DIP Episode 105 - USMLE Step 1 Rapid Review Series 7 (Neuro)

Okay, welcome. My name is Divine. I am a PGY1 transitional year resident that's ultimately going into ideology. This would be the 105th episode of the Divine intervention podcasts. And in today's podcast, I'll be doing a rapid review series for the USML Step 1. So this will be Series 7. And I'll be focusing again on New Year. And again, like I said, these rapid review series. It's why I basically talk about the classic clinical presentations of things on NBME exams. So let's jump right into it. So what if you get a question about a lady that she has like, you know, a few days of like painful vision, blurry vision, and she has kind of like scanning speech. That's another boss phrase. What are you thinking about? Well, I hope you're thinking about multiple sclerosis. Right? Remember, that's a central. Excuse me. Excuse me. That's a central demilaneet in the solder. Okay. Now, what if you get a question about a patient that is beginning to forget things? They don't remember where their drawer is and they get lost on the way back from the store. And you get an MMSE and it's like 22 over 30. And this people like like 35 years old. But let's assume that these people have like, they have like a single parmarx crease and stuff like that. What are you thinking about? I really hope you're thinking about Alzheimer's, right? So remember early on set Alzheimer's like this. You really want to think about the association with a with a Down syndrome. Okay.

Now, what if you get a question about an archaeologist? You know, he studies Asian animals. And then they tell you that over the last like six weeks, he's become like super forgetful. And then they tell you that on physical exam, this patient has myoclonus. What kind of rapidly progressive disease are you thinking about? Well, I hope you're thinking about crow's feldiacop disease, right? That's the classic presentation. The almost always put the the myoclonus that's evident on physical exam. And it's a rapidly progressive dementia, right? And remember that crow's feldiacop disease. It's associated with elevated levels of the protein known as 1433 in the CSF. That's a very high your piece of trivia. You want to know for the USMLA exams. Okay. Now, what if you get a question about a person patient that has like a you know, like a family, he's strong like chronic liver disease. And then this patient has like a movement disorder down the line. Later in life, especially like in their teenage years, what kind of what what are you thinking about? Right? I hope you think about Wilson's disease. Remember Wilson's disease a copper metabolism problem, right? Sort of screws up your liver. Sort of screws up the bizzle ganglia as well, right? And then remember your classic a Kaiser fly sharing when you're looking at the person's eyes. And also, please don't forget that Wilson's disease. You can sort of make the diagnosis by checking serum levels of seroplasmic, right?

And you can actually trade Wilson's disease with an agent known as a try and team. So T R I E N T I N E, or you can use zinc as well. Okay? Very high your to no those. Now, what is the drug of choice used in the treatment of absentee. That's if the soxamide, right? And what's the classic EEG finding in a kid with absentee. You do it up sun seizures, right? That's the three hertz spike and weave pattern, right? Remember, um, the way it presents is like the describe absentee. Is like a kid that's not paying attention in school or has like these multiple staring spells during the day, right? That's an absentee. So many kids grow out of it. But yeah, you can treat it with it. If those soxamide remember that if those soxamide is a tea type calcium channel blocker. Very high you remember that versus your cardiac calcium channel blockers, right? Your entire it makes your class two agents. No, sorry. Really a class two your class four agents that are L type calcium channel blockers. Again, those are evil things that your friends at the NBME could do to you on an exam. Now, what is the most, I guess, consenere involving like I guess hearing loss in the order of your NBME? That's press by Q says right? That's press guy press by Q says so that's basically like a high frequency here in loss. Okay, now what is the most common cause like in trying to get in in things of mechanism, right? For central or it no later occlusion right it's a symbolic phenomena. Okay, it's a symbolic phenomena.

One thing I would just encourage you to sort of keep at the back of your mind is the classic quick central or it no later occlusion presents versus central or it no longer occlusion, right? So the thing is if you talk about like sodium onset loss of vision and the patient has like fondle power, right? So let's say you perform a funoscopy exam and you note like power of like the optic disc. That's a central or it no later occlusion, right? But if you see like engorge vessels, blood and thunder, appearance and all that crap, you're thinking more about a central or it no Venus occlusion. I would encourage you if you're listening to this podcast and you're taking like an exam that will likely test like neuro, opthal, whatever. I would encourage you to listen to the ophthalmology podcast. I have a podcast that's specifically for ophthalmology and it basically covers essentially all the high ophthalgies you could see tested on a USMLE exam. Okay, now what if you get a question about a patient that you know has a detail that when she wakes up in the morning, she feels like the room is spinning around her when she turns her head to one side, she feels like the room is spinning around her. And she does not have hearing loss, but she has like really bad ready go, no hearing loss. What disease are you thinking about? This is BPPV, right? So benign positional, no benign peraccessimal positional, right? So positional means changes in position triggered disease positional ready go.

Okay, that's BPPV. And remember it sort of arises because your or your or your or your or let's right sort of like displays from the anomalous locations. Now, what if they give you a question about like a six month old kid that has that has a fast calculations and is not medium auto milestones. What are you thinking about? That's where the cough man disease, right? So that's like your spinal most philanthropy. Remember it's an autozomer recessive disorder, right? And it arises from having issues in chromosome five, the survivor of motor neurone 1 G. If you see fast calculations in a little kid, you can pretty much stop reading the question. It's spinal most philanthropy also called redney cough man disease. Remember it tends to affect the anterior horn of the spinal cord or you can also call that the ventral horn of the spinal cord. So present primarily with lower motor neuron symptoms. Okay. Now, what if you get a question about a patient, you know, that's being treated for TB. And then it sort of develops like a tingling sensation in his upper extremities. What are you thinking about? I hope you're thinking about like the peripheral neuropathy or with isonias it, right? That's why for person is being treated with isonias it for TB. What kind of vitamin should they be on? That would be vitamin B6, right? Vitamin B6 or pyrodoxyl or phosphate. Very high. You'll know that. Okay.

Remember that isonias it right can also cause a cerebral elastic anemia because remember in the synthesis of remember that he is made of iron and proto porphry. So one of those him components, proto porphry is made through like the kind of like the him synthesis pathway. Right. And remember that the first enzyme in that pathway is alas, right? So amino level, liniac acid synthetase. And that takes like glycine from non mistaken and then ultimately converts it to things like glycine and succ, glycine and succino coa from non mistaken and takes those two and then ultimately converts. Wait, is it glycine and succ, oh, but I talk about it my biochem podcast, but it takes two things uses vitamin B6 as a cofactor and makes delta amino level liniac acid synthetase. So that enzyme again uses some uses a vitamin B6 as a cofactor. So if you take isonias it, you depleted vitamin B6. You don't have cofactor for alas. You don't need proto porphry. So you get a cerebral elastic anemia. Okay. Remember that isonias it can also cause seizures. Right. So easy way to remember this is I and each is neurotoxic. So I isonias it and each because that's what's called it's called in the hospital. So I and each and for neurotoxicity H4 hepato toxicities also hepato toxic. But yeah, the neurotoxicity is the peripheral neuropathy. But please also don't forget the classic seizures. Remember if remember that glutamate is excitatory to the brain.

Gaba is inhibitory to the brain and inhibitory neurotransmitter. But the thing is it so happens that GABA is made from glutamate by an enzyme known as a glutamate decarboxyls. So glutamate decarboxyls converts glutamate to GABA. But it so happens that glutamate decarboxyls uses a vitamin B6 as a cofactor. So if you have a B6 deficiency, then glutamate decarboxyls doesn't work. And if it doesn't work, then you cannot convert glutamates to GABA. So glutamate will build up and that can cause seizures. So that's the potential pathophysiology behind isonias it potentially causing seizures in patients that are taking it for TB. And then remember that you make antibodies against glutamate decarboxyls. So anti-gather antibodies in type 1 diabetes. So like insulin dependent, let's call it type 1 diabetes. So like the autoimmune diabetes if you may. Now, one last thing I want to say about isonias it. Remember that isonias it is also associated with drug induced lupus. I don't know why isonias it and it's high yield. USMD connections are just sort of bumping in my mind this morning. But isonias it is a drug induced lupus. So that's one thing I want to keep in mind. And actually I for one more thing about isonias it is you see this whole ishrabal people that have problems with metabolizing isonias it. With like slow acid and later and faster as early later as acid and later. Right with those by model it's like a classic example of a by model distribution.

That's like a very classic m m equation where the essentially infused isonias it for describing it like give you a question that describes a bio statistical phenomenon. Right. Another way to do that seem like by model distribution concept is what is it called is with lymphomas. I believe it from let me speak with like the hotkins lymphomas because they shop in young people and then they shop in the incidents sort of dies down significantly and boom it then shows up in old people as well. So just something to keep at the back of your mind. Okay. Now what are the bugs I guess that are associated with CNS lymphomas in patients that I'm not compromised right that's HIV and EBV. Okay. Now what is the part of the brain. They love to test this on step one step two step three even and then they love this on the side shelf and the neural shelf in 30 for some reason. What's the part of the brain that's that degenerates in Alzheimer's disease. So think about it. Let me lead you to the answer. What's the neurotransmitter that is low in Alzheimer's. That's a pseudo calling right I mean it makes sense. That's why you know that a pseudo Alzheimer's you treat it with with colonnestries inhibitors right because I'm inhibiting colonnestries you build up your levels of a pseudo calling and you can sort of help help her almost like you're basically like treating the pathophysiology right so like don't epithelial gallantamine, reverse dig mean those are your classic a colonnestries inhibitors.

Remember that a pseudo calling is actually meeting the bison nucleus of minor. Okay. Minority spelled as MEY and ERT. So if you have a deficiency of acetylcholine if you if you basically destroy the bison nucleus of minor right we are. So colonnest produced that's kind of indicated in the pathophysiology of Alzheimer's. Okay. Now what is the disease that's associated with like you know like a ton of demilination in the central nervous system and then they tell you that all this person is accumulating like long chain fatty acids. That's a adrenal local dystrophy right. Okay. Now what if you get a question about I guess since we're talking about in my initial what is like the big big big demilinating disease of the peripheral nervous system that you know can affect shuan cells and it can arise after you have like an upper respiratory infection or you have like bloody diarrhea with a Campylo-Bacteria Juno.

That's Guillemboris syndrome right already talked about MS affecting oligodendrocytes right it's like the big big big demilinating disorder of the central nervous system on MB Ms and remember that your cranial nerves all of them but cranial to at the right from from neuro crest right so in general MS the classic cranial nerve it affects because remember MS is a central demilinating disorder the classic the classic what I want to say here the classic cranial nerve that's affected by MS is cranial to because the optic nerve actually does not come from neuro crest and actually comes from neuro tube remember cranial nerve trees are derivative of the diencephalon. Okay. Now what if the the give you a question about a patient that has complete like parapige on one side of the body and then they tell you that oh on imaging they say like an an infact in the posterior limb of the internal capsule what's the vessel that's all screwed up.

That's the lenticular stride artery right remember it's one of those branches of the middle cerebro but the lenticular stride artery supplies the posterior limb of the internal capsule so if a person has problems with the lenticular stride artery right so some classical name is decoded a shackle bushard micranyorism that can lead to issues with the posterior limb of the internal capsule remember that you're descending a corticospinal tract right so those fibers also like come together and squeeze in that posterior limb of the internal capsule and then go down and remember that those fibers that you say try the level of the medallary pyramids so because there's a decusation you have like contra lateral so let's say your left posterior limb of the internal capsule is all screwed up you have like your right like your your your upper and your lower extremities on the right to be knocked out okay and remember that will be an open motor neuron problem right so like hyper reflexia increase muscle tone and stuff like that okay now what if they give you a question about a patient that has they tell you that all that he became very weak and his speech was slurred for like five minutes and then he returned completely back to baseline and then they asked for your next step in diagnosis right so obviously this patient has a TIA right and for those patients you want to go ahead and do a caraded ultrasound on NVME exams and I'll say that usually for person has like a TIA they will usually tell you that all CT was done and it was negative or whatever but if they've not done a caraded ultrasound I will encourage you to get the caraded ultrasound that is usually the correct answer like 95% of the time on NVME exams okay now what if I guess if a person so this is a basic science question again that you love to test on like like the neuro like shelf exam that people taking like the first

years of medical what if a person and if you ever see me say like neuro shelf I mean the third year neurology shelf example like the actual neuro clerkship but if you ever see me saying you're like if I'm referring to the neuro shelf in the like preclinical years I will be very specific I like see that right now so this is like a neuro preclinical shelf are kind of kind of deal what do you tell you about a patient and the describe the scenario the person has a brain infarction and the ask you for the kind of necrosis that's associated with infarction of the brain what kind of necrosis is that that's actually like with active necrosis right that's like with active necrosis okay now what if a patient you know gets in an accident and they have like contusion of the cerebral cortex at the site of impact what kind of injury is that called that's a cool injury right so like CO U P right but if you haven't like contusions of the cerebral cortex on the opposite side that's a contract cool so C O N T R E C O U P injury okay so just something to keep in mind now what if they tell you about a patient they tell you that this patient is CD4 count is 50 and the tell you that own brain CT you find like ring enhancing lesions on MRI you see ring enhancing lesions and this patient CD4 count is 50 what's the bug you're thinking about I hope you're thinking about toxoplasma gondii right a toxoplasma gondii remember your magic CD4 count right so if you person has eats CD4 count less than 200 you should give them TMP SMX so try method from a thox is all to cover them against the necrosis is your vetsi right if you're using for count drops below 100 right you want to cover against toxoplasma gondii okay and you also do that with TMP SMX but if a person has toxoplasmosis right you definitely want to treat them with Pyramethamine and Sofodysine okay that is the correct answer on Indian is n

ot TMP SMX Pyramethamine and Sofodysine TMP SMX is for prophylaxis Pyramethamine and Sofodysine is for treatment okay now what if they and the thing is if a lady is pregnant and she has toxoplasmosis you can treat with a drug known as Pyramysine just something to keep in mind that's probably lower yield but it definitely does show up occasionally in exams okay now what is the bacterial infection that will be associated with a positive rhombus test double neuro syphilis right remember it causes a TBS Dorsalis so it screws up your Dorsal column amelial and niscasa system okay now what if they give you a question about a patient that has like like eye pain and then they tell you like they also have like you see vesicles in their ears that's a kind of like herpes right so that's like almost like shingles of the face they call it I believe it's known as a Ramsey hern like Ramsey hunt syndrome again classic just one of those really like what what is this and it's an actual thing you see on the exam so keep that in the back of your mind remember right herpes skin vesicles from a tumble distribution right now what if they talk about a patient that has like hemorrhagic macrosis of the temporal lobes what bug are you thinking about that's HSV right that's HSV as well remember that's why if a person has like meningel symptoms like no corgi to know that crap and then let's say you do like a lumber puncture and you see like a lot of red blood cells right you kind of want to think about herpes right it's classically known on mbm is to cause a they tell you that all you do CSF studies and you see like 600 red blood cells you want to think about herpes on the little circumstances what if the person presents with like the worst headache of the life and the LP shows like a ton of red blood cells that could also be a sub-rocknery hemorrhage okay so kind of look at the clinical picture t

o be able to sort of like tie things together and make the right diagnosis okay and because HSV right and cause like hemorrhagic macrosis of the temporal lobes that's why on a lumber puncture it can actually potentially see like blood okay I mean C-ray blood cells now what if they tell you about a patient that you know they tell you that all that she has trouble keeping eyes open in the evening and she's been having like some difficulty swallowing what kind of disease are you thinking about that be my Estinia Graves right so remember that's where you're making like auto antibodies against the acetylcholine receptor other neuromuscular junction okay now what if a patient always fall sleep eater feel sleepy during the day and then he has like occasionally has like like let's assume he's laughing with his friends and boom he just sort of falls to the ground or sometimes he has like syncopal episodes during the day let's think of them as like pseudo syncopal episodes during the day what are you thinking about right that's that's narcolepsy right that's a narcolepsy okay so basically the whole thing about where they lose most auto with the left that's what's known as a carablexi and remember that you can treat a narcolepsy with a drug known as a sodium oxybit on mbms just something to keep in mind and then what's what's the source what's the cell that makes CSF right those are your core plexus cells right those are your core in a plexus cells okay now what if they tell you that chest x-rays is showing like a long mass in a patient with toses myosis and antidropses right that's a painful struma right that's pretty easy please don't get that wrong it's like a like a mass in the epics of the lung that's causing a hornar syndrome what's the kind of headache that's as you know the passion hornar syndrome that's a that's a cluster headache right okay now what is the most common

cause of permanent vision loss in the elderly that's actually a rmd right so like macular degeneration remember there's the wet type and there's the dry type the wet type is the one you treat with like a vegeph inhibitor right so like the vasizumap or like random bisumap the dry type you can try like vitamin E antioxidants and all that crap okay and what if they tell you about a patient that you know they cannot extend their toes and they cannot either or dorsiflex their foot what's the nerve that's all screwed up so basically patients have food drop what's going on here that's the common perineal nerve right that's being screwed up right so remember if a person has foot drop right so dropped that's a nice demonic there dropped right you lose you have problems with like evening your foot and dorsiflexing your foot so those are the last two letters and then the pee you should help you remember there's the common pair or new nerve okay remember that's like L4 to S2 and then what if they describe a kid a newborn that has like a waiter's tip the formatee right that's herb de shane paulsey the classic video presents that question is it can be an infant of a diabetic mother right so that kid may have like macrosomy and stuff like that's like things that may be big that predispose the baby to getting those kinds of problems in the process of delivery and remember that's c5 c6 that's all screwed up okay so I think I'm gonna go ahead and stop here it's about time where I go to work you probably know my schedule at this point from my pattern of podcasting the last few days if you just get up at 4.30 pray and then make a podcast and then prepare for work so I'll see in the next podcast as I always do before I round up I go for one on one tutoring for all the usml exams step one two ck two cs step three and then the medicine training exam medicine board exams pre clinical med sch

ool exams 30-year-shelf exams and also a bunch of like college classes so like physics, jenkem, okem, biochem, physiology, histology, stuff like that and then if you're a medicine or plant or residency so like an irisap or college and applying to med school like an amk sap I go for one on one like consulting for those so like application prep, mocking reviews, writing personal statements and stuff like that I've been on an admissions committee for a top two med school for a year so I've shifted through thousands of solid applications and I know the things that make you stand out so if you need help with any of those things don't be afraid to reach out have a wonderful day God bless you and I'll see you in the next podcast thank you

Engorged vessels and "blood and thunder" appearance (due to venous congestion).

Rapidly progressive cognitive decline in an older adult; CSF testing often shows elevated 14-3-3 protein.

Liver dysfunction/disease, basal ganglia involvement (movement disorder), and Kayser-Fleischer rings.

Vitamin B6 (Pyridoxine).

Common peroneal nerve injury/compression.

Cluster headache (due to Horner's syndrome).

Issues in Chromosome 5.

Acetylcholine; Cholinesterase inhibitors (e.g., Donepezil).

Displacement of otoconia (calcium carbonate crystals) from the utricle into the semicircular canals.

Lenticulostriate artery; Leads to an open motor neuron problem (e.g., right-sided weakness with hyperreflexia).

Pyrimethamine and Sulfadiazine.

Ethosuximide (or similar T-type CCB); It differentiates it from cardiac L-type CC Bs.

Issues in Chromosome 5.

Acetylcholine; Cholinesterase inhibitors (e.g., Donepezil).

Displacement of otoconia (calcium carbonate crystals) from the utricle into the semicircular canals.

Lenticulostriate artery; Leads to an open motor neuron problem (e.g., right-sided weakness with hyperreflexia).

Pyrimethamine and Sulfadiazine.

Ethosuximide (or similar T-type CCB); It differentiates it from cardiac L-type CC Bs.