DIP Episode 92 - USMLE Step 1 Rapid Review Series 3 (Neuro)

Okay, welcome. My name is Divine. I'm a PGI One Transitioner here resident that's going into our radiology. In this podcast we are going to be doing another USML step one rapid review and this will also be again in Europe. This will be relatively short because unfortunately I'm not feeling super well today. Okay, so let's just jump right into it, right? So what if you get a question about a person that you know they have like some kind of a tear rupture that's causing like a rapidly progressive increase in intra-cranial pressures. I really hope you're thinking about like an epiderohematoma, right? I remember that it's associated with like a temporal bone fracture and a rupture of the middle meningel artery. Remember that's one of the terminal branches of the maxillary artery which is a branch of the external carotid. So that's kind of like the big relationship you want to remember then don't forget your lenshape lesion on a non-contraste as CT, right? For those people you want to emergently refer them to neurosurgery. And then what if you get a simple question a person that has you know like they've smoked for like 60 years and then they have like a droopy eyelid and they have like popular meiosis and they don't sweat on one side of their face, right? I really hope you're thinking about a hornar syndrome, right? Remember that this thing they have is likely like a panko stumer that's compressing the cervical sympathetic tracts, okay?

And it's causing an Ipsilateral hornar syndrome, hornar syndrome lesions actually Ipsilateral to the side where you see the the deficits. And then what if you see what's the cranial nerve that could lesion that could give you like toses and my dry asses? So remember hornar syndrome is toses and meiosis, right? So, pupillary construction, what's the cranial nerve lesion that will give you toses and my dry asses? I really hope you're thinking about an oculumurone nerve lesion, right? So cranial thre lesion, the toses, right? You'll get that because remember you'll live little popover superioris, no longer works because that's integrated by cranial nerve three. And then the my dry asses you get because your sympathetic nervous system is acting on a post. Remember that cranial nerve three carries sparse and pathetic nerve fibers that relates to the eye, right? And those sparse and pathetic fibers cause popular reconstruction of meiosis. So if you knock out cranial three, you have to blur my dilution out of my dry asses, right? So that's the whole thing about the blown pupillal. That's like the pathophysiology behind that. And then what if a person has like a lesion to the sub-thelomic nucleus? What would they have? Right? I really hope you're thinking about like a hemibalismus, right? So they'll have like flailing movements of the of one arm and the arm will be contralateral to the side where the sub-thelomic nucleus lesion.

Now what if a person has a lesion of the frontal eye field, right? So a lesion of the frontal eye field, where will their eyes deviate? This is actually kind of high you to know for step one and step two. And the neural shelf has a third year, right? So for person has like a frontal eye field lesion, right? Their eyes will actually deviate towards the side of the lesion. So you may see divine how does that make sense? The thing is the frontal eye field, right? Say for, let's just choose one side of the brain. Let's say the right frontal eye field and actually goes down from the cerebral cortex and projects to the left, um, PPRF, right? So the left paramedian, pontin reticulum formation. So the left PPRF is connected to the left cranial six, the left abducense nucleus. And then somehow through some pathway, no more likely like the MLF, it is connected to the right cranial three nucleus, right? So basically let's map it out this way. So right frontal eye field is connected to the left PPRF, the left paramedian pontin reticulum formation. And then the left PPRF is connected to the left abducense nucleus and the right oculumodonucleus, right? So basically the whole point of this system is for horizontal conjugate gaze, right? You want to go from, let's say you want to look all the way to the right without having any issues, right? If you're right PPRF, if you're, I mean, let's say you want to look all the way to the left, right?

Like conjugate horizontal gaze to the left, your left PPRF will fire, right? That will help you activate your left cranial six, your left abducense nerve. So you will ab dock to your left eye, but you will ad dock to your right eye, right? So if you think about it, if you have to ad dock to your right eye, that means your right cranial three has to be working, right? So really instead of memorizing this, you can just sort of work it out in your brain, kind of mix, uh, mix a lot of sense, right? So if you sort of think about it, if you lesion like your right frontal eye field, your left PPRF will not work, if your left PPRF does not work, that means your right PPRF will act on a post. If your right PPRF is acting on a post, right? That means you have connections to the right cranial six and intact connect, so intact connections to the right cranial six nucleus and intact connections to the left cranial three nucleus, right? So your right eye will ab docked and your left eye will ad docked, right? So basically if you have a frontal eye field lesion, your eyes will deviate towards the side of the lesion. That's the path of physiology behind that. If you sort of bring up an analogous question like, oh, what happens if you scrub your PPRF itself? Right? So let's say you scrub your left PPRF, right? Again, if you scrub your left PPRF, that means your right PPRF will be acting on a post and with your right PPRF acting on a post, right?

Remember your right PPRF is connected to the pseudo lateral or the right cranial six nucleus and the control lateral or the left cranial three nucleus, right? So that means your eyes will deviate to the right, right? So that means whenever you have a PPRF lesion, because your right cranial six, right, is causing your lateral, your right lateral rectus to AB docked and your left cranial three is causing your left medial rectus to AD docked. So whenever you have a PPRF lesion, your eyes will deviate towards, I mean your eyes will deviate away from the side of the lesion. So frontal eye field lesion, that's a critical issue. Your eyes will deviate towards the side of the lesion. PPRF lesion, that's more of a brainstem issue. Your eyes will deviate away from the side of the lesion, okay? It's actually kind of high up to know that and the thing is I expand on like these concepts in the neuro podcast, I actually have for 30 years. So if you're if you're a med student that's actually studying for step one and you have like eight or nine three hours on your hands, I would actually kind of like recommend listening to the neuro podcasts that I have for like 30 years. It's actually super helpful. Like it will make you like super well grounded in neuro, but again, I will also do neuro podcasts for that are specifically targeted towards towards a step one.

The only thing is that those 30 year podcasts, they're just very clinical because that's kind of the way your 30 year show of exams are. Now what if you get a question about a patient and they have trouble like with upward gaze, right? So they have like paralysis of upward gaze. What's the structure in the brainstem that's potentially lesion? Well, I really hope you're thinking about the super colloquialis, right? Remember the super colloquialis is in the door so mid-brain, right? And if you have like paryno syndrome, right? So let's assume you have like a you can have paryno syndrome or let's say you have like a piney luma, right? Because remember that the pineal gland is superior to the super colloquialis. So whenever you have like a paryno gland tumor, right? That can compress the super colloquialis and you can have paralysis with upward gaze. Now what if you get a question about a person, you know, they say that, oh, a commodition is just fine, but when you try to do the popularly, popularly light reflex, it's not working out so well. And let's assume they're a sex worker. I really hope with that you're thinking about tertiary syphilis, right? And the argol or rubbery sin, a pupil. Now let's assume you get a question about a guy, you know, gets into a super severe accident and then for some reason he cannot form new memories, right? So what's the portion in the brain that's lesion that helps you form new memories, right? That's the hippocampus, okay?

That's again, a high-o thing you want to keep at the back of your mind. Now what if you get a question about a patient? The, let's say like their acquaintance is say that this person has been acting super weird, making like sexually suggestive comments. And then let's say the person dies, got for a bit, right? And then you're doing like pathology analysis, right? And you look at their brain grossly and you see like this, basically let me give you the boss phrase, knife edge atrophy of the cerebrum, right? So the cerebral cortex. If you see that what kind of dementia are you thinking about? I really hope you're thinking about frontal temporal dementia, right? Remember, classically on exams, shows up in like guys in the 40s, 50s, early 60s and then over like a one to three year period, they begin to have just weird, weird, weird behaviors like the have issues with like executive function, but usually like they just begin to like just do a lot of inappropriate things. If you see that think about frontal temporal dementia, that's also not a spics disease. Now what's the vasculolision that's associated with like you know, they tell you that okay this person has a vasculolision and they have like complete quadriplegia. So like all their low extremities, all their upper extremities just like just gone in terms of our motor function. Think about some kind of like locked-ends syndrome, right?

Remember I told you that this kind of rise from like a basilar artery stroke or like a basilar artery aneurysm, right? But a more metabolic cause of that of a locked-ends syndrome will be like will be if you correct a hyponitremia too quickly. I'd remember the numonic that if a person goes from low to high, the the ponds will die. Okay now what if a person you know has trouble, they give you a question about a patient and they can write, they cannot calculate and they cannot tell which finger is which like oh they don't know like this is this finger, this is that finger. What kind of parietal lobe lesion are you thinking about? I really hope you're thinking about a dominant parietal lobe lesion, okay? In fact there is a term for this disorder is actually known as Girstmann syndrome, okay? Basically it's a lesion to your dominant parietal lobe. So you have trouble like doing math, trouble like writing and then sort of like telling like oh these are this is this finger, this is that finger, that's kind of how you know. So you want to be able to contrast a dominant parietal lobe lesion with a non-dominant parietal lobe lesion, right? Because basically if you lesion your non-dominant parietal lobe, you basically have issues like recognizing one side of your body, okay? So these are people that will like comb one side of their hair or they would apply makeup to one side of their face, that's more of a non-dominant parietal lobe lesion.

Now and the thing is just a high-yield thing to know is you may see divine. How do I know what parietal lobe is dominant for me? Well the thing is most human beings are right-handed, right? If you're right-handed that means your left parietal lobe is your dominant parietal lobe. If you're left-handed you're kind of like swimming in like weird waters. Those people may have like co-dominant parietal lobes or whatever, it's just kind of weird situation but I'll say for most people your dominant parietal lobe is your left parietal lobe. Again being left-handed does not confer any disadvantages to you. Actually I think it's kind of cool for people, people that are right with their left hands. It's actually kind of difficult to do but that's a different story that we can have on another, a different conversation and can have on another day. Okay now what if a person has a brain stem lesion and they just completely lose consciousness? What is the brain stem structure that has been lesion? So what's the system that activates you? Right? That's your reticle activating, your reticle activating system. Okay? Now what if you get a question about you know like a super tall athlete has the worst headache of his life, right? Super tall. That's the key thing there. Super tall athlete, worst headache of his life. There will be a thing about Marfans and Drum, right? Remember in Marfans those people tend to get a lot of like anterior communicating artery on your symptoms, right?

And those on your symptoms if they are ruptured that can cause like a subarachnoid hemorrhage and that can present as the worst headache of the patient's life. Okay now what if you get a question about patient with elevated creatinine? Right? So the acradinines clearance is not great and they also again present with the worst headache of their lives. I really hope you're thinking about like ADP-KD, right? So like autosomal dominant polyacistic kidney disease. Remember that those people again, right? Remember classically it's associated with having like cis and the kidneys, having cis and the liver. That's actually kind of high you to know. It's also associated with mitral valve prolapse, right? And it's also associated with aneurysms in the circle of willis. That's very high you to know for exams. Now what if you get a question about a patient with a connective tissue disease that has the worst headache of his life, right? I really hope you're thinking about EDS, right? So like Earl's Danlos syndrome, probably the one we're most concerned about is like the type three, Earl's Danlos syndrome. That's like the vascular, Earl's Danlos syndrome that arises with like a defecting type, type four collagen if I'm not mistaken. So remember those people tend to have like hyper extensible skin and all that crap. Okay, so remember that Earl's Danlos syndrome, Marfan syndrome, and I don't know, I feel like this Earl's Danlos syndrome involves type three collagen. Yeah, I don't know.

I'm thinking that Earl's Danlos syndrome involves a type three collagen defect. Yeah, you know what? I be, yeah, I'm 99.9% rates. It's a type three collagen defect, not type four, not type four collagen. Yeah, I'm gonna go with a with a type three collagen defect. That's that's that's the correct thing. Okay, sorry again, these again, sort of kind of like off the cough lecture. So yeah, but I'm pretty sure it's it's type three, so type three collagen defect. Okay, what if you get a question about, or you know what? Let's just put it this way. What if a person has an arterial lesion, right? And they kind of have like a basal ganglia hemorrhage, right? Just think of this boss phrase is like a French, French term. So it's high over test, right? So a Shaco Bushada micro aneurysm, right? Now, what if you get a question about a patient, right? That has a brain bleed and the lesion on C Ts on CT imaging does not cross suture lines. What are you thinking about? I would really hope you're thinking about an epidural hematoma on that those are circumstances. What's the analogous lesion? I guess that does that actually does cross suture lines, right? That'll be more of like a subdueral subdueral hematoma, right? Now what's the blood vessel lesion, right? That'll be associated with the person like an old person that falls. So an old person that falls. I would want you to think more about a subdueral hematoma with that.

Remember that happens when you have like a rupture of your bridging veins. Classically, if a person is an alcoholic, or if a person is an old person that falls or a person or you have like a non-accedental trauma in a kid, think more about subdueral hematomas with those three classic exam scenarios. Now what's the, I guess, all the physical exam finding being a victim of a severe accident who has severe uncle herniation, right? That'll be like a down and out eye, right? That's the classic way and it will usually be like you'll see like the bloon poopy old, usually put pictures on exams to highlight those things. Now what's the bug, I guess, that'll be associated with paralysis in an immigrant, paralysis in an immigrant, right? So you really want to think about like a polio virus, right? Remember that polio loves to affect the anterior horn, also called the ventral horn of your spinal cord. Now what if you see like, you know, like a sensory ataxia in a person that has like a pass medical history of a painless shanker, right? I really hope with that you're thinking about like TB's door salus and syphilis. Remember syphilis can basically screw up the, your door, the door so horn of your spinal cord, okay? So your door so column medium, medium, and niscos pathway at the level of the cord can be all screwed up by, all screwed up by syphilis. Okay, now what is the drug of choice in the treatment of like a 25-year-old female that has like headaches and photophobia?

What's like the acute treatment for those for those patients, right? So really bad headache that's worse in by like loud noises, louts, by bright lights and whatnot. What do you think will be able to treat, what would you use to treat that lesion? Acutely, right? I really hope you're thinking about a trip 10, right? Like so much trip 10 for example, you can also use like an ergonomy compound, but trip 10s are the most common answers on exams. Remember trip 10s, are contraindicated in people that are taking like SSR Is. Remember you can trigger serotonin syndrome because trip 10s, right? They have serotonin receptor agonist activity. And remember they also contraindicated in people that have a history of like renotes phenomenon. So you probably don't want to give it to a person like Crests, Clare, Derma, right? Or a person that has like a prince metal also called a variant angina because remember that so much trip 10, right? Is a visospastic compound. So basically if a person has any kind of visospastic disease, right? You probably want to make sure you avoid so much trip 10 or like an ergot compound in those kinds of patients. Now what if you get a question about like a college student that has like no core rigidity and then he presents with like massive abdominal bleeding? I really hope you're thinking about like my serotonin syndrome, right? And like how the waterhouse of Friedrichsend syndrome.

Remember that can arise in the setting of a in the setting of an isothermine, in jididis, meningitis. Yeah, so remember right? Waterhouse Friedrichsend syndrome. You can basically like have like adrenaline, hemorrhage and then those the mortality is actually pretty high but like more than 50% or some crazy number like that. Now what if you see a patient that has like a rapidly fatal dementia? Let's see they recently had like a corneal transplant or something weird like that and they tell you that all that on physical exam you observe myoclonus. What are you thinking about? I really hope you're thinking about a CJD, right? So like Croixfeld, Iacob disease. Remember that if you do like a lumber puncture on these patients and you check via CSF, you'll find elevated levels of the protein known as 1433. Believe it or not that is floridly high yield to know for exams, right? And remember that those people if you do like pathological analysis of their brains, you'll see like beta pleated sheets, right? Because of the weird, excuse me, the weirder protein afforded. And I promise I'll round this podcast option. Yeah, I'm not feeling I'm not really feeling well. So what would your diagnosis be for a person has like this triad, right? Where they have like, you know, like scanning speech, like they're like, my name is this, right? So like scanning speech, right? And they have like intention tremors and they have like stagmas. That's like a triad, right?

In multiple sclerosis, there's like, it's like shackles triad of multiple sclerosis, right? Remember there are many triads in medicine, right? Probably the two biggest ones to remember, like the shackles triad of MS, right? So like the scanning speech, the intention tremor and the stagmas. And then there is also like shackles triad of like ascending colongitis, like the fever, right? Of a quadrant pin and John this, I guess you've sort of threw in the altered mental status and hypotension, then you're jumping to the land of Reynolds pentat. Now, what if a person has, like, let's say you perform a lumber puncture and a patient that's like paralyzed from, that's having like an ascending paralysis, like a symmetric ascending paralysis. And they tell you that you perform like a lumber puncture. And in the CSF, you see like very high levels of protein, but the cell count is like normal. That's, that's aberrant, right? Because normally if you have like a very high white blood cell count in your, in your CSF, your protein will be really high, right? But if you see like, you're like, wait, man, this protein is super high, but the cell count is normal. I really hope you're thinking about Guillembury syndrome, right? This phenomenon is basically what's known as abumino cytologic dissociation, right? So, abumino is the protein cytologic at the cells, right?

So normally, the protein level and your cell level sort of going, they're like directly proportional in your CSF, but if your protein level is high, well, your cell count is normal, that, that is not agreeable, right? That's why it's called an abumino cytologic dissociation, okay? That's pathonomonic for Guillembury syndrome. Now, what if a patient has like a combination of like, you know, like a sensory ataxia and hyperreflexia, right? So what kind of vitamin deficiency are you thinking about? I really hope you're thinking about a B12 deficiency, right? Then like a subacute combined degeneration of the court. Remember, if you have a B12 deficiency, you kill your dorsal columns and then you will also kill your lateral corticospinal tract, right? So you have hyperreflexia because you have an upper motor neuron issue, right? At the level of the court. And then you have a sensory ataxia because remember, your dorsal columns, right, help you sense like fine touch, vibration and proprioception, right? So you will not know where your joint sign space. If those people are sort of close to your eyes, they can actually have like a positive, like a positive, um, um, rumberg test. I already, I will explain the mechanism behind the rumberg test in a future podcast. Okay. Now, what is the enzyme lesion that's associated with like, you know, like progressive paralysis with no sensory deficits. So this person is having progressive paralysis and no sensory deficits.

So first thing is first, what's the diagnosis, right? I really hope you're thinking about ALS, right? So like Lou Gehrig's disease, right? In my atrophic, a lateral sclerosis. Remember, it's associated with mutations in a superoxide at dismutease. Now, what if you get a question about like a patient, right? Let's say this patient is now having is like a 40-year old patient having like behavioral changes. And let's say like this patient's dad died at like 45 and then the grand dad died at like 50, right? Can you see that like where things are happening with like earlier ages in this generation? I really hope with that you're thinking about Huntington's disease, right? Remember that Huntington's disease, it's otosomodominant inheritance and it demonstrates the genetic principle of, of anticipation, like many other otosomodominant disorders. Okay, now what's the drug of choice in the treatment? I remember that's like a chromosome 4 G effect. It's a trinocryphaloid repeat prop issue like C-G repeats, right? So that's kind of easy to remember for exams. Now, how do we treat ALS? What's the drug of choice? Remember, right? ALS is Lou Gehrig's disease, I introduced Lou Gehrig's disease with Ryluzol, right? I remember that's like an NMG receptor antagonist. And then how do we treat Alzheimer's? Right? So what are the drugs we use to treat Alzheimer's? Right? Remember, Alzheimer's, the pathophysiology kind of involves degeneration of the basal nucleus of minor.

And the basal nucleus of minor, it so happens, produces acetylcholine. So if your basal nucleus of minor, it's not working, right? Then you, you own produce acetylcholine. So you need as much acetylcholine as possible, right? And one way you can boost your levels of acetylcholine is by inhibiting the enzyme acetylcholine that breaks down acetylcholine, right? So there are certain drugs like Donepesil, Galantamine, and River Stigmin, okay? Remember your D or G and your R? These are again super high you to know for exams. Donepesil, Galantamine, and River Stigmin, the acetylcholine mysteries inhibitors that I used to treat Alzheimer's. Now, what would you find grossly in a patient that has like a 760 guy that has like cobalt rigidity? I hope you're telling me that you you will observe the pigmentation of the substantiate migra, right? So this is Parkinson's disease. Okay. Now, what would be the gross anatomical finding in like a 40-year old guy that has hyperkinesia? I hope you're thinking about like atrophy of the codi, right? Like atrophy of the basal ganglia, right? So again, this is a phantantins disease, okay? Now, what if you get a question about like an old guy, you know, he's kind of like forgetful and he has like visual hallucinations, right? So he's seeing things that are not there and he has like multiple syncopal episodes. What are you thinking about? That's Louis-Body dementia, okay? Very high yield to know that for exams.

Now, what if you get a question about like a 27-year-old like I guess, I know like medical student that sort of complains of like a pain that sort of feels like a band around his head? What kind of headache is this? That's attention headache, right? And then let's assume you get a question about like a patient that has like a headache at 9 a.m. every day for weeks on end and you have like a partial hornet syndrome. So let's say they have only like the tussis and meiosis. What kind of headache is that? That's a cluster headache, right? And I mean like this cluster headache was like the quickest abortive therapy for a cluster headache. That's 100% oxygen, right? Again, the all these things, I promise you all these things are very high yield to know for exams. That's why I like these rapid review series. You can sort of go through a lot of material in a very short period of time. And what's I guess the drug of choice? So let's assume you have to prescribe a medication on an exam for a patient that has like transient like electric shock-like facial pain. What's your diagnosis for starters? I hope you're thinking about like trigeminal neuralgia, right? Like tick-to-lure. So you treat that with carbamase, a pain, remember carbamase, a pain is a sodium channel blocker. It's one of those anti-penetica medications. Now, what if you get a question about like an Asian male that has like a rock heart super-edite and he's just coming from a cinema. He went to watch like a movie.

That will be closed and go glaucoma. Very good. That'll be closed and go glaucoma. That's a medical emergency, right? Those that patient would need like a like a lazy redotomy. You can also give them like pylocarpine because pylocarpine, right? It's a most chronic receptor agonist. So it will by causing public constriction. It will dilute the canals of shlenn. Okay. Now, what if you get a question you know about a patient that you know they have a headache and they were recently rescued from a house fire, right? If you see that, what are you thinking about? I really hope you're thinking about carbon monoxide poisoning, right? Another classic with this shows up on exams. You know, talk about a patient that was like found unconscious at home in the winter. Basically, the mbm tells you about something going on in the winter. You really, really want to ask yourself why will this question not be tested carbon monoxide poisoning? So if you see a winter, you really want to think about carbon monoxide poisoning on your mbm exams. That's like the first thing that should come to the surface of your mind before you even think about any of the things on your differential. Now, what if they give you a question about a patient that has like, you know, like a 60-year-old guy for the last six weeks, he's been weak enough with like severe headaches in the morning. So it gets better as the day goes by. And then they tell you that, oh, they perform an MRI of the brain.

And they say like, we are tumor, like they say like a tumor crossing the corpus callusum and it has like central neurosis, right? It's bad news, right? This is a, this is glioblastoma. This is a glioblastoma multiformy. This is just awful, awful, awful. I have not seen anyone with, I have only seen one person with GBM that has survived the month and a year. GBM is a terrible disease. You would not wish that on anyone. Okay. And my, I guess, I guess also lend me my support to any families that if you have any friends or relatives that have GBM, it's a tough, it's a tough thing to go through. Yeah, I would know wish that on anyone and I hope you get like some, some comfort. And I hope the person gets better. Okay. So back to this, right? So what if you get a question about a patient that has like, you know, they've been having like chronic headaches for a few months. And then let's say you perform like a brain biopsy of a legion that you found and you find like some umma buddies. What are you thinking about? Right? That's a, that'll be what? I mean, Juma, right? And a lot of the boss phrase you want to recognize on exams with that is like a parasagital tumor. Remember that, I mean, Juma's love to grow like around the dura. They usually have like a drill tail. That's like the classic boss phrase. That's why you can find them like parasagitally. Remember the, if you sort of like caught sagitally through the brain, you'll see like the fox cerebride.

That's a girl fort that basically separates the two cerebrola hemispheres. Now, what if you get a question about a patient that has a brain tumor and they tell you that oh, and histology, you find cells with a fried egg appearance, right? What would that be? That'll be what? And, oh, Ligo danger glioma. Okay? And oh, Ligo danger glioma. Okay. Now, what if they give you a question about a patient that has a history of like neurofibromatosis? And then they tell you that, oh, um, uh, uh, do you have a lesion at the cerebellic pontine angle? And then they're trying to ask you for the embryologic origin of that lesion. Am I really hope you're thinking about neurocrest? I remember, uh, these people can have like acoustic neuromids, right? So those are schwanomas. Remember that your schwan cells that are right from neurocrest? And these tumors classically sting positive for S100. Okay? Now, what's the, uh, what would, uh, what if they give you a question about a like a kid that's having like visual problems, having like signs of like hypopituitarism? And then they tell you that on imaging, you find like a calcified supercella mass. Uh, what are you thinking about? Right? So this will be a craniofarinjoma, right? Um, some people call this an adamantinomato scriniofarinjoma. Um, remember that it's very, it's actually very high, you'll remember that this is derived from, uh, from a ratkey spouch, okay? And it's the thing that classically drains a mudo oil fluid on pathology.

Uh, that's actually like cholesterol crystals and all that crap. It's not like real like mudo oil. Okay. Now, uh, I guess to sort around up today, what if you get a question about a patient that has like a GI malignancy, like a stomach cancer, and then they have a headache, and then they show you like, um, they say like, oh, this is a histological section from like a brain biopsy or something, and you find like, homerite rosettes. What are you thinking about? I hope you're thinking about a medallule blastoma, right? Remember, um, remember, um, this syndrome, right? Torco syndrome. It's as usual, like, GM malignancies, like visceral tumors and also brain tumors, classically on exams, a medallule blastoma, okay? Um, so I'll just sort of keep those at the back of your mind. Um, if you have any questions, uh, please feel free to reach out to me, and as I always say, if I need any podcast, I offer, one on one, T-Derm for the USM at this step one, two CK2 CS and three exams, um, preclinicumid, uh, exams like your first years of med school, shelf exams, um, medicine training exams, the medicine board exams, um, organic chemistry, physics, I tutor all these things pretty much, also general chemistry. And then I also do application advising, right? So if you're a med student applying for residency, like ERS apps, or college students applying for med school, so like Amcas apps, I do offer like, uh, application advising.

I've been on the admissions committee of like a top two medical school in this country of like a year, right? So, um, I have certainly helped a ton of people with that, and pretty much everyone I advice has matched. Um, so free of free to reach out to me anytime, send me a message and uh, and uh, well, and then one thing I recently put up on the website is like a 12-day USMLE course, uh, where it's like an in-person like class, like five to seven people, and we basically review everything in an integrated format that's tested on the USMLE Step 1 exam, or the two CK exam, or the step three exam. So if that's something you're interested in, if you have like a small group of like five to seven people that will need any of that kind of, the the interest in that kind of class, just send me an email, um, uh, you'll basically take place over like 12 days, um, it'll be an in-person review. Um, we can also do like an online thing, but um, that's if every member of the class is agreeable to it, but again, just sort of reach out to me, um, it's something I can arrange, and then we can go from there. So I wish you the best, have a wonderful rest of the day, and uh, God bless you. I'll see you in the next podcast.

Ptosis, miosis, and anhidrosis.

The superior colliculus; conditions like pineal gland tumors or pineocytoma can cause compression.

Frontal Eye Field lesion causes deviation towards the side of the lesion; PPRF lesion causes deviation away from the side of the lesion.

High protein levels with a normal cell count (albuminocytologic dissociation).

Vitamin B12 deficiency, leading to subacute combined degeneration.

Epidural hematomas do not cross suture lines; Subdural hematomas typically cross suture lines.

Type III collagen defect.

Cysts in the kidneys and liver, mitral valve prolapse, and aneurysms in the Circle of Willis.

Donepezil, Galantamine, and Rivastigmine (DGR).

Albuminocytologic dissociation (high protein, normal cell count).

Frontotemporal Dementia.

Elevated levels of 14-3-3 protein.

Cluster Headache.

"Shaco Bushada" microaneurysm.

Type III collagen defect.

Cysts in the kidneys and liver, mitral valve prolapse, and aneurysms in the Circle of Willis.

Donepezil, Galantamine, and Rivastigmine (DGR).

Albuminocytologic dissociation (high protein, normal cell count).

Frontotemporal Dementia.

Elevated levels of 14-3-3 protein.

Cluster Headache.

"Shaco Bushada" microaneurysm.