causes a hemorrhagic meningitis, hemorrhagic in cephalitis. So those people, if you check their CSF, you're going to see a lot of red blood cells. So please be careful.

It's not only a sub-arachnoid hemorrhage that can cause red blood cells in a person's CSF. A person having HSV in cephalitis or HSV meningitis will have a lot of red blood cells as well. Not in every case, but in many cases on the USME Ls. One other thing I will also say about the temporal lobe, and with HSV is that again, you're going to see lymphocytes in the CSF. Why are you going to see lymphocytes? Well, the reason you're going to see lymphocytes is because HSV is a virus. What arm of the immune system helps us deal with viruses? It's going to be our lymphocytes. You're going to see a lymphocytic predominance in the CSF. That's something I want to keep in mind for you, exams. If you have bacterial meningitis, you're going to see more of a neutrophilic predominance because neutrophils help us handle bacteria. But if you have a problem with viruses or fungi or TB, you're going to see more of a lymphocytic predominance. That's pretty high up to no for exams. Then we know that the occipital lobe is the primary visual cortex. If you infarge the occipital lobe, typically from a PCS stroke or posterior cerebral artery stroke, the person is going to have a cortical blindness. The person is going to have cortical blindness. The person is going to have cortical blindness. I think I've kind of hit the lobes. I know you may be like, man, if I didn't really talk about the pride of the lobe, but again, I will kind of hit it in some respects.

The other ones are the ones that have a lot of specificity with them. The best way to discuss the pride of lobes is to look at it from a vascular perspective. So just again, maybe let me brush up a few more mid-igridity things that you miss on your exams. And it's kind of high up to no. Remember, if you look at the cortex, it's the central sulcus. The central sulcus is pretty much something that, you know, demarcates anteriorly your muro cortex. Your muro cortex is in the pre-central gires, the pre-central gires. The sensory cortex is more in the posterior central gires, right? In the posterior central gires. And again, one thing I want you to keep in mind is that the temporal lobe is the primary auditory cortex. A lot of you hearing comes from the temporal lobe. That's something you want to keep at the back of your mind for your exams, right? Again, I said that the visual cortex is going to be your occipital lobe. It's going to be your occipital lobe. And the thing is, if we're looking at the cortex, one thing that is helpful to emphasize is knowing your arteries, right? Knowing your arteries and what they do. Knowing your arteries and what they do. I mean, what if they give you a question about a patient that, you know, has a history of chronic hematuria. And this person is on dialysis for end-stri-drenal disease. And then they give you some labs. And the persons they left is elevated.

But then they tell you that, oh, you, this person comes in because for the last 12 hours, they've been having severe headache. And they tell you that they have, you know, severe headache, you know, very, very severe. And you'll notice that you don't have a fever, but you have no corrigidity. What should you be thinking about here? And then they ask, like, oh, what's the underlying mechanism behind this patient symptoms? I'll hope you're going to see something along the lines of rupture of a barri aneurysm rupture of a barri aneurysm. So what in the world am I getting at here? Well, the thing I'm getting at here is this person has a rupture of the anterior comichinin artery, an aneurysm of the anterior comichinin artery. But first things first, what disease did this person have? This person clearly, clearly, clearly has a lot more dominant polycystic kidney disease. Remember, in ADP-KD, they're going to have cysts in the liver, they're going to have cysts in the kidneys. So those cysts in the liver that explains the high left is they get, those cysts in the kidneys, you may notice that they may have hematuria. In fact, over time, those people proceed to endstidri-known disease. Now remember that people that have ADP-KD, they tend to have other problems like my trovov prolapse, they tend to have aneurysms in the circle of willis. And let me ask you this, what is the most common location of an aneurysm in the circle of willis? It's going to be the anterior comichinin artery.

Again, I know some of you, the people studying first step, when you're like, oh, divine, this is great. Those of you studying first step, they're saying like, divine, this is too much detail. I don't need this for my exams. Well, I wish you all the best on whatever exam that you're taking. But I'm telling you, these things are things we've just put in a little work. It could make a big difference. It could be the thing that separates you from, wow, okay, I've been getting in the 240s too. I got this extra 7 or 8 questions right because I listened to this podcast and then boom, you're elevated into the 250s. So you're just going to keep that in, keep that in mind. So the anterior comichinin artery is the most common artery that is associated with aneurysms in the circle of willis. And remember, it's not only people that have or dozomo dominant polycystic kidney disease that can get aneurysms in the circle of willis. You can also see these in people that have morphine syndrome, right? Morphine syndrome, morphine syndrome, morphine syndrome, morphine syndrome. Okay, so again, let's kind of talk about the homonculus. I think it's an important thing to discuss. And if I discuss it, I'm going to discuss it in the context of some of the vessels. So the homonculus is, you know, there's like the lateral side and there's like the medial side and there's the in-between side. So I'm going to discuss how I like to chisel that out.

There's the lateral side, there's the medial side and then there's the in-between side. So, be honest with you, if you really think about it, the lateral side basically controls things like the hands, the fingers, you know, your jaw, your tongue, your upper extremities, right? If I let me classify the lateral and the in-between together because they're supplied by the same vessel, the lateral and the in-between side, right? So the lateral and the in-between side, that handles upper extremities, hand, fingers, jaw, all those things, right? But the medial side does morph your lower extremities and your genitals, your lower extremities and your what, your genitals. So what does the lateral slash in-between side is going to be the middle cerebral artery. So whenever you have a middle cerebral artery stroke, you're going to have control lateral deficits in these structures that I've mentioned, your upper extremities, your hands, your fingers, right? Your jaw, things like that. But the medial side is supplied by the anterior cerebral artery. That goes more with things like your lower extremities and your genitals. You may wonder, man, why you keep going on and on and on and on about these genitals? It's actually very important. The US Emily's there is this party trick they play with the anterior cerebral artery on the ex-apps. Many people know that the anterior cerebral artery supplies the lower extremities. They know that that is in every on-key deck known to mankind.

One thing that many people don't realize is that the EC actually controls like migration. So if you see a person that has a cerebral artery stroke and you see a lot of urinary incontinence, I want you to strongly consider an ECA stroke. Another weird thing you may see on your exams with an ECA stroke is a return of primitive reflexes. Or you see a person that is struggling with executive function that usually falls under the purview of an ECA stroke on the US Emily exams. So kind of keep those things at the back of your mind with an ECA stroke. But don't forget your medial cerebral artery, those upper extremities, hand fingers, your jaw and all those things. And honestly if you actually think about it, the hands, it may sound crazy to you, but the hands and the face, they actually take up a pretty big chunk of the homon killers. They actually take up a big chunk, maybe like your hands are small compared to like your arms and stuff, your face is small compared to like your trunk and stuff. Why are they taking up such huge pieces in the homon killers? Can I tell you the reason? The reason is that all those things require very fine movements, very complex control of movements. Like for example, your fingers, look at the gross mood, fine mood, all those fancy things you can do, all those muscles, all those things. You better believe that you need a big chunk of brain to handle that.

Or your face, your frowning, your sad, your happy, your burst out in laughter, your chewing, you'll have all these facial expressions. All those things to get that fine control, you need a big chunk of brain to make that happen. It's something you kind of want to keep at the back of your mind for, for example. Okay, now, okay, so I guess we've kind of talked about the cortex. I feel like I've hit the cortex pretty, pretty hard. And again, remember if you have an MC stroke or an EC stroke, you're going to have contralateral deficits on your exams. You're going to have what? Contralateral defects. You're going to have what? Contralateral defects. Please keep that at the back of your mind. Okay, so now that we've kind of gone through the cortex, let's descend a little bit. Let's descend to the Bizoganglia. Again, I'm trying to be a little methodical in this so that you can kind of build up this story for yourself. Well, let's look at the Bizoganglia. The Bizoganglia has a bunch of parts. Like one big one. And honestly, this, I will say that on image in all your exams, you want to make sure you can identify things like the Codid. You want to make sure you can identify the Globus Paladis. You want to make sure you can identify the putymin, the Codid, the Globus Paladis and the putymin. If you can identify those things, you're in pretty good shape. So what are some critical integrations to make here with these structures? Well, first is the Codid.

Well, we know that that Codid is atrophys. Then we know that you'll see it in a person that's probably in their 40s. That has these choreform movements. That's seeing all these inappropriate things. That has this burst of anger. That's clearly Huntington's disease. Remember, Huntington's disease sometimes on the exams they call it Huntington's Corial. It's an Orozomo dominant disorder. It's a trinocrystallia-repeated disorder. We have these C-EG trinocrystallia-repeats. That causes atrophy of the Codid. It's a problem with chromosome 4 on the USML Es. You're going to see choreform movements and all these bad things. Those people are unfortunately going to die. The thing is, in the future of spring, the condition is going to show up earlier and it's going to show up in a worse form. That's a genetic principle known as anticipation. We tend to see that a lot with trinocrystallia-repeats disorders. Because the trinocrystallia-repeats expand over time. They become more and more in future generations. Let's see. That's what I have in symptoms at 45. Let's see. For five years. The offspring will probably start in symptoms like a few years earlier and they will probably die a lot quicker. That's something you want to keep at the back of your mind. That's the big, big thing you want to know with the Codid on your test. The Globus Paladus.

One thing that's actually pretty high to know about the Globus Paladus is that you're going to have abnormalities within the Globus Paladus in a person that has carbon monoxide poisoning. Carbon what? Monoxide poisoning. Carbon what? Monoxide poisoning. Carbon what? Carbon monoxide poisoning. The pathophysiology behind that, you don't really need to worry about for purposes of your exams. What are some other kind of like assist structures in the visual ganglia I think I should discuss. I think I should discuss the subthalamic nucleus. The subthalamic nucleus is kind of high yield because if you see a person that has these involuntary flailing movements of like the arms of the upper extremities, think of a subthalamic nucleus problem. That's what we call hemibalismus. That's what we call hemibalismus. You're going to get that when you have a contralateral subthalamic nucleus problem. So if your left subthalamic nucleus is all screwed up, you will have right-sided hemibalismus. And then another thing to keep at the back of your mind with the visual ganglia is the internal capsule. The internal capsule actually has an anterior limb and a posterior limb. The posterior limb is the critical part you want to know because your corricose spinal track for the other side of the body cross it literally goes through that region. And that region of the brain is supplied by the lenticular stride artery. So think about it in a person that has hypertension.

And you know the lenticular stride artery, you know the formal aneurysm and the liticular stride artery ruptures. You have an aneurysm of the lenticular stride artery. That can destroy that posterior limb of the internal capsule. And the person is going to have a pure motor stroke. They can have a pure motor stroke. The contralateral side of the body will be completely paralyzed, upper extremities and lower extremities. Let me back up here a little bit to kind of help you understand something. As you go from cortex and you descend down, things are going to start coming together. So like for example, in the cortex everything is separated nicely because your cortex is huge. Right? You have a massive cortex. Right? So it's like, hey, you have this region, the handles just operate extremity. Hey, you have this region, the handles just lower extremity. But the thing is space is a little more cramped in a place like the basal ganglia. So you can be separating everybody. You can be putting people, people have to start kind of pairing up. Right? So your upper and lower extremities, they pretty much merge once you get towards the basal ganglia. Especially at that posterior limb of the internal capsule. Right? So the corticospinal tract fibers now control the other side of the body. Remember, they cross at the condom dollar. They're going to kind of merge there. And when they merge, if you mess up that region, it's a small region, but boy, you're going to get devastating consequences.

The person is going to have a pure moral stroke. They're going to be paralyzed in the upper extremities. I mean, the lower extremities control lateral to the problem. Now, one thing our friends at the MBM is can ask is they can ask you, what is the biggest risk factor for a lenticular stride artery aneurysm? I would hope you're saying that divine, this is hypertension. People that get those aneurysms, those are microneurysms, that rupture, it's almost exclusively found in people that are hypertensive. That's why half an hypertension is actually really bad. If that's why hypertension is the biggest risk factor for a stroke for purposes of your test. That's something you want to make sure you truly, truly know for your ex-apps. Something you want to truly make sure you truly know and you truly understand for your ex-apps. And then another thing that just kind of floated in my mind now with the Bisoganglia is they can give you a question about a person that has these a choreforme movements. And they'll tell you that maybe a few days ago or a few weeks ago, the person had so throat and fever. Well, I would hope you're thinking that this person has, you know, strep-firing gides. And remember, strep can cause problems because they are certain strains of group-y strep that we make antibodies against. And those antibodies that can destroy group-y strep, they also cross-react with the Bisoganglia. And why would that cross-reactivity happen?

That cross-reactivity will happen because they are certain group-y strep antigens that look very similar to antigens you'll find on the neural structures of the Bisoganglia. So sometimes those antibodies that we create in the setting of group-y strep infection, they can actually attack the Bisoganglia. And they can cause things like sydenamyschuria. They can cause things like pandas. Pandas we know that has pediatric autoimmune neuropsych disorder associated with group-y strep infection. So that phenomenon is actually known as molecular mimicry. Molecular mimicry. Many times they will ask you on the exam was the most likely outcome. Just reassure the patient's, those group-y movements are going to disappear over time. But again, it's from pretty much antibodies attacking the Bisoganglia. And also if we're still talking about the Bisoganglia, the Bisoganglia is kind of high yield. I feel like people just kind of brush it off. That would probably be a mistake for your test. But another high yield thing to know the Bisoganglia is that the Bisoganglia has this amazing, amazing thing where, I guess it's not an amazing thing for the patient's offering from it. But bilirubin loves to deposit in the Bisoganglia. Bilirubin loves loves loves to deposit in the Bisoganglia. And when he does, that can cause things like chronic disorders. So this is why when a child is born and they have jaundice, we cannot take it seriously.

Because that bilirubin can deposit in the Bisoganglia, the indirect bilirubin can deposit in the Bisoganglia. And that can cause chronic disorders, right? The child will have seizures, they'll have poor brain development, they'll have a bunch of issues, which are not obviously not ideal. Obviously not not ideal. So there are many things that can deposit in the Bisoganglia. You can even have things like copper deposit in there, things like copper deposit in the Bisoganglia. And that can certainly cause problems, right? What's the copper disorder that you know about? I hope you're saying it would be fine. That sounds an awful lot like well-sense disease. It sounds an awful lot like well-sense disease. It sounds an awful lot like well-sense disease. All right. So again, please don't forget all these integrations with the Bisoganglia, right? We talked about the putamen, is a part of the Bisoganglia. We talked about the coriic nucleus and haunting things. We talked about the globus pallidos and carbon monoxide poisoning. We talked about the internal capsule, the posterior limb, lenticular straight artery, stroke. Another thing actually you may find in the, is not you may find, you do find, in the Bisoganglia is the substantianiaigra. Remember the substantianiaigra is the part of the brain that has issues in a present that has Parkinson's disease. In fact, grossly, what would you observe with the substantianiaigra in a present that has Parkinson's?

You're going to observe deep pigmentation of the substantianiaigra, deep pigmentation of the substantianiaigra, pars compacta, right? So keep that at the back of your mind for, for example. And then don't forget the subthalamic nucleus with this cost in the context of hemibalismus, a contralateral hemibalismus, right? That's like a flailing movement of your upper extremities, okay? A flailing movement of your upper extremities. And again, if you like the way that I explain things, if you like the way I make integrations, you're really, really going to love my classes. I have a bunch of classes, like a series starting next Tuesday, testicking class, have a bio-stats class on Wednesday. I have a social sciences ethics and QI class on Thursday, step two, step three last minute review on Friday. And then the week after that I have a 20 hour step two class. If you're trying to get your scores back on time for Euras, your step two, step three scores, they should definitely take that class, that 20 hour class coming up. I believe it's from the 26 to the 29th. And you should also strongly consider the classes taking place next week. Those are probably the last classes that would hold, that would fit in with the timeline, if you're trying to get your scores in ahead of Euras, just something you can keep at the back of your mind as you prepare. So please, please, please, please, please, and don't forget another kind of important thing that's in the Bezo Ganglia is the Thalamus.

And again, if you're interested in any of the classes, just shoot me an email, be all over Zoom, I can give you some more information. Again, tons of people have taken these classes and found it to be extremely helpful. Alright, so I think another thing I should discuss about the Bezo Ganglia is the Thalamus. The Thalamus is really, really important. The key thing I want you to know here with Thalamus is the following. What are they going to really hone in on with step one, step two, and step three? The things they're going to really hone in on are one. The Thalamus is a big sensory place. It's a very, very big sensory place. Very, very big sensory place. So if you have a phalamic stroke, you have a pure sensory stroke. And what is like the big time blood supply to the Thalamus is actually a posterior cerebral artery. So if you have a PC stroke, you're really going to mess up your Thalamus. And if you mess up your Thalamus, you're going to get in a lot of trouble. You have a pure sensory stroke. You have a pure sensory stroke. Another thing to also know about the Thalamus for purposes of the USML exams is that the Thalamus, so all your ascending pathways, and this kind of explains why people get a lot of problems with sensation when you have a Thalamus stroke. If you actually go to the Thalamus, there's all these, all these, your drosal columns, feeds into the Thalamus. Your spinal phalamic tract feeds into the Thalamus, right?

So again, whenever you have a Thalamus stroke, you're going to get in a lot of trouble. And I don't think to also keep at the back of your mind with Thalamus strokes is this whole concept of aloeudinia. You know, when they have, because think about it, if your Thalamus is like your sensory big, big wig sensory place, you can see that if you have a Thalamus stroke, you may begin to have aloeudinia. You may begin to have a, sometimes they call this post Thalamus stroke pain syndrome. You see a person air blows on an extremity and they're like, oh, he hurts so bad. Usually in the distribution of a stroke or trauma, whatever, right? That thing has a lot to do with an impaired Thalamus signalling, okay? Impaired Thalamus signalling, impaired Thalamus signalling, impaired Thalamus signalling. All right. So again, I've kind of started talking about the circle of wiles in a sense, right? There are many parts to it. And again, there's a lot of high-yield stuff to know there. I've kind of touched on many of the arteries, but again, let me just kind of touch on them again and touch on a few new ones so that you can just kind of have everything here. Again, I want to meet this podcast to be something where you listen to it and you're like, oh, gee, I'm grateful I listened to this podcast, right? So don't forget your anterior cerebral artery, right? I said that literally the anterior cerebral artery supplies your low extremities and your genitals.

We talked about executive function with that. And then we talked about the anterior communicating artery. It's the most common location of an aneurysm to be formed in the circle of wiles. And then we talked about the middle cerebral artery that does the low extremities, that does your face, those things like that, right? And don't forget that the posterior cerebral artery is another part of the circle of wiles. The PC supplies the thalamus and it supplies your primary visual cortex. And remember, actually, whenever you have like a PC stroke, you're going to have this thing called macular sparing. So your visual field from your macular is still going to be intact because your macular has bilateral blood supply. It gets blood supply not just from the posterior cerebral artery, but also from the middle cerebral artery, also from the middle cerebral artery. And then don't forget another part of the circle of wiles is the superior. I'm pretty much going from like the top and going down. The superior cerebral artery is also kind of important. The big thing to know about that is that that is the blood supply. Look at it has superior in the name. That's the blood supply to the superior colliculus. Why is the superior colliculus important? The superior colliculus is important because it's the vertical conjugate gay center. It's the vertical conjugate gay center, vertical conjugate gay center.

So whenever you have any problems with the superior colliculus, you're going to have a vertical diplopia. You tell those people to look up and down, they're massively struggling with it. Right? So because the superior cerebral artery is the blood supply to the superior colliculus, if you have a superior cerebral artery stroke, you can have a vertical conjugate gay's palsy. But let me ask you this, is that the only thing that can cause a vertical conjugate gay's palsy? I hope you're saying divine, not really, because there is this fancy gland that is superior to the superior colliculus. I like to say this, it kind of rolls off the tongue well, superior to the superior colliculus. That's the pineal gland. The pineal gland can become a mess, right? You can have a pinealoma. That pinealoma can compress the superior colliculus and cause a vertical conjugate gay's palsy. So guess what I'm going to do? There are two things that can cause a vertical conjugate gay's palsy. You can have a mass like a pinealoma, compressing the superior colliculus causing that problem. We can have more of a vascular cause, like a superior cerebral artery stroke. And then, don't forget that the basilar artery is like the big, big, big blood supply to the ponds, right? The big, big, big blood supply to the ponds. And before I actually go there, let me not forget something. It's almost like the thing that links the anterior part of the circle of willis to the posterior part of the circle of willis.

The thing that makes that communication happen is the posterior communicating artery. And what is high utonabal p-com? What's high utonabal the posterior communicating artery? The thing is, it can form an aneurysm. When it forms an aneurysm, it's going to compress cranial nerve three. You can get an oculumodon nerve palsy. Many times when that happens, you're going to paralyze your extra ocular muscles. Your what? Your extra ocular muscles. Your what? Your extra ocular muscles. Remember, the easy way to remember the ocular muscles is that cranial three, pretty much supplies all of them, except like two. It doesn't do the superior oblique, which is done by the troclear nerve. Remember that with S-O-Four. If you did any chemistry class, you probably remember so far, it has it H-2-S-O-Four. So S-O, meaning superior oblique, and then the four for cranial nerve number four, that's the troclear nerve. Then the other cranial nerve that does another trocleomosol is cranial six. Just remember L-R-6, lateral rectus six, that's the abducent nerve. The abducent nerve supplies the lateral rectus muscle, which does abduction of the eye, which does abduction of the eye. Now, so if you have a p-constroke, you're going to compress cranial three. Many of your extra ocular muscles are going to be paralyzed. One thing I want to say about the PC that I think I kind of... Let me put it this way, I think I... kind of forgot to mention, let me just kind of run through this in my brain.

Again, I'm seeing these things from memory. But the PC supplies, we've said it supplies the thalamus, we said it supplies the primary visual cortex. Okay, this is the thing I forgot. It supplies the midbrain. If you have a PC stroke, you're going to mess up your midbrain. You're going to have Weber syndrome. Some people pronounce it as Weber syndrome. But the PC is the primary blood supply to the midbrain. And usually when you have a midbrain stroke, the thing that's going to tell you, you have a midbrain stroke is that a lot of your extra ocular muscles are kind of paralyzed, right? Because cranial three, cranial four are in the midbrain. And then many times those people are going to have like contralateral, upper motor neuron symptoms. Because obviously the corticosterino tract also curses through the kind of ghost through that... The midbrain. Some that keep at the back of your mind for, for example. Okay, now let's jump back to the basilar artery. Remember we said the basilar artery is the primary blood supply to the ponds. And it has two branches that are not worthy. It has the paramedium pointin arteries that supply the midiopons, right? If you mess up the midiopons, you're going to injure cranial six. Because cranial six runs in the midiopons, so you see an abducent spalsy. I also going to see a lot of corticosterino tract problems. Because the corticosterino tract runs in the midioprene stem.

But another branch of the basilar artery is eica, the anterior inferior cerebral artery, the anterior inferior cerebral artery. That supplies the lateral ponds. If you mess up eica, your lateral ponds is going to get screwed over. And the big thing you're going to notice, you're going to see a lot of cranial seven problems. But you're going to see issues with pain and temperature for the body and for the face. Because the spinal thalamic tract travels through the lateral brain stem. So if you mess up the lateral brain stem, you'll see pain and temperature problems for the body. You'll see pain and temperature problems for the face. And also you'll see problems with cranial eight. Because cranial eight is also in the lateral brain stem. And then remember if you infact the basilar artery, that can cause you to have locked in syndrome. Because the basilar artery, if you infract it, then your entire ponds is gone. Your entire ponds is literally gone. And if your entire ponds is gone, that's a huge, huge, huge, huge problem. Because all you are sending pathways, bye bye, all you are sending pathways, bye bye. The only things that will work are the things that are in the midbrain or higher, like your extraoclomozo, cranial nerves, like cranial three and four, your occipital nerve and your troclear nerve. And remember, I know that I think that it also caused locked in syndrome is if you're correct, type one, it's extremely too quickly.

Many of you have probably heard of this numonic that from low to high, the ponds will die. From low to high, the ponds will die. Now let's keep going further. So we'll go down to the vertebral arteries. The vertebral arteries, they have two branches. One big one to notice is the paika, the posterior inferior cerebral artery. The posterior inferior cerebral artery, so it plays the lateral medulla. So if you have a stroke of paika, that's called coloamberc syndrome. That's a lateral medallery stroke. The critical thing you're going to see is you're going to see a lot of cranial nine and ten problems, sort of dysphysia, things of that nature. And again, because it's a lateral brainstem stroke, you're going to see pain and temperature issues. Those pain and temperature fibers, the spinal thelamic tract, the running the lateral brainstem. But another branch of the vertebral artery is the anterior spinal artery. The anterior spinal artery. Okay? The anterior spinal artery. The anterior spinal artery. The anterior spinal artery also plays the medial medulla. If you mess it up, you're going to get in trouble. Right? The big thing you're going to see is cranial 12 issues. The hypoglossal nerve is going to be all messed up. And again, you're also going to see upper moron neurons symptoms, because again, as I've said many times, the corticospinal tract runs in the medial brainstem.

And also whenever you have any medial brainstem stroke, you're going to have issues with fine touch, vibration, and perception. You're going to have drosocolon issues, because the drosocolon medial lemneska system also runs in the medial brainstem. All right. Now, if we descend a little further, because that anterior spinal artery, I don't want to give you this impression that it's only from the vertebral artery. There are some anterior spinal arteries that are branches of the artery of a damcoids. The artery of a damcoids is a branch of the aorta. And the anterior spinal artery, none of itself, especially those ones that are branches of the artery of a damcoids, which are branches of the aorta. Disapply the anterior to thirds of the spinal cord. So if you have an anterior spinal artery stroke, or you have a problem with the artery of a damcoids, or you have a problem with the aorta itself, you can have anterior cord syndrome. And anterior cord syndrome, pretty much everything your spinal cord stops working with the exception of your drosocoloms, because your drosocoloms are in the posterior third of the spinal cord. Your drosocoloms are in the posterior third of the spinal cord, and the posterior third of the spinal cord. Again, please, I'm really, really begging you. You've got to know some of these things. Let me actually slow it in a few more things. Maybe I should maybe try to stop bringing this podcast to an end, Neuro.

If a person really wants to go to town on Neuro, you can keep talking and talking. And I love Neuro, as you can probably tell from this podcast. So maybe let me throw in a few more tidbits that I may have kind of neglected a little bit, to keep in mind. But one thing to remember is that if a person has a problem with the anterior comichetin artery, you can compress the optic chiasm. The optic chiasm kind of runs underneath the anterior comichetin artery. And if that happens, that's a problem. That's literally a problem. You can have bite temporal hemianopsia. You can have bite temporal hemianopsia. You can have bite temporal hemianopsia. And another thing you may also find around that general region are the mammillary bodies. The mammillary bodies, they are kind of under the pitruderic gland in a sense. What do you know about the mammillary bodies? Well, think about a person that drinks a lot. And in the person who is confused, the person has like an estagmas, the person who is swimming from side to side, that's where any keys. People have where any keys, remember, it has this very strong association with hemorrhagic infarctions of the mammillary body. And the mammillary body is hemorrhagic infarctions of the mammillary body. That's pretty high, or to not the back of your mind for, for the exam. So again, I think I've kind of hit on a lot of things. Again, I really hope you found this podcast to be helpful. You know, I'm just trying to think of like any structures.

I feel like today I kind of hit like cortex, bisoganglia, and brainstem. You know, I guess another structure I can talk about is the corpus callusum. The corpus callusum pretty much connects both cerebral hemispheres. The critical thing to know about that is gliblastoma multifomii. It loves to cross from one side of one cerebral hemispheres to the other through the corpus callusum, through the corpus callusum. Right? And then don't forget your ventricular system, right? We have the lateral ventricles. The lateral ventricles, they go down through the interventricular fremen of monorool. They connect to the third ventricle. And then the third ventricle, they then connect through the cerebral aqueduct of sylvios to the fourth ventricle. The fourth ventricle trains out lateral through the fremen of lusca and immediately through the fremen of magendi. But again, not so fast. Let's not just run through these ventricles. There is actually a bunch of weird things to know about the ventricles. Because I guess it's technically part of the cortex slash brainstem. So we kind of have to talk about it. Let's talk about the lateral ventricles. First thing to know is that the lateral ventricles, what is the psychiatric disorder that's associated with those lateral ventricles being large? I hope you see in schizophrenia. Schizophrenia has a very, very strong association with enlargement of the lateral, not just the lateral, also the third ventricles. And then think about it.

If we're talking about the cerebral aqueduct of sylvios, that is actually the most common region of stenosis within the ventricular system. So when a person has, if you see a person having a non-communicating hydrocephalus, which record an hydro-obstructive hydrocephalus, especially in a newborn, the most common location of obstruction is going to be in the cerebral aqueduct. Many times on exams they call it aqueductal stenosis, aqueductal stenosis. Another thing to know with the ventricular system as well is that remember after the CSF drains through the lateral fremen of lusca and the medial fremen of magendi, it gets reabsorbed into the sagittal sinuses with the arachnocrenol lesions. But if those arachnocrenol lesions are fibroost or they have issues, then you may have problems with reabsorbing CSF. That's actually the primary mechanism behind communicating or non-obstructive hydrocephalus. So remember an obstructive hydrocephalus is also known as a non-communicating hydrocephalus. There is an actual obstruction to flow of CSF. But a communicating hydrocephalus or a non-obstructive hydrocephalus, there's no obstruction to flow. The primary problem is that you have issues with reabsorption of CSF at the arachnocrenol lesions. People can get those kinds of problems from like meningitis because of the inflammation. But that's also the primary mechanism behind the hydrocephalus in normal pressure hydrocephalus.

And that's also the primary mechanism behind the hydrocephalus or the CSF build-up in people that have a pafficking trocranial hypertension. It's a pafficking trocranial hypertension. Although one thing I want to see is how can you differentiate MPH on your exams from idiopathic intracranial hypertension? Well people that have MPH look at the name normal pressure hydrocephalus. They're going to have normal CSF opening pressures. If a person has high CSF opening pressures on your exams, they don't have normal pressure hydrocephalus. They have idiopathic intracranial hypertension or some other disorder. Again, these things seem like they don't matter, but I promise you they're pretty high yield to know for for your exams. And then what is the brain tumor that loves loves loves loves to occlude the fourth ventricle especially? I hope you're seeing the findings and it's an appendi-moma. And what genetic disease is so you know that an appendi-moma? It's going to be neurofibromatosis type 2. People that have NF2, they tend to get schwannomas, they tend to get meningiomas, and they tend to get appendi-momas. Those if you see a person that has a four ventricular mass on your exams, one of the first things you should almost like reflects to is saying or divine, this is probably an appendi-moma. Remember those appendi-momas have those are perivascular pseudo-resets on histology. Make sure you can identify those perivascular pseudo-resets.

Make absolute certain you can identify those perivascular pseudo-resets. I think this is going on for like 41 minutes now, so I'm going to go ahead and stop. Again, if you like the way I teach, if I want to want to learn for step 1 to 3, level 1 to 3, let's go to exam show, exams, I have these podcasts on all the major podcasts apps, I have a You Tube channel you can check out. And then I also have another website called divineinterventionlifelessens.com. Every week, roughly every week, I post like a podcast or two away from a biblical perspective address a life lesson. There's an Apple podcast associated with that. And then if you're interested in any of my classes, just shoot me an email, be all live over Zoom. Again, tons of people have taken them, they're pretty comprehensive, found them to be extremely helpful. If you're trying to get in your scores before you hear us, you really want to consider the classes that are coming up. So thank you for listening to this podcast. Again, please, I really hope that you listen to this thing. This podcast is really, really high-yield. I'm telling you, if I were in your shoes, if I were a med student studying for a new US Emily exam, I will probably listen to this in the last week. I'm going to listen to this multiple times through my dedicated period. I may have only listened to it the night before my exam, because it's something that I know is going to score me a lot of points.

This podcast alone can easily give you about seven or eight questions right on your exams, like no question about that. Seven or eight questions may not seem like much, but step two is a 320 question exam. That's like 2.5% of your test. So these little things matter. Those are the things that separate the people that are average scores at the end of the day from people that end up being pretty high scores. So thank you for listening to me today. I'll see you in episode 547. God bless you. Have a wonderful rest of your day or weekend or whatever. I'm bye for now. Thank you.

The anterior communicating artery (A Comm).

The temporal lobe.

CN IX (Glossopharyngeal) and CN X (Vagus), leading to dysphagia/hoarseness.

Lymphocytic predominance (lymphocytes > neutrophils).

The subthalamic nucleus (damage causes contralateral flailing movements).

N/A (Focus on clinical presentation, but remember that the lateral medullary syndrome is key here).

The caudate nucleus.

Pure motor stroke; contralateral paralysis affecting both upper and lower extremities.

Bilirubin (jaundice) or Copper (Wilson's disease).

Posterior cerebral artery (PCA); Pure sensory stroke.

CN XII (Hypoglossal nerve); leading to tongue weakness/paralysis.

Molecular mimicry.

Communicating (or non-obstructive) hydrocephalus.

The caudate nucleus.

Pure motor stroke; contralateral paralysis affecting both upper and lower extremities.

Bilirubin (jaundice) or Copper (Wilson's disease).

Posterior cerebral artery (PCA); Pure sensory stroke.

CN XII (Hypoglossal nerve); leading to tongue weakness/paralysis.

Molecular mimicry.

Communicating (or non-obstructive) hydrocephalus.