DIP Episode 96 - USMLE Step 1 Rapid Review Series 5 (Neuro)

Okay, welcome. My name is Devine. I am a PGY-1 transitional year resident that's going into our ideology. This will be the 96th episode of the Divine Intervention Podcast. And in today's episode we'll be continuing our rapid review series for the USML Step 1 exam. I believe this will be Series 5 and I'm going to be focusing on Newer. And again, note, this is not... Obviously, you should use this to review for your Step 1 exam. But this is not part of the comprehensive new review series that I'm going to be continuing. And I promise I will continue that. I promise I'll finish that up. It's just timing. I'm on a fairly intense medicine rotation right now. And then I'm jumping right into ICU. So it just makes things a little difficult. So let's just get right into it. So what if you get a question about a patient that has like increased intra-cranial pressures, they have like obstructive hydrocephalus, and they tell you that you see a mass, and then you let's assume you do like a biopsy or whatever. And then on the histology you'll find like a perivascular pseudo-resets among histology. What kind of brain tumor are you thinking about? Really hope you're thinking about an ependimoma with that. Okay. Now what if you get a question about a patient? Let's say it's a baby, has like really bad chronic headaches. Oh let's say it's like a young kid, really bad chronic headaches. And let's assume this child, I don't know, let's say... Oh you know, let's not make it a baby.

Let's say it's really bad chronic headaches. And this patient's hematocrit is like 18 grams per deciliter. Normal hematocrit is about like 12, 13, maybe 14 max. So let's assume this person has like really high hematocrit. What are you thinking about here? What kind of brain tumor are you thinking about? I really hope you're thinking about a brain tumor that produces epo, which will be a hemangioblastoma. You'll be a hemangioblastoma. Remember, hemangioblastomas can produce epo as a panoplastica phenomenon. And remember that hemangioblastomas, right? They usually shop in the posterior fossa in kids. And the associate that one like VHL, right? So like if one hipola lends out, it's like an autosomal dominant disorder. Remember, those people also tend to have like multiple other problems. Like they can have like the hemangioblastomas as I just mentioned. They can also have like early onset like bilateral renosel carcinoma, especially like the clear cell kind of a renosel carcinoma. So those are all things you kind of want to keep at the back of your mind with a VHL. I remember that renosel carcinoma as well can also produce epo as a panoplastica phenomenon. And also like a liver cancer, right? So like epatocellular carcinoma can also produce a epo as a panoplastica phenomenon. Now, what is the, I guess, facial finding that will be associated with lesion to the trigeminal nerve? Well, I really hope you're thinking about like your jaw deviation. Where does your jaw deviate?

Does it deviate towards or away from the lesion? It deviate towards the side of the lesion, right? So again, something to keep in mind just a quick thing to remember there. Now, what would the orifying jaw finding be in a patient that has like a vagus nerve lesion? Think about deviation of the uvula. What do you think? The uvula will deviate towards or away. What do you think? It will deviate away from the side of the lesion. The thing is the path of physiology behind these like two things. Again, this is our rapid review, but I promise when I get to those neuro-comprancival neuro reviews, I'll talk about it, I promise. I'm obsessed with neuro. So we'll talk about it down the line. Okay. Now, what if you get a question about a patient that sort of has like a shoulder droop on the right side so they have like right shoulder droop and then they have difficulty turning their head to the left? What's the cranial nerve that's lesion and on what side? Right? So this patient has a cranial 11 lesion, right? So they have a lesion of the spinal accessory nerve. And if you want to be a little more exact, they'll be a lesion to the right spinal accessory nerve. Because the thing is you have shoulder droop on the hipsilateral side to the lesion. And then you have difficulty turning your head to the contralateral side as the lesion, right? Because remember, one of the muscles you need to turn your head is like your sternoclidomastoid muscle, right?

So it's all screwed up when you have a cranial 11 lesion. So shoulder droop on the hipsilateral side to the lesion cranial nerve. And then you have problems turning your head to the contralateral side. So those are both, those are different ways they can test the same thing. Okay. Now, what is the orifice in geolision that will be associated with the lesion to I guess the hypoglycemoner of the cranial 12? So think more about your tongue deviation. Where does your tongue deviate? It deviates towards the side of the lesion, right? Remember like kind of like licking your wounds. That's a nice fancy way to remember that. Okay. Now, what if you get a question about a Harvard student that sort of presents to the emergency room? And this Harvard student has a facial droop, right? So think of Harvard student, Harvard, Harvard. Where's Harvard? Harvard is embusted, right? So it's in New England, right? So what does this patient have? Well, I hope you're thinking about Bell's palsy, right? So remember like Lyme disease can cause like Bell's palsy. Or remember again, New England. So like Maryland, Connecticut, Boston, New York, potentially, right? Those are new hamshires, right? Main. Those are like classic places where people can get Rhode Island as well. Those are classic places where people can get a Lyme disease, right? So whenever they give you like geography on NV Mes, they're not giving you for the fun of it, right? It actually like means something towards the answer. Okay.

Now, what if you get a question about a patient and they have like pupils that do not respond to light, but they can accommodate? And they tell you that this patient has like a brain stem mass, right? So again, these persons pupils does not respond to light, but the patient has like intact accommodation. And they have like a mass in the brain stem. What kind of mass are you thinking about? Really, we're thinking about like a Pinyloema, right? We'd like Pinyloat Syndrome. Remember, the Pinylo gland is superior to the superior coliculus. And remember that around that superior coliculus area, you also have like your pre-tectone nucleus. And your pre-tectone nucleus, it's like directly above the midbrain. Actually, it's a part of the midbrain. It actually helps with your, what is this reflex called? Your popularity light reflex, okay? So if you have like a mass compressing the superior coliculus, you could potentially involve the pre-tectone nucleus. So you have problems with your popularity light reflex, right? So that's why this patient in this question has pupils that do not necessarily respond to light, okay? Just one of those rare things you want to keep at the back of your mind. Now, what if you get a question about like a bite temporal hemianopsia in a child? What kind of brain mass are you thinking about? Creative fire in Gioema, right? Remember what I talked about it in the previous like a rapid review series?

I think it was like series four, something like that four step one. Remember you add a mantinomatos, a cranioferin giumus. Don't forget the other right from a rackeys pouch, right? So they can compress the optic chiasm and cause a bite temporal hemianopsia. So basically like tonal vision, right? So that's an example of a heteronimus hemianopsia. Okay, now what if you get a question about an adult that has like bite temporal hemianopsia? And let's say they've stopped having the menstrual periods, or let's say it's a guy that has like a gallactoria, so like a guy that's like basically like peanut milk from his breasts. What are you thinking about? I hope you're thinking about a prolactinoma, right? Or if they don't put prolactinomas and anastrochroids, they can put a pituitary adenoma. Remember the most common pituitary adenoma is a prolactinoma. And how do you treat those? I hope you're thinking about like a burglino bromo cryptin, right? Remember, those are dopamine receptor agonist. Remember, I know the name for dopamine is a prolactin inhibiting factor, right? In fact, that is like the first line treatment for prolactinomas. It resolves it in like some ridiculous number, like 80, 90% of people. But if that doesn't work, then you can try like a transphenoidal resection of the pituitary. Okay, so I think that's all I'm going to say there. What is the most common pediatric brain tumor? That's a Pylocytic astrosyptoma, right?

And again, remember, it's classically in the posterior fossa. A cranial farongioma is different though. It's a superatintural mass. But contrast that with a Pylocytic astrosyptoma that's usually in like your posterior fossa, like around like the cerebellum area. Okay? And don't forget your classic arousinthal fibers with a Pylocytic astrosyptoma. Now, what is the most common adult brain tumor? That's glioblastoma, right? So that's GBM, glioblastoma multi-form. Remember, it's a GFAP positive. And the classic way they were described on an MBM is they were described like a mass that's crossing the corpus callusum, right? And it has like a lot of visogenic edema and central necrosis. Look for that boss phrase. If you see that, you really want to think about GBM. GBM is a nasty, nasty, nasty, nasty brain tumor. Okay, now, what if they tell you about a patient that has like a... They tell you that all they perform brain imaging and they find an extra axial mass that has a tail. It has a tail attached to the dura. So it has a dura tail. What kind of brain tumor are you thinking about? Are you be thinking about a meningioma? Okay? Hope you're thinking about a meningioma. M meningiomas, they love to attach to like derivatives of the dura, like the folk cerebrae, for example, right? So if they describe like a parastagetal mass that has a dura tail, you can pretty much stop reading the question. That's a meningioma.

And don't forget that your meningiomas have those fancy schmancy, someoma bodies. That could also be described as laminated calcifications on an MBM example. Okay, now, what if they give you a question about a child that has like... Like the child has to like crank up the TV like really loud so he can hear like doing an MBA game, for example. And they tell you that all the perform brain imaging and they find like by like masses at the cerebellopontin angles, by lottery. What are you thinking about? What syndrome are you thinking about? Well, I hope you're thinking about NF2, right? So like neurofibromatosis type 2. I remember it's again, it's an ozomodominant disorder, chromosome 22 issues. Remember NF2, chromosome 22. And those people, they can get like bilateral acoustic neuromas, right? Actually, it's kind of high you to know that NF2 is not associated with caffeine-related spots. It's just one of those like abranthines, people sort of putting their minds for tests. It's not a thing. The neurofibromatosis syndrome that has caffeine-related spots and like acronurophybromas is NF1. In NF2, you don't have caffeine-related spots. In NF2, you do not have neurofibromas, okay? So those are higher things you want to keep in mind for, for example. Okay, now, what if you get a question about a, and I guess since I talked about NF2, I remember that those people can, they can also get many genomes as well.

But most commonly think about the bilateral acoustic neuromas or acoustic surenomas or whatever. Okay, now, what if you get a question about a child that sort of has like a trunkally taxia? And they tell you that on brain imaging, they see like a mid-cerebellum mass. What tomorrow are you thinking about? I really hope you're thinking about a medulloblastoma. Remember medulloblastomas, they love green in the cerebellum. It's a posterior foisermas. In fact, if I'm not mistaken, it is the second most common pediatric brain tumor after a pylocytic astrocytoma. So, mineraloblastomas, they love to bring the cerebellum, so they almost always present with etaxia. In fact, if you see a question about a kid that's presenting with etaxia, right? And like chronic headaches, I really want you to think about a medulloblastoma. If you don't see a pylocytic astrocytoma as an answer choice. I will say that usually brain tumor in a kid with etaxia, almost like 90 to 95% of the time. On NV Me exams, it's a medulloblastoma. Okay. Now, what if they give you a question about a kid that has a brain tumor and you perform a biopsy and you find a legion that has solid and cystic components? What kind of tumor are you thinking about? This tumor is derived from reky spout. That's a cranial foreign tumor. I'm just basically thinking of this as the brain tumor rapid review. Although, obviously, I'm going to talk about some other high-yield stuff, but this stuff, it's like easy points on an exam.

If you can just recognize the buzzwords. Okay. Now, what if you get a question about an adult? This adult has a lot of like neurological deficits and they tell you that you see a mass in the frontal loop. Notice the loop I'm talking about, the frontal loop. What kind of tumor are you thinking about? It's an oligodendroglioma. Oligodendrogliomas, they can shop in many parts of the brain, but classically on NV Me exams, they shop in the frontal loop. Okay. And remember that they have that fried egg appearance on imaging. I mean, sorry, on histology. So it's one of those things you want to keep at the back of your mind. Okay. And then you see a mass crossing the corpus callosum. Don't forget your GBM, right? Remember this visoginic edema, central necrosis, very high u to know that blue blood stomamotiform. Okay. Now, what is the, I guess, property that underlies an aesthetic having a rapid onset of action? I'll give you a hint. It relates to the blood gas partition coefficient. Would it be a high blood gas partition coefficient or a low blood gas partition coefficient? Okay. If you want to be like, oh, divine, can you explain? I encourage you to go back to my neurofarmacology podcasts. They're like back, back, back on the website. I explain this in like excruciating detail. Basically, if you understand the explanation I give in that podcast, you will never forget the concept. Okay.

Now, what if, what is the, I guess, the property that on the lion and aesthetic have a rapid onset of action? How do I put this? I want to put this in a way that will not confuse you. Okay. Let me put it this way. What if you're trying to compare two anesthetics? Okay. And one has, you know what? I don't want to confuse you guys too much. Let's put it this way. Okay. So what is the property of an aesthetic that will sort of underlie needing like a smaller amount of that an aesthetic for a given like a fixed effect? All of that be. That would be like the lipid solubility, right? If an anesthetic has high lipid solubility, right? That means you can cross the blood-brain barrier pretty easily, right? It will have like, it'll be more potent. Okay. So it will potentially have like a lower map. Now, what if you, so MAC, right, means like minimum of your concentration, because you don't need to give a crap ton of that an aesthetic? Now, what is the anesthetic class that increases the duration of opening of gamma receptors? Right? Those are your barbedo rates, right? So your barbiterates. So like phenobarbital, for example, remember there is no reversal agent for phenobarbital. If a patient has like phenobarbital intoxication, you basically have to intubate them and pray for the best. Okay. Now, what is the anesthetic class that I guess increases the frequency of opening of gamma receptors? Right? That's benzodiazepine, right? Remember the numonic, right?

That Ben likes to have it more frequently and barb likes it to last longer, right? So Ben, right, more frequently increases the frequency of opening, barb last longer, right? So increases the duration of opening of the gamma receptor. Okay. Now, what if a patient, you know, they tell you that this patient was recently intubated and then the temperature is like 105, right? And they have like muscle rigidity. What's your diagnosis? That would be malignant hypothermia, right? So remember, this probably being intubated with something that contains like a succinocholine or like halothene or whatever, and then they get into trouble. And while I'm on this, so they get like the malignant hypothermia, remember, it arises from a person having either like a, it's like an orosomo dominant disorder and it arises if you have like a ryanodin receptor mutation or a dihydropyredine receptor mutation. Okay. And just one quick thing, right? So I guess on the whole topic of a succinocholine. Don't forget that if you're hyper, this will be a question that I can pretty much some ice most people get wrong and named me. But basically if you're hyperarchylemic, you should not get a non, you should not get a depolarizing and your muscular blocking agent like succinocholine. Okay. Because succinocholine right technically keeps the nicotinic acetylcholine receptor like open, right?

So the cell is like, basically like the muscle cell is like basically like wasting its cell soup into the surrounding environment. I talk about this in my neuro pharmacology podcast, but it's just something you want to keep at the back of your mind because if potassium is leaking out of the, remember potassium is an intracellular ion. If it leaks out of the cell, right, you can get a worsening of hyperarchylemia. So that's why these drugs, they are classically contraindicated in patients that have hyperarchylemia, right? So like drugs like succinocholine. And then another like classy one, they can put on an exam is like a recent like burn victim or a patient that has like rapdominolysis. Those patients should also not get any kind of depolarizing your muscular blocking agent. Because remember if you're a burn victim, right, remember burns can cause like muscle damage and whatnot. And if you get muscle damage, muscles can release the potassium into the circulation and that can cause a lot of trouble. Alternatively, if you have rapdominolysis, you have muscle cell necrosis, remember from pathoma whenever a cell dies, right? It can explode, when it explodes, it cells soups, sips into the circulation and that can basically present as a hyperarchylemia, right? So either if you have like legit hyperarchylemia or you have anything that predisposes you to hyperarchylemia, that is essentially a contraindication to get in a depolarizing your muscular blocking agent on an NVME exam.

I know you're like, divine, this seems low yield. I promise you it's not. I won't be saying it if it was low yield. Okay. Now, what is the drug of choice in the treatment of malignant hyperthermia on an NVME? What do you want to give? You want to give like, don't really remember, don't really need basically a calcium channel blocker, right? It basically like block calcium channels and that will present like, because think about it, right? If you block the release of calcium from the sarcoplasmic reticulum, right? The muscle cell will stop because let me put it this way. The thing that causes a lot of the problems in malignant hyperthermia is that you have the mutations in like the reanidine receptor or the dihydroperidine receptor, so you have like the muscle being in a hyper contractile state. So if you blocked the channel that helps you release calcium from the sarcoplasmic reticulum, remember that is the endoplasmic reticulum of muscle, then you do not release that calcium and then the muscle does not contract, right? And that can sort of like dumb down symptoms for a while. Okay. Now, what if they give you a question about a patient that is recently intubated? And then after the intubation, their liver enzymes begin to rise like severely. What kind of anesthetic are you thinking about? I hope you are thinking about how to think. Remember, how to think and cause a hepatic necrosis? Remember the H and how to think for the H and hepatic.

So that is an easy way to remember that for example. And how do you reverse a benzoyl overdose? You give a rubber receptor antagonist like flumasenil. Very good. And what is the reversal agent for an opioid overdose? It is like naloxone or naltrexone. So here is the thing. Your friends at the MBA me have been known to write questions where they put naloxone as an answer choice and they put naltrexone as an answer choice. In the same like five answer choice you see in a loxone and naltrexone, do not pick naltrexone. Naloxone has a faster onset of action. If you give your patient naltrexone and they have what is it called? So you give your patient naltrexone and they have opioid toxicity. Before the naltrexone kicks in your patient will probably be dead. So you do not want to do that. In fact I will tell you this. Naltrexone, classically on MBA me exams, is used in the treatment of alcohol like if a person is addicted to alcohol. That is when you give naltrexone on MBA me exams. You classically do not use naltrexone to treat opioid intoxication. So that is one thing you want to keep at the back of your mind for a test. Very very high you to know that. You want to give naloxone, not naltrexone. Naloxone is like a new opioid receptor and tagineus because remember your friends at the MBA me they love you to know those opioid receptors and their agonist. So remember beta and dorphine is for like the new receptor and caffeine is for the delta receptor.

So it is just one of those things you want to keep at the back of your mind. So the new opioid receptor I believe is a common divine thing. It is the copper receptor and the copper receptor has dynorphine as its agonist. You may see again divine these things are high. I promise you I have seen this that said multiple times. Copper receptor dynorphine as its agonist, delta receptor and caffeine as its agonist. And then the new opioid receptor has beta and dorphine as its endogenous agonist. So these are things that all exist in the brain. And one more weird thing you want to sort of keep at the back of your mind with beta and dorphine is that beta and dorphine is also derived from a compound known as pomc. So pro opioid melanocortin. Why is it important to know about pomc? So pomc is a precursor to three high yield things you want to know for your MBA me exam. You want to know that pomc is a precursor to acth. Okay. Okay. Pomc is a precursor to MSH or melanocytes stimulating hormone and pomc is a precursor to beta and dorphine. And you may see it define how to remember all this crap. Well actually there is a nice way to remember it. If you literally see what pomc stands for, pomc stands for pro opioid melanocortin. If you break down those words, pro opioid opioid. Right. So opioid agonist like beta and dorphine. Pro opioid melanocytes stimulating hormone and then melanocortin. Cortin like a corticotrophine like acth, which is adrenal corticotropic hormone. Okay.

So that's a nice way to sort of remember that if you sort of break it up nicely. And don't forget, right. And there is impome c is important is if a person has like other sense disease, right. So like primary adrenal insufficiency and the adrenal cortex is not working. Right. Those people have like elevated acth because there's no negative feedback from cortisol because they're not making cortisol. But another thing they will have is like skin hyperpigmentation because if you're making acth, right. So the acth has to come from somewhere you can like pull acth from thin air, right. So the acth has really come from like the pomc. If you come from the pomc has you're making a, because you're making a ton of acth, you need to make a ton of pomc. So if you're making a ton of acth, you'll be making a ton of fse, I mean, you'll be making a ton of MSH as well. So you still live your melanocytes and you get the skin hyperpigmentation. And the skin hyperpigmentation is something that can help you tell between primary adrenal insufficiency versus secondary adrenal insufficiency. In fact, one of the series I'll be starting on the USML Step 1 where like literally I covered in detail like I did for like biochem and I've done for renal will be endocrine. I'll start an endocrine review a relatively short. Okay, now what is the enzyme that breaks down soxinocolid? This is just a factoid question to know that'll be pseudo-colonesterase.

And what is the, what is the anesthetic I guess that has this property where the patient who have like no pain. So it's like a great anesthetic. They have no memory of the event but they are completely awake when under anesthesia. So it's like a dissociative and an aesthetic. What kind of drug are you thinking about? I hope you're thinking about a ketamine. And then remember I talked about soxinocolid being a depolarizing near a muscular blocking agent. Don't forget your non-depolarizing, your muscular blocking agent. So these are drugs like the or ending like churronium or churronium. So like churronium, vechurronium, panchurronium, panchurronium is kind of like on shortage because these use for like lethal injections or some red crap. So tubercorcharine is another one as well. Okay. And actually how do opioids work? This is just something that people don't really understand. But you sort of using this question as a leading to another question. So how do opioids work? So you know that opioids are opioid receptor agonist. So like mu receptor agonists. The thing is when you bind to the mu receptor, the thing that happens is the mu receptor is coupled to a signaling cascade that leads to the opening of potassium channels. So when those potassium channels open, right? When those potassium channels open, the cell basically hyperpolarizes, right? Because as the potassium channels open, remember potassium is primarily an intracellular ion.

So the potassium flows out of the cell, the cell stops firing and that sort of quiets down the neuron. Okay. So that is how opioids work. So this is actually why corned in can be used in the treatment of opioid redraw, right? But let me backtrack a little here, right? So I said opioids will act on mu receptors. The act on those mu receptors, those mu receptors cause the opening of potassium channels. And when you open potassium channels, potassium flows out of the cell. So the cell hyperpolarizes and basically shuts down, right? So that's how you know. And the thing is when the cell hyperpolarizes, right, if it's like a sympathetic neuron, right? So like a post gangrionic sympathetic neuron, right? By hyperpolarizing that cell, you have a decreased release of caracolomins, right? So that is sort of how if you understand that mechanism, you'll see why corned in is used in the treatment of opioid redraw. And the reason behind that is cloning in basically works like an opioid. The only thing is it works through a different receptor to achieve the same effect. Because think about it, right? I just said that opioids bind to mu receptor, open up potassium channel, cell hyperpolarizes. If you give cloning, remember cloning is an alpha-2 agonist, right? Remember that those alpha-2 adrenergic receptors are GI coupled, right? So they are kind of G-protein coupled receptor, but they are coupled to an inhibitory G-protein, right?

So when you give cloning, cloning will bind to those alpha-2 receptors. When it binds to those alpha-2 receptors, you'll activate GI, when it activates GI, you'll have like a, basically like a decreased... You basically have like an inhibition of a denolid cycle, so you mix E-clique and Piano, all that stuff. So that will sort of cause like hyperpolarization of the neuron, right? And if you hyperpolarize that neuron, then you will stop releasing caracolomids, right? So basically it's like cloning in is acting like... ...is giving you the same ultimate effect, decreased release of Norepinephrine from a neuron. But it's acting through like a different signaling cascade, through a different receptor. So it's walking through an alpha-2 receptor versus an opioid that works through a mu receptor. In fact, that's why cloning is like a straight drug, because basically if you're going through opioid withdrawal, if you take cloning in, most of those symptoms will effectively disappear, okay? So that's one thing to keep in mind. And while I'm on this topic, a brilliant idea just came into my mind. A closely related concept where you get the same effect from something through two different receptors, is also the concept of treating like an overdose of a beta blocker. So remember, beta receptors, especially like beta-2 receptors, those receptors, they work through a G protein coupled receptor as well, right?

So if for example you give a beta agonist, you can act on that beta-2 receptor, activate G-sobess, you activate a dendrit cycle, you make more cyclic AMP, and all that fun stuff, right? So the thing is, if a person overdoses on a beta blocker, one problem they have is basically, if you look downstream of the receptor, they have decreased activity of cyclic AMP, because they're not making as much cyclic AMP, right? So that's a problem. So if you could potentially give something that will act on a different kind of receptor that is not a beta receptor, or would basically prop up your levels of cyclic AMP, then that can fix a beta blocker overdose, right? So the classic drug in this case would be glucagon, right? Glucagon acts on a glucagon receptor, and it so happens that that glucagon receptor is G, is a G protein coupled receptor, and it's G-S coupled, right? So when glucagon acts on that G protein coupled receptor, that will increase the release of cyclic AMP. So basically getting like a beta agonist-like effect, we are getting it through a different receptor. That is the mechanism behind glucagon being the reversal agent for overdose on a beta blocker. Okay? So I know, rumbled, rumbled, rumbled for a bit, but I promise you all these things are floridly high yield for the USML exams. Okay, and I promise I will be ending this podcast on Relative Edition, right? And then I guess some easy questions to round things out. What is the model area of the cerebral cortex?

That's the pre-central gyros, right? And then what's the sensory area of the cerebral cortex? Now be the post-central gyros, right? That's pretty easy. Now let's do some vascular stuff real quick. What is the arterial lesion that will lead to like a contralateral low-extravity, like weakness and paralysis? Now be the anterior cerebral artery, right? Because remember, if you look at your homonculus, right? So like in the middle of the brain, like sort of close to the middle of the cerebral cortex, sort of close to the fork, cerebral right? That's where you have like your leg area in the homonculus. And remember that leg area is supplied by the anterior cerebral artery, right? So if you have like a stroke of the anterior cerebral artery, that can cause a contralateral lower extremity weakness, right? Because remember, if you infarge that part of your cerebral cortex, the reason you get contralateral symptoms is because remember that your... What is it called? Your corticospinal tract will study in the cortex, but it will take you say that the level of the pyramids, right? So because of that deaccusation, right? You have like contralateral symptoms. Okay. Now what is the arterial lesion that can... that will lead to like upper extremity or like facial weakness and paralysis? What kind of artery are you thinking about? That's the middle cerebral artery, right? The MCA. Because again, think about your homonculus, your face and arm area is in MCA territory.

And remember, this is actually a factor you want to know with regards to the middle cerebral artery. Whenever a person has an embolic stroke, the most commonly occluded artery is the middle cerebral artery. Okay. Now what if you get a question about a patient that can understand what is spoken, but they start in response. What kind of aphasia do they have? That is Broca's aphasia. Okay. Good. Now what if you get a question about a patient that you know speaks fluently, but basically says gibberish, right? So most of what he says is like senseless. What kind of aphasia is that? That's a... where any keys aphasia. Okay. So that's more of like a sensory aphasia versus Broca that's more of like an expressive aphasia. Okay. Now if a patient has a lesion to the frontal eye field, in what direction will their eyes deviate? The eye will actually deviate towards the lesion side, right? So let's just sort of walk through this, right? So let's talk about the normal first. So basically your frontal eye field projects it in your cerebral cortex, it projects to the contralateral, a PPRF, the contralateral, paramedian, pontine reticular formation, and then the contralateral PPRF activates the... So this is looking from the perspective of the PPRF, the contralateral PPRF will signal to like the abducense nucleus on the same side. So cranial six on the same side as the PPRF and cranial three on the opposing side as the PPRF.

So I think to make things a little clearer, let's just pick one side. Let's say we're talking about the right frontal eye field. Your right frontal eye field, which is in the cerebral cortex, projects to your left paramedian pontine reticular formation. And your left paramedian pontine reticular formation, projects to your left abducense nerve, and your right oculumuro nerve. Because the whole point behind that system is if you want to have like conjugate horizontal gaze, because think about it. If your right frontal eye field projects to your left paramedian pontine reticular formation, and your left paramedian pontine reticular formation, and your right oculumuro nerve, by projecting to your left abducense nerve, that means your lateral rectus for your left eye will be abducted. And then by projecting to your right oculumuro nerve, that means your medirectus for your right eye will cause abduction. So you have abduction of your left eye and abduction of your right eye. So that means you basically look to the left. So your right frontal eye field controls your ability to look left. Right again, right frontal eye field, left paramedian pontine reticular formation, left paramedian pontine reticular formation, left paramedian pontine reticular formation, left paramedian pontine reticular formation, and your right frontal eye field gives you the ability to look to the left. So think about it.

If you lesion your right frontal eye field, there's actually one of these things that are high out for step one, and also high out for step two, and your neuroshelf in third year. Okay, now what if a patient has a lesion to the pprf, in what direction will their eyes deviate? What do you think? Your eyes will actually deviate away from the side of the lesion, right? So again, very easy if you understood what I just explained. Your left pprf controls your left cranial six, and your right cranial three. Okay, and your left cranial six will cause a b-duction of your left eye, and your right cranial three will cause a d-duction of your right eye. So your pprf on your left side makes you look left. So if you have a lesion to your pprf, you lose the ability to look left, so your eyes will deviate right. So your eyes will deviate away from the side of the lesion. These are things I highly recommend, just sort of write it down, and try to like reason three to yourself as well, it will make sense. Okay, I know I've explained this in like maybe two or three of the podcasts in the past. Whenever I devote like multiple podcasts to explain the same concept, that should probably tell you something about the importance of that question on an MBA meexcept. Okay, now, what is the special sensation, right? So like special sensations like, special sensations of like smell of taste and all that stuff. What is a special sensation that does not have a really new clearest in the thalamus?

That's actually the sensation of smell. Okay, and then just I guess one thing I'll just say around this, because I feel like this is probably going on for a little longer than I planned for. But basically if you have, if you have like a lesion to like your prefrontal cortex, you'll basically begin to have like reemergence of like primitive reflexes. So I think I'm going to go ahead and stop here. And again, as I round up, I do offer one and one tutoring for the USML Step 1, two CK, two CS and Step 3, and then like pre-clinical medical exams, and then like third year shelf exams, and what else like tutor? I also tutor like the medicine, training exam, and the medicine board exam, so like for medicine residents, you may say to find, how do you tutor these things? And you're just a TY. Just send me an email and I'll do some explaining. And then if you're a college student applying to med school so like an Amcass application or a med student applying to residency, so an ERAS application, I do offer like consulting for that, like interview prep, personal statements, preparing your application, because I mean, I've been on the admissions committee for a top two med school for a year, so I have a lot of experience with that. And like I said, this current cycle of people that just matched, pretty much everyone advised, matched, so I guess I'll take that for all you will.

And then if you rarely have like an acquaintance, that's a studying for like organic chemistry, or general chemistry of physics, or physiology, or biochem, I do offer tutoring for those things. I'll have a wonderful rest of your day. And I'll see you in the next podcast. Have a great week and God bless you. Thanks.

VHL syndrome (Von Hippel-Lindau). Remember that they can produce EPO as a paraneoplastic phenomenon.

Meningioma. The "dura tail" is highly suggestive of this diagnosis.

Vagus nerve (CN X) lesion. This is due to paresis affecting the pharyngeal muscles.

Craniopharyngioma. It compresses the optic chiasm.

ACTH, MSH (Melanocyte Stimulating Hormone), and Beta-endorphin.

Wernicke's aphasia (Sensory/Receptive Aphasia).

Primary AI will show skin hyperpigmentation because ACTH must be produced by the pituitary, and high ACTH levels stimulate melanocytes via MSH.

Ataxia (truncal ataxia) and chronic headaches; it loves the cerebellum/posterior fossa.

High lipid solubility, allowing easy crossing of the blood-brain barrier.

Binding to $\mu$-receptors opens potassium channels ($\text{K}^+$ efflux), causing the cell membrane potential to become more negative (hyperpolarized).

Bilateral acoustic neuromas and association with chromosome 22 deletion.

Naloxone. Naltrexone is primarily used for alcohol addiction; naloxone has a faster onset of action required in acute intoxication.

Oligodendroglioma.

Pinyloblastoma/Superior colliculus compression. The pre-tectal nucleus is involved in the pupillary light reflex pathway.

Ataxia (truncal ataxia) and chronic headaches; it loves the cerebellum/posterior fossa.

High lipid solubility, allowing easy crossing of the blood-brain barrier.

Binding to $\mu$-receptors opens potassium channels ($\text{K}^+$ efflux), causing the cell membrane potential to become more negative (hyperpolarized).

Bilateral acoustic neuromas and association with chromosome 22 deletion.

Naloxone. Naltrexone is primarily used for alcohol addiction; naloxone has a faster onset of action required in acute intoxication.

Oligodendroglioma.

Pinyloblastoma/Superior colliculus compression. The pre-tectal nucleus is involved in the pupillary light reflex pathway.