This on-demand teaching session is relevant to medical professionals and will discuss topics of anatomy, visual pathways and investigation methods. It will focus on identifying and understanding the visual field defects in patients with monocular visual loss, such as optic neuritis, compressive lesions, central retinal artery occlusions and vascular issues. The video will discuss the shape of different visual field patterns, effects of macula and fovea, and the afferent/efferent pathways. It is applicable to neurological disorders such as Multiple Sclerosis, Idiopathic Intracranial Hypertension and Thyroid Eye Disease and will also touch on issues concerning the orbit, optic nerve and the cavernous sinus.
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Oliver Wroe Wright is a neurosurgical registrar and South London neurosurgical trainee.

Learning objectives

Learning Objectives 1.Identify the anatomy and physiology of the visual pathway 2.Recognize the different visual field defects due to retinal, optic nerve, and compressive lesions 3.Distinguish between monocular and binocular vision 4.Understand how relative afferent bilial defects can occur 5.Outline the role of the posterior ciliary/central retinal artery in maintaining visual acuity
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

And you can see, you can see different stimuli of varying size intensity to get an idea about not only the the field shape, but also um how um sensitivity is in different areas. And that's where you end up with a a chart like this. This is a humphreys field and there's the Goldman test which requires a perimetry. So you have to have someone there. It's kinetics. So rather than having static things flash from the visual field, it's uh something that's moving, it's brought into the field. And the patient taps the table when they see the stimulus coming into their field. And the perimetry just marks where that was and you can measure the scotoma, the blind spot by doing the opposite. So starting in the center and moving outwards, this is the um Goldman's field. So just in terms of the retina, so the visual field corresponds to a topographic arrangement of uh the photoreceptor in the retina. So when the light hits the, the retinal surface, it starts the kind of photo transduction cascade which ultimately results in the ganglion cells being activated and the fibers from the ganglion uh or the fibers from the activator photoreceptors head to the optic nerve head and the optic nerve, there's no receptors. This corresponds to the physiological blind spot. And we know the maximum uh uh the macula has the highest density of receptors um and the fovea is the central portion of this. So this just demonstrates that the fibers run from the fovea to the disc that's pass the Palo macular bundle. Um but uh it's more in the realm of the ophthalmologists in terms of the visual pathway. Key things to remember are that the nasal retina sees the temporal field, the temporal retina sees the nasal field and similarly the inferior retina see the superior field and vice versa. So when light hits the the retina, it activates that signal transduction. So light hitting the um temporal retina travels posteriorly to the chiasm and then backwards to the optic tract into the visual cortex. Light hitting the nasal retina from the temporal field crosses over something called the optic chiasm and then travels along the other side along with the fibers from the um temporal retina of the contralateral eye and then the electro nucleus, the optic radiation and the visual cortex. And based upon this pattern or how these signals are transmitted, you can get an insight into um the different visual field defects you get with lesions in each of these locations. Just a a brief word on the the light reflex. This demonstrates that the ret pathway and you have an afferent and an efferent limb as with every reflex pathway. So, when light hits the retina, the afferent limb is the optic nerve to the chiasm and then to the optic tract and fibers from the optic tract before it reaches the later geniculate lus heads, the pretectal nucleus which is in the dorsal midbrain, then to a den adeno S valve, which is the um parasympathetic nucleus of the third cranial nerve. And the efferent limb is those fibers in the third nerve, going to ci ciliary ganglion and they stimulate pupillary constriction and that's crossed. So if light hits the left uh left eye, it's got bilateral representation. So the right eye will also constrict. So that's where you get a direct and a consensual um light reflex. If you have an uh an afferent apiary defect, it just means that the efferent function of part of this reflex arc is less good in one eye than the other. Uh this video on youtube shows that. So you see this patient, if you shine the lights uh in the in this patient, you will see that the right pupil consistently dilates as the light is. Uh So if you light in the left pupil, it constricts. And if you shine a light on the right people, it paradoxically dilates, that tells you that there's an afferent defect in the right eye. And because it's relative to the left eye, it's called a relative afferent pail defect uh that's important for later. So, scotoma, um so this is basically talking about the size and the shape of the blind spots. So, scotoma comes from the Greek Scotto which means darkness and there are various different shapes. You can um get, they tend to be due to retinal optic nerve lesions and dependent on the underlying cause. They can be unilateral or bilateral. The shape says the ring scotoma, which is meant to be indicative of optic nerve degeneration. Oh, sorry, retinal degeneration, the cents fecal scotoma, you see, there's a scotoma that's involving the physiological blind spot that's seen in toxic Gambia. There's a scotoma which follows the pattern of those papilloma b um papilla macular fibers we talked about earlier. Um and that's seen in glaucoma and then central scotoma, which is the thing that we're more concerned with in terms of compressive pathology and also um optic nerve or, you know, inflammatory knee lesions, macular degeneration, things like that. Sometimes you can have a patient who has um bilateral scotoma. Um And in a pa this patient has bilateral papilledema on fundoscopy. And if, when they did the um Humphreys field test, they had a constricted visual field and then enlarged like blind spot. And if someone has this bilaterally, it's a sign of kind of optic atrophy. And that could be the end stage result of chronically raised intracranial pressure, for instance, in idiopathic intracranial hypertension. So it's a bit about kind of the the underlying anatomy, we'll go through each step of the optic or the visual pathway now and talk about the shape of different visual field patterns um at each stage. So firstly, in a patient with monocular visual loss, you're basically looking at a retinal, an optic nerve lesion and in its mildest form or in its milder form, you can get an enlarged blind spot to the central scotoma. The patient may have reduced acuity or color vision and they may have that relative afferent biliary defect. We talked about if the underlying pathology progresses um to its ultimate stage can cause ocular blindness. And Monis just means alone in Greek. And if you shine a light in a an eye that's completely um blind, you'll have an absent direct reflex because the afferent limb is not functioning at all, but the consensual reflex. So if you shine a light in the other eye, it should still constrict because the um the the stimulus from the cranial nerve three is crossed from the other eye. Um So if you look at the field defects, you just have a monocular. So that means it's in front of the chi under the problem, uh it can be due to optic neuritis. So, characteristically in your medical school, multiple choice questions, it will be a patient coming in with reduced visual acuity, eye pain, color desaturation, young woman, and then later develops, you know, limb weakness. You're thinking about multiple sclerosis or other demyelinating processes. Um when the neurosurgical team get involved, it can be due to compressive lesions. So another cause of slightly weird and wacky visual field defects are vascular issues. So if you look at this diagram and all the diagrams I'm using are from Ra's um dissections this artery here. So that's the ophthalmic artery that provides the predominant supply to the optic nerve and the retina, it has multiple branches. The, the two really that are of note with vision are the central retinal artery of the retina, which as you see enters the optic nerve sheath and travels to the eye and also the ciliary branches. And you have anterior and posterior ciliary arteries. The central retinal artery travels with the nerve to the eye and it has branches that supply the upper and lower bit of the retina. But if you look interestingly, the veer which we said is where the highest density of um uh photoreceptors are is can be supplied by branches from the ciliary arteries. The postero ciliary arteries, what they're called Celio retinal branches. So sometimes you can get a situation like this. So on fundoscopy, there's a patient there optic um I'm sorry, the retina is pale but this which is the fovea is cherry red. This is a cherry red um spot on the visual field, the effect they've got peripheral constriction, but a reserved central uh field. This is seen in central retinal artery occlusion. So you get a monocular peripheral constriction in the pre preserved central vision. And that's due to that differential blood supply. I mentioned, you can see how if you cut your or you block the ophthalmic artery, you get monocular blindness. But if you just lose a um circulation from the central re artery, you have still preserved poster arteries and they're supplying the veer, which means that that central area of vision is preserved um similar, you can have AAA problem like this. So this fundoscopy shows that there's a superiorly kind of pale retina. And on the visual field defects, there's an inferior um field defect affecting both sides, that's called an altitude inal field defect. It's an inferior altitude defect. In this, in this case, it's due to a superior retinal artery branch occlusion. So the retinal artery branch that was supplying the upper bit of the retina was blocked. And because the superior retina is the inferior visual field, you get an inferior altitude field defect and it depends on which branch is affected. It can be obviously superior, inferior, just a word and compressive pathology. So going back to that um picture in neurology and in medicine in general, it's always good to have a structure. So thinking about compressive pathology affecting the optic nerve, it can do things within the orbit. So you may see proptosis if that's the case because the orbital contents are increase in the eyes bulging out. It can due to tumors such as optic nerve sheath, meningioma, inflammation. So, thyroid eye disease, granuloma infection, or rarely, you can have kind of retro orbital hematomas and secondary to trauma. Then you can have problems in the optic canal. And again, tumor granuloma or the bone around the optic canal can, can become a hyperostosis like fibrous dysplasia. And you see on this picture, it's a bit small but in the CT above the optic nerve and the frontal and spinal bones are hypertrophy narrowing, the canal, which naturally would put pressure on the nerve compared to someone who doesn't have that hyperostosis and then you can have intracranial. So the portion of the optic nerve before the chiasm and again, the differentials are quite similar, you can differentiate sometimes between problemss in these different areas. So there's a syndrome called orbital apex syndrome, which is. So this is the orbital apex. That's where the optic nerve and the optic uh sorry, the optic nerve enter the optic canal and the nerves in most the superior orbital fissure and the nerves as we know that exit the skull through the superior fissure R 346 and B one. So if you have a tumor or a lesion that's pressing in this region, it can affect both the optic nerve as it leaves the optic canal and also those fiber or those nerves as they enter the orbit through the superior to fissure. There is another or another structure in this area, the cavernous saus, which contains very similar nerves, those running through the orbital apex. So 346 V one um and V two, but the optic nerve doesn't travel through the cavernous sinus. So if you have a lesion here, you shouldn't have visual um visual compromise compared to syndrome. Also, the sympathetic fibers run with the carotid artery. So you may get oye dysfunction, Ie Horna syndrome. And then there's something called superior tal fissure syndrome, which is due to pathology within the orbit, but it's sparing optic the canal. So again, you have that constellation of 346 and V one, but no optic nerve involvement. And you can contrast that from the cavernous sinus um because the maxillary branch of trigeminal and also the ocular sympathetics are relatively spared. So that's pre cosmetic lesions, then cosmetic lesions. And this is um again, the raum slide from the optic chiasm. So down here, that's the top of the head. That's the bottom. This is the optic chiasm, cranial nerve two. This is the orbit optic canal. This is the optic tract down here's the pituitary, the clivus has been removed. So, actually, what you're seeing here is the brain stem. That's the basilar artery, that's the carotid siphon. And this is the anterior cerebral artery complex or Acom complex here. So this is the classic um medical school exam question. Um So, a lesion here which is impacting the nasal retina from both eyes. So the temporal feel from both eyes will give you that classic bi temporal hem here. And so that localizes to the optic chiasm. It comes from um well, it's Greek. So hemi means half and without an opus seeing. And it's a form of heteronym hemianopia. So it means that different sides are involved as opposed to homonymous hemianopia where both side, both the same sides involved. So here, it's the right field in one eye and the left field in the other with the homonymous hemiopia. It's the right field in both eyes. There is another form of heteronym hemianopia, which is just the reverse of bi temporal hemianopia. And that's a bi nasal hemianopia and that's been on nasal. He Yeah. Um So I look at questions at the end because it's quite hard to click between two of them using the pointer. So that's the optic chiasm. In a simple term. It's actually, it's a three dimensional structure and the visual field defect you get from cosmetic compression are a bit more complicated than that. This is a sagittal um side from Rogo tos as well. That's the sphenoid sinus is the pituitary. We see the brain stem, third ventricle. Um This is the Antero artery or Acom complex. Again, this highest thing is the optic chiasm. That's the infundibulum, the tubular, uh the pituitary ST and that's the optic nerve getting into the canal there. So if you look at actually an anatomic relationship to the optic chiasm, there's um the, the fibers of the optic nerves are distributed slightly differently between the two. So, fibers from the um inferior nasal field are more anteriorly and um inferior and fibers from the superior nasal field are more superior with macula running through the center of the chiasm. So you can see how if you have compression coming from different areas around the Chisum, you can have differential field defects. So for instance, if you have a lesion in a pituitary that's pushing up, it's going to impact upon those inferior nasal retinal fibers first. The inferior re uh as we said shows the upper visual field. So with a pituitary tumor, you may see that the patient loses the superior portion of the temporal field first and then develops a complete bi temporal hemianopia or maybe he just has um hand motion in one bit but can count fingers in the inferior bit. Similarly, if you have compression that's coming above the chiasm, um the superior um fibers are affected first. So you may get an inferior field defect. So you can predict based on the pattern of the bitemporal hemianopia weight that the compressive lesion is going to be. And the differential for the lesions in this area. I mean, it's classically it's pituitary adenoma or craniopharyngioma. And the pituitary adenoma is what's meant to give you the um bitemporal superior field defect and craniopharyngioma because the eyes com press on the posterior fibers uh at the top and we'll get the inferior field defect. And I have seen consultants change the surgical or the same operative decisions based on that. Um Because if you come transsphenoidal and actually you're trying to get a craniopharyngioma, the optic chiasm is going to be in the way, it's not going to be able to manage that. So I've seen someone switch from uh a trans to a Teron for a kind of seller lesion which wasn't clear where, where it was arising from on the MRI scan. Um because of the pattern of the visual field defect. And it ended up being I think it was a juice seller meningioma um which is one of the other causes. And then you see we've seen on a couple of sides, the close relationship of the Antero cerebral arteries um to the chiasm. So, aneurysms particularly the Acom complex can cause bi temporal field defects. Um But then if you look at the optic chiasm or or defects around the optic chiasm in a bit more detail, it's it's slightly more complicated than just having a central lesion giving you by temporal hemianopia. You also get these slightly strange um field defects called junctional scotomas. And when they say junction, it just means the junction of the optic nerve with the optic chiasm. And there are two main ones you need to know about. The first is called a juncture scotoma. So if you have a compressive lesion pressing here, you get a monocular central scotoma. And then because the superior retinal sorry, the inferior nasal fibers from the contralateral eye can be impacted on. You can get a superior quadrantanopia which looks like this. So central scotoma, ipsilateral, superior chemical quadrantanopia in the contralateral eye. And this used to be due to something or thought to be due to something called Willebrand's knee, which is where fibers from the optic or the nasal portion of the optic nerve bends into the contralateral optic nerve, which will make them vulnerable if there's compressive lesion here, before heading backwards into the optic tract. Actually, that was based on some anatomical studies where they cut out the uh the eyes of a monkey and then look at the fibers of uh fibers in the chiasm. And it was found to be an artifact of the enucleation of the eye. So when you cut the eye, when you cut the eye on the right hand side, the fibers retract into the nerve. Um regardless for whatever reason, you still get this visual field defect due to um compressive lesions in this area. Then there's another form of junctional scotoma, which is called the junctional scotoma of tra, which is in the same region. But rather than having a, a large compressing lesion causing a central scotoma on one eye, you have a lesion that's causing pressure on one side of the, of the optic nerve near the chiasm. So if you have a, a medial lesion, pressing on the nasal retinal fibers, you're gonna get a monocular right uh side of temporal hemianopia. If it's pressing on the lateral side, it'll be the nasal field. So in monocular right sided uh nasal hemianopia and that's called a junction talk about and the lesions or the differentials for lesions causing that uh are the same as for uh kind of cell maes. It's just their geographical or their anatomical relationship to the Chis. And whether it's near the um the nerve, the Chisum itself or towards the optic tract, then in terms of retro cosmetic problems, we're talking about things behind the chiasm. Now, once you're behind the chiasm, as we saw earlier, the fibers, it's not, you can now have fibers in both eyes. So you have the left or sorry, the right nasal retina and oh yeah, the the the range of left from one eye, the temporal retina from the other, which means you have the um temporal and the nasal field and they've crossed over. So it's s it's rever is crossed. So, retro defects on the right leads due to visual field defects on the left. So we call that homonymous as opposed to heteronym, but it's the same side that's affected. So any lesion behind the chiasm will give you a homonymous hemianopia. The shape of the field defect depends where exactly in this uh retro spasmatic pathway is affected. And there are other ways to localize lesions in this area as well. You're basically trying to work out if it's the optic tract nucular nucleus, the radiation or the cortex that's involved. Um So this again is from Raton. So that's the optic nerve optic chiasm, infundibulum, these mammillary bodies, third nerve midbrain, this is the optic tract, that's the la nucleus. So if we're talking about optic tract lesions, as we said, you can get a homonymous field defect and these can be described as congruous or incongruous. So congruous just means the field defect is the shade the same shape in both eyes. If it's incongruous, that means that they have different shapes and generally the field defect in the eye, uh contralateral to the side that's affected. Uh So the the field defect in the eye that's on the same side as the tract lesion is worse. So you have a worse field defect in the same eye basically. So if you have a left-sided lesion, the the uh nasal field in the left eye is going to be uh have a bigger defect in the temporal in the right eye that makes sense, the more posterior you are on the retro spasmatic pathway, the more the defect. So as you get back and back the field shape, so the fi the shape of the field defects in both eyes becomes more and more similar. Similarly, if you remember the um afferent limb of the light reflex, the fibers leave the optic tract before they reach the later nucleus. So if you have a lesion in the optic tract, generally, you'd expect to see an rapd. So that can help you distinguish it from something that's in the optic radiations. And because the later nucleus contains the cell body of the optic nerve, if you have any lesion in the retro cosmetic pathway, you'll have optic atrophy. So if you look at the retina, there will be evidence of atrophy of the optic nerve. The pattern of this depends on where exactly the lesion is. And for, for reasons, I don't fully grasp it's more an log thing. The pattern of a atrophy is characteristic. So if there's a left-sided lesion in the optic tract, the atrophy in the temporal retina, the atrophy in the retina ipsilateral to the the lesion will be in a temporal in temporalis patterns like this. Whereas if it's the contralateral eye, you get a bow tie pattern of atrophy. It's to do with the arrangement of fibers and how they arc around the um for which is the for is the vertical meridian of the eye. I've never actually had to use that in clinical practice. So then the ate body. Um so this is something I'd really heard of in medical school. But the fi the way the fis and the layers are arranged in the L GB you have these lamina and the central portion of the visual field is um that kind of carried to the the central lamina and then the peripheries are these peripheral lamina here and they have a differential blood supply. So the central portion gets supplied from the lateral, posterior cord artery and this lateral portion comes from the anterior cord artery. And if you look at this diagram, you see that these come from different parts of the circulation. So the anterior cord artery comes from the anterior circulation, which is a branch of the or terminal IC, a communicating portion of the IC A and then the um posterior cord artery comes from the PC A. So it makes sense that you could have a differential occlusion of one of these vessels and not the other. So if you have a lateral, posterior cord and artery occlusion, you lose uh vascular, apply to that central core or central lamina. So you get loss of the central field, but preservation of um the peripheral field. So that's called AAA sector. A right homonymous wedge sector and here and it's um crossed and pola so crossed and homonymous um to the side of the defect. So if it's the left side, you're gonna have a right sided wedge set to an opium. And that's what a Pacman field cos it looks like Pacman if the lateral. So if the anterior coid artery is affected, then it's the peripheral lamina that are affected. So you're going to get a peripheral visual field loss with sparing of the sector and that's called se sparing S um sorry homonymous sparing se So it looks like this, that's pretty characteristic of la genicular nu nuclear lesions. You can get this as this is an hour glass visual field defect. So both eyes are affected on both sides and this is seen in bilateral extranuclear nucleus lesions. And it's been described as that an all fascial field defects and this is seen in or can be seen extra pon time mys. So if you remember your osmotic demyelination syndrome, so if you overcorrect rapidly, someone's hyponatremia, you can get rapid fluid shift and demyelination of the axons. And we always talked about central pon time, myelinolysis um which is where, you know, in the worst case scenario, you can get locked in syndrome, but you may also get ophthalmoplegia or other problems because of um the involvement of pontine fibers. I think there's a push now towards calling, calling it an osmotic demyelination syndrome to affect the fact that all of the demyelination isn't just in the ponds, you can have extra pon time, my lysis. So some portions of the brain are more vulnerable than others. And one of those is the Laar nucleus. So if you have rapid correction of, so you can have myelin lysis of the later or or, and you can get end up with these bilateral visual field defects along with all of the other manifestations of, you know, osmotic demyelination syndrome. So that's the lateral genetic nu plus and then this is the optic tras optic radiation, sorry optic radiation optic tract. This is the optic tract. So chiasm optic nerve tract ma nucleus radiation, this is the medulla, this is the ponds there. So the optic radiation. So there's Cusco of teachings that there are two main loops. So you have a loop of uh white matter bundling through the temporal lobe and one through the p prior lobe, also known as the genicular cac tract, which is basically how fibers travel from the lateral nucleus to the um the calcine fissure, which is where the primary visual cortex is in the occipital lay. There's Mayer's loop which is where you have these fibers that arch forward into the front of the temporal lobe and then backwards. And that's now called or you see that described as the ventral um tract, it runs anterior and then posteriorly parallel to the atrial, the lateral ventricle. Then you have non Mayers loops. That's the portion that passes through the parietal lobe that's called the dorsal tracts. And then uh and that travels along the posterior hall of the la to do. And then the central tract which carries fibers in the macula and just travels directly backwards. So you have a ventral central and dorsal bundle for medical school purposes, you have Mayer's loop which is temporal and then there's a portion or non Mayer's lo that travels through the parietal lobe. You can see these bundles here. So it's not just two fiber tracts. So that's Lanus there, the back of the thalamus that's may as lo at the front. This will be the dorsal tract and you have the central tracts. These are the fibers that patent of the corpus callosum. And you're seeing here into the lateral ventricle and they've done some nice white a dissection around that. So what happens if you get lesions in the optic radiation? Well, if you have one that's affecting Mayer's loop, so that ventral loop that goes into the front of the um uh temporal lobe, these Mayer's carries fibers from the superior quadrant or the inferior quadrant of the retina. So you get a contractual superior uh quadrantanopia. So if you have a left Mayer e lesion, you have a right, superior quadrantanopia that's called A P in the sky defect because that wedges is like a wedge of pine. If it's the non Mayers and you get an inferior Proia that's called P the floor. I've never seen anyone actually call it that. If you have both sets of um op radiation is affected, you're gonna get a homonymous hemianopia and it's contralateral to the side of the lesion. The way to remember that is pneumonic pits. So parietal was in the inferior, the inferior field and temporal is superior. I remember it obviously, if you have lesions in the par lobe with the temporal lobe, skin to have other manifestations of lesions in those areas. And how that manifests depends on whether it's dominant or nondominant. And um uh yeah. So you may have other signs. These things are involved last but not least we have the visual cortex. Um This is in the occipital lobe. So again, it's a sagittal s size, corpus callosum, frontal lobe, para lobular there, a cingulate gyrus parietal. This is occipital lobe here and the cal coin fissure um is the location of the primary visual cortex. So we can so cause it's where the optic radiation converge from the temporal um fibers and the parietal fibers, uh it doesn't show up that well. So the le lesions that are posterior, the retro cosmetic pathway are more congruous than those that are anterior, which I think we, we mentioned that's because as the fibers leave the la because they play out and they come closer together again. So if you have a lesion, um that's more uh anterior, it's less likely to catch all the fibers in one go. Um If you have a lesion in the occipital lobe or affecting the visual cortex, again, it's crossed over. So you have a contralateral hemianopia and there may or may not be macular involvement if you look at the topographical arrangement of fibers in the retina. So you said that this fibers in the inferior field travel through the part lobe. So those fibers terminate in the superior bank of the cal sulcus fis from the superior field travel through the temporal lobe and they terminated in the inferior bank of the cal sulcus. They find in the central bundle or the macula terminate towards the occipital pole of the tip. So that's why you get something called a homonymous hemi that spares the macula that's characteristic of occipital lesions. The reason that happens, well, there are two main theories. The first um is that there's bilateral representation of the, the macula in, in both occipital lobes. I think that's less accepted. Now, I think the the predominant thing, the thing that I was taught was that there's a dual blood supply. So the occipital lobe is predominant supplies from the posterior cerebral artery or the posterior circulation, but it has collateral supply for the middle cerebral artery, the middle cerebral artery supplies the tip. So you have a PC A stroke, you'll lose predominant arterial supply to the septal lobe, but you may have collateral supply to the middle cerebral artery which is supplying the tip of the occipital lobe or where that central push to the macular field is which can be spared. So when you have the field defect, you've lost the occipital lobe, but the central macula is still preserved. Um Yeah, so I I appreciate him going quite quickly. So if anyone has any questions, now, let me know, just catch on the questions. So perception diagrams are from protons. OK. That's it. No other questions. Um So then in regards to cortical field defects. So, so now we're, we're not really talking about the, the visual part where we're talking about the cortical process. Um, so maybe I'll make it a bit more interactive now. So, can someone ex describe what this CT scan shows? Danielle Ramsay or anyone watch the CT show? So, it looks like a occipital area of hyperintensity, particularly on the left hand side, hyperintensity or hypodensity. Hypodensity. Yeah. Hypodensity. CT. So, it's all about density, not intensity. but you're right. Yes, there's bilateral occipital hypodensity worse on the left. So, what would you think's going on then infarction? Yeah, that's right. Exactly. So, bilateral six lab infarction, it's not that clear on the, the CT uh but generally with infarct, you have sparing of uh you have involvement of both the gray and white matter whereas the vasic edema um the uh cortex is spared. So this is b bilateral o septal lobe infarction and this can result in things like cortical blindness. So, cortical blindness is defined as a loss of the vision with intact ophthalmological function, intact Pupi reflexes. So basically the the opposite apparatus is working, but the brain isn't able to interpret it properly and germinates due to bilateral occipital lesions. This can manifest as some weird and whacky things. There's something called Anton syndrome, which is also known as a visual ans agnosia. So, a meaning without noss disease and knowledge. So the patient doesn't have insight into their, their defects. So they're basically blind and uh but they'll deny visual loss and can fibrillate. Despite clear objective evidence that they can't see that's anatom syndrome, then there's other things again to do with processing. There's something called Riddock phenomenon, which is essentially you get stato kinetic dissociation, which means that the patient can perceive things that are moving in their visual field but not static objects. So if you test someone visual field defects and are moving, you may overestimate how much they can see where if you look at it with static testing, um you may uh demonstrate a more significant visual field defect and you can see how that might be a problem when you're comparing the Goldman and the Humphrey because the hump is a, a static um test, whereas Gould is kinetic. So that could be a um a source of inaccuracy in your visual field testing that's generally seen as lo disease. Uh Then there's something called balance syndrome that's characterized by the triad of Si Tasia. So that's the inability to perceive simultaneous subjects in the visual field. So if you tested someone's visual field and you showed them two things at once, they'd only be able to see one. Um the ocular moray pra, they can't voluntarily guide their eye movements. And that's because um the smooth pursuit centers in the parietal or Parpi region and then optic ataxia. So again, there's a problem with coordination of what they are seeing to their hands. They can't pick up objects that they can see due to optic dysfunction and that's uh due to bilateral parietal problems, then you have some weird, well, some um causes of color blindness. There's two main categories, the cerebral achromatopsia, that's where due to a cortical defect, there are functionally color blind. And again, that's an occipital lobe and it's, it's um it's uh crossover. So if you have a unilateral lesion causing cerebral achromatopsia, then may just have a hemi achromatopsia effect on the contralateral side, that's different from color agnosia. So in color agnosia, the patients able to perceive the color, but they can't recognize it due to a problem with naming. So it tends to be dominantly because it's to do with language and um kind of language and processing of vision and, but you can differentiate between the two because if you ask someone with color agnosia to source a load of red and blue pens, they'll be able to do it into different categories. They won't be able to tell you the name of the color. Whereas someone with cerebral a chromatopsia wouldn't be able to um sort them. And then there's Alexy without graphic, a with a, without a graphic. So basically the patient can't read what they can write. So if you tell them to write something down, they'll be able to write it. And then if you ask them to read what they've just written, they can't. But if you spell out a word and ask them to tell you what the word is. They're able to tell you what the spell that word is and that's the dominant occipital lesion that's involving the spleen of the corpus callosum. Does he? I'm sure the neurologists have many more um weird and wacky visual field defects. But I thought these ones were quite interesting. So then just brief you on some case examples. Um So, yeah, can I pick on someone to describe the MRI scan and then tell me what field defect they would have? I think that's tey is in the core, isn't she? Oh yeah, it is. Well, I go to the floor. I don't mind and someone in the comment say what they think the lesion is and what visual field defect they might get. Um There's a mass in the midline church. Adenoma church. A yeah. Any advances cream from ja Yeah, by temporal he opposite. That's right. Uh Yeah. So, so yeah, there's a central cellar lesion. Um It's a t one post contrast corona and axial. Um You can't comment to whether it's enhancing because you can't see a pre contos we assume it's enhancing. Um pituitary a name is probably the top differential but um you know, this could be, it's relatively homogenous enhancement. It could be a a seller or juice meningioma could be a craniopharyngioma Amanti subtype. Oh sorry papillary subtype. Um But yeah, cio um macroadenoma in the top differential things that would help you determine that if you looked at a Sagi might the expansion of the seller or bone erosion and the optic chiasm is affected. So you get a by temporal hemianopia, that is correct. And you can see the chiasm displayed over the top of the tumor here, depending on the relationship of this tumor to the chiasm. You may have one of those weird and whacky field defects or you know, like a juncture scotoma. If it's more anterior, if it's more posterior, you can get things that look like an optic tract lesion. So an incongruous contralateral hemianopia, uh You won't get to pine the sty lesion. That's um well, no, you won't. That's a bit, that's, it's a bit too far forward for that. I'm afraid. So, next. Uh So yes, this is just showing. It's a bi temple hem A P and would it be a superior um temporal he Mlapa and inferior hemianopia. Take care. Yeah. Well, it's pretty big. So you probably have both in this situation. But yeah, you'd imagine based on what we've heard about the anatomy is a cosmetic region that the superior field was the one that was affected first? Good. So then next. So A and B can someone tell me what A shows and then what B shows and then what field defects might you expect with this lesion? He is? Yeah. Which septal lobe is that in left? Yeah. Um That's right. So yes, it's probably an inter axial. So, I haven't been very fair because I haven't given any physical history or any other cuts. But yeah, so it's the T one axial post contrast. And a so there's a kind of a ring enhancing, enhancing lesion with an area of central hypo intensity. Again, you're gonna assume that it's enhancing because we haven't seen a precontrast MRI scan. The top differential obviously depend on the clinical history should probably be an uh glioma or actually with the central hyperintensity, high grade glioma such as a GB M. Uh an abscess is possible but the pattern of enhancement is not quite the same. Uh How would you differentiate between abscess and GB M on the MR any sequences that would help you tell the difference between an abscess and a tumor borders in shape? Yeah, but there's a particular sequence that you can use. Uh Well, no, because flare shows edema, doesn't it? So you're still going to see edema with. Yeah. So that's right. So, so DW I um so because there's restricted movement of water in an abscess and it's less restricted in the GB M, you expect to see um high signal on the DW I um less see less restriction on the um for the GB M and with the abscess CC um diffusion from the DW I. So yes, that's A then B uh again, so not much clinical history given by myself, but the um B is actually a POSTOP MRI scan Um So you can see that there's a tumor or the lesions been resected. Um And there may be some enhancing residual that might be blood product. So, what field defect would you get if you cut out someone's left occipital lobe or cut out a tumor from the left occipital lobe? Yeah, he, he, that's right. Um And it may or may not involve the macula. So, you know, I said the macular uh well, the macular may or may not be spared because you may have cut out the the occipital tip or the portion of the occipital li that corresponds to the macular. Um But yeah, you definitely have a contractual he like yeah ORAC birth defect which probably be a hemi and that would look like this. So that's the right I one of a Semak you OK. So now on to the slightly more interesting, more interesting specific stuff. So what is this field defect? And where does this localize? Do this is a temple filled in one eye? Sorry. Uh So typically this is the temporal fi in one eye. So there's a superior temporal quadrant contractual and there's complete visual loss in one eye. So what type of um field defect is that the church? I don't know. Well, yeah, it's near the SM so well it yeah, so that's right. So it's in the the junction. So this is a form of junctional um field defect. So rather than having a scotoma because it's so advanced, there's blindness in one eye and the inferior retinal fibers from the contralateral eye start to be involved. So there's a contralateral superior temporal quadrantanopia. So it localizes the cosmetic region but junctional cosmetic region. Um So here, so this is a, well, again, it's an axial M RT one post contrast diff some any different tools for this lesion. Yeah there. And it could be, could it be this one over uh short of which? No optic N you? Well, you can't have a Schwannoma of the optic nerve. She can you because the optic nerve is part of the central nervous system. So it has um dendur cells rather than Schwann cells. So you can't get an optic nerve one. Yeah, this it's probably a meningioma. Yeah, it could be a short name of five. Could be doctor Pale there. Um I think, well, the, the asked the summer said it was a medial sphenoid wing meningoma. It's probably involving the cavernous sinus. And one of the indications that this patient's blind in the left eye. But if you look at the visual field defect, it start can get compromised in the right eye. Sometimes you might see, despite the lesion itself being far away from the contra optic nerve, you can get signal change developing in your contractual optic nerve. So that can be an indication to operate on something even when someone's blind is that there's a risk to, to vision from this, in this case, operable. Um Well, it could be, it could be operated. I don't think it's completely resectable because it's involving the cavernous sinus. Um, but I'm sure there are some skull based surgeons who would be able to weigh on that. Um, so that was pretty much everything for me. A bit of a whirlwind tour. Um, just in terms of the references I used or suggested reading. So, for any people who had any junior people interested in neurology or neurosurgery, I'd really recommend this book, which is Lindsay. That's the fifth edition. It's got some nice diagrams that talks about how to structure um your approach to localizing lesions and some very broad strokes on pathology. I mentioned all of the, all of the dissection slides are taken. They're from the RO to collection, which is, well, when I stand up, it was free. Um And he's also got some videos on youtube where he talks through his dissections. Another good resource is neuro ophthalmology with Andrew Lisa. He's an American nephrologist who does kind of three minute five minute videos on youtube talking about specific things. So he'll talk about Congress field defects or the motor nerve palsies and things like that. And the I Wikipedia, if there's anything specific or specific field defects, it's probably got a bit too much information for me or my interest in my limited interest in your ophthalmology. But it can be quite helpful if you want to try and get your head around some of the more um complicated things. Uh Yeah, that's good. Any questions just going to chat? Thank you so much, Mister, right? For such an informative session. Um If anybody does have any questions, please ask, um go ahead or pass um whi on the chat and um if everybody could fill out the feedback form, which is in the chat, I will also bring up a QR code as well. Thanks. Uh Just got any questions. So someone can you please repeat why the ma for the spa and straight? So uh I'll go back, you still see my slide. So I'm sorry, could you perhaps share again, please? Uh fine. So just going back, can you do this now? Um So going back to the macular. So if you look here, so this is the occipital lobes, the superior bank of the cal sulcus that's taking fibers from the um the op radiation passing through the lobe, the inferior from fibers through the temporal lobe, the fibers from the central bundle go to the, the tip of the occipital lobe, that portion there. And if you look at the vascular supply of the occipital lobe, its predominant supply is from the PC A. But the MC A also provides collateral supply if I can draw a picture. So that's the brain, it's just the brain on the sagittal frontal occipital lobe. So the PC supplies this strip here and the outer surface of the cortex is supplied by the MC A. So the MC A and then the central band at the top is the AC A. But basically, there's a watershed zone like around here where the MC A and the PC A both supply a portion of the occipital lay. So if you have a PA A PC A stroke, you can lose vascular supply to this portion of the oci lobe. But the macula can be relatively spared because it's getting colla supply from this kind of external branch of the middle cerebral artery. So that's the theory as to why it happens. But it's probably more complicated than that because if you go back to that case where um they've done an occipital, you know, taken out an occipital GB M, the macular, the port of the o theoretically um carries uh or presses the foid fibers in the macula has been cut out here. But they have done studies in patients who've had kind of oci lobectomy or partial OPI lobe removals where the portion of the Oslo that thought to correspond to the macula should sit and they will still have a degree of macular sparing. So that's why there's that theory about bilateral um representation. I think really as with lots of neurology or neuro, we probably oversimplify things um based on our limited understanding of the brain. Um But for the purpose of your medical school examinations, it's due for your blood supply and that's what I was taught and that's what I was original um university. Um How does it typically take to recover from visual dysfunction following compressive pathology? Well, it depends on the acuity of the compression. So how quickly it's developed the severity of the defects. Um and lots of other things generally in neurosurgery as a as a mantra, we operate to stop things from getting worse. So if you had a patient, you had a, you know, compressive optic nerve problem and you're doing an operation to take the pressure off, the intended benefit would be to prevent the visual function from getting worse. We would never guarantee when consent to the patient that things would get better. There are certain things that would suggest the patient is less likely to get better. Um One of those is I mentioned earlier, optic atrophy, that's where you basically have had chronic compression and the optic or the retina is basically dead. So if you take off the, if you take or not dead, but you know, severely um atrophy, it's not going to be able to s to see functionally see. So if you take off pressure, you think the eye is not going to have any functional use. If someone has a very rapid progressive or compressive problem and they go blind very quickly and then you're able to operate and decompress it very, very quickly as well. The degree of reversibility, I think it probably be perceived as higher, but there isn't any hard and fast rule. So generally if someone's getting blind from a compressive tumor and it's, you got evidence either radiologically or clinically that it's progressing, you'd counsel them about the need for, you know, decompression or to, to relieve the pressure effect. Are there any other questions? No, the uh no worries. Thanks for dining in. I'll leave it with the, um your anatomy committee to close out. Thank you again, mister. Um So I'm just going to set up a QR code for everyone. We would be really grateful if you could fill this in just so we know how we can improve our sessions for next time.