DIP Episode 58 - Neurology Clerkship Shelf Review Part 7

Okay, welcome. My name is Devine. I'm a PGY one, a transitional year resident. This is the 50th episode of the Divine Intervention Podcasts. And in this episode I'll be doing the seventh part of our Neurologic Clutchip Show for Views. Let's just jump right into it. So the first question says, discussion of the pathway, slashing formation, carried by the three high-yield spinal cord tracts. So that's like the DOSO column medial, the MISCO system, the spinal phalamic tract, and the cortical spinal tract. So let's talk about this real quick. So the DOSO column medial and MISCO system carries information relating to like fine touch, vibration, and proprioception. Okay. And if you sort of want to talk about the pathways, I think it's probably, it probably makes sense. So it's causing in the context of the upper and lower extremity, right? So for the lower extremity, we have those fibers coming in carrying that information, they first ascend in the spinal cord, okay? And the fibers, I mean, you see them as they constitute like the fasciculus, gracilis, if you're dealing with the lower extremity. And then for the upper extremity, you have something that is the fasciculus conidas, okay? Both in the DOSO, like the more DOSO part of the spinal cord, but those fibers don't synapse yet. They continue their journey, they ascend it salarily, okay? To the Codomidola, and then they meet via first synapse, right?

So the second order neurons for fasciculus, gracilis, that deals with the lower extremity. We have nucleus gracilis, and then for fasciculus conidas, that deals with the upper extremity, we have nucleus conidas, okay? So you have those fibers synapse, and then after that, those fibers decusate the crust, as the fibers of the medial lemniscus, and then continue all the way up, contralaterally, very high, or contralaterally, and go the way to the thalamus, okay? And then they synapse in the thalamus, and then the third order neurons, right? They go from the thalamus to the post-central gyros, very high, you to know that it's not the pre, it's the post-central gyros, those are sensory fibers. And then for the spinal thalamic tracts, the spinal thalamic tracts carries pain, pain prick, so like pain and pain prick, and inflammation, and temperature information, and the way that tract works is, again, kind of in single deal, carries that pain and temperature information. Only problem is, it actually, when it gets into the spinal cord, it actually synapses almost immediately, although it can rise like one or two levels, whatever, that doesn't really matter much. But basically, it will synapse almost immediately when it gets into the spinal cord. After, initially, it comes in, excuse me, initially, it comes into the spinal cord as less hours tract, rise this one or two levels, doesn't really matter, and then it synapses immediately.

And then those second other fibers, the cross in the anterior wide commission of the spinal cord, and then they ascend, contralaterally, as the fibers of the spinal thalamic tract. And it's actually very high, you'll to know that they travel in the lateral brain stem, not the medial brain stem, lateral brain stem, unlike your doso-colon-medial-limniscus system that actually travels in the medial brain stem. And then, again, going back to the spinal thalamic tract, and then the lateral brain stem contralaterally, goes to the thalamus synapses there, okay, third other neuron, then starts from then again, goes to the post-central gyros, because those are sensory fibers. And then, for the coricospinal tract, it carries motor information, right? So, that starts in the pre-central gyros of the cortex, right? Because, again, remember, those are motor fibers, and then those fibers continue down, and it's allaterally, they go through like the interpandomular fossa, blah, blah, blah, blah, blah, blah, and they all travel immediately in the brain stem, until they get to the medulla, okay? And then, you have something known as the pyramidal deucetion. Those fibers that you see at the level of the medillary pyramids, at least 90% of them, okay? And then, those fibers continue downwards to the lateral, I mean, to the dorsal part of the spinal cord, they keep going, get to the ventral horn of the spinal cord, and synapse on anterior horn, motor neurons, that then send fibers, right?

Remember, like your smart nervous system, basically, those are the lower motor neurons, they go to your skeletal muscle. Okay. Now, the rhumbar test, right? So, the rhumbar test is really many people say, it's a test of a servile function, it's not. Okay, the rhumbar test is a test of dorsal column function. Okay. Basically, it's a test of perceptive ability, and the thing is, to know where you are in space, you need two out of three things to be working. The three things are your vision, your vestibular system, okay, and your dorsal columns. Okay. Out of those three, you need two out of three to follow over. Right? The rhumbar test is just where you close your eyes, stand together, boom, you can fall, you either stay standing or you fall off, right? So, the thing is, say, for example, a patient has tertiary syphilis, right? And they have tibis dorsalis. Tibis dorsalis knocks out your dorsal columns. Well, those people, they walk around just fine, no problem, because two other things are working for them, vision and the vestibular system. When you then tell those people to close your eyes, you think vision out of the equation. So, it's now just one of those three things that are working, and then we topple over. It was a test developed by a physician back in the day. This name was like Dr. Romburg to sort of screen people for tertiary syphilis.

And to test your develop function, you can do those things that you've probably learned in your physical diagnosis courses in med school, where you can tap your hands rapidly on your laps, right? That's like testing for this diadococainecia, right? Or you can do the finger to nose business, or you can tell people to sort of like take the heel of your legs, and sort of rub it up and down along their lobe extremity. And then the homonculus, right? The homonculus, don't forget that if you're looking at the homonculus, on the lateral side of your homonculus, you have your face, and then on the middle side, sort of like descending down the fox area, right? Is your leg area, okay? And then kind of in the middle, you have like your upper extremities, okay? Very high u to know that in the context of localizing lesions with vasculine salts in the brain. And then dronkallitaxia is indicative of a lesion to the serbalovermis, okay? Serbalovermis, very high u to know that. Now, the circle of willis, right? So I'm going to discuss this. That's question two. And pathologies associated with vasculine salts, right? So let's talk about the circle of willis. So basically, the circle of willis is, you know, high u to know for exams. It's a high u to know for exams. So let's talk about it in pathologies associated with vasculine salts, right? And they will talk about one high u to know the association. So the circle of willis starts as the vertebral arteries, right?

They come off of the subclivian. So you have the vertebral arteries, they come together, okay? To form the basilar artery. But before they come together from the basilar artery, they give off two arteries, right? They give off your eica, your anterior inferior cerebral artery, okay? And then they give off your anterior spinal artery, okay? And then they join together from the basilar artery. The basilar artery gives off paika, the posterior inferior cerebral artery. And then the basilar artery continues, okay? You have like some paramedium-pointing arteries from the long the way. And then you have the superior cerebral artery, okay? And then after that you form the posterior cerebral artery. And then the posterior cerebral artery joins up, sort of gives off the posterior comricating arteries by lottery. Then join up with the anterior cerebral artery. And then those two anterior cerebral arteries, I kind of joined together by the anterior comricating artery. So what are the high u things you want to know about these different arteries, right? So let's start with anterior spinal artery. The anterior is the anterior spinal artery, right? If you have an infarction of that artery, you have problems with your medial medulla, okay? I've talked about this in a previous, in one of the previous neuro podcasts. But you have issues with your, you have issues with your, with your medial medulla, okay? So you have like crinion of 12 problems, right?

So your tongue will like a divide towards the side of the lesion. You will also have contralateral hemiparysis, right? Because you have involvement of your corticospinal tract. Remember that goes in the medial brain step, okay? And then if you have issues with, let's assume you get a weird question about a patient that is getting a triple ear repair, okay? In the process of repairing a triple, you can actually, so that's like an abdominal, an anterior abdominal, an aortic aneurysm, okay? You can, in fact, I'm not even known as the artery of a dhamcoids. The artery of a dhamcoids is a precursor artery to the anterior spinal artery, kind of a little lower in the spinal cord. So if that happens, you can actually get something that was anterior spinal cord syndrome, okay? Where basically you lose every spinal cord function with the exception of your drosal columns. It's another high you think you know, but that's more of a spinal cord pathology as against the cerebral cortical pathology. And then if we go further to a aica, I mean, sorry, yeah. Paica, sorry, paica. The posterior fira cerebellar artery, okay? Paica, remember those come off the vertebrates, okay? Paica supplies the lateral medall, right? So if you have an infarct of paica, you would have issues with cranial nerves 9 through 12, okay? I mean, sorry, cranial nerves 9 through 11. You would have problems with cranial 12.

And the reason is, again, remember cranial 12 runs in the medial medalla, not in the lateral medalla. So you have problems with cranial 9, okay? So you can have problems with like your jaw or anything like your uvula, or you can have problems like tasting stuff in the posterior third of your tongue. You can have like shoulder droop from like cranial 11 issues, right? Stuff like that. And then if we go on to aica, if you have a problem with aica, you have a problem with your lateral ponds, okay? Remember, aica comes off of the basilar artery. You have problems with your lateral ponds. If you have issues with your lateral ponds, basically cranial nerves 7, 8, really is your cranial nerve 7 and 8 will be all screwed up, and also cranial nerve 5, okay? And the reason you have those problems is because you have a lateral pontein problem, right? Remember cranial 6 runs in the medial ponds, but all those other like like 5, 7, and 8, they all run in the lateral ponds, right? So you have problems with like facial droop and all that badness. You will have, you actually have pain and temperature problems as well, okay? Because your spinal phylamic tract runs in the lateral brain stem, okay? And one of the high you think you will actually get is honor syndrome, okay? Honor syndrome, honor syndrome, because your hypothalamus sympathetic pathway also runs in the lateral brain stem.

In fact, any lateral brain stem syndrome will cause problems with pain and temperature, because the spinal spinal phylamic tract runs in the lateral brain stem. You have problems with honor syndrome because your hypothalamus sympathetic tract, right? The thing that does the superior cervical ganglion business runs in the lateral brain stem, okay? And you have problems with the specific cranial nerves that run in the lateral brain stem, okay? Again, it's very high you have to know that. So if you have like a pica infarct or an ai-kin infarct, those are lateral brain stem issues. Those will all cause those associated problems in addition to the cranial nerve deficits. I promise you we see it all divine. This is low yield, no one cares. Trust me, I would actually not take your neural shelf exam. If you don't know this thing I'm talking about, you will get localization questions where you have to actually use this knowledge. Same thing with your medicine shelf, your surgery shelf, and your step 2cK exam. So you might as well just go ahead and learn this pretty well, right now. And also on step 3 as well. I'm saying this because I've seen questions like these on all those kinds of exams. Okay, so if you affect your bazzle artery, that person is in trouble, right? Your bazzle artery controls so many high yield functions, right? Well, basically your pons is gone. Or if you have like a paramedium pointin artery lesion, your medial pons will be gone, right?

Your paramedium pointin arteries. So for example, you can imagine a person having like an abducent nerve issue with that. Okay, although that is really if ever tested on exams. And then the next set I want to discuss at the superior cerebral and posterior cerebral arteries. In fact, I also sort of discussed the one high yield cranial nerve association right of the bat. The thing is cranial 3, the oculumur nerve crosses between the, it sort of is kind of like a sandwich, is between the superior cerebral artery and the posterior cerebral artery. High yield to know that. And I'll say some weird stuff about cranial 3 down the line. Okay, so, and then the posterior cerebral artery. Remember that it supplies the primary visual cortex right in the occipital lobe. So if you have cortical blindness, right? But don't forget that you basically lose vision in every part of the eye with the exception of the macula. Because remember the macula gets collateral blood supply from the middle cerebral artery. Which is a branch of the internal carotid. Okay, so, and then the posterior communicating artery. The high yield thing I want you to know is that it runs alongside the oculumur nerve that's cranial 3. So if you have a p-com aneurysic, okay, that can actually compress cranial 3. At least the fibers on the outside for starters. Okay, so, and the fibers on the outside are the things that carry parts and pathetic function. So those people can basically lose their, what is it called?

They lose their popularity like reflex. At least the efferent limp of the popularity like reflex. Okay, and then the anterior communicating artery it's important, right? Because it's, it's, it's, it's the most common location of aneurysms in the circle of willis. Okay, and then the anterior cerebral arteries. If you infarct your anterior cerebral arteries, right? Obviously, if you sort of think of the homonculus, remember your anterior cerebral. This is why the homonculus is IELT. The anterior cerebral is run kind of like in the middle of the cerebral cortex, right? So, they supply the late area of your homonculus. So if you have an EC in fact, you have issues with your legs. Okay, you have like motor and sensory issues with your legs. Again, super high you to know your homonculus. Okay, next slide. So heading that is worse with sitting upright and better with lying down after a lumber puncture. So this is something called a post lumber puncture headache. Some people call it a spinal headache. Basically, it arises because you have like a CSF leak, like a persistent CSF leak after a lumber puncture. The pathophysiology basically involves if you have like a CSF leak that lowers your intra cranial and intra spinal pressures. Okay, because those pressures are maintained by your CSF. So if you have a leak, those pressures will be low.

And I sort of think of the brain and the spinal cord sort of like banging up against all those structures because there is not that nice warm fluid around them. So you can get a spinal headache with that. The way you treat that is it's usually self limited. Usually you don't need to do anything. But if it's not going away after like a while, right? You can do like a blood patch, okay? Sort of patch up that CSF leak. And then the second thing you can do is... You can actually give caffeine. Caffeine actually works pretty well for these spinal headaches. Next slide. So what is causing the cranial three, the oculumodonerv lesion, right? So the first one says, I solidified my dryassis with sparing of other cranial three functions, right? So if you just have my dryassis, right? Remember, I told you that I think I mentioned this in the previous podcast, that the oculumodonerv cranial nerve three has fibers on the outside and fibers on the inside. The outside fibers carry the parts and pathetic functions, right? So like a commodition, pulmonary constriction. And then the inner fibers carry the motor fibers, right? So like the somatic motor fibers, okay? So the stuff that controls all those extra oculum, or so's like inferior bleak, inferior rectus, superior rectus, medial rectus, and the levator, papal bris superioris, right? So if you have just isolated my dryassis, you want to think about a compressive lesion from the outside, right?

So like a p-com, a posterior communicative artery, aneurysm. Although, I mean, obviously the aneurysm gets bad enough, right? You compress the outside fibers and then compress the inward fibers. What you see, like isolated my dryassis, the number one thing I want you to think about on your exam, which regards to the oculumodonerv is a p-comaneurysm. Next one is down an outpupil without my dryassis, right? So now, if you have a down an outpupil, that means your extracurricular muscles have been knocked off, right? But your passing pathetic muscles are just fine, right? So that will arise more from an ischemic lesion. Remember, other ischocationally run inside nerves. So let's say a person has like diabetes, that's the classic demographic on exams. A patient has diabetes, and then they have like a schemia of the oculumodonerv. Okay? That can specifically target the inward fibers, right? So they won't have my dryassis, but they will have issues with the other cranial three functions, the monosomatic motor functions that deals with the extracurricular muscles. And then if a patient has down an outpupil, plus notice, these are all different things that are causing the same cranial nerve issue, right? So you can see how this is just tempting for the mb-n. Next one is down an outpupil plus my dryassis, plus weakness of the other trochlamosomes, plus sensory loss over the forehead. That's kind of weird, right? Because it's like you're having cranial three problems, right?

But you also have weakness of all the other trochlamosomes, or pretty much most of them. And then you also have sensory loss over the forehead, right? So what's the cranial nerve that controls sensation over the forehead? Well, I hope you're telling me that it is the trigeminal nerve, the trigeminal nerve, right? It's first branched the ophthalmic nerve, okay? Control sensation over the forehead, okay? So if you see that cluster of symptoms, where you're seeing like trigeminal nerve problems, you're seeing cranial three problems, you're potentially seeing cranial four problems, and cranial six problems, right? That all tells you that, okay, these are all structures. This lesion was being a spot that carries all those things, okay? Which happens to be the coronasinus. So if a patient has coronasinus thrombosis, they can have the specific deficit. This specific lesion is in the coronasinus. Next question says, down an outpropel plus my dracis plus contralateral muroperesis. Okay, so if you're having cranial three problems, we're also having contralateral muro problems, and you know this has to be a critical issue, right? Most likely at the oncus, okay, remember? So if you have like an oncoherenation, for example, that's the classic way this presents, the oncus can compress cranial three, okay? But it can also compress the brainstem, and if you compress the brainstem, right? You can screw up your corticospinal tract.

Remember, that's prior to the deaccusation, so you have a contralateral muroperesis. So make sure you can explain why all these deficits are much up with these are four different locations. Next slide. So differentiating between an opromodon neuron and a low-modon neuron cranial seven lesion, right? So the facial nerve. So this is high-yield, obviously, right? That's why it's in this slide, right? So if you have an opromodon neuron cranial seven lesion, okay? In fact, you know, let's put it this way. Let me talk about the last point of this slide. I think that will help a little more. So let's talk about a subtle principle relating to opromodon neuron versus low-modon neuron cranial nerve deficits. Okay, so here's the deal. Whenever people think about, and I've talked about this in a previous podcast, actually, whenever people think about opromodon neurons, they just think of the corticospinal tract, right? They're like, oh, opromodon neuron, mostly the anterior horn of the spinal cord of the ventral horn of the spinal cord, same business. And then you send fibers to the neuromuscular junction, big deal, okay? The thing you should try to not forget, right, is that, yeah, there's skeletal muscle everywhere in the body. But, you know, there's also skeletal muscle in the head and neck, okay? And just like the skeletal muscles of the body need low-modon neurons, the skeletal muscle of the head and neck also needs low-modon neurons.

Those low-modon neurons for the skeletal muscles of the head and neck are cranial nerves, okay? Cranial nerves are the low-modon neurons for the skeletal muscles of your head and neck. So, if those, if your cranial nerves are low-modon neurons, right, first off, you should know that, that means they are derived from the neuro crest, higher to know that, with the exception of our cranial tube. Cranial tube is actually an outgrowth of the diencephalon, so it's derived from neuro tube. But, those lower-modon neurons, right, the stanza reason that they should have upper-modon neurons, okay? But those upper-modon neurons are not known as the corticospinal tract, you know, as the corticobobotract, okay? Corticobobotract, okay? So, the same way that the upper-modon neurons for the corticospinal tract travel, they quease it, and then go to the lower-modon neurons, corticobobotract works the same way. The fiber study in the cerebral cortex, they travel down, they dequease it, and then they synapse on the nuclei of the respective cranial nerves. So, if you have an upper-modon neuron cranial nerve issue, okay? You have contralateral problems, okay? Because you have those contralateral problems because those fibers ultimately dequease it, before they synapse on the nuclei of the associated cranial nerve. But, if you have a lower-modon neuron cranial nerve issue, you have etsylateral problems, okay? Because those fibers don't dequease it, right?

They go from the nucleus straight to the associated skeletal muscles in the head and neck that they innervate. But there is one exception to that, I know. So, the one exception is the trochlear nerve. The trochlear nerve is the one lower-modon neuron cranial nerve that dequease it's in the brain, so it gives crust findings. So, if you have a left cranial for, left trochlear nerve lesion, you have problems in the right eye, okay? So, let me make this even more annoying, and again, I apologize in advance. Well, let's assume you have an upper-modon neuron trochlear nerve lesion, right? We said that the upper-modon neuron, that's just the way it works, it will dequease it, but we said that cranial for, also dequease it's as well. So, that's like a double-cross kind of issue. So, if you have an upper-modon neuron trochlear nerve, let's say you have a trochlear nerve lesion on the right side of the cerebral hemisphere, right? That will screw up your left trochlear nerve, right? If you have a left trochlear nerve issue, that will screw up your right eye, okay? So, I mean, the superior bleak of your right eye, right? So, that means that upper-modon neuron trochlear nerve lesions, okay? Affect the Ipsilateral eye, lower-modon neuron trochlear nerve lesions, affects the contralateral eye, okay? It's a high-od exception to not. Okay, so now, let's go back to differentiating between an upper-modon neuron and a lower-modon neuron cranial 7 lesion, right?

So, the upper-modon neuron cranial 7 lesion that arises in the setting of, like, a corticoline fart or something, right? The thing is, you have a contralateral issue, again, because remember, those upper-modon neurons will dequease it, you have a contralateral like facial droop, well, that facial droop will actually just be for the lower face only, it will not be for the upper face. And again, I've discussed all this stuff in a previous podcast, so I'll move a little quickly through this, okay? The reason that you have contralateral droop of just the lower face, even if your facial nerve controls all the muscles of facial expression, is that to wrinkle your forehead, that function is controlled by the frontalis muscle. The frontalis muscle is one of those skeletal muscles on the head and neck. The frontalis muscle actually has binilateral innervation from basically like there are two upper-modon neurons, right, for cranial 7, right? There's the upper-modon neuron on the right that goes to the left cranial 7, there's the upper-modon neuron on the left that goes to the right cranial 7, okay? Those upper-modon neurons, both of them, go to the fibers of cranial 7 that control the frontalis muscle specifically. So because there is bilateral innervation, you literally have to infect the whole brain to get like an upper-modon neuron, cranial 7 problem that will affect both the upper and lower face.

Let's assume you don't infect your whole brain, let's assume you infect one side, okay? You will just have contralateral lower facial droop, okay? But in addition to that, if you wanted to localize that smartly, right? If you know that you're infecting one part of the brain, right, you have hemiparesis on the same side as the lower facial droop, right? Because your corticospinal tract will also be screwed up, right? So to make sure you can convince yourself that that is true. Okay, but a lower-modon neuron cranial 7 lesion will scrub both the upper and lower face, okay? So you have a droop of both the upper and lower face, okay? How you to know that? Now the common causes of Bell's palsy, right? Bacterial cause, you're thinking of Lyme disease or a little bit of Dophory, right? Carried by the exodistic. Remember the exodistic I think also carries a Babesia Microdi. Remember that multi-scros business in your red cells and also an aplasma, okay? And then viral cause you're thinking of her piece, okay? In fact, some people for Bell's palsy have actually seen them get a cyclover, okay? Has like some benefit. Bell's palsy also usually steroids help, okay? Although for the most part, Bell's palsy results on its own, right? So the way we'll present on the exam, a person will not be able to like close the mouth on one side. They won't be able to close their eye on one side, right? So for those people, you want to like patch that eye or put like eye drops, right?

So they don't dry out the eye and destroy it, right? And then inflammatory causes, right? So like multiple sclerosis, sacoidosis, sacoidosis, actually a pretty common cause of Bell's palsy. So Bell's palsy is basically a low motor neuron, a cranial 7-0 issue, okay? And then the cranial nerve that's most susceptible to elevated ICP, that will be your abducense nerve, okay? Next slide. 55-year-old female presents with a severe headache that appears to be concentrated over her right eye. Okay? That's bad news. She has a history of job pain, wentch-wing nuts, and proximal shoulder pain. So job pain wentch-wing nuts, right? So that's job litigation. And proximal shoulder pain that was relieved with low-dose pregnancy. I'm hoping you're thinking of pulling my algebra America, okay? So this lady has temporal arteryitis, right? And your next step in management, they will always put an answer that says to do a temporal artery biopsy. Don't do that, okay? You need to give high dose of, like high dose of corticosteroids, okay? And then after that, you can then do an biopsy of the temporal artery. You may say, oh, divine. But if I do a biopsy of the temporal artery late, I will be missing out. No, you're not. You can actually do this biopsy up to like 72 hours later, I think. And you'll still get good results from the biopsy. And this will be more of a step three question, or I guess a medicine boards question.

But if you biopsy one temporal artery, and it's negative, the biopsy is negative, your next step in management is actually to biopsy the temporal artery on the other side, okay? On the other side. Even if that's not the side that has the issue. And the elevated serum markers, it's an inflammatory disorder, right? It's a kind of vasculitis. So your ESR and CRP will be elevated, okay? Next slide. 39-year-old female with a pass medical history of MS presents with severe lift, eye pain and decreased vision. The right and left eye do not constrict when light is shown in the left eye, right? So hopefully this gets you thinking of optic neuritis, okay? Optic neuritis is an inflammation of cranial too, right? So the afferent limb of your pulmonary light reflects. It's not going to work, right? Remember, if you have a problem with the afferent limb, macranial too lesion, right? If you shine light in the eye that has the problem, vision has like left-light pain, so the problem has to be the left eye, right? You cannot carry that afferent, basically the information relating to the pulmonary construction. The pulmonary light reflects does not go in. So if no information is coming in, remember, the information comes in through cranial too and then it projects bilaterally, after from the pre-tecton nucleus, to both cranial nerve-3s. Remember, cranial-3 constitutes the efferent limb of the pulmonary light reflect.

So if cranial-2 is all screwed up, then you're not bringing the information in. So that bilateral projection to a cranial-3 on both eyes, in both eyes, doesn't happen. And if that doesn't happen, right? You will not have pulmonary constriction of either eye when you shine light in the afferent eye. Okay? So this is optic neuritis, you make the diagnosis, but you don't feel like a slit lump exam. And then the way you treat this is with a conical steroids. Now, next question says 65-year-old male with a pass history of diabetes. That's a high-yield history to note there. So pass history of diabetes and coronary artery disease presents with a 5-day history of decreased vision and floters in his right eye. Okay? From the scopic exam reveals retinol-venosengorgement and diffuse hemorrhage. So if a patient is having decreased with a history of diabetes, for like 5 days, they're having like decreased vision. And then you do a phondoscopic exam and you're seeing floters and you're seeing retinol-venosengorgements, diffuse hemorrhage. I really hope you're thinking about retinol detachment. Remember, in diabetic retinopathy, right? You promote this like weird blood vessels in the eye and all those weird blood vessels in the eye can begin to exert like a pooling force on the retina. So that can actually cause a retinol detachment. And really the way you make this diagnosis, you can do like an ultrasound of the eye actually, or you can do like ophthalmoscopy if you may.

But an ultrasound is just fine. You can make the diagnosis pretty well. And really the way you treat this is you can do like a sclerod, we call them like you can do like a lizard, like a lizard, the trectomy. You can do something like a scleroboccal, you can inject like gas bubbles or something like that into the eye. Those things all work. Okay? You basically want to reattach the retina, right? And that's pretty much how that's taking care of. But let's assume we have this inpatient, right? Again, notice we have a history of coronary artery disease. It presents with sudden loss of vision in his right eye. Okay? From the scopic exam is notable for optic disc power. Okay? And the cherry red spot on the macula. I really hope you're thinking about the central retinol artery occlusion. In fact, I have an ophthalmology podcast. Now you should probably listen to before you take your medicine exam, before you take your surgery exam, before you take your neuro exam, and before you take step two, see, and step three. Okay? I talk about all these ophthalmologic pathologies in that podcast. So this is a central retinol artery occlusion. You make the diagnosis with, you can do like CT angiogram. That could work. And the thing you want to do is you want to do like a Doppler ultrasound of the coronary artery, right?

Because many things that have that cause a central retinol artery occlusion, the embolite usually start from like the, start from the coronary arteries and then sort of flick off to the, to the central retinol artery. Okay? So this is how a central retinol artery occlusion presents, right? So like fondle power, I mean optic disc power, cherry red spot on the macula, right? But if you see like a blood and thunder appearance in the eye, that's more of a central retinovino occlusion. And really the way you treat C-R-A-O is you basically begin to massage the eye, okay? And you, you can permanently lose vision. Remember, this is a painless vision loss. And permanently lose a vision. And the way you sort of want to like fix that is you want to inject TPA into the blood vessel directly. Okay? So that's something we want to call your interventional guys for. And then the next question says transient loss, but your initial step in my name is to just, you know, oculum massage. Okay? And then you, that's a, it's a medicine of thermological emergency. People can lose their vision within two hours permanently. Next one says transient loss of vision in the same patient with a curtain, with a return to baseline after 10 minutes. Right? So this is like a TIA of the eye almost. And he says that he felt like a curtain coming down, right? That's amorosis, few gaps. And really the potential complications you could have like a big time stroke in the future.

So if a patient has amorosis, few gaps, you probably want to go ahead and do like some kind of vascular workup so they can figure out whatever is going on with, with a, with a, okay. So you want to check the carotid blah, blah, blah. Now, next question says time we know for TPA administration, right? So if a patient has an ischemic stroke, remember you don't give TPA for hemorrhagic strokes, right? You have a bigger problem with your hands if you did that. So don't do that. So if a patient has an ischemic stroke, you try to give TPA within four and a half hours. Okay? That's like the hard cutoff. All those, you can also give it up to six hours, but that, that has like some red criteria where if you can like get directly into the blood vessel, but that's probably beyond the scope of our conversation here. And then in general, the same drug answer on exams for most strokes is aspirin. Is any kind of anti-plit lead drug? It could be aspirin. Sometimes it could be diperidomal, even diperidomal is an anti-plit lead agent, right? It's a force for diastries inhibitor. And usually in the question, you say like, oh, you hear corroded breweries or something. Okay? Use, I will say like 98% of the time on exams, aspirin is the safe drug to give. However, if a patient has a specifically tell you that the patient has like a fib, okay? And they tell you that, oh, you oscotic the corroded and it's just fine. Okay? That is the only time you give an anti-quagulant.

Notice I did not say anti-plit lead. I said anti-quagulant. Anti-plit lead drugs and anti-quagulants are not the same thing. Right? So for those people, you give anti-quagulants like warframe, okay, or heparin. That's the only time where that will ever be correct. But pretty much every other time, anti-plit lead drugs are the answer like aspirin or diperidomal or really clopidogram. Okay. So next slide. So this just shows you like the visual field defects, right? So like lesion A, if you kill the optic nerve, you're not going to see that eye, right? So if you kill the right optic nerve, right? The eye labeled right? Kill the right optic nerve, you're not going to see that eye. If you have a temporal, if you have a chiasm lesion, right? So like from a pituitary adenoma or from a craniofaringeoma, sometimes an anterior communicating artery and urethane can actually also compress the optic chiasm. It's actually kind of high up to now. So you transsec the optic chiasm, right? You have tonal vision, right? The pathophys behind that is if you look at this diagram, you're basically killing the fibers that come from the, from the nasal retina bilaterally. Okay. So if you're killing the fibers that are coming from the nasal retina bilaterally, you're going to kill your temporal visual fields bilaterally. Okay. So that's why you have a, that's why you have a tonal vision, right? So you're losing the, yeah, you're losing your, need your temporal visual fields bilaterally. Okay.

Tonal vision. That's known as a bite temporal heteroanimus, not homonymous heteroanimus hemianopsia. And then for option C, if you transsec the fibers of the optic tract, okay? Remember, the optic tract is the term used when you're distal to the chiasm. If you transsec the fibers of the optic tract, right? You have a bite temporal homonymous, okay? Homonymous hemianopsia. The reason it's called the homonymous hemianopsia is that you lose the same visual field in both eyes, right? So if you look at B, right? In B, it's called a heteroanimus hemianopsia because you're losing two different visual fields. You're losing the left visual field in the left eye and the right visual field in the right eye. That's why it's a heteroanimus hemianopsia versus C. That's a homonymous hemianopsia because you're losing the left visual field in the left eye and the left visual field in the right eye. So you're losing the left visual field in both eyes, okay? That's why it's known as a homonymous hemianopsia. And you have that if you have lesions distal to the optic chiasm, right? And then if you have a lesion of your lower fibers, so that's like lesion D, you have something known as, basically just reverse things. Although I think actually this diagram, just listen to what I'm saying here. Let's assume that lesion D is a lesion to the lower fibers, okay, of the optic raditions, the lower fibers. If you have lesions of your lower fibers, then your upper visual field will be gone.

If you have lesions of your upper fibers, then your lower visual field will be gone, right? So in this case, because the upper visual field is gone, that means you must have had a lesion of your lower fibers, okay? So if you have a lower fiber lesion, you have something known as a superior quadrant anopia, okay? Superior quadrant anopia, right? It's like a quadrant because like a quarter of a circle. And it'll be a homonymous hemianopsia as well, right? Because it's like the other visual field, right? So if you have a lesion on the right, you lose your left visual field. If you have a lesion on the left, you lose your right visual field in both eyes. And then option E is if you translate like your posterior cerebral artery, right? You'll spare the macula again because you have a collateral circulation from the middle cerebral artery. And remember that this will be a... This would have a macula sparing, okay? Because again, remember the macula gets supplied from the MC and the PCA, okay? And again, it will be a homonymous hemianopsia. Okay, now question 10. What should you consider as an underlying mass in the child that presents with bite temporal hemianopsia? I really hope you're thinking about a craniofarinjoma. There's this pathology professor at the medical I graduated from. He loves to pronounce the full term Adamantinomatos craniofarinjoma. Okay? But remember, it's a tumor that comes from raffi's pouch, okay?

So classically, classically, calcified mass on brain imaging, you have your diagnosis. And it leaks a motor oil fluid. I've talked about that in a previous podcast. In an adult, you're thinking about a pituitary adenoma, likely a prolatinoma, okay? And then in a cerebral cortex stroke, right? The eyes will actually deviate towards the side of the lesion, okay? So why is that? The thing is, I believe I've talked about this in a previous podcast. There is something in the cortex known as the frontal eye field, okay? So let me just describe the path we real quick. The frontal eye field on the right goes down in the brain, decusates, and then goes to something known as the pyramidian pointin reticular formation. The PPRF on the contralateral side, so like the PPRF on the left. And then the thing is the PPRF on the left controls cranial six on the same side and cranial three on the opposing side through the medial longitudinal facicular. So why would that be important? Right? That'll be important because if, for example, you want to look to the left, okay? If you're looking to the left, if your two eyes are moving to the left, one eye has to abduct your left eye and one eye has to adduct. That's your right eye, okay? So you need one structure that controls both. The one structure that controls both is your PPRF, okay? But the go between, right? Like the thing that talks to the cranial three on the opposing side is the medial longitudinal facicular.

So let's assume you lesion the cerebral cortex on the right, okay? Your left PPRF will be screwed up, right? So your left cranial six and your right cranial three will not work. So you have on opposed activity of your right cranial six and your left cranial three. So the eyes will divide towards the side of the stroke, okay? But away from the PPRF, okay? Away from the PPRF, right? So that's what I mean by the brainstem stroke lesion, right? So let's say you have like a brainstem stroke on the left. Your left PPRF will be gone. If your left PPRF is gone, then again, your left cranial six and your right cranial three will not work. So you have on opposed activity of your right cranial six and your left cranial three, okay? So your eyes will divide away from the lesion in a brainstem stroke or your eyes will divide towards the lesion in a cortical stroke, very high to know that. And the thing is if you have... If you have a stroke in the cortex, right? You have like a contralateral hemiparesis. I've talked about that path already. If you also have a stroke in the brainstem, you also have a contralateral hemiparesis, right? Because again, these are all prior to the deaccusation, right? So let's just summarize real quick. If you have a cortical stroke, your eyes will divide towards the side of the lesion and you have contralateral. So you have epsilonateral deviation of the eye and contralateral hemiparesis.

But if you have a brainstem stroke, you have a deviation to the eye to the opposing side. So you have a contralateral eye deviation, where you also have contralateral hemiparesis, okay? Make sure you can reason through that in your mind. And then you have a question for your free to reach out to me. Now, a patient with a history of MS presents with right abduction as stagmas and impaired left eye adduction when asked to look to the right, where's the lesion, right? So this is an MLF lesion. This is interneucleoptermopleasion, okay? So it's an epsilonateral MLF lesion, right? So basically the easy answer to this is find the eye that has adduction issues. In this case is the left eye, so it's the left MLF that is all screwed up. And then horner syndrome, you can have the lesion in multiple spots. You can have the lesion in the spinal cord, right? So if you have like a lateral cord of the spinal, lateral horn of the spinal cord issue, right? So like let's assume you have like a pancus tumor. You can have those kinds of problems. If you have a lateral brainstem stroke already talked about this, you can also have a horner syndrome, okay? Remember, horner syndrome is tosis, myosis, and unhydrocysis. And remember that your claustro headaches can present with a partial horner syndrome. So you have tosis and myosis, but no, and hydrocysis. And then the last question here, a 19 year old male visited the chiropractor for some neck massages. So think of like a neck trauma.

Two hours ago, he was brought to the ED by ambulance after completing of right-sided neck pain, okay? Physical exam is notable for right. So he has pain on the right side of the neck. Physical exam is notable for right-sided, popularly tosis and myosis, right? So he has like a partial horner syndrome on the same side, okay? There are no left-sided findings, right? So this is just a scenario that you just need to recognize on exams. If a patient has any like neck trauma, right? So let's say we're brushing their teeth too violently, or doing a motor vehicle accident that involved the neck, right? Or they went to a chiropractor, right? And they got these kinds of problems. You want to think about a chronic already dissection, okay? And really, the classic findings are you have like Ipsilateral neck pain, Ipsilateral partial horner syndrome, okay? And really, the way you diagnose this is you do like some kind of angiography. Most physicians prefer an MR angiogram, right? So like MR angiography, but you can also do a CT angiogram. That's fine as well. And then the way you treat this is you can treat this with... Treat me will probably not be tested on exams, but you can give like anti-plated leg drugs. You usually go to surgery. I mean, sometimes you can do medical management, but sometimes you also do need to go to surgery, okay? So that's where I'm going to stop today. I hope you've gotten something from this.

I probably will have one more podcast, and that will complete our new series, and then you have a complete review for your new shelf exams. I wish you all the best, and just a reminder, I also offer a private 101 tutoring for med school curse work and the step one through step three exams, okay? Just reach out to me at Divine Intervention Podcasts at gmail.com, and I can point you in the right direction, and also review applications and do like application advising. So have a wonderful rest of the day, and God bless. I'll see you in the next podcast.

Dorsal column function and overall balance/proprioception (requires 2 of 3 systems: Vision, Vestibular system, Dorsal columns).

Posterior inferior cerebellar artery (PICA), due to its supply of the lateral medulla.

Loss of pain and temperature sensation, plus Horner syndrome (due to involvement of the spinal trigeminal tract and sympathetic pathway).

Contralateral lower face droop only (because the forehead receives bilateral innervation).

Bitemporal hemianopsia.

Ocular massage.

Dorsal Column-Medial Lemniscus System.

UMN lesions cause contralateral weakness (except forehead); LMN lesions cause ipsilateral weakness.

Abducens nerve (CN VI).

Loss of pain and temperature sensation plus Horner's syndrome.

Homonymous hemianopsia (loss of the same visual field in both eyes).

Anterior communicating artery.

Dorsal Column-Medial Lemniscus System.

UMN lesions cause contralateral weakness (except forehead); LMN lesions cause ipsilateral weakness.

Abducens nerve (CN VI).

Loss of pain and temperature sensation plus Horner's syndrome.

Homonymous hemianopsia (loss of the same visual field in both eyes).

Anterior communicating artery.