DIP Episode 361 - The Eye Part 1 (for Step 1-3) + Step 2CK/3 Course Reminder

Okay, welcome. My name is Divine. This is episode 361 of the Divine Intervention podcasts. And in this podcast I'm going to be discussing the I. This is going to be a very comprehensive review for pretty much all the USML exams, step 1, step 2, CK step 3. And as a reminder this month we're going to be having two different review courses. So the first is starting on the 24th of this month I have the MBME Testicking Strategy course. It's two and a half hours. It's going to be from 2 to 4 30 PM Mountain Standard Time. Again, if you're taking step 2, see your step 3. That's a course that will be really helpful to you. Many people, the reason they don't do well on the USML exams is just poor testing strategy. So there's tons of people that are taking these courses. They've done extremely well on the exams. I mean I've literally seen people jump 30 points in a week just from attending a testing strategy course or you see if your U-World Q-Bank percentage is jump over by like 20 to 30%. They just start doing really well. Again, it's a class that is very high level but it's extremely helpful. Again, and you know, answer many of the questions that you also have on just a test-ticking process. And then for step 2, see again step 3 and also, you know, if you're taking complex level 2 or 3, I do have a 24-hour review course. That's going to be taking place from the 25th, so the 28th. It's basically going to be six hours, four days, right?

So six hours, six hours, six hours, six hours, 24 hours. We cover internal medicine, PEEDS, surgery, OB-guine, psychneural, biostatistics, ethics, communications, professionalism, and ethics and also multi-system processes and disorders. Again, many people have taken these courses and if don't really well on their tests. And then I also have a foundation's course. That's going to be taking place from the 31st of this month. To the 4th of February, it's targeted to people that are taking the USML Step 1 exam. And it's also targeted to people that are taking step 2 or step 3 that have poor foundations. So let's say for example, if taking step 1 or let's say your first two years of medical screening horribly met school, if your foundations are weak, then that's a course to attend. It's targeted mostly to people taking step 1, but it's going to be extremely useful to those taking step 2, CK and step 3. Again, if you have a weak foundation from step 1, then the course is for you. Basically, we're going to be going over just different pathologies using clinical vignettes, and we'll talk about the physiology and pathophysiology behind those things. And I'm going to make it a point to make integrations. It's going to be like a very integrative course. We're going to integrate like physiology, pathology, pharmacology, many different things across different body systems. So again, it's a 25-hour course. It's five hours every day from the 31st of January to the 4th of February.

So if you're interested, again, in any of these courses, they are all held via Zoom. Just shoot me an email through the website, and I'll be happy to give you some more information. Okay, so let's just go ahead and jump into the eye. And again, I'm going to talk about the eye in just many different formats over the course of this series on the eye. So the first thing is, let's maybe look at how the eye, like from just a structural perspective. So what are the layers of the eye? Well, remember the eye, let's maybe go from outside to inside. I think that will make a lot of sense. So the first thing is, remember the layers of the eye from outside to inside. First, you have the scleror. The scleror is the thing that is on the outermost part of the eye. It's primarily collective tissue. And please don't forget, when you see people that have blue scleror on your exams, that should make you think about something potentially. That should make you think about something potentially. What is that? That. Well, I hope you're saying, oh, divine, blue scleror makes me think about osteogenesis in perfect. So blue scleror is something you should think about with, you know, osteogenesis in perfect. Remember, it's a deficiency of type 1 collagen, right? So I remember that collagen we find it in the scleror. Right? So the thing is, when you have the deficiency of type 1 collagen, basically you have less collagen in your scleror.

So your choroidal vessels, like the blood vessels in your choroid, we'll talk about that in a bit. The blood vessels in your choroid, they just become more visible. That's why you see the person having blue scleror is those blood vessels in the choroid that are just more prominent because there is like a collagen, a type 1 collagen deficiency. So again, if you're looking at the layers of the eye from outside to inside, we have the scleror. Remember, that's connective tissue. And then after that, we have the choroid. Remember, the choroid contains blood vessels. And then if you go further inward, you know, you have the retina, right? The retina is a neuro layer, right? So we have the scleror first, and then the choroid second, which contains blood vessels. And then we have the retina, which is a neuro layer, right? So remember the retina, you know, it's a bunch of neurons, right? Those things just converging the back of the eye. And as it converges in the back of the eye, it forms the optic nerve. That's cranial nerve 2, right? It forms the optic nerve cranial nerve 2. Remember, cranial nerve 2 is derived from the diene cephalon. It's very different, right? From the other cranial nerves. Pretty much every other cranial nerve is derived from neurocressels, right? But your cranial nerve 2 is derived from the diene cephalon. So it's derived from like the neuro 2. Now why is that important?

There is in that, that's important is that the optic nerve is mainly needed by oligodanger sites, not shwan cells like you see for the other cranial nerves. So common mistake, common thing, just many met students just don't understand, I've even heard, right? But the optic nerve is mainly needed by oligodanger sites, right? Because again, it's derived from the diene cephalon. It's derived from your neuro 2. But your neurocressels give rise to all the other cranial nerves, cranial 1 and then cranial 3 all the way to 12. Those ones are mainly needed by shwan cells. In general, as a general rule, not always accurate, but as a general rule, things that are derived from neurocressels are going to be mainly needed by shwan cells. Things that are derived from the neuro tube itself are going to be mainly needed by oligodanger sites. The reason why that's important is if you look at, for example, the demilinating diseases that are friends that the NBM is love to test. If a person has multiple sclerosis, which is a central demilinating disease, right? It's a problem with oligodanger sites. You'll notice that those people tend to have a lot of eye problems, right? Optic neuritis, intranucleopthamuoplisia, blah, blah, blah, blah, blah, again, cranial 2 is innervated by cells by a malinitine cell that's affected in MS, right? But you see people that have Guillembray syndrome. People that have Guillembray syndrome, they almost never have like cranial 2 problems. Why?

Because again, in Guillembray, that's a periferal demilinating disease. That's a shwan cell problem. It's not an oligodanger site problem. Again, it seems like a subtle point, but it actually explains a lot of things that we observe in many different disorders. So again, we have the sclerosis, we have the coroid, and then we have the retina. Again, the retina, again, those things converge in the back of the eye to form the optic nerve, right? It's going to be cranial nerve 2, right? And the optic nerve goes through the optic disk, right? And essentially, as it goes through the optic disk, it forms the afferent, right? So afferent as an A, as an apple, right? The afferent part of our visual system, right? So that we can see, like the thing that's bringing information in. Remember, the cranial nerve that brings information in for you to see is cranial 2. The cranial nerve that gets information out for you to see cranial 3. Cranial 3 is the efferent ear as an egg, is the efferent part of the light reflex, right? So again, so, you know, the retina converges in the back of the eye, forms the optic nerve, goes through the optic disk, right? And that begins your afferent visual system, right? And again, it's actually very high, you'll to know that the convergence of the retina in the back of the eye is actually what gives rise to the blind spot. We do have blind spots in our eyes. It's just from that region where the retina converges, right?

Now, it's also high you to know that the area of highest visual acuity in your eye is actually the fovea, FOVA. Well, what is this fovea part of? The fovea is actually part of a bigger structure called the macula, right? The thing is, this area, you have very good visual acuity because it's basically like just infested with a lot of sensory cells, right? Foto sensory cells that are called cones, right? Remember, the macula, again, is something that our friends at the end of the evening is love, love, love to test, right? They can talk about an old person on your exam that has a lot of blurry vision and the person is seeing a lot of like wavy lines when they're reading, right? When lines don't look straight to them anymore, obviously, and they say, oh, you know, when you look in those people's eyes, you see like a lot of whitish or yellowish deposits, right? That person has macula degeneration, right? That person has macula degeneration, remember, macula degeneration, the positive scene in the eyes, and on us, drusein, right? So you see drusein in the eyes, right? And that's the thing that causes problems, right? And you know, obviously, they can be wet macula degeneration, they can be dry macula degeneration, and we know that the wet macula degeneration, right? You know, it's all these blood vessels proliferating in the macula that's causing problems. So the thing you can do is you can give a vegeph inhibitor.

Vegeph is vasculine, the thylio-growth factor is the thing that mixed blood vessels proliferate. So if you give a vegeph inhibitor, like bevacizumab or anibezumab, that will prevent those blood vessels from proliferating. That's the treatment for wet AMD. Dry AMD treatments are not really great, but you can give anti-oxidants, like, you know, like vitamin E, vitamin K, beta-carotene, and things like that, right? So again, the area of high residual acute in the eye, raised the fovea, the fovea is part of the macula, right? Remember, the chair that's put on the macula things that you find in two of those, like, so some of the storage diseases where we find it in T-Sax disease, or also find it in Neem and Pick disease. But remember in T-Sax disease, they just have the chair-retz put on the macula. They do not have a pardustlenomagula, right? But people that have Neem and Pick disease, they have the chair-retz put on the macula, but in addition to having said chair-retz put on the macula, they also have a pardustlenomagula, right? Because the thing is in Neem and Pick disease, it's a deficiency of an enzyme called sphingomilines. Sphingomilines is an enzyme that we find not just in neurons, but also find it in the reticuloendothelial system. Well, what is the reticuloendothelial system? The reticuloendothelial system is basically a fancy term to be honest with you for the lever and spleen, right?

So the thing is, if you have a sphingomilines deficiency, then sphingomilines is going to build up. It's going to build up in the cells that are in the reticuloendothelial system and in the brain, right? So if those, if your hepatocytes or your spemic cells are getting bigger, then you're going to have hepato-megaly. You're going to have spleenomagaly. If you collapse those two terms together, you get hepato-splino-megaly, right? But in T-Sax disease, it's a deficiency of hexosaminatedase A, when you have a deficiency of hexosaminatedase A, you're going to build up GM2 gangliosite. Look at the name, gangliosite, gangliosite, ganglion. So that means it's only neurons, right? It's not in your reticuloendothelial system, so that's why you don't get hepato-splino-megaly, right? But again, basically, as we go through the eye as we talk to each layer or whatever, I'm just going to bring in the integrations that our friends at the USME Ls love to go after. So again, the area of high-visual acuity, again, is the fovea, which is part of the macula, and it contains a ton of cones. That's why you have amazing visual acuity, right? Now, the thing is, there are two refractory surfaces, because remember, you're probably learning this from college physics, you know, there's like reflection of light and there's a reflection of light. Don't worry, you don't need to panic, and we're not going into optic physics right now.

That can be a discussion for a completely different deal, maybe a different website. Anyway, what's it? Right? Well, they're basically two refractory surfaces in the eye, right? So the cornea, right? Remember, the cornea is the first refractory surface, it's fixed, and you really cannot adjust the cornea. Well, I mean, an ophthalmologist can, but the second refractory surface is the lens, right? The lens is something that your body can absolutely adjust, right? Because remember, your lens is on the other control of your autonomic nervous system. It has a very tight relationship with your autonomic nervous system. So that's something that can be modulated in the body, right? So knowing those modulations, understanding how they work, is something that's very useful for the USMLE exams, right? And then let's go to the iris, right? So the thing is the iris, basically, is a collection of muscles. And essentially, what the iris does is that it adjusts the amount of light that is getting into your eye, right? It adjusts the amount of light, that is getting into your eye, right? So really, let me tell you this, there are two main functions of the iris. And again, I'm going to, the thing is, things that involve neurology, people just tend to not understand it. So these podcasts, I'm just going to take my time and just really try to explain things out well for you, right? So the thing is, again, the iris has two jobs.

The first job is that it's a collection of muscles that adjusts the amount of eye, sorry, the amount, not the amount of eye, whoops, the amount of light getting into your eyes, right? So it's a bunch of muscles that will say, okay, let's come together and make less light enter the eye, or let's come apart and let's make more light getting into the eye, right? So that's one job description of the iris. Now, the second job description of the iris is that it demarcates a certain part of the eye. So let me tell you this, your eye is made of two segments. There's an anterior segment and there's a posterior segment. I'll say that again, the eye is made of two segments. There's an anterior segment and there's a posterior segment. Now, the thing is, the anterior segment contains two chambers. I'll say that again, the anterior segment of the eye contains two chambers. The first chamber is the anterior chamber. The second chamber is the posterior chamber. The thing that demarcates the anterior chamber from the posterior chamber is the iris. The iris demarcates the anterior chamber from the posterior chamber. But remember, the anterior and posterior chambers they are both parts of the anterior segment of the eye. Really, one very roughly to approximate and say that, okay, why do we call this anterior segment? Why do we call this posterior segment? The thing is, in the anterior segment, you have akeous humor. Remember, the akeous for the a and anterior segment.

But in the posterior segment of the eye, you largely have vitrious humor. Really, the thing that divides the anterior segment of the eye from the posterior segment of the eye is actually the lens. The lens demarcates the anterior segment of the eye from the posterior segment. But the iris only demarcates the members of the anterior segment in the anterior chamber from the posterior chamber. Those are the two jobs of the iris. Now, what is the pupil? Again, the thing is, some of you may be like, divine, why are you defining these basic terms? The thing is, if you understand the basic terms, a lot of what I'm going to teach you is going to make a ton of sense. Like, really, like, my goal with these podcasts series on the eyes, if the eye is something you're struggling with for any USML exam, after you listen to these podcasts, you'll never struggle with the eye again. That is the goal. Okay, so we're going to keep going, right? So, the pupil, so what is the pupil? Well, the thing is the pupil is not a structure. It's actually just a space between the iris on the left and the iris on the right. Remember, you have iris on both sides of your eye. So, the iris on the left, the iris on the eye, on the right. The space between them is the pupil. The thing is, the size of the space is pretty much modulated by your pupillary constructors and your pupillary dilators. So that, again, you control the amount of lights getting into the right now.

Now, the thing is the lens, your lens, you know, you can actually modulate the curvature. Remember, I said that the lens is your second refractory surface and its curvature can be modulated. Well, what is the thing that can modulate the curvature of the lens? Well, those are going to be your silery muscles, right? Those are going to be your silery muscles. Remember, your silery muscles, they actually are innervated by your parasympathetic nervous system, right? Your parasympathetic nervous system, right? And those, the fibers, right, they actually originate from the silery ganglia, right? From the silery ganglion. The silery ganglion is an example of a post ganglionic parasympathetic neuron. I'll say that again. The silery ganglion is an example of a post ganglionic parasympathetic ganglion, right? Because remember, in your autonomic nervous system, you have a two neuron system, right? We have the, you know, your autonomic nervous system, we know includes the sympathetic and the parasympathetic, right? And there's a pre-ganglionic neuron and there's a post ganglionic neuron, right? So the thing is for the silery ganglion, it's a post ganglionic neuron, right? So it may be my okay divine. What in the world is the pre-ganglionic neuron that sends fibers to the silery ganglion? Well, the pre-ganglionic neuron actually comes from the edinja wesfonucleus of crinionus 3, right? Remember, crinionus 3 is your oculumurinus, right?

So from the edinja wesfonucleus, you have fibers going from your, from your crinionus 3 into midbrain, going to the silery ganglion, the silery ganglion again has the cell bodies of those post ganglionic parasympathetic neurons. And then those neurons go on in our videos, silery muscles, and those silery muscles control the curvature of your lens, okay? So the thing is really the contraction of these silery muscles actually plays a pretty huge role in your ability to accommodate. I want to talk about a more decent in a bit, right? So now, again, light, when light enters the eye, right? Again, it gets refracted, it gets bent at many different interfaces, right? Again, the first place is going to get bent, right? Again, it's at the level of the cornea, right? That's like the air, tear film interface, right? Like your tears, you know, like your form of small room of tears on your eye, right? That essentially prevents eye trinas, right? And then another surface where light is refracted, right? Is the anterior lens, right? Remember the itchial tumor rests on top of the lens, right? So between your itchial tumor and the anterior part of the lens of the eye, you also have refraction, right? And then the post, you also have refraction at the posterior lens, right? But it's like the interface between the posterior lens and the vitra tumor, right? Those are the different places where you refract light, okay?

Those are different places where you, where you bend the light that is getting into the, into the eye, right? So now we know that the eye can move in many different directions, right? So, you know, what are those extrachylomusules that that really, really work on the eye? The first thing I'm going to say is, again, instead of memorizing, well, this muscle is integrated by this, that muscle is integrated by that. Let me spare you all the all those troubles, right? The first thing you need to remember is that most of the extrachylomusules are integrated by cranial nerve three, the oculumurnav. But there are two exceptions to that rule, that's it. So you just need to know the two exceptions. And they remember that everything else is integrated by the oculumurnav, right? So what are the two exceptions? Well, the first exception is the lateral rectus muscle. The lateral rectus muscle is integrated by the abducent nerve, right? Abducent, the abducent nerve is cranial nerve number six. Basically, it makes you AB dot, look at the name abducent. It makes you AB dot your eye. That's the six cranial nerve, right? Remember, it's in the middle of the ponds, right? So it makes you AB dot your eye. This makes you bring your eye balls outward, right? Outward, like lateral, right? Lateral to the midline, right? So you see that that's the lateral rectus muscle of the ducent nerve. And then the next one is your superior oblique muscle. Your superior oblique is integrated by the tropyon nerve.

Some people use the word S04, right? Like sulfate, you know, you probably remember, like in general chemistry in college, we're in about sulfuric acid. Remember sulfuric acid is H2, S04, right? Hydrogen tetraoxyl sulfate six acid, but that's a different story. But H2 S04, right? The SO stands for superior oblique, the four stands for cranial four, which is your tropyon nerve, right? Which is your tropyon nerve. Your tropyon nerve through the superior oblique muscle is job is to depress and AB dot your eyeball. It basically moves your cornea down and out, right? That's done again by the tropyon nerve, which is cranial nerve four, right? So what are your other extrachylo-muscles? Remember, you have your superior rectus, right? Again, that's going to be occipital nerve. It's going to elevate your eye, right? It elevates and adopts your eyeball. It moves your cornea up and in, right? AD dots, up and in, right? The superior rectus, again, is the occipital nerve. The inferior rectus is also occipital nerve. But again, you can also think about it again, inferior. So it pulls your eye inferiorly, right? So it moves your, it depresses your, your, your, your eye down and in, right? It adopts your eye, but it moves it down. It's almost like the exact opposite action of your superior rectus, right? And again, that's also going to be done by the occipital nerve. And then we said that the abducense nerve AB dot the eye.

Well, your medial rectus, um, medial, look at the knee, medial, it AD dots at AWD, right? AD dots your eye, ready? It brings your eye close to the midline, right? And then, you know, inferior bleak, you know, it's done by the occipital nerve, uh, but that one is kind of low yield. So I'm not really going to talk about that much. They almost pretty much don't test that on exams, right? And then remember, your eyelid, remember your eye is not the same time as your eyelid, right? Your eyelid is that of the has like the hairs like your, your lashes or whatever it's called, right? So if you want to elevate your eyelid, that is done by your levator, palpabry superioris, right? Your levator palpabry superioris muscle. And that's actually innervated by the occipital nerve, right? occipital nerve. Now the thing is, uh, if you think about it, if you're running away from a lion, right? You don't want to be squinting your eyes to run away from said lion. You want your eyes to be like, huh? You want your eyes to be like open, open, open, open wide. So the thing is, it's not just the occipital nerve, you know, remember, occipital nerve is, is a parasympathetically oriented nerve. It's not only your occipital nerve that causes you to elevate your eyelid, but when you have a fight or flight response, your sympathetic nervous system can actually work through the superior tarsal muscles, um, to cause you to elevate your eyelid, right?

That's something that's controlled by some fibers coming from the superior cervical ganglion. We'll talk about the superior cervical ganglion leader in this podcast series. So let's talk about some pathologies. Again, I'm going to wrap up here. So I'm going to keep these podcasts a little bit short, right? So let's talk about some pathologies as she did with the extraoclonal muscle, uh, extraoclonal muscle, uh, cranial nerve. So remember cranial nerve two, right? It's kind of like the big one, right? You know, whenever you have a cranial nerve two problem, you're going to have visual field deficits, right? You're going to absolutely have visual field deficits, right? Now remember, the way cranial nerve two works is that you know, you have cranial two, it travels in the brain, right? And then the fibers cross at the optic chiasm. And then after the optic chiasm, you then form the optic tracts, right? Or optical radiations, if you may, right? Now don't forget, whenever you have a problem that is proximal, a problem that is just before the optic chiasm, you're going to lose all the vision in that one eye, simple as that, right? So if you have a problem that is proximal to the optic chiasm, right? Before the fibers cross, uh, you're going to have, uh, just no vision in that same eye, right? So let's say, for example, your cranial two nerve fibers that are traveling from the right eye and you're going towards the optic chiasm. If you lesion them before the optic chiasm, right?

You're going to lose vision in your right eye. You're not going to be able to see squat in your right eye. Okay. Now, what if you have a lesion at the optic chiasm, right? So you have a lesion literally at the chiasm, right? What are the things that cause these kinds of problems or things that cause these kinds of problems are going to be pituitary at the nomeness, right? So, for example, you have a pronounctinoma, right? If you're an adult or, you know, you have like some kind of a cranial fire in geoma, remember, those are the things that leak muddle oil fluid, you know, they're the right from a rafky's pouch, those things can compress the optic chiasm. And also, if you have an aneurysm of your anterior communicating artery, right, that can also cause compression of the optic chiasm, right? Remember, whenever you have, whenever you compress, you know, you mess up the optic chiasm, you're going to have tunnel vision, right? But again, the thing is our friends at the NBM Es, they're very wise, it'll be very unusual if they put the term tunnel vision. If they put tunnel vision, everyone will get the question right, right? So obviously, they don't do that, right? So, what's the, what's what are some other terms that they use for tunnel vision on exams? So, they can call it a bi-temporal hemianopsia, right? They call it a bi-temporal hemianopsia, right? Or sometimes they can call it a heteronimus H-E-T-E-R-O-N-Y-M-U-U-S, they can call it a heteronimus hemianopsia, right?

So, what does it mean to be a heteronimus hemianopsia? Basically, the word heteronimus hemianopsia just means that you're losing different visual fields in each eye. I'll say that again, you're losing different visual fields in each eye, right? So, for example, if a person has a bi-temporal hemianopsia, a bi-temporal heteronimus hemianopsia, for example, they can be losing the left visual field in the right eye and the right visual field in the left eye. I'll say that again, they lose the left visual field in the right eye and the right visual field in the left eye, right? So, again, if you notice, one eye is losing like a visual field on the right, but the other eye is losing a visual field on the left, for example, right? So, when you have like different visual fields lost in each endowed in your two eyes, that's a heteronimus hemianopsia. That's what happens when you have a problem that is at the level of the optic chiasm. But, whenever you have a visual field defect that is distal to the optic chiasm, you're going to lose the same visual field in each eye. So, say, for example, you can lose the right visual field in the right eye and the right visual field in the left eye. I'll say that again, for example, you can lose the right visual field in the right eye and the right visual field in the left eye. Whenever you see stuff like that, then that should, that absolutely tells you that, oh, okay, this person likely has some problem that is distal, right?

So, the optic chiasm, right? Again, if you recognize those things, you should be able to answer most of the exam questions you're going to see, right? Now, also, you may see some visual field deficits where they tell you that, oh, this person has macular sparing, right? The thing is, most times, you're going to see this with a problem of the posterior cerebral artery, right? So, you're pressing the half problems with the posterior cerebral artery. Whenever you see something like that, right? Those people are going to have macular sparing. So, you may be like, okay, divine, why is the macular sparing? Well, the thing is, the macular gets two blood supplies. It gets blood supply from your posterior cerebral artery, but it also gets collateral supply from the middle cerebral artery. So, if your PC gets all messed up, your MC is going to be working just fine, right? Your MC is going to be working just fine, right? So, that's why you have macular sparing, right? Because again, you have adequate amounts of proficient to the, to the macular, right? Now, some other high-yield things I guess to kind of keep in mind, you know, if you, for example, if you upload the posterior ciliary artery, right? Remember the posterior ciliary artery supplies the corals of the eye, right? It also supplies the optic nerve head, right? Again, that can actually cause an african-populary defect, right? That can also cause an african-populary defect, right?

Because you're messing up the head of the optic nerve, right? And then, remember, cranial three, right? So, we've talked about cranial two. Cranial three delusions, right? Again, it causes your eyes to look down and out, right? To look down and out. Because basically, your meerectus, your superior rectus, your inferior oblique, your inferior rectus, and your levietal populary superior is they don't work, right? And remember, you know, there are two, actually a bunch of anatomical relationships that are kind of helpful here with cranial three. Well, remember the first one is that cranial three, you know, it travels very closely, you know, in proximity to the on the oncus of your temporal lobe, right? The oncus of your temporal lobe. So, the thing is, if you have on-call herniation, that can cause you to compress cranial three and you can get a cranial three lesion, right? So, that's where your bloon pupula down and out pupial is usually indicative of a person having, uh, um, increasing for cranial pressures, right? And also, remember that cranial three also passes between your super, the terminal branches of your, of your circle of willis, right? Especially of your terminal branches of your bazzle artery, right? So, it actually passes between your superior cerebellar and your posterior cerebral arteries. I'll say that again, cranial three oculumodonerve crosses between your superior cerebellar and your posterior cerebral arteries, right? So, why is it important to know that?

Well, if you think about it, if you have an aneurysm of any of these arteries, that can also cause an extrinsic compression of cranial three. So, if you have like a superior cerebellar artery aneurysm, or a posterior cerebral artery aneurysm, right? Those things can cause a person to have a cranial three defect, right? So, again, um, to wrap up here, I just want to compare, compare contrast between two disorders, right? Because I know I've kind of talked about, oh, wow, down and out eye cranial three, right? I just want to throw in a bonus for you. Remember, there is a genetic disease that's a pseudo lens dislocation. Actually, there are two genetic diseases. Actually, there's more than two. I'm going to focus on just two today. There are two genetic diseases where the lens dislocation pattern can help you differentiate one thing from one from the other, right? So, remembering homocysteinuria, those people's lenses are dislocated down and in, right? Now, contrast that with people that have morphine syndrome, right? Where the lens is actually going to be dislocated up and out. I'll say that again. Lens dislocation down and in is something you see with homocysteinuria, right? Remember, that's a deficiency of cystophion in beta-synthes. So, these people have intellectual disability, they get M Is very early in life. But then, morphine syndrome, right? That's an autosomal dominant disorder, right?

Malfeins is autosomal dominant versus homocysteinuria, there is autosomal recessive, but morphine is autosomal dominant and you have a fibrillin defect, right? These people, they have lens dislocation, but their lenses are going to be dislocated up and out and people that have morphine, they usually tend to not have intellectual disability on NBN exams, right? So, again, down and out, lens dislocation is homocysteinuria, sorry, down and in, whoops, down and in lens dislocation is homocysteinuria, up and out lens dislocation is morphine syndrome. So, I think I'm going to go ahead and stop here, and I'm going to pick up from here in the next podcast. As I do at the end of every podcast, I do offer one or one children for many exams. Step one, step two, CK, step three, preclinical medical exam, study a show of exams, and if you desire to do no children where, I tell you for all your like, your regular medical exams, but also children for your USML exams, that's something I also do. Again, I've had many people do this and find you to be extremely successful. And then, finally, I do have these podcasts on Apple podcasts, on Google podcasts, and on Spotify, at least the most recent 150. So, if you want everything before, you know, since this is episode 361, that means everything from episode one to episode like 211 is going to be on the website. You're not going to see it on any of these podcast apps. It's a podcast rules, it's not much I can do about that.

So, I'll encourage you if you've gone the website. Actually, if you sign up for the website, you will even get an email notification whenever I make a new podcast. And then, I have a You Tube channel, Divine Intervention, USML podcast and videos, that's where I post the videos that I make. And then, finally, I also have a new website called Divine Intervention Lifelessense.com. In fact, I have a podcast attached with this, if you go on Apple podcasts, you're going to see something called Divine Intervention Life Lessons, and you can learn a ton from it, right? So, the podcasts are short and sweet and they are dressed like some problem that is faced by humanity, right? I usually address it from a Bible perspective. They're short and sweet, many of them are like 10, 10, 15 minutes long, right? And I upload like two a week roughly, right? And again, the goal is to just teach you how to navigate certain challenges that many people, especially young people, are facing our world. So, thank you for listening to me today. Have a wonderful day. Again, if you want to sign up for any of the courses, should you email through the website and I'll give you some more information. So, thank you, God bless you. Goodbye for now. Have a wonderful weekend.

CN II (Optic Nerve) is derived from the diencephalon, while most other cranial nerves are derived from neurocords.

Oligodendrocytes. This is important because MS affects oligodendroglia sites.

The Lateral Rectus muscle (CN VI) and the Superior Oblique muscle (CN IV).

Drusen (whitish or yellowish deposits).

That the macula receives collateral blood supply from both the Posterior Cerebral Artery (PCA) and the Middle Cerebral Artery (MCA).

Homocystinuria.

Deficiency of Type I collagen, seen in Osteogenesis Imperfecta.

The anterior segment (contains aqueous humor) is separated from the posterior segment (contains vitreous humor) by the lens.

1) Air-tear film interface (Cornea); 2) Cornea-anterior lens interface; 3) Posterior lens-vitreous humor interface.

Macular involvement and accumulation of sphingomyelin.

"Down and out" gaze (paralysis of superior rectus, inferior oblique, etc.).

Marfan Syndrome.

Deficiency of Type I collagen, seen in Osteogenesis Imperfecta.

The anterior segment (contains aqueous humor) is separated from the posterior segment (contains vitreous humor) by the lens.

1) Air-tear film interface (Cornea); 2) Cornea-anterior lens interface; 3) Posterior lens-vitreous humor interface.

Macular involvement and accumulation of sphingomyelin.

"Down and out" gaze (paralysis of superior rectus, inferior oblique, etc.).

Marfan Syndrome.