DIP Episode 365 - The Eye Part 2 (for Step 1-3)

Okay, welcome. My name is Divine. This is episode 365 of the Divine Intervention Podcast. And into these podcasts we're going to be continuing our series on the eye. This is going to be the eye part two. And we're just going to jump right into it as a reminder. I do have an MBB Test Ticking Strategy course in February on the 21st of February from 2 to 4.30pm on Tentide. And then I have a 24 hour review course for step two or step three. Or people taking complex level two or three from the 22nd to the 25th of February. And also if you're taking the USML Es in the summer, especially step two CK or step three, I do have what I call a disc school is the Divine Intervention Step Two CK School. They'll be running from me second to me 13th, 2022. That one has a 40% cap on it. It's 75th. The total score on time is 75 hours. If you're interested in that, just shoot me an email through the website. There's a 40% cap for the school. And because I want to be able to invest in everyone that attends. So if you're interested in that, just shoot me an email through the website at our point in the right direction. Now, let's go ahead and continue. So the last time we met, we talked about the pathologies of the Etrocule Muscle Creature Nerves. So let's continue that we did a cranial nerve two, the optic nerve and cranial three, the ocular motor nerve. Now, when you have a cranial four problem, right? Cranial four is the trocular nerve. Whenever you have a trocular nerve problem, right?

You get a contralateral, extrocular movement deficit. Why is that? The reason is, if, for example, you had a Cranial three problem on your left side, is your left eye that's going to be affected. But cranial four, if you have a left-sided cranial four problem, you have a right eye problem. Because cranial four actually crosses in the brainstem. Why? It crosses because it actually exits from the back in the brainstem instead of exiting forward, like the others, like just going straight ahead. Instead of going straight ahead, it decides to like take a detour, come out the back and go out on the other side. It's almost like it's making a half a loop around the brainstem to come out on the other side. And the thing is, cranial four intervenes to the superior bleak muscle. And the easy way to remember that is with the term SO4, superior bleak cranial four. So the superior bleak muscle, what does it do? Well, it depresses and it intorts the eye. What does intortion mean? Intortion means to move the eye towards the 12 o'clock position. So when you lesion the trochlear nerve, the person is going to have trouble depressing their eyeballs. So that eyeball is going to remain elevated. So the thing is, as the affected eye looks up, and the unaffected eye looks down, images are going to appear double. Because it's like literally one eye is able to look down. And then the other eye is not able to do that. Because the superior bleak muscle on that side is impaired.

So especially in the vertical orientation, they're going to have diplopia. They're going to have a very poor diplopia, double vision. So the thing is, as a compensation, individuals that are affected, they tend to tilt their heads away from the lesion side. Or we can see the poor, the chin towards the lesion side. Why? Because they try to pull up the unaffected eye. Because again, if you pull up the unaffected eye, that would almost kind of balance things out. The almost balanced things out. When you balance things out like that, then the diplopia will almost like even out. So many times, how do we do that off to test screening or four? You love to test screening or four. And the context of an individual that has problems like reading books or getting downstairs. Because those are things that require good vertical vision. So those people will have diplopia in that orientation. Now, really, screening or five has many different problems it can cause. But most times, the classic way they love to test it is in the context of the corneal reflex or the blink reflex. In fact, sometimes this is something that you check people for before you declare them bring dead. You notice that those people have no brain stem reflexes. Remember, a person that is brain dead could have spinal reflexes. But the person that is brain dead is not going to have brain stem reflexes. The presence of brain stem reflexes essentially for purposes of the USML exams rules out brain death.

So it's very important to understand that the ophthalmic division of the trigeminal nerve. So that's like the first division of the trigeminal nerve controls the afferent. The information receiving part of the reflex while creating a seven, which is your facial nerve, controls the efferent of the information given a limb of the reflex. So again, that's kind of like a big thing. And so maybe like, oh, the brain death. Is this something the test on exams? Absolutely. They love to test brain death. You do need to know certain things. You need to rule out to see that the person is brain dead. Number one, the person must have no brain stem reflexes. That's very, very important. Right? Again, their quenial reflex should not be working. The popularly-like reflexes should not be working. Those people most likely have like a blown pupil because of increasing internal pressures. Those people that color it test should not work in them. And again, to the clear person brain dead, you need to have them maybe not on the ventilator. You get them up to a PCO2 of 60. Your PCO2 is up to 60. Right? And you're not taking spontaneous breaths. Right? You're probably long dead because most people when they experience hypercupnea, right? Is that breathing to blow that seer to seer around die? But if a person is not taking those measures, taking those steps, they're brain dead. And then another classic one is a body temperature over 90 firing heights. Right? 90 degrees firing heights.

Again, you cannot be cold and dead. You have to be warmed first before you declare brain dead. Again, just one of these rare things you see on the example you're like, well, what is that? Well, you just had it now. So again, very high yield to know that stuff, for example. Now, pre-new 6, which is the abducense nerve is very high yield in the sense that it plays many roles in many reflexes, many specialized eye movements, which we're going to very likely talk about in the future. Right? Specialized eye movements like the vestibuloocular reflex, the horizontal conjugate gaze, those are all things that can be discussed in the future. But it is very high yield to know that the abducense nerve eros in the center of the cavernous sinus. Right? And frequently it's lesioned in the setting of like situations of like high intracranial pressures, or let's say you have like an infection within the cavernous sinus, or you have thrombosis of the cavernous sinus. Remember, whether people that get thrombosis of the cavernous sinus, people that get thrombosis of the cavernous sinus are people that have hyperquagulable disorders. Right? So that for example, have factor five lighting, for example. Right? So the abducense nerve, remember it controls the lateral rectus muscle, right? It makes the eye ab-duct. It causes you to ab-duct your eye, right? And remember, cranial six, the abducense nerve runs in the middle of the ponds. Right?

So people get cranial six problems with a medial pontine lesion, right? Remember in the medial pontine lesion, those people are going to lose corticose final, like they're going to have opomodonium problems on the contralateral side of the lesion, right? But they're going to have cranial six problems, abducense nerve problems on the Ipsilateral side of the lesion, right? Because if you think about it, right? cranial six runs in the middle of the ponds. So if you injure the middle of the ponds, which is something you would get with a lesion of like the paramedian pontine arteries, right? Remember, those are derivatives of the basilar artery? The thing that happens is, first you infect the abducense, but again, the abducense, most cranial nerve deficits, things to be Ipsilateral, right? So you have like, let's say you have like a left paramedian pontine artery lesion, right? You're going to have a left cranial six problem, right? But remember, the corticose final tract, at least the opomodonium runs that constitute your corticose final tract, they run through the middle of the brain stem, right? So as they run through the middle of the brain stem, the thing that's going to happen is, you know, they're still going down the ponds, right? But then remember, when they get to the cordome, you know, the cordome dollar, right? They're going to cross, right? In those medallary pyramids, right? So the cross, right?

So like those fibers that are running down the left, they're automatically good to the right side of the body. So that's why you're going to get right-sided opomodonium run symptoms. So like right-sided hyperreflexia, right-sided hyperreflexia, right-sided hyperreflexia, right-sided, how do I put this? Babinski signs that are positive and all those are fun things, right? Babinski signs and those are fun things. Okay, so let's keep going, right? So again, don't forget your cranial six, right? It does your lateral rectus muscle, right? So now, let's talk about the process of accommodation and convergence, right? Let's talk about how a combination, how convergence happens, right? So the thing is accommodation, which we again, we also call convergence, is a reflex that makes it possible for you to focus on a near object, right? So let's say you've just been looking far ahead, but then something comes into your field of view like it's very close to you, right? So let's say we're looking at something really, really far. Let's say we're looking at a car that was coming from a very long distance away. And then that car starts driving a high speed towards you and you want to focus on that car as it comes down, comes your way, right? So you're going to need to accommodate, you're going to need to converge, right? And basically this process of focusing on accommodating, right? It occurs in three phases, right? It occurs in three phases.

So the thing is the first phase requires you making your lens round or thick, right? You're making your lens like rounder, like thicker, right? So that you can increase its refractive index. Many times this is actually accomplished by the, is not many times. This is actually accomplished by your ciliary muscle, right? Remember your ciliary muscle is under the control of your past and pathetic system, right? So it gets, since it's under the control of your past and pathetic system, that means there's a pre-ganglionic fiber somewhere. And there's a post-ganglionic fiber somewhere. So where's the pre-ganglionic fiber coming from? Well, the pre-ganglionic fiber is coming from the edinja-wessful nucleus that we find in the midbrain, right? It's starting from the edinja-wessful nucleus we find in the midbrain, right? So the fibers come from there, right? Pre-ganglionic, parasympathetic, right? They come from the edinja-wessful nucleus, the travel, and then these synapse on the ciliary ganglion, right? And then the ciliary ganglion is going to be the origin of the post-ganglionic parasympathetic fibers that go all the way to the ciliary muscle again. This is all parasympathetic, right? That's again, cranial or three territory. And then the second phase of accommodation is that you need to make the image of the object to be viewed, focused on the same portion of the retina in each eye. So basically, it's almost like that object you want to view, right?

You want to really focus hard on it. You want it to, I mean, you have two retinas, right? So you want it to appear at the same spot on the retina in both eyes simultaneously, right? So for you to do this, you essentially have to become cross-eyed, right? You need to become cross-eyed. And remember, for you to become cross-eyed, that means you need to pull your two-medial retinas muscles together. Remember the job of your medial retinas muscle, which is again also controlled by your oculum motor nerve, cranial three, is to adduct your pupil, right? It brings your eye close to the middle eye, right? Close to your nose, right? So you need to become cross-eyed by pulling both medial retinas muscles together, right? And then in the final phase, the depth of field, right? So the third phase, right? The depth of field, you need to increase that. And how do you do that? You do this by making your pupil's smaller. Well, how do you make your pupil's smaller? Well, you use your pupil's fingers. And again, remember your pupil's fingers also under the control of your parasympathetic, I mean, yes, they are under the control of cranial three, sir, your oculum motor nerve, right? So again, it should be super obvious to you at this point that cranial three, again, plays a huge role in convergence and in accommodation, right? Now, a quick sidebar I want to take here is not really a sidebar, it's actually a premier or logical extension of this conversation is.

How do you differentiate between MLS lesion? MLS means the medium longitudinal facculous and a cranial three lesion, right? Again, these are classic questions they love to test on exams. And most people, almost as a role, get this wrong. And they love to test this also on these med school exams, right? So let me explain, right? Because the thing is, who is the classic patient that we are used to having with MLS problems, right? Again, basically, intranucleophthalmoplesia. There's going to be people that have multiple sclerosis, right? People that have MS, people that have MS, right? Because remember, when a person has MS, one of the unfortunate things that happens is sometimes they can injure the medial longitudinal facculous, right? And I guess maybe what in the world does the MLF do? Maybe let's start there. Well, the thing is, if you want to look in one direction in the horizontal plane, so let's say you want to keep your head straight, but you want to look to the right, right? Your right eye has to AB duct, you need to look towards the right side. But for your left eye to follow your right eye, your left eye has to go closer to your nose. So it has to AD duct, right? So your right eye has to AB duct, like abs duct, and then your left eye has to AD duct, right? For that to happen, right? Again, think about it. You're literally having two eyes during the similar movements.

That means there must be a structure that connects those two dissimilar movements so that they can happen in one symphony, right? The structure that makes that happen is the medial longitudinal facculous, right? The medial longitudinal facculous, right? So the right eye AB ducts, that's cranial six controlling it. The left eye AD ducts, that's cranial three controlling it, right? The thing that makes cranial three that forces it to AD duct so that you can bring your left eye close to the nose as you're looking right, is the MLF, right? Is the left MLF, the MLF controls the Ipsilateral cranial three, right? So you want your left eye to AD duct, so your left MLF controls it, right? So the thing is your left MLF, right? Again, if you demyelineat it, right? Because you are destroying your oligodangerous sites because you have multiple sclerosis, that can cause you to not be able to AD duct your left eye, right? That's what's called inter-new clear of femoplegia, right? It's an ophthalmoplegia because the go-between, like the matchmaker between cranial six and cranial three during that conjugate eye movement is messed up, right? That's why it's called inter-new clear, right? New clear of cranial six, nucleus of cranial three, inter-new clear of femoplegia, right? It's messed up, right? So that's what happens with people that have eye anal, right? So if you see a person not AD duct their eye successfully on horizontal conjugate gaze, right?

And they say, oh, wow, this person's cranial three is affected. Even if it may just be the MLF that's affected but the cranial three is fine. So how do you differentiate an MLF lesion from a cranial three lesion? Well, the way you differentiate is by testing a commodition, right? Because the process of a commodition does not involve the medial longitudinal fasciculus. So by testing for a commodition you are pretty much excluding the activity of your medial longitudinal fasciculus, right? And you'll notice that if a person has an MLF lesion they're going to have normal accommodation. Well, you can't have normal accommodation if your problem was cranial three is ru in the first place, right? So the way you differentiate between an MLF lesion, right? This is extremely high yield. The way you differentiate between an MLF lesion and a cranial three lesion, right, is by testing a commodition. If you have an MLF problem you have impaired E Dduction on horizontal conjugate gaze but you have perfect E Dduction on a commodition or convergence of the pupils. Okay, so now to wrap up today I believe I'm going to go ahead and talk about this oculo sympathetic pathway, right? This whole business with honor syndrome. You know, honor syndrome is a high yield syndrome to know. Obviously, for exams, right? So let's talk about why this thing is so important to know.

Well, the first thing that kick starts this is that maybe you can kick start you understand you know this is just knowing that many of us were like, oh, honor syndrome is a sympathetic pathway lesion. That's true. Now, the first thing I want to establish is that the sympathetic nervous system. Many people think it's just a two-neuron system and that's fine to know for exams. But if you really want to dig deep, it's actually a three-neuron system, right? Where does the first neuron come from? The first neuron actually comes from the hypothalamus, right? Comes from some nucleus in the hypothalamus, goes all the way down, the lateral brainstem, right? That's why many times when people have a lateral brainstem stroke like Wallenberg syndrome, they have honor syndrome because you're basically killing the first neuron in that oculo sympathetic pathway, right? Coming from the hypothalamus. And then that first neuron then synapses on what will then become the pre-ganglionic sympathetic neuron, right? It synapses on it in the lateral horn of the spinal cord. That's why your sympathetic nervous system is called the thoracolomba system, right? In the thoracic and in the lomba spinal cord, right? So that second neuron is then what is the pre-ganglionic sympathetic neuron, right? And then it goes all the way to the superior cervical ganglion that is very close to the external correlated artery, right?

Actually, pretty close to the internal, before you buy, you know, it's close to the external, right? And then it synapses, right, to form the third neuron, right? The third neuron, which is actually the post-ganglionic sympathetic neuron, it then goes to many different things, right? So it goes to the superior trussal muscles, which are supposed to keep your eyelids up, right? It goes to the sweat glands of your forehead, goes to the throat muscles of your eyelid, right? Goes to your popularity dilators, right? So it does a lot of things, right? It does a lot of things, right? So if, for example, you lesion this nerve, or you lesion this oculus sympathetic system, then you're going to get a lot of problems, right? You're going to get a lot of problems, right? So that big problem you get is hunger syndrome, right? The hunger syndrome is an ophthalmic condition that there's associated with any lesion of the oculus sympathetic pathway anywhere along its length. So what are some things that can cause this problem? Well, if you have a pancus tumor, right? It's like a carcinoma in the apex of the lungs, right? That can compress these sympathetic fibers, or if you have like a chord hemisection, right? Like a brown sick heart syndrome, for example, right? Well, for example, you have like a lateral brinsteine lesion, right? Again, as I explained, like a pica problem or an aica problem, right? And during ferecerabella, or posterior ferecerabella artery problem, right?

Again, that can cause a hunger syndrome, right? So again, you're going to get the classic trato of toses, right? You're going to get a droopy eyelid, right? Because again, you've denervated the sympathetic nervous system, innervated, superior trussal muscles, right? You're going to get toses, right? We've talked about that. You're going to get meiosis, right? Again, because again, your sympathetic nervous system controls my dry assesses. So if my dry assesses is not there, your parasympathetic nervous system will operate unopposed. And you get meiosis. And you also get anhydrosis. Because again, remember, your sympathetic nervous system actually innervates sweat glands, although it does this weirdly through most chryonic acetylcholine receptors, right? Now, another thing that can cause a hunger syndrome, maybe like I call it a partial hunger syndrome, is something we call a claustra headache, right? A claustra headache, right? Is, you know, a headache where is unilateral is going to be a one side of the head. And those people are usually going to have eye findings on the same side, right? One of the things they have is partial hunger syndrome. So they have toses, they have meiosis, but they do not have anhydrosis, right? They have toses, they have meiosis, but they do not have anhydrosis. Again, this stuff very high you to know for, for example. So thank you for listening to me in today's podcast. Again, I hope you've got it in a lot from it. We're going to continue.

There's going to be an eye part three. But I wish all the very best as you study for your exams. I do have these podcasts again on Apple Podcasts, Google Podcasts and Spotify. So if you're interested, just sign up for any of those. Subscribe to the podcast and you're going to, you know, see the most recent 150 viewer. One everything from episode one to episode 365, which is to these episodes. You want to go on the website, the Vine Intervention Podcasts.com. I have a You Tube channel as well, the Vine Intervention, the assembly podcasts and videos. And then if you want more life lessons like I throw in these podcasts, you can also look up my new website, divineinterventionlifelessens.com. I do have, even it's actually an Apple Podcast as well, divine intervention, life lessons podcast. I have about 55 episodes where I address again, just from a biblical perspective, many problems that face a humanity. And then I also offer one of one to your first step one, step two, see again, step three, you know, pre clinical medical exams, 30-ishelf exams, and also help with ira's applications. And again, also offer these review courses and the step two CK school that's going to be studying in May that has a 40% cap. So thank you for listening to me. Have a wonderful rest of your day. God bless you. Thank you.

An MLF lesion impairs horizontal conjugate gaze, but accommodation/convergence remains normal. A CN III lesion affects all aspects of eye movement, including convergence and accommodation.

Cranial VI (Abducens). Deficits are typically ipsilateral to the lesion because it runs in the middle of the pons.

Ptosis (droopy eyelid), Miosis (constricted pupil), and Anhidrosis (lack of sweating) on the affected side.

Pancoast tumor or lateral brainstem stroke/lesion.

Testing for accommodation/convergence, as this process does not rely on the MLF.

Absence of brain stem reflexes and maintaining a body temperature above 90°F (or requiring warming first).

CN IV. The deficit causes difficulty depressing the eye, leading to vertical diplopia (vertical gaze palsy).

1) Hypothalamus (first neuron), 2) Lateral horn of spinal cord (second/pre-ganglionic neuron), and 3) Superior cervical ganglion (third/post-ganglionic neuron).

Horizontal conjugate gaze (the ability for both eyes to move together in the same horizontal direction).

To contract and change the shape of the lens, increasing its refractive index (making it thicker/rounder) to focus on near objects.

Because the abducens nerve runs through the middle of the pons, making it susceptible to local compression or damage from paramedian lesions.

The absence of brain stem reflexes (e.g., corneal reflex) is critical evidence suggesting irreversible brain death.

CN IV. The deficit causes difficulty depressing the eye, leading to vertical diplopia (vertical gaze palsy).

1) Hypothalamus (first neuron), 2) Lateral horn of spinal cord (second/pre-ganglionic neuron), and 3) Superior cervical ganglion (third/post-ganglionic neuron).

Horizontal conjugate gaze (the ability for both eyes to move together in the same horizontal direction).

To contract and change the shape of the lens, increasing its refractive index (making it thicker/rounder) to focus on near objects.

Because the abducens nerve runs through the middle of the pons, making it susceptible to local compression or damage from paramedian lesions.

The absence of brain stem reflexes (e.g., corneal reflex) is critical evidence suggesting irreversible brain death.