DIP Episode 49 - 3rd Year Neurology Clerkship Shelf Review Part 6

Welcome. My name is Devine. I am a PGY one transitional year resident. This is the 49th episode of the Divine Intervention Podcasts. We're going to be talking, we're going to be continuing on your OG clerkship as shelf reviews. This will be the sixth part. So let's just jump right into it. But I'll just give a forward warning. I will encourage you like... You really want to pay attention to this podcast and here is the reason why. And you'll see why as we go along. But I can almost promise you that for those of you taking a newer shelf, you'll probably get like 10 to 15 questions correct conservatively. This is me just speaking conservatively from this singular podcast. So I really encourage you to pay attention. I'll try to make it as short as possible. But try to make it as high as possible as well. So the first question. Multiple neurologic deficits in a kit after getting the VZV vaccine or after let's assume a viral operator infection. So what's the diagnosis? So this is just something you need to recognize. It's kind of like along the spectrum of multiple sclerosis. But it kind of resolves after a while. But this is something known as ADM, ADEM. Acute disseminated and cephalomyelitis. The classic association on exams is a kid gets the VZV vaccine or gets any kind of viral vaccine or gets like some weird viral infection. And then after that, they just have like just diffuse profound paralysis. Think about ADM.

It's basically you have like a ton of like inflammatory demyelinating lesions in the brain and spinal cord. I will imagine probably me the diagnosis with like MR imaging, right? So you get an MRI and the norm in general is a full is a full recovery. Okay. So next question. So this is the multiple sclerosis question. Right. You knew this was coming up. Right. And I'm going to talk about the demographics of for MS. I'll talk about the associated vitamin deficiency. And I'll give you some reasoning why that may make some sense. We'll talk about the diagnostic testing. We'll talk about the CSF findings with if you do a lumber puncture. We'll talk about the classic cranial tube pathology and how it presents. We'll also talk about the classic exam presentations, right? I'll mention some things with that in a second. We'll talk about how you treat an acute exacerbation and how you treat chronically. Okay. With like disease modifying therapies if you may. Okay. And then we'll talk about treating like the other stuff in MS like urge and overflowing continents. They love to test that on your exams and also on Ubi Gain shelves for some reason. And then we'll talk about how the muscle spasticity is treated. Right. So the thing is multiple sclerosis. The classic demographic on exams is a young female. Okay. And almost always it's a young female in her 30s that has these are disparate neurologic deficits. If you see that think I'm on multiple sclerosis.

And usually these patients have vitamin D deficiencies. I mean, it may not even necessarily mean that they have a vitamin D deficiency, but low vitamin D like supplementing vitamin D actually makes things better somewhat in multiple sclerosis. And this is how you sort of thought about it. Right. So it kind of makes some sense. Right. The thing is the incidence of multiple sclerosis. So I guess prevalence is much higher. The farther away you are from the equator. Right. And the thing is as you go farther and farther away from the equator, you have less sunlight. Right. If you have less sunlight, you have more risk of vitamin D deficiency. Right. And the thing is actually the farther away from the equator, actually the higher the incidence of I mean the prevalence. And I guess incidence of MS. Right. So if going away from the equator increases the risk of MS and going from the equator is as if she's a less sunlight, which is associated with less vitamin D, you can sort of imagine that given vitamin D may sort of like reverse that in some way, shape or form. So sort of keep that at the back of your mind. I mean, obviously does it reverse MS what it helps. Okay. At least many neurologies prescribe prescribed vitamin D to their patients. Okay. And the way you make the diagnosis of MS is within MRI. Okay. It's essentially a radiologic diagnosis. Patients with MS tend to get like MR Is. I believe every like three to six months to sort of track the progression of the allusions.

Right. So if you see multiple like demilinating lesions separated in space and time, that helps you make the diagnosis of MS. Right. And you again, you get a brain and spinal cord MRI. The lumber puncture is not necessary for diagnosis, but if they were to do an LP, you'll show something known as an oligoclonal band. Right. So it can be like a non specific. IGG elevation in the CSF and the classic cranial nerve to presentation, right. It's optic neuritis. Right. Do not choose U Vitis. Choose optic neuritis on your test. It's a super classic cranial nerve to presentation. Basically, the will present is a present as like I Pane in the setting of like a severe affroned popularity effect. It's an acute problem. Right. So you see like a severe profound unilateral decrease in visual acuity on one eye. Right. So classicly on exam questions, you'll say, oh, the visual acuity in the left eye, the eye without optic neuritis like 2020. But in the right eye, the eye with the I Pane, acute onset blurry vision, whatever in like 20 over 200 or something ridiculous. Okay. If you see a unilateral acute onset profound affroned popularity effect in an MS patient, you really want to think about, you really want to think about optic neuritis. Okay. And the other signs that you may see on exams for MS, right. They, if they describe a patient that, oh, when they flex the neck, they have like a shock like sensation going down the back all the way to the limbs. That's what's known as lermite sign.

It's a classic physical exam finding in the setting of multiple sclerosis. And then you may see that, oh, patients with MS, they may say like, oh, in the ground in the sun, or when they take a hot shower, their symptoms get worse. That's something known as utosphenominone. I'm not a hundred percent on this, but I think heat sort of slows down conduction through nerves. So if you already have a demilinating disorder, right. Remember, you need myelin to speed up conduction along nerves. So if you already have a demilinating disorder, and then you add a second hit by being in the heat, then you can sort of imagine that that would like profoundly slow down nerve conduction. And that can acutely worsen, acutely worsen symptoms. And really, the way you treat acutely exacerbations of MS, you give super high doses of our quadricosteroids, like a thousand mix per day or something ridiculous like that. And really, the disease, what to find therapies, you probably don't need to know the mechanisms of action, or there are some key things you want to know, right. So like you want to remember like weird names. And the thing is, their names are kind of exotic for the most part, right. So like, fengolimate is an MS medication. Nathalie's UMAP is another MS medication. That one I found in high yield, at least for people taking step one to know that it's an alpha-4 integrated inhibitor.

But a big, big, big thing you want to certainly remember, or not, at least UMAP is that it can cause a reactivation of the JC virus. So it can cause a progressive, multi-focal look and stuff, a lot with these. So PML, PML from JC virus activation. And then you also want to remember, um, gladiorama. Again, you don't need to worry about the mechanisms of action. Gladiorama is another treatment. Some physicians prescribe a toxin map for MS. It works pretty well. And interferon beta is also a good treatment for MS. Please do not confuse interferon beta for MS with interferon alpha that's used to treat more like HEPC, for example. And an easy way to remember that is like HEPCIA, right. So HEPCIA interferon alpha. So CIA, right. If you live in the US, you probably heard of the CIA. Okay, don't worry, I'm not a member. Okay, so next. So urgent overflowing continents. So urgent continents, right, is where a patient cannot get to the bathroom in time before the EP, right. And urgent continents, right. Think of urinary urgency. Usually put that buzzword in the Q-step. Okay, and urgent continents, right. It arises from your detrusome muscles being like hyperactive, right. So like hypertonic detrusome muscles, if you may. So you sort of try to quieten them down. And the way you can quieten them down is by just blocking the most chronic receptors that you find on their surfaces. Right. So you can give drugs like oxybutin, that's a most chronic receptor antagonist.

You can give a toterrhodene, right. You can give dharfenacene. You can give sulfenacene and trospia. In fact, if I'm remembering correctly, I think when I was studying for a step one, I learned a nomonic about on the darn toilet. Right. So the always for oxybutin, the teeth for toterrhodene, the teeth for like dharfenacene and sulfenacene, they kind of sound the same. And then the teeth for trospia. I've actually seen each of those drug names on exams. So you definitely want to know those. And then for overflowing continents, this is where it's kind of like the opposite of urging continents. So these people, their, their detrusome muscles have refused to contract, right. They don't sense when the bladder is full. So like urging continents where those patients have like detrusome hyperactivity, right. With low post void residual volume, contrast that overflowing continents where they have like detrusome hypotonia. So the detrusome muscles don't have enough tone. And the post void residual volumes, this is, that's more for an obi-gain shelf, is usually pretty high, usually more than like 300 cc's or 300 meals, for example. For those patients, you treat with, you treat, you give something that can activate those detrusome muscles. So if we give a muscronic receptor antagonist for urging continents, you want to give a muscronic receptor agonist for overflowing continents.

So you want to give drugs like, like Bethany call, or you can give something that can boost the levels of acetylcholine, like new stigmin. New stigmin is an acetylcholine esterase inhibitor. So by inhibiting acetylcholine esterase, you'll boost your levels of acetylcholine. And that those can activate the muscronic receptors on the surfaces of the, of the, of the detrusome muscles. Another thing you could also do is, you can do like a self-catheterization for, for overflowing continents, right? So like, periodic self-cath. One other thing you could do is, you could technically give like a tam-sulocene to sort of open up the bladder neck so that they can drain their, their, blooders easily. But that's really favorite tested on exams. And then the spasticity that accompanies MS, right? You can treat it with like a black baclofen, right? So baclofen is a gababir receptor agonist, I already talked about this in a previous podcast. So, right, gabba is a calming down neurotransmitter if you may, right? So it causes like, it reduces the rate of firing of neurons, right? So if you gave a gababir agonist, like baclofen, that can sort of quieten down those muscles. And you can also give tizanidine, right? Tizanidine sounds an awful lot like a clonidine, right? So that should help you remember that it's an alpha-2 agonist, okay? So it's a centrally acting alpha-2 agonist. That would decrease the release of neuropinephrim, right?

And again, sort of just think of it as, you remember neuropinephrim is something that you have if you're like in a hyper, think of it as a hyper state. And if you want to treat spasticity, you want to go to a hypostate. So give an alpha-2 agonist. Remember, those are GI coupled, right? So they are coupled to G-Protting coupled receptors, they are coupled to a GI, right? So those inhibits are then a little cyclase. So you do not convert ATP to cyclic KMP. So those low levels of cyclic KMP, you don't activate protein kinase A, and you decrease the release of neuropinephrim at the adjuenergic synapse, okay? You could also use dantrulline, I've talked about dantrulline in previous podcasts. It's a calcium channel blocker that you can use to treat malignant hypothermia, or you can also use that to treat an ureletic malignant syndrome, right? And then you could use benzoes. Remember, benzoes are kind of like baclofen, but benzoes are GABA air receptor agonist versus baclofen that is GABA-B receptor agonist. If it's like a localized spasticity, you can actually just inject Botox toxin into the muscle. Okay, remember, the botulinum toxin cleaves like SNAP proteins. So you do not release acetylcholine at the neuromuscular junction, right? So you get like a flassey paralysis. So effectively paralyze the muscle under the circumstances. Okay, so I know this was a long slide, but MS, in fact, I will tell you this.

If you finish a neuroshelf and you did not encounter any MS question, go back and look over your entire exam. Something has gone horribly wrong. You have to see MS questions and a neuroshelf exam. So just so that you keep that at the back of your mind. Okay, so next question. So this is slide three. So classic exam presentation of viso-vigal syncopy. This one shows up in a pretty classic way, right? So it can be a patient that sees blood or they undergo like a severe emotional stressor and then they pass out. That's viso-vigal syncopy. You can make the diagnosis with something known as the tilt table test. That's probably about as much as you need to know for exams. I mean, there is treatment. You can give like some synbathomimetics and all that stuff. Like middle drink. For example, middle drink is an often cited treatment choice in textbooks, but that's very, really tested. Remember the presentation like you see blood, you go through a severe emotional stressor, you pass out. Meet the diagnosis with a tilt table test. That's pretty much all you need to know. And you can treat with middle drink if you have bandwidth for that extra information. Now next one, right? So the most common cause of death in patients with factor eight and factor nine deficiencies. Well, I'm really hoping you're thinking of hemophilia A. Remember hemophilia A sounds like eight, right? Eight deficiencies. And then hemophilia B. Remember like vitamin B9, right? Fully casted, vitamin B9. Okay?

So hemophilia B is a factor nine deficiency. Those are both inherited in an excellent, recessive fashion. So if you see a girl with bleeding problems on your test, it's not hemophilia A or B. Okay? Hemophilia C can show up in girls because that one is autosomal recessive inheritance, right? And the easier we remember that is like, remember the like pronounced the word car like C-A-R. Hemophilia C is autosomal recessive. Okay? So if a patient has hemophilia C, right? They can show up in a boy and a girl, but in a, the only people that get hemophilia M beyond tests are guys. Okay? Because they are excellent recessive disorders. And really the most common cause of death in those patients is actually like hemorrhagic strokes, right? So they can have like intra-cerbral bleeds. Because remember if you have no activity of factor eight and factor nine, your, your intrinsic coagulation cascade does not work. So you cannot form clots. I mean, basically secondary hemostasis does not work. Okay? So you have an increased risk of bleeding. Remember, those patients can also have like hemathrosis from bleeding into their joints. And again, it's excellent recessive. So how you think to know that? So let's keep going. So the next, the next question talks about the stepwise diagnostic testing and stroke management, right? So this one, basically for patients with signs and symptoms of a stroke, like, oh, neurodefersed, stop talking.

I, something issue like sodium onset loss of vision in one eye. The first thing you want to do is a non-conhead CT. You want to do a CT scan of the head without contrast. Okay? The reason you do that first is because you want to differentiate between a hemorrhagic stroke and an ischemic stroke. Right? The thing is if you give contrast, then you don't know if you are looking at blood or you're looking at contrast in the brain because blood essentially serves as its own contrast, especially on a CT image. Right? So you do a non-contrast head CT first. Now help you determine is this a hemorrhagic stroke or is this an ischemic stroke? If it's an ischemic stroke, if, say for example, like worst headache of a patient's life, you don't have a non-conhead CT, you don't see anything, right? You want to jump to a lumbar puncture, right? To rule out, like a sub-archnoid hemorrhage, right? Because a negative non-conhead CT does not rule out a sub-archnoid hemorrhage, right? So for that, you want to go down the pathway of getting a lumbar puncture looking for zanctochromia. Okay? And remember for that, you lower the blood pressure and then you can give them my modepine so that you can prevent like the post stroke visospasm. But again, for just mainstream stroke, you do the non-conhead CT, it's negative. Then the next thing you do is actually do a combination of things at the same time pretty much, right?

So usually the next right answer on the exams is to get a doppler, like a duplex ultrasound of the carotid arteries. Okay? That will help you see if you have like, if you hear like, brewery or whatever, right? To help you see if you have any kinds of issues with the carotid arteries, right? Because for most of these schemic strokes, many of them begin from the internal carotid, not the external carotids, the internal carotid arteries. Okay? Remember the internal carotid, right? Please a big roll in the vasculature of the brain. And then another thing you can do is you can do an echocardiogram to look for like a thrombus, especially for schemic strokes. You can do for like a thrombus, like at the left echala appendage, for example, or to look for a, what is it called? To look for a PFO, right? A PATHEN for a mental valley that may cause like a cryptic stroke where things go from the right side of the heart to the left side of the heart and flick up to the brain. Okay? So first step, non-conhead CT, second step, get a carotid, like duplex ultrasound, a duplex ultrasound of the internal, not external, internal carotid arteries. And then you can also get an echocardiogram. Okay? And in general, if it's a hemorrhagic stroke, you try to lower the blood pressure, blah, blah, blah.

But if it's an schemic stroke, which is actually the most common kind of stroke happens at about 80% of the time, you give aspirin, if you don't see aspirin as an answer choice, give any antiplichlet agent that shows up in the answers. If you see aspirin and another antiplichlet agent, choose aspirin. But if you don't see aspirin, choose something like clopidogra or diperidomal. Any antiplichlet agent, remember, there's a big difference between an antiplichlet drug and an anti-quagulant. The anti-quagulant contains like warfarin, riveroxaban, bivalerodean, gabigatron and all that stuff. Those are anti-quagulants. Those target secondary hemostasis. Versus antiplichlet agents that target primary hemostasis like aspirin, like diperidomal, like clopidogra. Okay? Those are the ones you generally want to choose for strokes. The only time an anti-quagulant like heprin will be the correct answer in the treatment of a stroke is if they basically tell you in the Q-step that the patient, your scotate the chest and you hear like an irregularly irregular murmur indicating that you have E-fib. The patient has E-fib. That is the only time on exams or new exams where you give an anti-quagulant like heprin or warfarin for the treatment of the stroke. Very, very high yield to know that. Okay. So moving on to the next slide. I know some of you are probably hyperventilating by looking at this slide already. Don't panic. But this stuff is super high yield. You'll see it on your neural shelf.

You'll see it on step one. You'll see it on step two. You'll see it on step three. I promise you that. I promise you that. So you might as well just learn it now. Okay. So much to the lesion cream on her. And this is actually in two parts. So the first one is paralysis of the psyllateral upper and lower facial muscles. Dry mouth, loss of lacrimation and psyllateral upper and lower facial muscle weakness. So this one is kind of high yield to know. This is a cranial nerve seven lesion. This is the facial nerve. And remember for your NBM is actually like mega high yield to know the difference between an upper motor neuron cranial seven lesion and lower motor neuron cranial seven lesion. The thing is an upper motor neuron cranial nerve seven lesion, right? Effects. And upper motor neuron CN seven lesion affects the contra lateral face. Okay. But the lower motor neuron cranial nerve seven lesion affects the psyllateral face. So many times if people think of upper and lower motor neurons, the only thing they think about is like, oh, the cortical spinal track coming down to the anterior horn of the spinal cord. And then supply those anterior horn neurons, which are lower model neurons. The thing is your cranial nerves, all your cranial nerves are actually lower motor neurons. And well, I guess with one exception, I'll say, I mean, I have to do some research on this, but I'll see probably cranial nerve two.

It's kind of different because it's actually an outgrowth of the, of the diencephalop. But pretty much every cranial nerve is a lower motor neuron. The upper motor neurons that correspond to your cranial nerves constitute a tract known as the cortical boba tract. Okay. The cortical spinal tract is for the lower motor neurons that are your spinal cord, but the cortical boba tract. So cortical spinal, lower motor neurons spinal cord, what? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What? What?

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Bytemporal heteronomas, hemianopsia because you're involving the left visual field and the left eye and the right visual field and the right eye. I'll encourage you sort of diagram that sort of makes sense to you. You basically have ton of vision. Yeah. Okay. So next one. Contralateral facial weakness. Please don't get this one wrong. Take a pause here. Don't get this one wrong. Contralateral facial weakness with forehead sparing and loss of taste sensation with the anterior to thirds of the tongue, right? So this is an upper motor neuron cranial nerve seven lesion. Okay. So contralateral lower facial weakness. Contralateral lower facial weakness. That's a cranial nerve seven lesion. Well, that's an upper motor neuron cranial nerve seven lesion. Okay. And the sparing of the, again, the forehead is spared. And remember for taste from the anterior to thirds of the tongue, right? So the general sensation of taste from the anterior to thirds of the tongue is done by cranial nerve five. Okay. It's done by cranial five. Contrast that with the special sensation of taste from the anterior to thirds of the tongue. That is done by cranial nerve seven, the facial nerve. Okay. So that's why this patient has loss of taste sensation in the anterior to thirds of the tongue. And then the next one says horizontal deplopia with failed A Bduction on lateral conjugate gaze, right? So if you have problems with A Bduction, that tells you that you have issues with cranial six.

The abducent nerve, right? So the lateral rectus muscle has been knocked out, right? So you tell the patient, oh, look to your side. And they can adopt the contralateral, like one eye, but they cannot AB doc to the other eye. Think about a cranial nerve six lesion and abducent nerve lesion, right? So that can arise in the setting of, sorry, I'm trying to think through this. That can arise in the setting of like a cavernous sinus syndrome or something like that, right? Because remember, the abducent nerve runs through the middle of the cavernous sinus, right? Or if you have like elevated ICP, right? Remember, the abducent nerve has like the longest course of all the cranial nerves in the brain. So it's very susceptible to elevations and intracranial pressures. Now, the next one says vertical diplopia. So this is not horizontal diplopia. This is vertical diplopia. Vertical diplopia with the jaw tilt it towards the side of the lesion and difficulty going down stairs. This should hopefully get you thinking about a troclear nerve issue. Troclear nerve issue. Remember, the troclear nerve is the only cranial nerve that decusates in the like dorsally in the brain stem, right? So you can give your contralateral findings. So if you see a contralateral finding with cranial nerve for, that can actually be a normal motor neuron deficit, right? Because cranial nerve for decusates. It's actually the one cranial nerve that decusates in the brain stem.

Okay, and the mechanism behind like the jaw tilt in towards the side of the lesion, that is easily a 15, 20 minute lecture. It's something that I will need like an actual visual to describe. I'll probably describe it in a podcast that I'll make like in a few weeks or months. Yeah, that's a very complex phenomenon, but not necessary for a neural shaft. Just remember that your jaw tilt towards the side of the lesion. And you get vertical diplopia. If you see that combination, think about a troclear nerve, a troclear nerve cranial for issue. Okay, so slide 6b, right? So again, much of the lesion cranial nerve. Since we're in your role here in loss, ready go? And an abnormal caloric test result, right? So that's the vestibular cochlear nerve, right? That's cranial nerve A. That's pretty easy. The caloric test, I'll probably describe the mechanism in a different podcast, but that's like cows, right? Like cold opposite worms saying. Talk about that in a later podcast. So do I think they may have mentioned it somewhere? But I don't really remember a minute where 49 podcasts and this has been going on for a while, obviously. Okay, so, but that's a cranial at lesion. Now, division of the protrudeck tongue to the Ipsidial site, so think of licking your wounds. Remember, what's the cranial nerve that innervates all the intrinsic muscles of the tongue, right? That is, that is that is the hypoglycein nerve, right? cranial nerve 12.

Although remember that palatoglosus is actually one of the intrinsic muscles of the tongue, it's actually innervated by cranial nerve 10, the vagus nerve. There are certain rules that sort of like govern those naming conventions. They are known as, I'll encourage you to look up stern's laws. I don't have time to go into those studies. I'm going to keep going. What Palatoglosus is the only intrinsic talk muscle that is innervated, that is not innervated by cranial nerve 12. It's innervated by cranial nerve 10, the vagus nerve. Okay, next one. Wigness in shoulder shrug plus problems turning the head to the opposite side, right? So that tells you that I don't know, maybe like your sternoclidomastoid don't work or your trapezoids. Your trapezoid muscle doesn't work, right? So, hopefully you're thinking about the spinal lecesary nerve, that's a cranial nerve 11, okay? The spinal lecesary nerve. So you have shoulder droop on the Ipsilateral site, site, and difficulty turning your head to the Contralateral site. Okay, now, next one says, loss of taste sensation in the busier third of the tongue, plus dysphysia, plus an absente, gag reflex, right? So, hopefully you're thinking about a cranial 10. I mean, this can be a technically a cranial 9 or cranial 10 lesion. So you probably won't try to mess you up with that, but probably think more of a cranial 10 lesion, although cranial 10 does like the back, back, back of the tongue.

So really, I'll say that really, this is probably an ambiguous question. I'll see that yeah, cranial nerve 9 fits for this, the glosopharyngeal, the glosopharyngeal nerve, because the glosopharyngeal nerve, if I'm remembering correctly from, from anatomy, back in the day, the glosopharyngeal nerve does, um, um, it does one far in geomotol, I believe it's known as stylofaringeus, but cranial nerve 10, the vagus nerve does pretty much every other far in geomotol. So yeah, this could technically be cranial 9 or cranial 10. So glosopharyngeal cranial 9 or, or vagus cranial 10, okay, although for this one, I think I'll lean more towards vagus, um, but cranial 9 is also an acceptable answer. Okay. Now, um, it invades the superior bleak mossol, right?

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and then, um, the glosopharyngeal 10, and then, um, the glosopharyngeal 10, and then, um, the glosopharyngeal 10, and then, um, the glosopharyngeal 10, and then, um, the glosoph have bilateral construction of the pupils, because the information is just not making its way to the brain.

But, for those people, if you shine light in the left eye, you're getting the information into the brain through the left cranial nerve 2, and the left cranial nerve 2 for the pupillary light reflex projects bilaterally to the cranial nerve 3, right? So, those people, if you actually shine light in the eye that does not have the upper and pupillary defect, they will have bilateral, pupillary construction. That's an afferent, so an A, like an A, like Apple, A, Ferent Pupillary defect. Contrast that with an E, Ferent Pupillary defect, like an E, like an egg, right? So, like an E Ferent Pupillary defect, that's an issue with cranial nerve 3, okay? So, let's see, a patient has an E Ferent Pupillary defect on the left, for example. If you shine light in the right eye, the information travels to the brain, it's projected to both cranial nerve 3s, right? But, you only get construction of the right cranial of the right pupil, you won't get construction of the left pupil, because the left cranial nerve 3 is a little bit more difficult to do.

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The mechanism behind that is if you have a right frontal-eye field lesion by knocking out your right frontal-eye field that means you have knocked out your left pprf, your left paramedium pontine reticular formation If you have knocked out your left pprf that means your right pprf will act on a post If your right pprf is acting on a post that means you will have your right cranial 6 nucleus active that means your right eye will act on a post that means your right eye will act on a post that means your right eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that means your left eye will act on a post that like rewind this diagram this out it makes perfect sense okay but this again will be an example of like a brain stem this will be an example of a brain stem lesion okay now next slide to A B so complete sensory loss on the left plus severe pain on the right this one is just an association you need to know this is a lesion of the thalamus okay so again this will fall under the purview of a sub cortical lesion basically for patient has like control letter of severe pain if the letter of complete sensory loss think about

I mean so let me put it this way so I don't get things confused if a patient has complete like a dense sensory loss on one side of the body and severe pain on the alternate inside of the body think about a thalamic nerve lesion I'm not going to go into any mechanisms there but just think about a thalamic nerve lesion that's not very high you to know for example okay now ataxia pass pointing impaired rapid alternating movements right so remember the tremor this diadococaine is here right so nothing you tell your patients to sort of slap your hands on their on their on their thighs quickly right and an intention tremor right so hopefully this tells you this is a this is a cerebellar problem right it's a cerebellar problem and most cerebellar problems are ipsilateral okay the ipsilateral to the side of the lesion now bowel blooded dysfunction plus upper mureneuron and lower mureneuron findings plus a sensory level a sensory level this is floridly high yield for the neurochef if you see the boss phrase sensory level that is a mylopathy that's a lesion in the spinal cord okay it's a lesion in the spinal cord basically if you have like a sharp demarcation after which you've basically lost like sensory and mood information like oh it's like oh they say like right beneath the nipple the patient has lost all sensation lost all mood activity that's a spinal cord lesion that's what's known as a sensory level okay and the thing is the spinal cord in does control like bowel bladder function right so think about what I coined a scene from for example right so bowel bladder dysfunction upper mureneuron findings right usually the upper mureneuron findings are below the level of the lesion while the lower mureneuron findings are at the level of the lesion if you see that combination you really really really want to think about you really really want to think about a spinal cord spina

l cord problem okay next one is trouble swallowing plus problems with eye adduction on conjugate gase plus sensory loss on the left face plus sensory loss on the right body right so this is again a brainstem problem okay so why is this a brainstem problem right the thing is if you see sensory loss in the itsylateral face and then sensory loss on the control lateral side of the body that's pathonomonic for a brainstem lesion right because remember that your spinal trigeminal tract that controls a pain and temperature sensation for the face runs lateral lateral in the brainstem right it runs like itsylateral and it runs like in the lateral brainstem right but your body the pain and temperature sensation of the body that's your spinal phyllamic tract right that runs also lateral in the brainstem remember that you've had an initial deaccusation at the level of the anterior white comasher in the spinal cord so so this patient that has trouble swallowing that's kind of like cranial 9 through 10 and 12 territory so this is probably a problem like in the lateral meddala right if you're using that algorithm I mentioned like I think one or two podcasts ago so this is a lateral meddlerary problem right so this is probably like the posterior inferior cerebellarory that has been looked this I believe is known as Wallenberg or Syndrome remember that posterior inferior cerebellarory is a branch of the vertebral artery okay so if you don't see paikas an answer show is big vertebral but if you see paikas vertebral pick the most direct answer to the question pick paika okay and then a hemibalismus bradykinesia so let me if you make this more complete control lateral hemibalismus and bradykinesia think about sub-tolamic nucleus issue right this is a sub-tolamic issue and again the sub-tolamic nucleus is a deep brain structure so that's a sub-cortical lesion okay now next one stocking an

d glove distribution of sensory loss plus fluctuating the pleopia dysphysia dysatria plus lower moron neuron findings so the thing is I'm just gonna um in fact probably forget about the fluctuating the pleopia dysphysia dysatria blah blah blah this patient basically has diabetes but the thing I just want to mention here is that if a patient has a stocking and glove distribution of like sensory deficits you really want to think about a peripheral nerve issue that is the pathonomonic finding in a peripheral nerve lesion if a patient has lesions in a stocking and glove distribution you really want to think about a peripheral nerve problem okay but it's one nerve that is effect there's not multiple nerves multiple nerves that's a radical empathy one nerve that's a peripheral neuropathy okay again you may see divine this is all you I promise you if you don't learn the stuff you'll regret on your neural shelf and likely on step two seek as well okay now the next one says trouble rising from the seated position so like a proximal muscle defect if you may plus an elevated ck this is a problem with actual muscle right so this could be polymyocytis or dermato myocytis or inclusion body myocytis I talk about this in an earlier podcast and also in the medicine videos um but yes this would be a muscle problem if you see like proximal ish like proximal extremity issues think about a muscle problem it's a problem at the level of the muscle one I did not include here if you're thinking about a neuromuscular junction problem uh so like a myon neural junction problem if you may so myon neural uh think more about uh neurologic symptoms that are fatigable right so like they get worse with uh further activation of the muscle right so like uh my austenia gravity so be an example of a neuromuscular junction problem or lumbar it in my austenic syndrome although uh lumbar it in is not a fatig

able disorder something where if you actually stimulate the muscle more and more you uh it gets better right so you have an incremental response of the muscle with repetitive nerve stimulation I talked about that in a previous a neuro podcast right so um that'll be a myon neural junction issue okay so if you see fatigable symptoms that's pretty pathosmotic for a neuromuscular junction or a myon neural junction issue good so nine four signs of a busiler skull fracture there's something you need to memorize right so like battle sign right so like uh like basically like bruising behind the mastoid process um raccoon eyes right so like bruising around the eyes right raccoon eyes that's another sign of a busiler skull fracture um if you see like css frainuria right so like css literally like dripping from the nose uh that's a sign of a busiler skull fracture or if you see like css otoria right so like css dripping out from the ears that's a really bad sign again that's also pretty pathosmotic for a busiler for a busiler skull fracture you may have that diagnosis by like doing a head CT right you can see bone really well with CT imaging okay now uh and I've talked about how your differentiate between a peripheral neuropathy and the radicalopathy right so a peripheral neuropathy one nerve involved stocking and glove distribution radicalopathy multiple nerves involves dermatomo distribution radiating pain from like one place to another okay think about a radicalopathy that's a nerve root issue okay now um last question right so question 10 weakness in shoulder abduction and deltoid paralysis right so that's an axillary nerve problem that's c5 c6 right so that's uh that's a nerve that's a peripheral nerve issue okay now weakness in foot eversion and dorsiflexion um that will be hmm that will be a perineal nerve problem right so remember the first ebnomonic dropped foot dropped

like the last three letters of dropped this p ed so a perineal nerve problem will cause problems with eversion and dorsiflexion okay and then the next one says weakness in foot inversion and planter flexion so remember the first ebnomonic tip right so tip tb-on-erv if you have a tb-on-erv injury you have problems with i inversion and p planter flexion now weakness in wrist extension that's pretty easy that's your radio nerve right um and remember you can injure the radio nerve if you have a uh mid shaft fracture of the humerus a mid shaft fracture of the humerus can cause a radio nerve uh injury and axillary nerve injury usually arises in the setting of a surgical neck fracture of the humerus or in the setting of an anterior shoulder dislocation okay um remember that your radio nerve does your triceps reflex does your supinator um kind of high your things do there okay now problems with thomb eb-duction with sensory losses on the ventral agro three and a half digits right it's pretty easy this is capotoneal syndrome that's a midion nerve issue right uh it's a compression uh uh by the flexor etenaculum right in the capotoneal and remember that classically on exams the classic populations that get a capotoneal people that have like a like a dim a causing conditions right like pregnancy very kind of swell up everywhere in pregnancy right or um rheumatoid arthritis right from all that inflammation and also um hypo thyroidism those are like the classic classic demographics for capotoneal syndrome on exams and then also people that do a lot of like furious typing uh like office workers or i guess uh coming a little closer to uh to medicine right like match students or people that are using epico furiously during the day so i guess like residence and uh interns maybe not attendance okay moving moving on so um uh problems with hip flexion it's pretty easy that's a femoral ne

rve so remember the f in femoral for the f in hip flexion okay problems with hip adduction this one is easy they'll tell you that the patient cannot the way i think about it is i think of it as like an air problem right so like markbook air for example so they cannot ad docks their hips and they cannot internally rotate their hips that's an obturator nerve lesion okay that's an obturator nerve lesion now weakness with a finger spread and problems with flexion at the mcp's right so the method couple phalangeal joints and extension at the ip joint right so your proximal and distal interphalangeal joints that's pretty classic for owner nerve lesion okay so if you have problems with finger spread that's an owner nerve injury and their nerve roots controlling the following reflexes uh you you basically need to know this like there's nowhere around it if you don't know it uh you'll be doing yourself a big disservice on your neural shelf right so uh basically let's talk about these are reflexes right so the biceps reflex it's like c5 c6 the triceps reflex that's like radio nerve territory that's like c7 c8 okay the achilles reflex that's a s1 and s2 and the patelli tendon reflexes l3 l4 so repeat that again your biceps reflexes c5 c6 triceps is c7 c8 achilles is s1 s2 patelli tendon reflexes l3 and if i'm not mistaken there is actually a numonic yeah let me try to remember there's a numonic in first date i believe that makes this super easy to remember it's like like s1 to buckle shoe uh so that's like achilles reflex um l3 for kick the door something like that so that's a patelli tendon reflex and then c5 six has something to do with sticks um that's your biceps reflex and then uh latem straight so c7 eight right that's your triceps reflex right it's extension of your upper extremity right so yeah s1 to shoe something i'll encourage you to check for stadium see the exact nu

monic um for step one for say for step one l3 foys like the kick the door 5 6 c5 6 that's biceps that's something with sticks and then c7 eight that's like something with like lean them straight or something like that okay so that's all i would say with that and then just some high-yodermatomes you probably should commit to memory for your exam i'll talk about them real quick the big ones you want to know you want to know about your your nipple line right so that's what i do remember the numonic from first date it's kind of like the hope kids are not listening to this but t4 like the t the tit poor right so like tit's like breasts um so t4 tit poor that's t4 for the nipple line the zyfoid process is t7 okay and then the umbilikus is uh is t10 the umbilikus is t10 okay so i know this was kind of long but please um all the stuff is high in in fact i'll see all the neuro podcasts have made this is the highest yield one like i can almost guarantee 10 to 15 questions on your neural shelf will come from this and you'll see some questions on your step 2 ck that will come from this one so it's super super super super super high yield to learn this podcast i wish you all the best i will probably make two or three more for neuro and then i'll be done okay i wish i could make a video but i just don't have that technological capability right now uh but i have some good stuff coming down the pipeline within the next few days for step one and uh hopefully uh more students across the country can uh get some benefit from that so please feel free to share the website it's uh www.divineintervention podcasts so there's an s at the end.com and if you have any questions or need uh guidance and stuff or like uh tutoring you can reach out to me and uh we show the best have a wonderful rest of the day and god bless i'll see you in the next podcast thank you

Young female in her 30s, presenting with disparate neurologic deficits.

Optic neuritis (unilateral, acute onset profound afferent pupillary defect).

A sensory level (a sharp demarcation of lost sensation/motor function).

Cranial Nerve VI (Abducens nerve), as it controls the lateral rectus muscle.

Antiplatelets (e.g., Aspirin, Clopidogrel) target primary hemostasis; Anticoagulants (e.g., Warfarin, Heparin) target secondary hemostasis.

Hemorrhagic strokes/Intracerebral bleeds, due to failure of the intrinsic coagulation cascade.

Oligoclonal bands (OCB) and elevated IgG.

Optic chiasm compression, often by pituitary adenoma or craniopharyngeoma.

UMN affects the contralateral face; LMN affects the ipsilateral (peripheral) face.

Antimuscarinic agents (e.g., Oxybutynin). Mnemonic: "The teeth for toterodine, the teeth for dalfenacene, and the teeth for tropia."

Raccoon eyes (periorbital ecchymosis), Battle sign (mastoid ecchymosis), CSF rhinorrhea/otorrhea.

Patellar tendon reflex; part of the "First Date" mnemonic (L3 for kick the door).

Peripheral neuropathy shows stocking-glove distribution; Radiculopathy follows a dermatomal pattern.

Oligoclonal bands (OCB) and elevated IgG.

Optic chiasm compression, often by pituitary adenoma or craniopharyngeoma.

UMN affects the contralateral face; LMN affects the ipsilateral (peripheral) face.

Antimuscarinic agents (e.g., Oxybutynin). Mnemonic: "The teeth for toterodine, the teeth for dalfenacene, and the teeth for tropia."

Raccoon eyes (periorbital ecchymosis), Battle sign (mastoid ecchymosis), CSF rhinorrhea/otorrhea.

Patellar tendon reflex; part of the "First Date" mnemonic (L3 for kick the door).

Peripheral neuropathy shows stocking-glove distribution; Radiculopathy follows a dermatomal pattern.