DIP Episode 59 - Neurology Clerkship Shelf Review Part 8 (Final Part)

Okay, welcome. My name is Divine. I am a PGY1 transitional year resident and this is the 59th episode of the Divine Intervention Podcast and I'm actually pretty excited this morning. I'm going to be completing the Neurologic or Khipa review series, right? So this will be part 8 and this is actually going to be the final part. Very high yield lecture and I'll try to make it as short and as quick as possible. Although there's lots of high yield stuff here. So we'll see how that goes. Okay, so the first slide, right? So it says a parastegias in a patient who is being treated for TB. Well, I really hope you're thinking about isoniasitoxicity. Remember, you can prevent that by giving a vitamin B6, right? Which is also an aspiridoxal phosphate. And then the next one says parastegias and lots of joint and position sense. Okay, in addition to like low extremity hyperreflexia in a patient with a 15 year history of polytreated Crohn's disease, right? So I'm asking for the diagnosis, what kind of testing do you do and how do you treat this? Right? So this is obviously B12 deficiency, right? Remember Crohn's disease loves to torch the terminal ilium, right? And that's where B12 is reabsorbed in addition with its partner, I guess, intrinsic factor. Okay, and remember that B12 can cause like a subacute combined degeneration of the cord, right? So basically you scrub your dorsal column, medial laminuscus system, it doesn't work.

And then you also scrub the lateral corticospinal tract, right? So basically if you have a subacute combined degeneration, you have like lots of vibration, fine touch, preperception, right? And then you also have upper moron neurons symptoms, right? So like spasticity and like hyperreflexia, right? Because your lateral corticospinal tract constitutes the upper moron neurons for those low moron neurons that you find in the anterior horn of the spinal cord. And I mean, there are many like surrogate tests you can use to diagnose B12 deficiency, right? I mean like if a non-stickin would potentially check a B12 level, don't really show about that. But I'll see classically on exams, right? They may give you a person that has like a macrosidic anemia. If you want to be a little more specific, they potentially have like a megaloglastic anemia, right? And you also have elevated levels of methylmalonic acid, right? Remember, if you want to convert methylmaloneauquay to succinoquay, you need an enzyme known as a methylmaloneauquay in mutates, and that depends on what I mean B12 as a cofactor. And then there's this other test, no one pretty much no one does it in the real world anymore, but it shows up actually quite commonly on NBM means, okay? The shilling test, I mean there are many steps, but it's basically like a fancy way of figuring out the cause of a B12 deficiency, right?

And the thing you really do, and I'll give you like the Clifsonose version of this test, at least tell you what you generally need to know for exams. Basically you inject B12 into a human being, right? You basically saturate every store of B12 in the body, okay? And then after you've saturated them with like IVB12, you then give them OROB12, right? Because everywhere is saturated, you expect to find the B12 that you just give them in the urine, you give them like radio labeled B12, supposed to find in the urine, right? So, let's say you give the OROB12, you're like, wait, I'm not seeing any B12 in the urine, what's up with that? Right? I'll say there are many potential causes for that, but on exams you probably think of two major ones. One is pernishacinemia, okay? Well, another one could be that you have a disease in the terminal helium, right? Classically from like Crohn's or like Tropical Spur, for example, okay? So the next step is you give them that radio labeled OROB12, and then you give them intrinsic factor, okay? Radio labeled OROB12 within intrinsic factor, and if that essentially, if you're giving intrinsic factor and you're like, oh wait, I can see all this B12 in the urine now, right? You then know that the indienent pernishacinemia, because the addition of intrinsic factor, fix the problem. But if you give intrinsic factor and it does not fix the problem, probably think about more of a terminal helium disease, okay?

And I'm not going to go into this right now, but if you have an absorption defect in the GI tract, you have something known as an abnormal DZLOS test, okay? So, it's just one of those weird things you kind of want to keep at the back of your mind. And obviously, if a patient has B12 deficiency, you should clearly give vitamin B12, right? Okay, now next one says, ataxia and hemolybic anemia in a patient with a history of A-beta-lipoprotinemia, okay? And a brain MRI is revealing cerebelli atrophy. This is kind of a weird one, and it's one that many people get wrong on exams for some reason, but it's actually kind of high yield. And this is actually a vitamin E deficiency, okay? So, vitamin E deficiency. I remember that if you have A-beta-lipoprotinemia, please don't forget that's an autosomal recessive disease. You have a deficiency in something known as a micro-somal transfer protein. I believe I've talked about that in a previous podcast, or I will talk about it in a previous podcast. So, you basically cannot make Epo B48 and Epo B100, right? So, you essentially have troubles like exporting like kylomycrons and LDL and stuff, right? And you have all the parts of the body. And if you have those issues, obviously, right? You're basically not able to move like fatty products around, right? So, like your fat soluble vitamins, for example, like vitamins A, D, E, and K.

So, that can cause a vitamin E deficiency and vitamin E deficiencies can cause like hemolybic anemia, they can cause problems with the cerebellum, right? So, patients with vitamin E deficiencies tend to get it taxi and whatnot, okay? And please don't forget the association between E-beta-lipoprotenemia and acampusitis on a bloodstream. That's a very high-eat hematologic association. You sort of want to keep at the back of your mind. Now, the next one says, mammillary body infarcts in a chronic alcoholic, right? So, you're thinking of maybe like grannies or something like that. But alcoholism, right, is classically associated with a B1 deficiency, a thiamine deficiency, right? So, like this enzyme, transkydolids, right? From the non-oxidivity phase of the HMP shunt, also called the pentosephosphate pathway, doesn't work so well, right? So, you can have like infarction of the mammillary bodies. And then, the next question, let's see, there's so many things here. So, dermatitis and dementia in a patient with a long history of carcinoid syndrome, right? So, if you have carcinoid syndrome, right? You have a tumor that's secreting at ton of serotonin. Remember, the most common location is in the appendix, right? So, if you have carcinoid syndrome, you have a secreting at a crap ton of serotonin. Remember that serotonin is also known as 5-HT, 5-hydroxy-triptofen, right? So, that tells you right of the bad that it comes from triptofen. And if serotonin comes from triptofen, right?

If you have a tumor that's secreting at ton of serotonin, right? You see a ton, you're basically diverting all your triptofen to the production of serotonin. So, the triptofen will not be diverted towards the production of niacin, which is vitamin B3. So, you can have pelagra, right? Which is what the patient has, right? Which has the 4 Ds, right? Like dermatitis, diarrhea, dementia, and the bad D, which is death. And then, also, don't forget that if a patient has heart and op disease, remember, it's like a... It's a amino acid, a neutral amino acid, transport a defect. You don't reabsorb neutral amino acids like triptofen, right? That can also go ahead and cause a carcinoid... I mean, that can also cause a pelagra, right? Because, again, you're not reabsorbing the feedstock that you need for the production of niacin, which is vitamin B3. Okay, and remember the way you diagnose carcinoyous syndrome is by checking for 5 HIA in the urine, right? That's a metabolic tough of serotonin. Okay, now, the next one says, child with chronic abdominal pain and food drop, whoever the past six months has been performing poorly in school. Okay, that's not good. Right, so food drop, abdominal pain, this is a classic, classic, classic, and BME presentation. It's pretty classic for lead poisoning, right? Remember that on exams, you may also see, like, they may give you a picture of a ring, a cedar blast, or they may describe whether like weird, like, isolate that mononiropathy.

So, okay, think about lead poisoning, okay? And remember that the way you treat lead poisoning is you give like a lead killer, right? So, like calcium ETA, you can give a DMSA, you can give succimer, you can give B... L, I think that's known as like, British anti-low sight or something weird like that. And basically, right, if you check out child's blood lead levels and it's high, right? Usually the next test you do to sort of like confirm is to get a venous lead level, okay? And then you treat one of those modalities that I've described. Now, the next question says, where the lines on the finger, plus Gallic breath? So, Gallic breath should hopefully bring some good memories from step one for you. In relation to arsenic poisoning, okay? Remember that arsenic poisoning can also cause like some weird like horizontal lines on the fingers, they're known as meselines, M-E-E-S, meselines, okay? They're pretty classic for arsenic poisoning. And for those of you that, if you remember from step one, arsenic messes with like lipoic acid in the pyruvy dehydrogenase complex. But that's more of a step one discussion. Okay, so I think we're done with this real large slide. So, yeah, on the verge you look up a picture of meselines. It's a pretty classic a picture that shows up on exams. Okay, the next one. So, a child with declining grades and many staring episodes, right? So, hopefully this gets you thinking of an absent seizure, okay?

Remember, classically, that's associated with like a three-hertz spike and slow-wave activity on EEG. You don't need to be able to recognize it, you just remember the buzzword. And you treat that with Ethosoxamide. Don't forget that Ethosoxamide is a T-type calcium channel blocker, not L-type. T-type calcium channel blocker. And remember that absent seizures, right? Doesn't show up in adults on MBM Es. If you see an adult question seizures, don't pick up Sons, right? Absons is a Pete's question 100% of the time for the most part on MBM Es. Okay, let's say 99.9% because you can maybe never truly be sure of something. But I have never seen an absent seizure question that was not in a Pete's patient, okay? And I've done, trust me, I've taken lots of exams in my life and I've treated a crap ton of people. Yeah, absent seizures, pediatric question on MBM Es. Okay. Now, next question says, actually an absent seizure is a kind of generalized seizure. I'll just throw that out there. Okay. So, seizures heralded by olfactory hallucinations and the rise in sensation in the abdomen, right? It's been like weird symptoms, right? The thing is, I want you to think more of a simple, partial seizure. These are basically like weird horrors. Actually, the horrors people have, like horrors, actually a kind of simple, partial seizure. Just think of them as like weird, bizarre phenomena, like rising sensation in the abdomen, right? Basically, they're starting the originating, the temporal lobe, okay?

Very high, you'll know that association that they're originating in the temporal lobe, right? And if you kind of remember from previous podcasts, I mean, as you look at the next question that says seizures with sensory motor problems, those are more for like the frontal and parietal cerebral cortex, right? I've sort of talked about this in previous podcasts. Basically, these are seizures that you can kind of look allies with like classic neuro and atomic op principles, right? So, see, for example, the patient has like an infarct in the left MCA. They can have like a right-sided, like motor seizure or right-sided sensory seizure, okay? So, they have like, basically they have like seizures that are contralateral to the side of the infarct, okay? That's a pretty classic thing that shows up on exams. It's something you kind of want to keep at the back of your mind, right? And then the next one is a focal pole seizure paralysis and weakness. That's something known as a tauts paralysis, just something you want to remember. It's fine. You generally don't need to treat it. Just go through it after a while. Okay. Usually like hours to days or something like that. Okay. So, let's sort of talk about like generalize than focal seizures, okay? So, focal seizures. You have the seizures that we're called, partial seizures, back in the day, okay? And really, there are two kinds of like, partial seizures. And again, I've talked about this in a previous podcast, right?

You can have like a simple, partial seizure. The new term, I believe, is like, focal seizure without loss of awareness, right? You can have like the model simple, partial seizure, right? Then you have like, muscle rigidity. Then you have like this like weird, like movement of the arms. Or you may have like a sensory simple, partial seizure, right? Those people tend to have like just like bizarre sensations that sort of fit like they're hearing, or their smell, or their taste, or like the vision, right? Or they can say, oh, I hear a hissing sound, right? Think about, think about a sensory or simple, partial seizure. There's also the autonomic kind of a simple, partial seizure, right? Where the people can have like sweating, or they may have like, flushing, or like, they're... Or they may have like, popular dilation, right? So, like, autonomic symptoms, think about a simple, partial seizure with that. Or they may also have like, psychic seizures, right? That one really shows up on an exam, so we're gonna keep on moving from that. And then, under the focal seizures, right? So, the partial seizures. There's also those, the complex, partial seizures. The other term for complex partial seizure is like a focal seizure with loss of awareness, right? And the thing is, the NBA may sort of place on this trick with people, right? Because we're like, oh, loss of awareness. So that means the person passed out. No, they don't necessarily have to pass out.

The thing is that the patient may appear weak in the question, but they actually know that we're of their surroundings, okay? That is still a complex partial seizure, although again, the new name is focal seizure with loss of awareness, right? And the thing is, these seizures, they usually have like, you know, like weird automatisms like chewing or like swallowing or like smacking their lips. Or sometimes you may actually see people like disrobing. Those are all like automatisms that can happen with a complex partial seizures. Again, also known as focal seizures with loss of awareness, okay? They may have like some weird hallucinations, like they may hear like some weird music playing in the background. Or they may say that, oh, they feel fooling the abdomen, usually in the epigastrum. Think about a complex partial seizure with that. And again, those are both like simple partial seizures, complex partial seizures, the examples of partial seizures, right? So focal seizures. So the simple partial kind is the one that's focal without loss of awareness. The complex partial kind is the focal kind that has loss of awareness. And then the general life seizures, there's many kinds of general life seizures, right? I already talked about the absent seizures. Don't forget the three per second, the three herds, the spike and slow wave activity on EEG. They can have like chronic seizures. There's like tonic seizures where they have the predominance symptoms like muscle rigidity.

Or there's like tonic chronic seizures. That's like the seizure that everyone knows to be a seizure, right? Where like they're shaking from everywhere and all that stuff. And you may have like myoclonic seizures or they can have like drop seizures. Drop seizures also known as a tonic seizures where patient, like just like loose muscle, loose muscle tone and just boom. Drops to the ground. And if you remember from a previous podcast, right? I've talked about there's a weird disease condition that's associated with atonia. So let's assume they tell you a question about a patient that falls asleep at like weird times of the day. And sometimes when they smile or when they hang out with friends, they sort of like just like loose muscle tone and fall to the ground. I hope you're thinking about cut up lexia, right? That's a classic finding in narcolepsy, right? Remember you make that diagnosis with polysomnography, a sleep study. And those patients tend to have like low levels of hypochritin. I think that's also known as a rixin in the cerebral spinal fluid, okay? So one of those weird things to know. Okay. Now the next question here is a quick discussion of brain death and syncopy. These are just things that you kind of want to know for the neuroshelf. So I'll just give you like just a few like high-yield things relating to like brain death and syncopy, right? So I mean, if your heart stops, you're probably dead, right?

But the thing is brain death is more aware like you've basically lost all functions of your entire brain, right? Including your brain stem. And the thing is if you've lost all brain functions, there are certain things you can use to sort of like tell yourself that, okay, maybe the patient is brain death on an exam, right? So the thing is they'll essentially have like no brain stem reflexes, right? And the classic ones are like the vestibular ocular reflex may be gone, right? So you can sort of do the caloric test or you can check like the popularity right, light reflex that could also be gone in a brain death. Another thing you can actually do is something as the apnea test, right? So basically you confirm that those people don't have any kind of like spontaneous respiration. After their sealed has been allowed to rise, we can think about it. If you're carbon dioxide has risen to like 70, right? We long, long, long before that your medulla will kick in, right? And force you to breathe, right? If you remember from step one, hypercarbia is a powerful stimulus of respiration, right? So if you're hypercarbic, but you're still not having spontaneous respiration, it means like your brain is no longer responding, okay? That's known as the apnea test, that's really a pretty good test for the diagnosis of brain death, okay?

I mean an EEG, it should like a flatline, but I'll tell you that in general on exams, if they want you to make the diagnosis of brain death and they're trying to get you to pick an answer, think more of like absent brain stem reflexes, like the vestibular ocular reflex. There is one known as the ocular cephalic reflex, but think more of the VOR, the vestibular ocular reflex. I think I've described this in one of the neuro podcasts, and then think about like the absence of like a popularly light reflex, okay? And then the apnea test is a pretty good test as well, which I've already described for the diagnosis of brain death. And then syncopy, syncopy is a long topic, there are many kinds of syncopy. I mean there's like a viso-vigose syncopy where usually the trigger is like the patient may see like blood, or they may have like a very strong emotional event or like severe pain, and then they pass out, think about viso-vigose syncopy. Carotid sinus hypersensitivity, right? It may be a patient that oh they are trying to weirdize, or you do like a physical exam, we are scotidium for carotid bruise, and then they pass out. Think more about like a carotid sinus hypersensitivity, or you may see like a maturation syncopy where the patient is like trying to pee, and then they pass out, okay? These are all kinds of like a kind of like a big kind of syncopy, known as like reflex syncopy, if you may, okay?

So those are kind of like key things you want to keep in mind, and don't forget that viso-vigose syncopy, you can actually make the diagnosis by doing something known as the tilt table test, okay? Tilt table test, and I mean some of you may say like divine, how do I recognize a cardiogenic syncopy? Cardiogenic syncopy, like there's usually like no real pro-dram, right? The patient usually just suddenly like just loses consciousness, he just pass out, no warning, no pro-dram, and the thing is sometimes they may have chest pain with the syncopy, and usually in the MBME question they may tell you that the patient has like risk factors for like vascular disease, right? So they may have like a history of MI, or coronary artery disease, or stroke, or whatever. If you see that, think more about like cardiogenic syncopy, as the potential cause of the patient syncopy. So I think those are just sort of key things you can sort of like latch onto to help you make the diagnosis pretty much for most cases you'll see on your exam. So let's jump on to the next question. So I'll go ahead and for the management of a patient in status epilepticus, and then the anti-peleptic drug with the strongest risk of neuro tube defects. I'll just answer the second question right off the bat. For pre-cass it is not good. In general, if you can make a pregnant woman not take for pre-cass it, do that. Because it has a very high risk of neuro tube defects.

But while I'm talking about that, on your MBME, they may actually give you a question about a patient that has had seizures for a long time that has been well controlled for pre-cass it. And then they can tell you that the patient gets pregnant. And then they stop taking the avalpric acid. Or let's say the taking of avalpric acid, but you're having like multiple seizures in pregnancy. The thing is, usually the right answer there is actually to continue the anti-peleptic that they're taking. So you may like have to like increase the dose of avalpric acid or something. And in the question usually they'll say that, oh, these people have tried multiple anti-peleptics and none of them are working. It's only avalpric acid that's working really well for the patient. Even if you're worried about neuro tube defects, seizures are very fatal to the baby. So you want to keep that avalpric acid going during pregnancy. Like a right answer maybe to increase the dose or restart the avalpric acid. Sometimes it won't tell you that all the drug level is suboptimal. You want to increase the dose of the drug. So that mom does not have seizures during pregnancy. But avalpric acid is the anti-peleptic with the highest risk of neuro tube defects. Now, how do you manage status epilepticus? I mean, there are many things you're supposed to do. But I'll say for MBM is the key things you want to recognize are that. First, you start with lorazapam. You basically start with a benzodiazepine.

And then if that's not doing the trick for the patient, you then jump to the next option. You give them like IV, like phytonin or like phosphytonin. You usually give two doses. If that doesn't work, you should probably be calling like your friends in neurology and anesthesia at this point. You want to go for the new hair option. You basically sedate them with a barbiturate phenobarbital. And then the next question says, as an aside, involuntary flailing movement of one arm. This is hemibalismas. This is a sub-tolamic nucleus lesion. A contralateral sub-tolamic nucleus lesion. If the patient has involuntary flailing movement of the left hand, think about a right sub-tolamic nucleus lesion. And then the next one says involuntary movements of the jaw with northern neurodeficities are relieved with gentle stroking of the jaw. This is just something that you should be able to classify recognize on exams. This is like a focote estonia. That stroking, the jaw, I think there's like a Latin term they use for. That stroking to relieve the symptoms, I think, is known as a g-e-s-t-e. G-e-s-t-e. G-e-s-t-e. Something like that. Like weird stuff. That's a focote estonia. Really, like it's like a sustained muscle contraction. And again, the classic way it presents on exams is the way I just described it. Actually, treat a focote estonia by just injecting Botox, like the Botulinum toxin, into that muscle group. Remember, Botulinum toxin works by cleavants and proteins, right?

So you don't release acetylcholine at the neuromuscular junction. Okay? Okay. So let's go on to the next slide. So what is going on? So fever had a stiff neck, right? Hopefully you know that this is meningitis. In general, you can do a lumbar puncture from meningitis, but before you can do a lumbar puncture on exams, look in the Q-stem. Ask yourself, do they have any signs of increase in trocranial pressures? If they do, you need to do a CT scan first before you do the L-P, right? Because you don't want to do an L-P, and the patient that has high C-P, they need and die. You don't want to do that, right? So if there are no signs of increased ICP in the Q-stem, do an L-P. There are signs of increased L-C-P on your Q-stem. So you need to do a CT scan first before you do an L-P. Okay. Next one says, Sodden onset, severe headache, and next stiffness, right? So I'm asking for the diagnosis here and diagnostic testing, right? So hopefully you're not thinking meningitis with this. Hopefully you're thinking more of a sub-arachnoid hemorrhage. So sub-arachnoid hemorrhage can actually present with no coregidity. Okay? So don't get dinged by that on an exam. So this is a sub-arachnoid hemorrhage, right? Again, obviously, you meet the diagnosis with a non-contrast CT scan on the head. And then you also do, if that's negative, you can jump to a lumber puncture to look for example chromia.

And I guess with this question, I kind of want to highlight a useful testic embrace bullet that has helped me like many times to eliminate answers on exams, right? So it's differentiating between a problem that is acute and a problem that is like chronic, right? So think about this question I just talked about. Sodden onset, severe headache, right? You cannot be sort of like walking on the street and boom, you get meningitis. No, it doesn't happen that way. It will be something that sort of like develops over hours, right? But if a patient has like sodium onset, worst headache of their life, that's a more sinister acute problem, right? You want to think more about like a brain bleed, like a sub-arachnoid hemorrhage with that. So the thing is when you're analyzing exam answers, divide them if the question is giving you an acute problem, an answer choice that is like a chronic issue is probably not the correct answer, right? That's like a very useful testic in strategy that helps me a ton on many of these NBME questions and also I guess in your word. Okay, now next question is a triad, right? So like fever, headache and focal neurologic deficits, this is the classic triad. This is almost always the way it presents on exams. You're thinking more about a brain abscess, okay? So fever, headache, neurologic deficits, think about a brain abscess. You can make the diagnosis with like a brain MRI. Don't you see Tscandua MRI?

And you want to give a prospect from antibiotics, use imaging to aspirate the abscess that's usually done by the neurosurgery of people. Okay. And then the next one says recent history of a tightest media would focus on neurologic deficits and papillodemon of fundoscopic exam. This is also potentially a brain abscess, okay? So same treatment as I already described, right? And then just I guess while we're on this topic, if you see the triad of a patient that has a history of being an IV drug user and they have fever and then they tell you in the question that, oh, they have back pain and they have like some weird neuro deficits. Think about a spinal epidural abscess, okay? Treatment is the same as a brain abscess, right? So you give a blood spent trauma antibiotics and if you can drain it, you try to drain it. Again, call your neurosurgery folks to help you with that. Okay. And then the next question says, eight-taxia urinary incontinence and dementia. Hopefully this gets you thinking about like waky wet and wobbly. This is normal pressure hydrocephalus, it's just something you need to recognize. You treat it by decreasing the ICP, right? So you can put like a VP shunt in the brain or something like that. And then the final one here, elderly patient, mini mental status exam of 20 over 30, with no post neurological history of to manager last night, right? So on your example, you're not going to see a manager, you're going to see difenhydramine, okay?

But this should hopefully get you thinking about delirium, okay? Remember that difenhydramine has powerful anti-colonurgic activity. In fact, you've probably heard this warning like more times than you care to remember in med school. Don't give drugs with anti-colonurgic activity to the elderly, right? So like difenhydramine, all these many of these first generation anti-histamines, they have anti-colonurgic activity, drugs that are useful like urinary and continent, because guess what? Who gets urinary and continents, old people, right? So drugs like oxybutamine, toteuridine, dharfenacin, sulfenacin, trospium, those are all like most chronic receptor antagonists, okay? They can cause delirium in the elderly, okay? So they can give you a question about a patient that has like urgent continents and then they act delirious, okay? So they can give you a question about those drugs as potential inciting agents, okay? And then the next question, kind of dementia. So the first one, in fact, I guess let me just sort of see right off the bat. And basically gonna answer the questions on this slide and the next slide together, okay? So the first one is MMSC in 1930, plus difficulty speaking, plus inability to perform AD Ls, right? So activities of daily living, right? Mascam for the diagnosis, how do you manage this? Was the APOE association? Just one of those bizarre things that you love to throw on exams. So for this patient, I'm talking about Alzheimer's disease, okay?

And I guess one thing I'll say is this is actually like a low-yout factoid, but it's a weird thing that makes you open an exam. Before you formally make the diagnosis of Alzheimer's, you actually need to do some kind of brain imaging. You usually do like an MRI, right? Usually you do an MRI. Sometimes you can use those cuts, can a CT scan, or you can do like spectimaging, but usually you do an MRI, okay? And please don't forget that Down syndrome has an association with Alzheimer's, right? Because remember that the amyloid precursor protein is on chromosome 21. If you have Downs, you have trisomy 21. So you have three copies, right? So patients with Downs tend to get like early on set Alzheimer's, right? So like Alzheimer's in their 40s, for example. And Alzheimer's, right? If you do like a brain biopsy, let's say when the patient is dead, classic things you'll see is right? You can see like a synoplock, right? Those are basically like extracellular deposits of like amyloid in the brain, right? You can see like neurofibralary tangles. As against the synoplock that are extracellular, the neurofibralary tangles are actually intracellular, okay? The amyloid of like hyperphosphorylithid and tau protein, okay? And the thing is remember in Alzheimer's in general, if you want to treat, you give a drug that has pro-colonurgical activity, right? So you give like you are pseudo-colonestero-inhibitors.

And you don't like on the example of the poor paridosigmen as a treatment for Alzheimer's, don't choose that even if it's an acetyl-colonestero-inhibitor. You want to choose one of three drugs, right? So like donepesial, galantamine or rivestigmin. They are all anti-acetyl-colonestero-inhibitors. They boost your levels of acetyl-colon and treat Alzheimer's because Alzheimer's is associated with low levels of acetyl-colon. In fact, on exams, classically the neuro-shelf and the side-shelf, they love to test neuro-anatomic associations with certain diseases. I will encourage you if you have the chance, look at the last slide, one of the last two slides of my psych video review. I sort of cut a lot of those associations for you, but for Alzheimer's, which is I guess what we really care about in this podcast. For Alzheimer's, I told you that there are low levels of acetyl-colon in Alzheimer's, right? That's why you give acetyl-colonestero-inhibitors to treat. So the thing is, one nice way they can test the pathophysiology of Alzheimer's on your exam, is they can tell you that, oh, is there a part of the brain that is not functional in Alzheimer's? Think about the Bisonucleus of minor. Remember, the Bisonucleus of minor is where acetyl-colon is produced in the brain. And if you actually think about acetyl-colon synthesis, acetyl-colon synthesis has a real-mething enzyme. The real-mething enzyme of acetyl-colon synthesis, I believe, is a colon acetyl-transferase, okay?

If you have mutations in that enzyme or dysfunction of that enzyme, that's potentially behind the pathophysiology of Alzheimer's disease. Just one of those weird things you want to keep at the back of your mind, for exams. Okay, so, when Alzheimer's, I mean, I said, you can give a colon esterase inhibitor, donepazel, galantamine, or restigment, there's one other drug known as tachrin, but that's really used. I don't know if it's been banned or something, but I didn't just in general, maybe not don't choose tachrin on exams. If you have those other options, like donepazel, galantamine, or restigment, I should probably look that up some more. But donepazel, galantamine, or restigment, are your good two drugs. You can also use mementine. That's like an NMD receptor antagonist. Okay, so next question here says, so kind of dementia, in a patient, has like Parkinsonian features, they have like visual hallucinations and syncopal episodes, think about Louis body dementia, that's a pretty classic presentation there. And then the next one says, dementia plus choriform movements, and for this, I actually need the pathophys, I need the findings on imaging and the treatment. So this hopefully gets you thinking about haunting things disease, right? haunting things, Korea. Remember, it's a trinucleothide repeat disorder, right? And like most trinucleothide repeat disorders, not almost, it's inherited in an autosomal dominant fashion, right?

And the trinucleothide repeat here is a CAG, okay, like CAG repeats on chromosome four. Okay, and classically, if you do imaging, the vision that has haunting things, right? You can find like atrophy of the codic nucleus, remember, it's right, smack dab begins the lateral ventricle. And haunting things disease, I really don't have the time to go into describing mechanisms. I don't know if I've done in a previous podcast or something, but haunting things disease, I think of it as a high dopamine disorder, like a disorder that is as high levels of dopamine, at least initially in the disease, right? So you treat it with like a dopamine antagonist, you can give like caloparydol, or you can give something that inhibits the transporter, that basically like packages dopamine in vesicles before you dump it in the synapse. That transporter I believe is known as V-MAT, you can inhibit it with a drug known as tetrabenazine, okay? Or like, yeah, tetrabenazine is probably the big one you want to remember for tests. Okay, now the next one says, mild dementia plus difficulty speaking, plus inappropriate behavior, plus knife's edge appearance on brain imaging. Hopefully this gets you thinking about pigs disease, right? So like frontal temporal dementia. Yeah, that's pretty much all you need to know about that. And then the next one says, stepwise deterioration in cognitive function with neuro deficits. This is a vascular dementia.

And by stepwise, this decline in neurologic function, here's how it will present on an exam. The basically you have a question about a patient that is like, oh, you can, because I mean, think about it. A patient that has dementia, I didn't say, oh, on December 7, 1992, I stopped, I studied having troubles remembering stuff. No, they're not, they were just sort of say like, yeah, don't, couple of the last couple of months, couple of years. I don't see me remembering stuff very well anymore, right? Vascular dementia is more like, oh, they were seeing the question like, oh, five years ago, this patient studied being forgetful. Four years ago, this patient studied having social and social issue, right? Usually it's like dementia in the setting of neurologic deficits. And you can almost always pinpoint like an exact time where the symptoms started, like specific symptoms started. That's what's the stepwise decline in your logic function. Think about a vascular dementia with that. And really vascular dementia, usually on exams, they will give it in, they will give it as a question in a patient that has like, again, risk factors like hyperlipidemia, coronary artery disease, histral stroke, blah, blah, blah. Okay. And again, there's not much you can do to treat, but you can give like the drugs you give Alzheimer's, the colonistries inhibitors, like donepizel. Okay. So next question says rapidly, rapidly.

So let's say over like a six week period, for example, rapidly progressive dementia in a patient that got a corneal transplant a year ago with, and this patient also has myoclonus on physical exam. This is the bad, bad, bad, bad, bad disease. There's no treatment. This patient is in big trouble. This is Croitsfall Diacob disease. Okay. Remember that in the CSF, they will have elevated levels of the 1433 protein. It's a very high yield thing to know, for exams. And then this last one I've talked about it again, but again, I'm not repeating it for fun, Z's, it's kind of high yield to know this, right? So urinary incontinence, bloods-gate problems, think about normal pressure hydrocephalus. And early onset Alzheimer's, again, remember that it's in patients that have a Down syndrome, right? So like trisomy 21. And if you're thinking about apo E with Alzheimer's, don't forget that if you have like the apo E4 polymorphism, that actually renders you susceptible to Alzheimer's, versus the apo E2 polymorphism that is actually like a protective factor against Alzheimer's. So the lower number is protective, the higher number is, renders you susceptible to Alzheimer's. Okay. So apo E4 Alzheimer's, apo E2 protective, apo E4 renders you susceptible. Okay. And I think that's all I need to talk about on this slide. So let's jump to the next one, right? So next one says inability to calculate plus left right disorientation. You want to think about like a parietal lobe lesion, okay?

And I guess let's sort of talk about these parietal lobe lesions because they're kind of high up to no for exams, right? So you can scrub your dominant parietal lobe or your non-dominant parietal lobe, right? If you scrub your dominant parietal lobe, that's something known as Gerstmann syndrome, okay? Basically, these people will not be able to calculate, they can do math, right? So Ecalcolia, right? They'll have problems writing, right? So they'll have like a graphia, and they'll also kind of have trouble telling like left from right, okay? Like left right disorientation, think about a dominant parietal lobe lesion. That's known as Gerstmann syndrome. And then if you think more about neglect, think more about a non-dominant parietal lobe lesion, okay? So remember that most people use their right hands, right? And the right side of your body is controlled by the left side of your brain, right? So most people are left parietal lobe dominant, right? So if you have a lesion of your left parietal lobe, which is like your dominant parietal lobe, okay? Then you have Gerstmann syndrome and all those symptoms I described. But if you have like a lesion of your right parietal lobe, which is your non-dominant parietal lobe, you have like neglect, right? So they can like basically not be attention to one side of their body, like they can like brush one side of their teeth, you know, like just neglect, right? You kind of know how that presents.

Okay, wow, we're on 30th, we need it already. Well, okay, let's keep going. Next slide says, Hi-Yo, the anti-pelptic drug side effects. So like Valparate, Carbamazepine or Orx-Carbazepine and also Phenetone. These ones, they're kind of high-yield, just very few things you need to know. Well, Precarsid already said, Hyastrophneural 2 D effects. Now, very high-yield to know for your neuron, your side-shoff, that Valparate Acid is hepatotoxic, okay? It's bad for the liver. And then your Carbamazepine slash, I guess, Orx-Carbazepine, think about it, granoloseitosis. So they are terrarogens, right? So you don't give them to pregnant women. They can also cause SID, remember SID, he's a cause of uvolemic hyposmolar, hyponitremia. Remember, I talked about this in one of the medicine videos. And, right, so basically these patients will have like low sermostmolarity and high-irinosmolarity, okay? And then again, it's a terrarogen. And then phenetolin can cause neuro 2 D effects. It can cause arrhythmias. Actually, phenetolin is actually a class 1 B antirithmic. If you really dig down, drill down on its pharmacology, it's basically a class 1 B antirithmic. So you can actually cause arrhythmias. It's a terrarogen. You can actually cause like some weird visual issues. So if they usually write it as like a non-descript question on exams, or like a patient is like weird visual issues, like a stagma. Just like weird stuff. Think about phenetoin toxicity.

In fact, that's like usually like a telltale sign of phenetoin toxicity, like just weird visual problems. And then don't forget, you can actually measure like a blood phenetoin level to see if like it's like therapeutic, subtherapuric, or like in toxic range, right? And then don't forget from step one, you'll feel like high-dentoin syndrome. This can show up on a pitch shelf as well. Usually they have like mycosephaly, like a small head. They'll have like a flattened isle bridge. They can have like clef lip and palate. Those things all go along with fiddle high-dentoin syndrome. Remember high-dentoin kind of sounds like phenetoin. So it's kind of easy to remember that way. And then also very high yield to know that phenetoin can cause gingivol hyperplasia. And then there's also this weird immunosupperson that causes gingivol hyperplasia. I believe that's a cyclosporing. Yes, cyclosporing can cause gingivol hyperplasia as well, but also phenetoin can. And then don't forget that phenetoin can cause like dermatologic issues like Stephen Johnson syndrome. And also kind of a weird one to know. There's probably more for step two, CK and step three. And I guess step one, if you're listening to this podcast. Drug-induced lupus. Phenetoin can cause drug-induced lupus, just like hydrolyzean and sulfonamides. And isonize it. And I believe it's a turner-sept. And then I'll give you the association with anti-histona antibodies. Okay. Next question here. 15-year-old with hand with...

Let me correct this right now so I don't forget. With jerky hand movements in the morning. An occasional generalized tonic clonic seizures. This is just a weird one you want to be able to remember. This is like druvanala, myoclonic epilepsy. Just literally all you need to know. There's just something you want to be able to recognize on a test. Okay. Now, this next one is kind of bizarre, but it's actually very high-yield for exams. Recallant seizures plus a contralateral, homonymos hemianopsia, plus problems on the standing speech. So think about like... When it is aphasia, if you may. Recallant nose bleeds, positive fecal occult blood test. This is just a weird thing that you want to be able to recognize. This is a disease known as a hereditary hemorrhagic telangectasia. You probably know it as osla-weber-randu disease. It's in herethan and arrozomodominant fashion. Classically on exams, it presents with like telangectages. Classically it's on the lips. So don't get fooled by a pure it's a yeager syndrome. Because remember, pure the yeager syndrome can also cause like black lip lesions, if you may. But if you give your picture like those black lip lesions, but they tell you that this patient has like bleeding and they have like a positive fecal occult blood test. You probably want to think more about HHT, which is also again known as osla-weber-randu syndrome. So again, it's got classically on exams, presented like telangectages. And they may also form like AVM's, right?

So like AVM are formations in like multiple organs, right? So in the example I'm giving in this question, this patient has the AVM in the brain. And if you want to be a little more specific in the question, we have like the AVM in the temporal lobe. AVM's usually you can see them pretty well on imaging with like an MRI. They actually tend to have like weird calcific, like dystrophic calcifications within them. Okay, if you see that, again, if you see those cluster findings, think about osla-weber-randu syndrome. Okay. Now, the next one again, another bizarre presentation, right? So, sodium onset of redness in the eye plus bulging eyes plus a humming sound on a quotation of the skull. Plus a visual acuity of like 20 over 100 in the affected eye, right? So again, this is just a weird thing you want to be able to recognize on your exam. This is, in fact, instead of the humming sound, you could see like, oh, you osculted the skull or even like the eye, like you put a stereoscope literally over the eye or like over the skull. And you hear like a brewery. You want to think about something known as like a carotid cavernos fistula. It's super rare. It's super weird. But it's essentially an EVM. And again, I'm putting this here because I talked about EVM's redness level around. It's basically an EVM, but you'll find it more in the cavernos sinus. Remember, there are many veins in the cavernos sinus, right? So you can actually have EV Ms in the cavernos sinus.

And that can cause a carotid, a carotid, a carotid, a carotid, a fistula. Because remember, your carotid arteries actually run through your carotid sinus. And they're like some veins and like cerebral sinuses. And again, run through the cavernos sinus. So if you have an EVM in the cavernos sinus, that can begin to compress all that like surround instructors and that can cause lots and lots and lots of problems. So again, it's just one of those bizarre things you want to keep at the back of your mind. Usually you make the diagnosis by doing like an MRI. You can do like an MRI and geography. And really, the treatment is surgery. Okay. So now that we're done with that, let's go on to the next slide. Okay. So 12-year-old male, that stands from a seated position by moving his hands over his legs. Right? Here I'm asking for the diagnosis, the pathophys and the less severe from the disease. So hopefully this gets you thinking about the Doshin muscular dystrophy. Okay. Remember, it's an X-ling disorder. So you'll shop in boys on tests. And the pathophys involves like a distrofinging mutation. Distrofing is an important cytoskeleton protein. And so you basically have issues anchoring the cytoskeleton within a skeletal myocytes. So that's the pathophys behind the Doshin muscular dystrophy. And unfortunately, many of these kids, they die like in their teenage years or like early 20s. I mean, you try to give them like high nutritional support.

Many of them become wheelchair-bounder pretty early. Yeah, it's just a pretty unfortunate disease, but thankfully it's pretty rare. Although it's the most common kind of muscular dystrophy. DMD is the most common kind of muscular dystrophy. And then the less severe kind of muscular dystrophy is like the becker muscular dystrophy. Okay. It's less severe. And really, the pathophys here is that you have problems with distrofin. So you have like a mutation in distrofin literally. Just like DMD, it's just the mutated dystrophy you form has like some function left. These kids versus those that with the shins that die like in their early 20s or in their teenage years, kids with beckers can actually leave to like old age. Many of them leave to like their 50s and whatnot. So that's I guess a less severe phenotype if you may. But again, it's also excellent. So you only shop in boys on your tests. A girl cannot get the shin muscular dystrophy or becker muscular dystrophy on an NVME exam. Again, I just threw that out there. Now, the next question says a kid that is hypotonic at birth. And then they tell you that the pediatrician, this is like classic exam presentation here. Pediatrician has trouble releasing the grip, releasing his grip from his kids mom during a three month well child check. Or they may present this as well on an exam as like an older male that has like balding, like premature balding. I mean, you probably shouldn't be bald at the age of 25, right?

If you see like premature balding on an NVME, you want to think about my electronic dystrophy. Remember, it's a try nucleotide repeat disorder. I believe it's a CTG, try nucleotide repeat. Also, it was a more dominant inheritance. And don't forget the gene mutation, right? It's like a DMPK gene mutation. There's also this weird gene like the CNBP gene that can also be a metedigene in my electronic dystrophy. And again, don't forget, it was a more dominant inheritance. It's a kind of muscular dystrophy. But unlike DMD and BMD that are inherited in an excellent fashion, my electronic dystrophy is inherited in an orzomo dominant fashion. And then the next one says 18 year old male presents with a chief complaint of facial weakness, okay? And opera extremity weakness that have progressively worsened over the past 18 months, okay? So I'm asking for the diagnosis, the inheritance, and the weird demographic exception. It's not really weird, but I think it's just something high you'll sort of talk about, right? So this patient has problems in the face, and then they have problems in the opera extremities. Remember, this capula is kind of around the opera extremities. I'm using this to give you a hint. This is something known as a facial scapolo-humero dystrophy. It's a kind of muscular dystrophy. And the weird thing about it is, it kind of shows up like in the initial presentation, usually in like teenage years. And again, facial, right, problems in the face, capula humoral, right?

So problems in the opera extremities. That's kind of a nice way to remember that. And it's also inherited in an orzomo dominant fashion. And it actually affects boys and girls, right? So like the shamelessly dystrophy, becker muscular dystrophy affects only boys on exams. But my authentic dystrophy can affect boys and girls, but usually on NBM is its boys. But facial scapolo-humero dystrophy actually affects both boys and girls on NBM exams. Okay, again, that's kind of a nice distinction from like the shins and beckers muscular dystrophy. Okay, now, quick discussion of the proximal muscle weakness disorders, right? So hopefully you're thinking about like polyandromyocytes. I've talked about these extensively in my medicine video, but I'll just give it like the cleaves notes version for your neural shelf. Basically, these disorders, I guess one other thing I guess I could kind of talk about is inclusion body myocytes. That's another weird one that, occasionally, I pop up on on exams. Now, the thing is, polyandromyocytes, they're like inflammatory myopathies, if you may. So the problem is that the level of muscle, they usually present on exams like proximal muscle weakness, right? So the metelol like, oh, the patient has trouble like coming their hair or rising from a chair, right? Those are just all indications of like proximal muscle weakness. Contrast that with inclusion body myocytes is that usually is like can have like both proximal and dystomal muscle weakness.

In fact, if I'm not mistaken in inclusion body myocytes, the dystomal muscle weakness usually shows up first before the proximal muscle weakness. And in contrast with polyandromyocytes is that tend to be symmetric, right? So like symmetric proximal muscle weakness, inclusion body myocytes is usually asymmetric, usually presents as an asymmetric proximal muscle weakness. In fact, for inclusion body myocytes, the metelol exams are initially before they had the proximal muscle weakness like their finger flexors or like their forearm flexors or like their knee extensors, we're kind of like all screwed up. Think more about inclusion body myocytes, if those were the first things that kind of shop again, the dystomal muscle weakness showing up before the proximal muscle weakness, right? And really the way you treat, I guess I can sort of talk about some more things, for polydromyromyocytes don't forget your autoantibodies, right? So like your anti-jouwan, anti-MI2, there's another one known as anti-signal recognition particle, anti-bodies, right? Those are classic anti-bodies in polyandromyromyocytes and really the way you make the diagnosis of these disorders is you check the creatine kinase first, right? So the creatine kinase will be elevated on exams, okay? If the creatine kinase is normal on an exam, those patients don't have an inflammatory myopathy, I'm just gonna throw that out there. So you check the creatine kinase and then after that you do an MRI of the muscle, okay?

You may say you're a different, come on, it's a muscle biopsy, muscle biopsy is no longer the diagnostic test for the inflammatory myopathy. You screen with the creatine kinase level and then you do an MRI of the muscle, if the muscle MRI is equivocal, then you can jump to doing a muscle biopsy, because I mean obviously a muscle biopsy will be like a good standard diagnostic test, okay? And don't forget, on polymyocytes, the dermatomyocytes will show up with dermatologic findings on an exam, that's why it's called dermatomyocytes. So you may shop with the racoon eyes, you may shop with the gut trans papules, you may shop with the shell sign where you have a v-shape like erythema, like around your neck or your chest or your upper back, right? And don't forget that polyandromatomyocytes is, they may actually be like a presentation, they may be a panoplasmic phenomenon in the setting of lung cancer. So usually, if a patient has polyodromatomyocytes, usually try to do some kind of chest imaging to roll out like some kind of malignancy, usually lung cancer. Usually they also scan like the abdomen, just make sure they don't have like a visceral malignancy going on. Let's see, what else I want to say? Polydemyocytes, you can treat them with steroids, inclusion polymyocytes, usually does not respond to steroids. And polymyocytes, it's classically more in adults, first of all, the dermatomyocytes that can shop in adults, but can also shop in kids.

Polymyocytes is like super, super, super, super in kids. Polymyocytes is a lot more common in adults, right? So those are just again weird high-yield things you want to keep at the back of your mind. Okay, now let's go on to the next slide. So, quick discussion of the high-yield toxic drones. Okay, so let's talk about this real quick. I'm gonna try to keep the spot gas below an hour. Let's see how that goes. So, a co-inergic toxic drone, excuse me. This may show up in the context of like nerve gas on an exam, right? Or organophosphate poisoning, right? Remember your nerve gases could have weird names, usually start with S, like saryn, soma, non-exams. Really, the way it will present is you'll be licking from everywhere, right? So like diarrhea, rhinorrhea, sweating. Also, because it's a co-inergic toxic, you have to have like, popularly myosis. You want to treat this by basically blocking the acetylcholine receptor, right? Because you have too much acetylcholine going on. Because organophosphate, remember the inhibit, or nerve gas, remember the inhibit acetylcholine esterase. So that boosts your levels of acetylcholine, right? So you can treat those by giving an atropine to block most chronic receptors. And then you can also give prelydoxin, right? To regenerate the acetylcholine esterase that's kind of like dead. I sort of think of it as resurrecting acetylcholine esterase from the dead. Okay, give prelydoxin to make that resurrection happen. Okay.

And then for an anticholinergic toxic drone, it's kind of the opposite. So they'll have like, popularly my dry asses, they'll have like constipation, they will have like, like flasid paralysis and it will be like a symmetric descending flasid paralysis, right? So think about like botulism, right? If a patient is like infected with botulism or they're exposed to like the botulinum toxin for some bizarre reason, they'll have like a symmetric descending flasid paralysis. Contrast that with Guillembray syndrome, right? That presents with a symmetric ascending paralysis. Okay, so symmetric ascending flasid paralysis without sensory problems. Think about Guillembray syndrome and please don't forget, I believe I've talked about this in a previous podcast, one of the neuro podcasts. Guillembray syndrome is associated with something known as a Abuminocytologic dissociation, right? So you'll find very high levels of protein in the CSF, but you don't find an increase the number of cells. Okay, I talked about like what that term, Abuminocytologic dissociation means in a prior podcast. So I'm gonna keep going. Okay, and then you can basically contain the presence, you'll be a patient with like a psych history, classically on exams, it will show up with like great neurologic deficits, they'll have like arrhythmias and they may even give you an EKG showing like a white curious complex. That's a classic presentation there, and really you want to treat that toxicity with a sodium bicarb.

And then cocaine, also known as cocaine, cocaine, I like that term. Okay, so cocaine, right, your cost hypertension on exams may present with like perforation of the meso-septom, right? Those patients will tend to have like my dry asses, it may present with like a like a myocardial infarction on a test, okay? And the patient blood pressure is a crazy high, right? Like in the 180s, 200s, a stoic. I'm really for cocaine toxicity, remember you don't want to give a bit of blocker, right? Persking with a JD after their name will be very happy to come and collect your license and throw you in jail. So don't do that. You don't give it a blockers for cocaine toxicity. You tend to give benzos first, okay? And then you can actually try to lower the blood pressure like an alpha one blocker like a phentolamine, for example, okay? And then glue slash a toluene, right? So like sniffing, this is something usually on exams, the classic presentation will be that you do like urine tox screen and you don't see anything. For that, think about like a patient that's like, you know, like sniffing glue. I mean, there are other things they could sniff as well, that sort of contain like they could sniff glue, they could sniff like gasoline, they could sniff like stuff useful like dry cleaning or like cooking sprays or like toiletries. Basically glue on all this badness, the big thing they contain is a toluene. And, um, classically on exams, right?

These patients, they may have like sores or like rashes around like their nose, around their lips. If you see the think about sniffing glue, and the thing is toluene can cause a type one RTA, it can cause a type one or another to Blasidosis. So on exams, it may actually present with like hypochylemia. And in some cases, it may also present with like hypophosphatemia, okay? Those are kind of like weird associations you want to keep at the back of your mind. But hypochylemia raises because you get like a type one RTA, a distal RTA, if you chronically a sniff glue. I mean, there's some other like badness that can also happen when you sniff glue. There's something called, um, what's this thing I read, read an article about this. It's called like, I think it's like, sodding sniffing death syndrome. Because the thing is one of the, the reason people sniff glue, right, is it gives you a high. And the high comes because glue sniffing actually causes like this hypochylinergic response. They're like this massive release of cadet colomines, right? So that's what gives you the high. Only problem is that hypochylinergic response can cause ventricular rhythms, classically V-fib, okay? And they can die, okay? So if you see a patient like sniffing weird stuff and then they suddenly die, think about a sodding sniffing death syndrome, okay? Usually the rhythm of the kills them is V-fib, right? So if you have friends that sniff, that's a sniff stuff, tell them to stop doing that, right?

It's something that can kill them pretty quickly. Okay. Next one is opioids, right? So opioids will present with pinpoint opioids, right? So like, popillary, myosis, and respiratory depression, right? So the respiratory will be like five or six on an exam. And remember the way you treat that is with, you give them a loxum, right? If you get an exam question, they give you an oxygen and an out-trick, so you have answer choices. Don't pick an out-trick, so your patient could be dead before the now-trick, so you can give them a loxum. Now, loxum is the treatment of choice for opioid toxicity. And opioid withdrawal is not life-threatening, so you really don't give anything for that. What do I think I want to say about opioids? Let's see. And opioids, yeah, okay. So I guess opioids, right? So you get me, you'll say, and you actually never get tolerant to like the meiosis and constipation that arises with opioids. Remember, opioids cost constipation, right? I mean, if you've ever taken inmodium for diarrhea, inmodium is basically lopera, my lopera is an opioid, right? So you use the constipation side effect to treat the diarrhea. And then your benzo diazapines, right? So your benzos, your benzos, they can cause respiratory depression, but you have like normal populationary findings, right? You won't see the pinpoint opioids that you find with opioids, right? So if you see respiratory depression and a decreased, so respiratory depression and populationary meiosis, think opioids.

If you see respiratory depression and no population meiosis, think about a benzo or a babiterate. Remember, you can treat benzos toxicity with a flomarzenel, okay? Babiterates can not be reversed with flomarzenel. If you have babiterate toxicity, all the best. And actually, while I'm on this, remember that flomarzenel can also reverse those toxicity of the Z drugs that I use for insomnia, right? So like Zopidem, Zalapone and Zobic Lone. Again, I apologize for all the arms and arms. Again, talking about this, basically off the top of my head. Okay, now LSD, LSD, right? Causes flashbacks, like intensified experiences. PCP, right? PCP on an exam will be a patient that is like Superman, basically, right? They'll push like security guards down. They want to jump off the top of a building. They'll be like hyper, like hyperviolet. Think about PCP with that and they'll usually have like an astagmas, like horizontal and vertical and astagmas, an NV Me question. And then meth, right? If you have like a busted mouth, like bad, like bad dental hygiene, patient is like super hungry. They have like redness of your eyes. So like conjunctival injection, that's the 5 word. Or if they have hyperreflexia, you want to think about methatoxicity. And you really don't need to treat that. And then opioid prep gone bad and thinking more about Parkinsonism. Remember, if you, if you prepare opioids wrong, right, you shouldn't take opioids in the first place.

But if you prepare opioids wrong, you can make an MPTP. MPTP has that nice added side effects of the strongest substantiant eye graph. Right? So that can cause Parkinsonism, right? So classically on an exam, and this can show up like on a newer psych exam, they may describe it as a patient that took drugs at a party and then they have like muteism, right? They kind of like stay still in their chairs. They don't move nothing. Think about Parkinsonism from like bad opioids, right? So that contains like MPTP. Okay. So let's go on to the last slide. So the last slide says, what is the next best step in the management of a seasoned patient with small cell lung cancer with a sodium of 115, right? I just put this in error here because this is the one time you give hypertonic saline on any exam on any MBME. You never, in fact, I was saying in general, never peak hypertonic saline as an answer. This is the one exception. If a patient has like profound hyponitremia, the sodium is less than 120 and they're seasoned, then you give 3% saline hypertonic saline for that purpose. But once the sodium is raised to like 120 or like 122, they're about stop the hypertonic saline and switch back to normal saline hypertonic saline can cause so from high to low, the brim will blow that can cause like a profound cerebral edema and like hernation, right? And you don't, you obviously don't want that.

Now, next one says to how you the electrolyte imbalance is that could cause seizures in the infant of a diabetic mother, right? So like if you're an infant of a diabetic mother, you have the infant to have a ton of glucose in your serum. So they'll have a ton of insulin, right? 12 year in year. Right? So they'll have like a ton of glucose. So that will cause the fetus to see good a ton of insulin, right? But when you extract that baby from mom, when the baby is delivered, right? Well, that high source of glucose is gone, right? You're not out of mom's body. That high source of glucose is gone. But the pancreatic eyelets cells may not get the message and the mistilets, you've hit on a ton of insulin, right? So those infant of the infant of diabetic mothers, they can actually get hypoglycemic seizures, okay? They can also have like hypocalcemic seizures. I don't really know the mechanism behind that. And I guess while I'm on this, don't forget, right? That hypocalcemia with seizures, right? Can be a presentation of the George Syndrome on an exam. Also like a kidney, like vitamin D deficiency, right? So they make sure you're like a picture, like a racially cruiserie, like an African American or a patient that like lives in a place that has like no sunlight, or I guess a radiologist, haha. They could all get like vitamin D deficiency that can cause hypocalcemia and they could get a seizure with that, okay? So just one of those weird things you want to keep in mind.

So I really hope that you've gotten a lot from this series of neuro podcasts. I know taking together, they're all kind of long, but really these neuro podcasts, I designed them to be extremely, extremely, extremely comprehensive. I feel like if you know the material in these neuro podcasts and you do like your practice questions, you do the clinical master series tests, I really don't see why you cannot do really well on the, on the newer exam. I mean, I, I, I will say that I knew a lot of this material and I did really well on my, on my neural shelf. I did extremely well on my neural shelf. Okay. And if you're free, if you have like added time to study, one thing I will say to maybe consider doing is to watch my psych review video, because the thing is on the psych on the neural mbme, they have, they put up some psych questions there. My psych review video, I think is like an hour and a half. Okay. So it's just something you can watch there, slight for it. And that will potentially help you get like the psych questions that they put on the neural shelf. Okay. So just again, a weird thing to keep in mind. Then as I found out, I offered tutoring for the USML is step one through three exams and shelf exams and like medical school coursework basically. So if you have any friends that need tutoring in those areas, don't forget to send me an email, divine intervention podcasts at gmail.com.

And if you have any feedback on the videos or any questions or any concerns, please don't be afraid to reach out. I'll be more than happy to help. So I am sorry, I did not pick my goal of keeping this under an hour. It's like 68 minutes, but I wish you a wonderful day. And God bless and have a wonderful week. And I hope a Manchester United wins their game tomorrow against Juventus. Okay. Bye for now. Thank you.

Elevated methylmalonic acid (MMA) and/or elevated homocysteine.

Sudden onset, "worst headache of life," or thunderclap headache (suggesting Subarachnoid Hemorrhage).

Carbamazepine/Oxcarbazepine.

Fever, headache, and focal neurological deficits.

Spinal epidural abscess.

Administering Atropine (to block receptors) and Pralidoxime (to reactivate acetylcholinesterase).

Gerstmann syndrome (acalculia, agraphia, left-right disorientation).

Vasovagal syncope.

Simple partial seizure (focal without loss of awareness) and Complex partial seizure (focal with loss of awareness).

PMD is typically symmetric proximal weakness; IBM often presents as asymmetric, distal weakness first.

3-Hz spike and slow wave activity.

Niacin/Vitamin B3, due to diversion of Tryptophan away from its conversion pathway.

Gerstmann syndrome (acalculia, agraphia, left-right disorientation).

Vasovagal syncope.

Simple partial seizure (focal without loss of awareness) and Complex partial seizure (focal with loss of awareness).

PMD is typically symmetric proximal weakness; IBM often presents as asymmetric, distal weakness first.

3-Hz spike and slow wave activity.

Niacin/Vitamin B3, due to diversion of Tryptophan away from its conversion pathway.