DIP Episode 101 - USMLE Step 1 Rapid Review Series 6 (Neuro)

Okay folks, welcome. My name is Divine. I am a PGI-1 Transitioner here resident who are going into ideology. And this is episode 101 of the Divine Intervention Podcast. And this podcast will be a short podcast. It will be the sixth iteration of our USML Step 1, Rapid Review Series. And we'll be talking again about neurology. But again, notice this is not my full neurology review for the USML Step 1. I'm going to make that series. Just being on ICU, mixing kind of tough. But think about this Rapid Review Series as an opportunity to get like clinical presentations of diseases very quickly. You get those down because that's the way the NVME classically tests those concepts. So let's go ahead and jump right in. So what is the, I guess, what's the lesion associated with ignoring one side of the world? So like, hemispation neglect. That's actually a lesion to the non-dominant Pridolope. Right? Remember, if you are right-handed, chances are your dominant Pridolope on your left and your non-dominant Pridolope on your right. Okay? So for most people, for the great majority of people, the non-dominant Pridolope is epsilon, to the hand that they use for the most part to write. Now, next one. What if you get a question about a lesion that's associated with like Paul, like the Abelid? These people cannot calculate, they can't write, they can't tell like, oh, this is this finger versus this other finger. So they have like eight calcula. What do you think?

What kind of lesion can produce those kinds of deficits? So that's actually a lesion to the dominant Pridolope. Right? So again, if you are right-handed for the great majority of people, and most of the time on the NBA means, right, it'll be your left Pridolope. Now, what would you have as the visual field deficit? They'll be associated with lesion in the Pridolope. So in the Pridolope, will it be a superior or inferior quadrantanopia? It'll be inferior, right? Remember, the Pridolope is higher than the temporal lobe in the brain, right? So, and remember that your optic pathway crosses a lot, and I'll say more things about this pathway when I finish up the four-neural reviews. But because the Pridolope is above, right, you'll have problems with your visual fields below. So you'll have an inferior quadrantanopia. And remember, you'll have an inferior, contralateral quadrantanopia. Okay, now, what would be the visual field deficit that may be associated with like compression of the optic chiasm? So let's assume a person has like a pituitary adenoma, that's compressing the optic chiasm, or in a kid you have like an adamantinomato screen, you find in juma, that's also compressing the optic chiasm, right? That'll be a bi-temporal heteronimus hemianopsia, okay? That'll be a bi-temporal heteronimus hemianopsia. And I mean, I just said that if you have a lesion of the Pridolope, you have like an inferior contralateral quadrantanopia.

What do you think would be the case if you had a lesion in the temporal lobe? Remember, the temporal lobe is below, right? So you have a superior contralateral hemianomus, quadrantanopia, okay? So just make sure you can sort of reason through it because again, I promise you all these scenarios, I'm not bringing them to the forefront because they are low-yodominiums, they're from cause-in-shop on exams, more specifically, NV Me exams. Okay, now what would be the visual field deficit that will be associated with PCA stroke? To them, really, I'm going to hammer these deficits in. So like a posterior cerebral artery stroke, right? It would be like a contralateral homonimus hemianopsia, right, with macular sparing. Remember that the macula receives two sources of blood supply. It gives blood supply from the posterior cerebral artery and from the middle cerebral artery, right? So you have a PC stroke, the macula will still get blood supply from its collateral system if you may, which is the MCA, so the macula will be spared. Okay, what if they give you a question? A person, they tell you that this person has been altered, has been disoriented, has like a fever, has no courage, GDT, and they tell you that on image in let's say like MRI of the brain, you'll find enhancement of the temporal lobes. What bug are you thinking about? Now be HSV1.

Remember, herpes love to torch the temporal lobes, and then in addition to that, you will also see a lot of rib blood cells in the CSF if you were to perform a lumber puncture. Okay, now what if they give you a question about a patient that loves to put everything in his mouth, like put everything literally in his or her mouth? So where is the part of the brain that has been lesion? That'll be the amygdala, right? That'll be like a bilateral amygdala lesion. What's that syndrome called? That'll be the clover bucy syndrome, okay? That'll be the clover bucy syndrome. Okay, and then if you have a lesion to the fasciculus gracilis, what kinds of deficits would you have? Would you have deficits in the upper extremity or in the lower extremity? You'll actually have deficits in the upper extremity, right? And remember that because it's a spinal cord lesion, right? So basically, right, I'm referring to the doso column media lemneska system because it's a problem at the level of the spinal cord. Remember that your doso columns do not cross until they get to the coda medulla, right? So they is sent it'silaterally and then they cross. So did they, you see, the level of the coda medulla? So because that's not the case, you basically have an it'silateral loss of fine touch and vibratory sense for the lower extremity. Remember the fasciculus gracilis controls the lower extremity and then the fasciculus conidas controls the upper extremity.

So if you, for example, lesion to the fasciculus conidas, you would have like an it'silateral loss of fine touch and vibratory sense for the upper extremity. And again, it will be it's lateral because you've not had the accusation happen just yet. Now, what is the spinal cord tracked that will be lesioned if you had like a problem with your lateral brain stem? What's the spinal cord tracked that will be lesioned if you had a problem with your lateral brain stem? That'll be a spinal phalamic tract, right? In fact, in my neuro podcasts for the 30th year show of exam, I basically just cost an algorithm for resolving brain stem lesions. Brain stem lesions like people are always scared by those things, but those things are probably one of the easiest things in neurology. And when I continue my full neural reviews for step one, I am going to spend a decent chunk of time just going over that algorithm. But it's a pretty nifty algorithm. Like, basically helps you essentially resolve every brain stem lesion, or you could see with like almost like 100 or 100% a degree of confidence. Okay, now what is the spinal cord tracked that will be involved in a medial brain stem lesion? Right? That'll be the corticospinal tract remember the corticospinal tract travels in the in the medial brain stem. And then the spinal phalamic tract travels more in the lateral brain stem. Another high yield track that sort of travels in the lateral brain stem is your hypothalamus sympathetic tract, right?

So whenever you have a problem with the lateral brain stem, one of the findings you'll see is you'll find an epsilon lateral hornar syndrome. Okay? Because that you're really your sympathetic, your autonomic nervous system in general, including like for your sympathetic, for example, they all study in the hypothalamus certain like nuclei in the hypothalamus. So for example, if you're doing your sympathetic nervous system to sort of trigger your thoracolumbar business, you're studying the hypothalamus, you decent lateral in the brain stem, and then make your week to like the thoracolumbar spinal cord. And then you have all those things that then ultimately go to the superior cervical ganglia and whatnot. So just sort of keep that at the back of your mind. Okay, now what if a patient loses pain and temperature sensation in a key plight distribution? What are you going after here? Right? I'll be sharing my earlier, right? I'll be sharing my earlier. Remember, sharing my earlier is associated with a type one and all key area malformation. Okay, so that's one thing I definitely keep at the back of your mind if I were you. What's a key area tumor formation associated with a lumbus sacral mylominin gocel? Okay, that's a question that's going to show up on step one on step two, CK and on step three. You better keep that at the back of your mind. Okay, now what if they give you a question and the patient has trouble repeating no ifs and or buts. So they cannot repeat the spoken word.

What kind of lesion are you thinking about? So they have poor repetition? That's a lesion to the acuate facicular. Okay, remember that's kind of like a go between your brookers area and your wrenky's area. Remember, kind of to repeat things you need to be able to sort of connect what you hear. I mean, what you understand to what you say. Excuse me. Excuse me. Okay, now. Let's sort of dig a little deeper with this brainstem problems because it's just one of these things that sort of almost like it's people alive on an MBA. So let's sort of like knock those out quite a bit. So I already said that if you have a lateral brainstem lesion, right, you have issues with the spinal phalamic tract. So you have like a contralateral loss of pin and temperature sensation. So pin temperature and pin prick sensation. And then I also said that you have an epsilon or a horn or syndrome, right. Now, that's all what you find with a lateral brainstem lesion. But what if you want to be a little more specific and say you know what to find? I know that it's a problem like in the lateral medulla, right. Remember the medulla is a part of the brainstem, right. The thing is you find like shoulder droop, right. So like a cranial 11 problem, right. So like an epsilon lateral shoulder droop or epsilon lateral like a cranial nine or cranial 10 lesions. So basically these lateral, I'll just tell you this. So basically figure out where you are.

Ask yourself, is there a hunger syndrome or pin and temperature problems? If the answer to that is yes, that's a lateral brainstem lesion. If the answer to that is no, it's a medial brainstem lesion. Or if you, the person has primarily motor weakness, right. That's more of a medial brainstem lesion because you're involving the corticospinal tract. And then to know exactly what part of the brainstem, like what part of the lateral brainstem or part of the medial brainstem is screwed up, find a cranial nerve or two that's mentioned in the Q-stem. So if for example, right, you see like shoulder droop, that's cranial 11, your spinal accessory nerve. Or you see like cranial nine, cranial 10 problems, right. That tells you it's the lateral medial. Because guess what, cranial 19 and 11 are found in the medial. Now, what is the cranial, what is the, so I said that a medial brainstem lesion will give you like motor weakness problems, right. From the corticospinal tract, that being screwed up. What is I guess one distinctive feature that can tell you that you know what I'm dealing with the medial medial. That'll be tongue deviation, right. I remember it to be tongue deviation towards the side of the lesion, right. So like leaking your wound, right. That'll be a cranial 12 problem or a hypoglossal nerve problem. Okay. Now, it will be a distinctive feature for a lesion in the lateral ponds. That'll be facial droop, right. So that'll be like a cranial 7 problem. Okay.

Now, it will be a distinctive feature of a problem in the medial ponds. So think of the cranial nerve that you find in the medial ponds. That'll be cranial 6, right. You have 2 cents nerve. So this people will have problems with, problems with an IAB reduction. So problems with I abduction. Okay. Now, what kind of stroke will be associated because the thing is, you know, in BAB, you can test these concepts in many different ways, right. They can ask you like, where's the lesion in the brain or they can ask like stroke of what blood vessel causes these same features. So basically you're just, you just essentially have to know like your circle of will is like this other tends to supply what part of the brain stem this other tends to supply what other part of the brain stem. So if for example, right, they're asking you for the stroke that's associated with like problems with a lateral medial, right. That'll be a paika lesion, right. So like a lesion to the posterior inferior cerebellar artery. How about the medium edulla? That'll be the anterior spinal artery, right. That'll be the anterior spinal artery. Remember that anterior spinal artery, right. Can arise from the artery of a dhamcoids, especially if you're like the upper spinal cord. So if a person has like a triple-lay repair, so a repair of an abdominal aortic aneurysm, they can actually get in function of the anterior to thirds of the spinal cord. They can get an anterior spinal artery syndrome, okay.

So I keep that at the back of your mind. So basically those people, the only tracks that will still be functional will be, um, um, will be like the dorsal columns. Those will be basically the only things that function. And then they may have like some lateral cortical spinal tract function as well. Okay. Now, what would the stroke be? That'll be associated with problems in the lateral ponds. That'll be an e-icast stroke, right. So an anterior inferior cerebral artery. Uh, what would the stroke be? That'll be associated with problems in the medial ponds. That'll be a stroke of like the basilar artery, right. So like the basilar artery, it's a paramedian branches, stuff like that. Okay. Good. So like the paramedian pointing, um, arteries. Now, what would be the stroke? That'll be associated with internal capsule problems. That'll be the stroke, uh, lesion to the lenticular stride artery, okay. It's actually kind of high up to know that the lenticular stride artery is a derivative of, um, of the middle cerebral artery. Uh, it's one of those tiny artery strokes that can cause profound deficits, right. Because remember, the posterior limb of the internal capsule, your cortical spinal tract fibers that are coming from the cerebral cortex, they also to crowd themselves into the posterior limb of the internal capsule. So if and the lenticular stride artery supplies that posterior limb of the internal capsule.

So if you infarct your lenticular stride arteries, um, you'll basically have like control lateral loss of all motor function on one side of the body. So if you leege, if you have an infarct of your left lenticular stride artery, you have right, like right-sided weakness of the upper and lower extremities, okay. So it's one of those small arterial problems that can cause big, big, big deficits. Okay. Now, what will be the stroke that'll be associated with infarction of the optic nerve head? That'll be the posterior ciliary artery, okay. It supplies the head of the optic nerve. Now, what will be the stroke associated with a complete loss of vision in one eye? Right. That's- this is basically a central retinal artery occlusion, right. So it'll be the central retinal artery. Okay. Now, what if you get a question about a patient that sort of loses his sense of smell? After getting in a fight, what has he fractured? He has fractured the cribiform pleats, right. Remember the cribiform pleat of the ethmoid bone? Um, it's kind of useful for what's the name of this nerve? Um, cranial one, right? Your factory nerve. Okay. Now, what is the arterial lesion? The arterial lesion that'll be associated with a loss of cortical hearing. A loss of cortical hearing. Now, be the middle cerebral artery, right. Because remember that you are part of what you used to hear, okay. Um, it's kind of concentrated in a part of the cortex that's supplied by the middle- by the middle cerebral artery.

So it's in the middle cerebral artery distribution. Now, what if they give you a question and detail you that they give like a super-dilithe amount of pylocarpine and it leads to a pupillary constriction? What's the diagnosis? So this is actually something known as AD's pupill. Um, the pathophysiology behind it is easily a five-minute lecture. So because, again, this is supposed to be a part of the rapid review series. I'm going to it. But the way I just sort of think about it is this way. I'll give you a very nice analogy, right. Let's assume your home like any normal, um, uh, look, let's say your home like any normal meds today and you're studying and all that crap. You have already access to a lot of food, right. So you can afford to be picky. You can say, you know, I don't want to eat this. I don't want to eat that and all that crap. You're not very sensitive to food, right. But let's assume that something bad happens and you're stuck in an island for like four weeks and you've not had food. If a person gives you food, are you really hate? He doesn't matter. You're going to eat it, right. So the thing is, in people that have a dyspropial, um, uh, they are cranial three fibers like they are post ganglionic, parasympathetic, uh, like cranial three fibers. Those fibers have not been getting a lot of stimulation from the pre ganglionic, um, uh, how do I put this? I don't know. I don't really want to go into a lot of, uh, explanation with this. Okay.

Let's just put it this way. So it's a problem with, uh, uh, with a parasympathetic system and the parasympathetic system is not stimulating, um, the cranial three parasympathetic involved fibers, enough. So because the parasympathetic system is not stimulating them enough, um, again, I promise I'll explain this more in my phone, your podcast. Those fibers become super sensitive. So if you give them like super dilute amounts of pile of carping, you would get a popularity construction. Whereas if you did that same test in a normal individual, um, you would not have full popularity construction because people are not that sensitive to the dilute amounts of pile of carping. I think I'm going to go ahead and, uh, and leave it at that. Okay. Now, what if they give you a question and the patient, uh, basically has lost taste sensation in the anterior to third of the tongue? That's a lesion to the facial nerve. Okay. Now, what if they tell you that a patient loses pain and temperature sensation in the anterior to thirds of the tongue? That's a lesion to what branch of the trigeminal? That's the mandibular nerve, right? Remember, in the anterior to thirds of the tongue, the special sensation of taste is handled by cranial seven. But the general sensation of taste, so like pain, temperature, pain, prick, all that crap, is handled by the mandibular nerve. Okay. That's cranial nerve V3, the third branch of the trigeminal.

Now, what if a patient loses like taste, pain, temperature sensation in the posterior third of the tongue? That's the glossopharyngeal nerve, right? That's cranial line. Remember, both the special and the general sensations of taste in the posterior third of the tongue, are handled by the glossopharyngeal nerve. Okay. What if a patient loses all sensation in the pharynx and larynx? That's the biggest nerve, right? That's cranial ten, and maybe, I guess maybe like a tinge of cranial nine as well. Okay. What if they tell you that a patient has an enlarged heart and wharseness? What's the nerve that has been lesioned? That's the recurring laryngeal nerve. Remember, if you have like lefty trill enlargement, that can actually sort of mess up the recurring laryngeal nerve on the... And that can then cause a wharseness. That's why I'm saying like a large heart and wharseness. That's actually a very common USMLE exam question. Okay. And how does the olfactory nerve get into the brain already talked about this, with the person getting into a fight and losing smell, does the crib reform plead, right? Okay. Now, what is the embryologic derivative of the thalamus, hypothalamus, and the optic nerve? That's actually the diencephalon, right? Remember that MS is like a multiple sclerosis essential, the maliniating disorder, and if you notice, the optic nerve, right? Optic neuritis is like a very commonly in common problem in patients with MS.

Because MS usually doesn't go after shuan cells, goes after a legal danger size. But it's so happen that the only cranial nerve that is derived from the di... Like the... From the neuro tube, okay, is cranial tube. The optic nerve, because it's actually derived from the diencephalon. Okay. The other cranial nerves actually are derived from neurocress, so cranial one through twelve. Other than two, cranial twis derived from neuro tube is derived from the diencephalon. Okay. Now, what is the... What if they give you a question about a patient that has a depressed eye that is AB docted in a fixed position? So the eye is down and out, right? That's a lesion to cranial three. Very good. That's an ocular motor nerve lesion, okay? What if a patient has trouble going downstairs or like reading a book? Was the nerve that is all screwed up? That's a trochlear nerve lesion. And again, I will explain the pathophysiology behind all of this in my full neuro... Step one, reviews. Okay. Now, what's the only cranial nerve that's associated with contralateral findings? That's the trochlear nerve as well, okay? And if a person has a lesion to the trochlear nerve, in what direction will their heads deviate? It will deviate away from the side of the lesion, okay? Away from the side of the lesion. Now, what's the cranial nerve that carries like the sensory portion of the popularity light reflex? That's cranial two, right? That's the optic nerve.

How about the motor portion of that popularity light reflex? That's cranial three. That's the ocular motor nerve. Again, I'll talk about the mechanisms behind all this fun stuff in my four-neur reviews. Now, what's the cranial nerve that carries the sensory portion of like the blink, or I guess lacrimation reflex? That's the ophthalmic nerve, right? That's like the first branch of the trigeminal. How about the motor portion of that reflex? That's the fission nerve, right? That's cranial seven. Okay. Now, what's the cranial nerve that carries the sensory and motor portions of the georeject reflex? That's the mandibular nerve, actually. It's the third branch of the trigeminal, okay? And what's the cranial nerve that carries the sensory portion of the gag reflex? That's your glossopharyngeal nerve, okay? That's cranial nine. How about the motor portion of that reflex? That's vagus nerve. So sensory portion, cranial nine, motor portion, cranial ten. And if you lesion your hypoglycer nerve, right? I already talked about this. Your tongue will deviate towards the affected side. But if you have like a vagus nerve lesion, like a cranial ten lesion, your tongue will deviate away from the affected side, right? I mean, your uvalus, sorry, your uvalus will deviate away from the affected side. And then, what's the jaw deviation that would be associated with a trigeminal nerve lesion? It will also deviate towards the affected side. Okay.

And then, remember that if you have a lesion of your cranial, of a, if you have like an obomoto, you know what? Let me leave this for the next podcast. If you notice, I'm sort of going fast towards the end here because I have to run to the ICU, right? I'm actually a ICU rotation. So I'll see some more things about cranial seven that are kind of confusing for people. I'll talk about that in the, in the next rapid reveal. I'll try to kind of maybe break it down there. So I'm going to stop here. As always, I offer one on one tutoring for step one, step two, CK, step three, step two, CES, and then, I'll show you some of the things that I've been doing. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things.

I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things. I've been doing a lot of things.

Non-dominant parietal lobe.

Bitemporal hemianopsia.

Glossopharyngeal nerve (CN IX).

Dorsal columns and potentially lateral corticospinal tract function.

Ipsilateral Horner's syndrome AND contralateral loss of pain/temperature sensation (Spinal Phalamic Tract).

Oculomotor nerve (CN III).

Ipsilateral loss of fine touch and vibratory sense in the upper extremity.

Dominant parietal lobe.

Kleinian syndrome (or Amygdaloid Syndrome).

Lesion in the non-dominant parietal lobe.

Mandibular nerve (CN V3).

Lenticular artery; causes contralateral motor loss.

Olfactory nerve (CN I).

The uvalar/tongue deviates away from the side of the lesion.

Dominant parietal lobe.

Kleinian syndrome (or Amygdaloid Syndrome).

Lesion in the non-dominant parietal lobe.

Mandibular nerve (CN V3).

Lenticular artery; causes contralateral motor loss.

Olfactory nerve (CN I).

The uvalar/tongue deviates away from the side of the lesion.