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Ok. Hi, everyone. Welcome back to the New Anatomy Collaborative. I'm Marma. I'm the chair of the series this year. I'm delighted to present. Yeah, we have started, just started. Ok. Delighted to present talk three of our 14 part series this year. And I now hand over to Dara who will be introducing our speaker and the talk for today. Uh Hi, everybody. I'm Dara. I'm part of the events team and thank you for joining us this evening. We have visual pathways. Who's going, that's gonna be delivered by the Mr Oliver Roe, who's a neurosurgical registrar from the S South Tame scenery. Who's a repeating speaker that's come, that's kindly agreed to come and join us this evening, delivered a talk again. Um If this is the first time that you're attending this series, this, this sorry, this year, we're completely running on metal. Uh this way, we can accommodate for our international audience. And we have also restructured the talks this year whereby we're going from the spine to the brain stem and beyond. And we're gonna have clinical case based talks like our next talk next week uh to kind of cement your neurosurgical learning as well. But with all that said, I want to thank Mr Oliver Roh in advance and hand the stage to him to get over the call. I forget. Yeah. Uh Thanks very much. Um I'm on an NHS computer so I'm sorry, I don't have a camera. Um But yeah, I'm gonna give the same talk I've given the past couple of years about the visual pathways. Um So the main idea is to give you an understanding about the co anatomy of the visual pathway, breaking it down into its separate constituent parts to allow you to help localize lesions based on the pattern of the visual field defect as a consequence. I'd hope that you afterwards, you're able to describe visual pathway um lesions with correct terminology and to identify which bit of the visual pathway is being affected based on the description of the field defect. OK, I break it down into assessing or how you assess vision, an overview of the visual pathway a bit or some specifics about the anatomy because I think that's why you're all here. Um As well as the no nomenclature, I've put a star or like a asterisk against somebody and asked me that's beyond the level of the medical student, but I've included for kind of personal interest, but that's mainly just kind of a an interest piece. So I wouldn't get too hung up on it. And then, as I said, localizing lesions based on the field defects. The caveat of this whole talk is that I'm not, not an ophthalmologist or a training neurologist. I'm a neurosurgical trainee. So I'm going to focus predominantly on compressive pathology. And if there's any um inaccuracies and the nuances of the way that the field defects are described by myself, I apologize. So I thought we'd go back to basics and talk about how you examine a patient's vision and this kind of reflects on how you approach this in medical school. I think if anyone ever asked you to describe how a patient's presenting or examine something, it's always best to go back to basics and stick to a structure. So as with all examination, we approach from the, the patients left, you start by inspecting, you examine the second cranial nerve and there's a pneumonic that we learned in. I don't know, I learned in third year, which is Afro C. So you check the acuity with the Snellen chart. It's helpful to practice using um MD CALC. It's got like a bedside chart that you can use on your phone. You test each eye and turn um getting the patient to read the lines and you score it based on the final line in which um they didn't make an error. And then you assess the field, you do that confrontational face to face by using uh fingers. But also um you can test the, the blind spot and the classical teaching as you do that with a red hat pin. Um, you look into the patient's eye and you ask them, you, you slowly move the, the hap pin across the field of vision and you ask them to tell you when the, the pin or the tip of the pin disappears and then when it reappears again. And the idea is that the, um, the point at which it disappears is the same for both of you. If the patient says the hap disappears much before um you see it disappear, then there's a suggestion that the blind spots increased in size. Then um you do can assess reflexes. There's the direct and consensual light reflex as well as the relevant uh the swinging light test and also accommodation and you can perform ophthalmoscopies. Look at the back of the eye. Finally, you can assess color vision using Ishihara charts. And again, I think there are um Ishihara charts integrated into MD calcs. You can do it all on your phone at the patient's bedside. Then whenever you finish a specific bit of a neurological examination, um you move on to kind of the associated structures. So around the eye and the orbit, you have the extraocular muscles which are supplied by cranial nerves 34 and six as well as the trigeminal. Um And then to complete any neuro examination, you can do a full cranial nerve, upper and lower limb neurological examination, looking for associated um signs that might point you to where the pathology is lying. When it comes to the objective assessment of visual fields. There are two main ways we do that. It's done by ophthalmology in an outpatient setting. Normally, there's something called Humphrey um which is an automated test where the patient sits with a head on the chin rest pointing towards us looking at a central point and there's a non mobile stimulus strain for a brief moment. And when the patient sees the uh stimulus, they press a button on a handheld remote control and it generates a map which looks like this with different stimuli, use of varying size and intensity to try and stratify the bit of the visual field that the patient can see, then there's the Goldman's field. So this requires someone to actually do it to someone called a perimetrist and it's a kinetic perimetry. So the patients um having a stimulus that's moved into the field of vision and they tap the, they tap the table when they can see um the stimulus and that's marked by hand on a field by the perimetrist, then they kind of do the reverse, starting in the center of the field and moving outwards. And that's to delineate the scotoma or the blind spots. And that ends up with a a field of like this when it comes to the visual field or what it actually represents, it looks at the topographic arrangement of the receptors in the retina. So when light hits the retina or the retinal ganglion, the retinal cells, it starts the phototransduction cascade, which ultimately results in the ganglion cell being activated. The fibers run to the optic nerve head, which has no receptors. That's what we call the physiological blind spot. Um And the macular has the highest density of receptors which is um found the FVE or sorry, the FVE is the central portion of this. So that's where you see the optic disc represents the blind spot. So when it comes to the visual pathway or the visual field, remember that the temporal field is seen by the nasal retina and the nasal field is seen by the temporal retina. Similarly, the bottom of the retina sees the superior aspect of the visual field and vice versa. So you have the light hitting the retina, it travels down the optic nerve to the chiasm, then to the tract, then to the lateral geniculate body or nucleus, the optic radiations and finally to the visual cortex. So my hope is that by the end of this talk, you're able to identify which bit of this pathway is being affected based on the pattern of the visual field defect, just the inside of of the light reflex. Does anyone know what this uh this video showing? What is it there? What are we looking at here? Yeah. And what's that, what's that demonstrating? Are people able to talk? Are people able to un unmute or is it uh just chat. Uh It's just chat for now. Uh OK, everyone's invited to, to the stage, but fine. So consensual and direct light, right? Light reflex. Yeah. And is there anything abnormal on the, we call it the swinging light test? Is there anything abnormal on the swinging light test? R APD? Yeah. And which eye has got the R APD? It says it doesn't, it, it's the, the right patient's right eye. So if you look at the, the swinging light, you see when the light shines in the left eye, the pupil constricts when it switched to the right eye, the pupil paradoxically dilates the reason that happens is because there's a relative defect in the transmission of the afferent aspect of the light reflex. So if you look at the uh light reflex, now when the light hits the retina, it sends fibers down through the optic nerve across the chiasm, the optic tract and then via the pretectal nucleus, which is in the back of the midbrain to um and they're doing a ves nucleus which is the parasympathetic nucleus of the oculomotor nerve. And then the efferent limb which is the oculomotor nerve to the ciliary ganglion which promotes papillary constriction. So, when this pupils paradoxically dilatate dilating, it means that there's an aspect or an issue with the consent, the afferent part of this party, which means that um it's dilating because the fibers or the signals are not traveling down the optic nerve as well as they are in the left eye. When you shine light in the left eye, the right eye is constricting as part of the consensual pathway, uh just a bit on scotoma. So, scotoma is what we call the blind spot. It comes from the Greek scotoma and in darkness, when you have a scotoma, it tends to be a problem with the rectal or the optic nerve lesions themselves. It tends to be unilateral um but it can be bilateral dependent on the underlying pathology. Um different patterns of scotoma point to different types of pathology. So you have this thing called ringing scotoma. And there's retinal degeneration, a central cecal scotoma which extends to involve the blind spots, um is seen in a toxic envelope with things like alcohol use and tobacco, arcuate scotoma extends from the blind spot to the f fya following kind of the the nerve fibers. You see that in glaucoma and in the central scotoma, it tends to be problems with the optic nerve leading to um an enlarging uh of the physiological blind spot that tends to be seen in cranial nerve to compression or macular degeneration. What does this show? So, it's papilledema showing blurring of the optic disc margins. So, if you have severe chronic papilledema, you get, can get optic atrophy as a consequence of uh basically compro compromise of the the optic nerves predominantly through venous hypertension. And these patients end up getting a constricted visual field um due to kind of peripheral atrophy and they can only see a small segment of the visual field and also the the the blind spot enlarges. So break it down into the different parts of the optic pathway. We can break the lesions down into prechiasmatic chiasmatic and postchiasmatic. So, when we're talking about prechiasmatic problems, we're talking predominantly about monocular visual loss that tends to be a problem with the retina or the optic nerve. It tends to have an association uh associated with scotoma. There's a reduction in acuity and color vision and they may or may not have an RA PD. That's for an incomplete lesion. If you have a complete lesion affecting the optic nerve or the reti, then you get blindness in the affected eye. Um and the patient will have an absent, direct but a present consensual reflex because the oculomotor nerve, the efferent limb of the, the light pathway is still intact. It tends to be the end result of inflammatory compressor pathology or you know, things like MS or if you have a tumor within the, the eye, uh sorry, within the orbit, causing pressure on the optic nerve. Um just as an aside a bit about the retina of the optic nerves, vascular supply. It comes from the ophthalmic artery which is a branch of the internal carotid artery. It has multiple branches um including the central retinal artery or central artery of the retina. The blood supply to the retina itself comes predominantly from the central retinal artery. It sends um posterior ciliary arteries that supply the retinal surface. Um but also the flavea, it's not a very good picture. The predominant supply to the FVE comes from retinal branches. Whereas the retina itself is from branch to the central retinal artery. So you have, if you have an occlusion of the central retinal artery, you get retinal um impaired supply to the retina. But the f is preserved. Yet this uh basically monocular peripheral constriction with a pre preserve preservation of the central vision. And if you do fundoscopy, you see there's something called the cherry red spot because the ve is still vascularized, but the whole of the retina is devascularized. And that's because of the differential blood supply to the retina versus the FVE. If you have an ophthalmic artery occlusion, obviously, the whole eye is going to be affected. If you look at this picture of the retina, you see there's kind of atrophy or um some pallor in the superior aspect of the retina. This is because the central retinal artery has two or predominantly two divisions that has a superior and inferior division, the superior division of the central retinal artery goes to the superior retina. So if you have an occlusion of the superior branch of the retinal artery, they'll have ischemic change within that aspect of the retina and they have an inferior field defect. In contrast to all of the other field defects we'll tend to discuss today. It's, we call it altitudinal, which means it's half of the visual field in the horizontal plane and that could be superior or inferior. So if you have, if you lose the superior aspect of the retina, you'll have an inferior field defect. Similarly, you know, if you have an inferior field, inferior retinal problem, then you have a superior field defect. So that's in contrast, if you have a altitudinal field defect, you're thinking it's something to do with the vascular supply to the retina, then it comes to through compressive pathology. So this all, all of the prosection pictures are taken from, wrote on. Um it's not really interactive or are people able to talk yet? Should I point out things? And people can tell me what it is. What's this is that the optic nerve? Yeah, that's the optic nerve. What's this then? So this is the optic nerve, this thing that splits into three branches or three divisions. It's a cranial nerve, trigeminal nerve, trigeminal nerve. Yeah, exactly. Uh what's this structure here? This vessel? This is the carotid artery. So if you think about the, the eye or the orbit, you can break it down into different compartments, you can have the orbit itself, the orbital apex where the structures, the neural structures are passing through to exit this cranium. So you have the optic canal which contains the optic nerve and the ophthalmic artery and then the superior orbital fissure which contains the, the nerves that supply the extraocular muscles. And the V one division of the trigeminal V two passes through um Framan rotundum and V three through Framan ovale, the extraocular muscle, uh innervating nerves and V one pass through the cavernous sinus, which also contains the carotid artery. Um These are the FM branches of your family artery. So when it comes to which bit of this pathway is affected, you can break it down based on the, the structures that are affected. So tend if you have problems within the orbit itself, you tend to get proptosis because the, the eye has pressure behind it and it starts to bulge out. Um We see that with uh things like meningiomas um or inflammatory conditions or in trauma, you might get a retrobulbar hematoma that causes that you can have problems in the optic canal. Again, it tends to be things like tumor or granuloma in this area, sometimes you can get hypostosis. Uh so the sphenoid bone, it can become hyperostotic and the the optic canal can start to become stenotic or we can have intracranial lesions uh adjacent to the optic nerve. And again, we're talking about generally the neoplastic or inflammatory things like meningioma or granulomas, which bit of this pathway, which bit is affected, you can work it out based on the structures that are affected. So, if it comes to the orbital apex, which is this portion here. If you think about it, logically, the orbital apex contains the optic nerve, the nerves, the extraocular muscles. So 34 and six and the V one division of trigeminal. So, if someone has an optic orbital apex syndrome, they'll have some visual loss with an ophthalmoplegia because all of the extraocular muscles will be affected plus minus numbness in the V one division of trigeminal or the forehead. That's in contrast, the cavernous sinus, which contains slightly different structures. It has V two, but it, and it doesn't contain the optic nerve. So they tend to with ca science pathology tend to have no cranial nerve dysfunction as well as ophthalmoplegia, numbness in the forehead and the cheek. And they get ocular sympathetic dysfunction because the sympathetic fibers that supply the people run on the carotid, which means uh and they go down the ophthalmic artery, which means that if you have a problem disrupting them, you would expect them to have a myotic or a constricted people because the parasympathetic fi is also run with the oculomotor nerve. You have loss of both parasympathetic and sympathetic innervation of the ciliary ganglion, which means that the people ends up being in mid position because there's no autonomic input on it. So, characteristic of a cavernous sinus problem is they'll have a mid mid position and fixed people. The caveat to the lack of cranial nerve two dysfunction is in pathology like cavernous sinus thrombosis or carotid, cavernous fistula where you end up having raised venous pressure within the cavernous sinus. Because the superior ophthalmic vein drains there. If you have venous hypertension, you can get visual loss because of um transmitted, raised venous pressure to the eye. This is the superior orbital fissure. So again, you can differentiate between superior orbital fissure syndrome and orbital apex syndrome because they're differential structures that are affected. If you see the superior orbital fissure doesn't contain the second cranial nerve. Um but it does contain V one. So if you have the constellation of 346 and V one, without cranial nerve two dysfunction, you think it's more likely to be a problem with the superior fissure rather than the orbital apex. I mean, when it comes to neurosurgery, this is slightly academic because lesions that are big enough to cause compressive pathology and and disruption of vision in the eye tend not to affect these quite small spaces. So I think the main dis discriminator is between cavernous sinus pathology and problems within the orbit itself. And that predominantly comes from um involvement of the optic nerve. So that's prechiasmatic issues and it comes to chiasmatic issues. Um This is uh the optic chiasm or so this is basically what you see from. Uh uh basically if you come subfrontal. So this is the optic chiasm, cranial nerve two coming out towards the orbit or the eye here. This is the pituitary, the pituitary stalk. This is the internal carotid artery, middle cerebral artery, anterior cerebral artery. With the Acom here, the optic tract is the bit behind the chiasm heading back towards the later genicular body. This is the basilar, the clivus has been removed. This is the basilar here. Uh This is the pons. You wouldn't normally see this because it would be covered by bone. Uh and this is the frontal lobe up here and you can't really see it, but the olfactory tract is around here somewhere. So when it comes to optic chiasm pathology, this is the classic picture that you get in your medical school exams. So if you remember that the fibers from the the temporal aspect of the retina don't cross over. But the fibers from the nasal aspect of the retina cross over, which means that the once you get behind the chiasm, the optic tract has fibers from both eyes. The classic lesion is a charismatic lesion that cause a bitemporal hemianopia. This is because the nasal retinal fibers from both eyes are affected the nasal retina, remember see the lateral aspect of the visual field. So if you have a central cosmetic lesion, you have bitemporal hemianopia, we say by temporal because it's both temple fields, hemianopia because it's on it's half the visual field we call that a heteronymous hemianopia because it's different size, it's different sides of the visual field. That's in contrast. Uh uh sorry, you can have a temporal hemilia. You can also have a binasal hemopure which looks like that it's much rarer. Again, this is a sagittal view. So this is the optic chiasm. This is the basilar, this is the pituitary sphenoid sinus, frontal lobe, anterior cerebral artery Acom complex. This is the third ventricle midbrain pons, cerebral aqueduct, tectum of the midbrain, fourth ventricle colum of fornix, fornix itself. This is the lateral ventricle up here, anterior commissure lamina terminalis. So if you think about the pattern of chiasmatic compression or the possible causes of chiasmatic compression, it could be any structures around this area. The main differentiator is whether it's compressive pathology that's arising below the chiasm or above the chiasm. And in simple terms, it's probably a little bit more complicated than this. If you have a problem that's coming from below the chiasm, the fibers in the inferior aspect of the visual field are affected first, which means that superior, sorry, the infer fibers from the inferior retina are affected first, which means the superior retinal field or the superior visual field is disproportionately affected. For instance, if you have a pituitary tumor that's growing upwards and pressing on the bottom of the chiasm, the inferior retina, uh the fibers from the inferior retina are preferentially affected. So the patient will have worse vision in the superior aspect of the visual field, they'll still have a bitemporal field defect. This is in contrast to pathology that's coming from above the chiasm. I mean a classic thing is a craniopharyngeal which tends to be more um ventrally orientated. But if you have a big ao ays or an olfactory groove or kind of parameningeal, that's causing compression on the top. Again, um the superior fibers from the retina are affected first. So the inferior field will be disproportionately affected. So you can try and you can try and gauge an idea when you examine a patient. Um which where the compression pathology is arising from. If you have a bitemporal hemi, a, if it's above or below the chiasm, that's a bit of a simplification. But for practical terms, it's quite an easy way of thinking about things when you have problems with bitemporal hemianopia. As I said, it could be anything in the region of the optic chiasm. Um The main ones you think about are pituitary, adenoma, craniopharyngioma or meningioma or aneurysms, particularly acho aneurysms. Again, as a kind of a point of interest, you can develop some weird visual field defects which are known as the junctional scotomas. There are two main ones you know about when we say junctional Coomer, it's basically a blind spot, but it's the junction of the optic nerve and the chiasm. The classic jun junctional scam presents with an IPSS, lateral, central, central scotus. So the blind spot in the affected eye is enlarged with a contralateral monocular superior temporal field defect. It looks like that. So you have compression on the right optic nerve adjacent to the chiasm, the blind spot is enlarged in the right eye and there's a contralateral superior quadranopia. This is thought or what used to be thought to be due to something called Willebrand's knee, which is basically the fibers from the nasal retina deviate into the contract optic nerve, which means that you get disproportionately affected, they get disproportionately affected if you have a uh sorry, the fibers from the nasal retina of this eye bend into the contractual optic nerve, which means if you have compressive pathology here, the blind spots increased and the temporal field is affected because the nasal retinal fibers are being caught. Again, that's a bit of a simplification. Um but that's the classic jun scotoma that was based initially on cadaveric studies in the optic nerves of monkeys. Um It's been shown to actually be an artifact because if you cut the nerve, the fibers get pulled into the contract optic nerve. But clinically, you do have this manifestation. So it's not quite clear why this contralateral superior temporal field defect arises. Then there's something called the junctural scotoma que, which is again, pathology, compressive um on the optic nerve. Um but it tends to present with a monocular hemianopic field loss, it looks like this and it can be nasal temporal. So if you have a monocular hemi field defect, it's called the junctural scotoma of que. And again, it's pointing to pathology around or near the optic chiasm, it's just pressing on one side of the optic nerve, that's the optic chiasm. Then when we go behind the chiasm, I mentioned that the the fibers from both eyes are on um are in the optic tract which means that both eyes will be affected, it's crossed. So if you have a problem in the left optic chiasm, it causes a problem in the right visual field and vice versa. The pathology or the visual food effect is on the same side. So we describe it as homonymous rather than heter heteronymous. The shape of the field defect depends on where in the retrochiasmatic pathway is being affected. And you can still localize retrochiasmatic lesions based on the pattern of neurological um findings. You can break the optic or the retro cosmetic pathway into the optic tract with electro geniculate body or nucleus, the optic radiation or the visual cortex. When we talk about congruity, you might hear people say there's an incongruous um homonymous hemianopia or incongruous um quadrantanopia. It just means that the visual field shape is different in both eyes. You see in this side, this eye is disproportionately affected. There's predominantly a superior quadrant quadrant um field defect here and a hemifield defect in this eye. So again, going back to the anatomy, this is the midbrain substantia, nigra, cerebral peduncle, cerebral peduncle aqueduct tegmentum of the midbrain. These are the oculomotor nerves, mamillary bodies. This is the pituitary stalk or infundibulum optic chiasm. Uh This is the optic nerve optic nerve. This is the temporal lobe, that's the uncus of the temporal lobe. You can see where that might catch the third nerve there. Um And this is the uh perforative substance, anterior perforator substance, posterior perforator substance ambiance system this bit. So this is the optic nerve. This is optic chiasm. This is the optic tract which terminates in the lateral body which is um lateral to the thalamus. When you have an optic tract problem, you tend to have a homonymous field defect and it can either be congress and in or incongruous, the more posterior in the retros pathway, the more congress the defect because the fibers come closer together. If you remember that picture of the um light reflex, the optic tract contains some fibers involved in the light reflex. So if you have a problem in the optic tract, they'll get a contract actual R APD because the light light fibers from um the contract I is poorly affected. So, if you have a homonymous hemin noia, you're saying it's retrochiasmatic and there's an R APD that's pointing towards an optic tract lesion, that's quite an important point. Um You also because the cell body of the optic nerve is in the lateral geniculate body. If you have any a lesion in front of that, they get atrophy of the optic nerve and that get get some characteristic pattern of retinal atrophy that you can see on fundoscopy. Um again, this is more in the remit of the ophthalmologist. So, II probably won't explain it very well. But basically the temporal fibers or the fibers from um the temple field are differentially uh represented compared to the nasal fibers. So, if you have um affect, if you have the nasal fibers being affected, they get atrophy in a particular pattern called bot atrophy. So the bo atrophy will be contralateral um to the lesion if that makes sense, probably not. Um So just to summarize optic tract lesions don't have con have a contract, actual homonymous field defect. It can be congress or in congress. But the presence of an R APD points heavily towards it being a problem in the optic tract. This is the lateral genicular body. It's topographically arranged. So the central portion of vision is located medially in the nucleus. Um and the peripheral portion of the vision is located laterally. These two areas have a differential blood supply. So the central or the medial portion of vision is supplied by the lateral posterior choroidal artery. And the lateral aspect of the periphery is supplied by the anterior cordal artery which comes from the anterior circulation. So, if you have disruption of either of these vessels, you can get different aspects of the lateral to the body affected. So, if you have a lateral posterior choroidal artery occlusion, because it's supplying the central portion of the um LGB, which is related to the central portion of vision, they can get a field defect that affects the central sector. And it's homonymous. If you have an anterior artery occlusion, it will affect the lateral or the peripheral aspect of the lateral genicular body. And they'll have a sector sparing, homonymous hemianopia. So if you have any form of sector hemianopia, you're pointing towards the lateral geniculate body. You can describe it as a wedge, the wedge sector anopia. So the the wedge involving is called a Pacman field defect because it looks like Pacman. So this is uh homonymous wedge ectopia and this is a homonymous sector sparing sorry, a homonymous sparing sector anopia because it's a sector of division that's affected any, any any questions about that. It's a little bit high, a little bit high level. No, they're moving on to lateral body lesions. You can have this where you see they have bilateral sector sparing. He uh field defects. This is called an hourglass defect. It looks like an hourglass. It's caused by bilateral genicular body um problems. There's a characteristic condition that gets this. It's something called extra pontine myelinolysis. If you remember from your first couple of years of medical school, you can have central pontine myelinolysis from overcorrection of of, of hypernatremia. Uh It used to be called osmotic demyelination syndrome. So this is basically a manifestation of that, but it occurs outside of the pons. So it's called extra pontine myelinolysis. So you might see this in someone who's had rapid overcorrection of hypernatremia developing this characteristic hourglass field defect because of bilateral later genicular body involvement. This is the optic radiation. So again, just to recap the anatomy, uh this is probably the medulla because we're, we're looking quite deep. This is medulla, this is the pons mamillary bodies, optic tract nucleus. The temporal lobe is gonna be here. This is one of the cerebellar peduncles. Um Yeah, the the surface of the optic radiation, it has two distinct portions, something called Meyer's loop which passes through the temporal lobe and then a superior radiation that passes through the Praet lobe. They both converge on the calcine fissure which is found on the occipital lobe. So that's the location of the primary visual cortex. It's also called the geniculocalcarine tract because it goes from the geniculate body to the calcine sulcus. It's a white metal white matter bundle. The may as it turns anterior initially and then posteriorly, it runs in the lateral aspect to the lateral ventricle adjacent to the atrium. The central portion of the there's a central portion of fibers that contains information from the macular which looks like this. This is a dissection. So basically this is just showing this is the thalamus, the lateral genicular body here. These are the optic, the white matter fibers that carry the optic um the other optic radiations terminating in the calcine sulcus. It's just the tip paum of the corpus callosum. This is the lateral ventricle. Um and this is the ulla that's been removed. So you can see the deeper structures. So when it comes to optic, sorry optic radiation field defects, it depends on which bit of that radiation is affected. So, if you have a lesion that's affecting the temporal portion or Mayer's le you get a pie in the sky defect. So you have a contralateral superior quadranopia, it's called pie in the sky because they've lost a segment of pi from their superior vision. Um If it's in the pra they get a non mayor's, uh they get an inferior quadrant defect that's called par on the floor. The way to remember that, sorry. And then if you knock out the whole of the optic radiation, you get a homonymous semia the way to remember that passive thing is that uh uh acronym or pneumonic pits prior to is inferior temporal superior field defect. Obviously, if you're having problems in the prior to label temporal lobe that are affecting vision, you're probably going to have problems or other evidence of cortical dysfunction. So you might have signs and symptoms that correlate with dominant or non dominant prior to lobe lesions like a Gerstmann's type syndrome or hemisensory neglect or in the temporal lobe. If it's dominant, they might have speech disturbance or having seizures or complex, you know, absent type episodes. So you have other signs um that are pointing towards a, a cortical or a labor issue with the optic radiation. Again, this is a kind of mid sagittal slice of the brain. This is the corpus callosum, lateral ventricle, frontal lobe, temporal lobe, the parietal lobes here. So you have cuneus, sorry precuneus cuneus. And then this is the calcine sulcus which is in the occipital lobe. This is the location of the primary visual cortex. It's where the optic radiations converge those that pass through the Pras lobe and those that have come through the temporal lobe as part of Myers loop. That's just to remind you of that the more posterior you go the more congress the lesion. That's because the fibers converge. If you have an occipital lobe problem, it results in a contractual hormon semin and there may or may not be macular involvement. That's because um the macular or the bit of the, the bit of the visual cortex that correlates to the macular is right at the tip of the occipital lobe. There are two theories why the macular or the central portion of vision might be spared. The first is that there's bilateral occipital representation. The second is that there's dual blood supply. So if you have a PCA stroke, a posterior cerebral artery stroke, you'll lose blood supply to the occipital lobe and have an occipital lobe stroke. But the MCA is, is part gives a watershed supply to the tip of the oil lobe. So that area may be represent may be relatively spared if you have a PC stroke. But the MCA is still patent. Uh Yeah. So to summarize with that visual cortex lesion caused contralateral homonymous field defect, it may or may not involve macular sparing. So then we come on to cortical visual field defects. This is basically where you're saying that all of the aspects of the visual pathway are anatomically intact. But there's a problem with the processing, which means that the patient manifests as having um signs of visual disturbance. Um So you can get things like cortical blindness. So basically, all of the eye structures are intact. So the people, the people reflex are intact. Um It's a problem with processing because the patient has bilateral uh ual lobe infarcts. So they can't see they're blind because they can't process the information. There's an extension of that which is called Anton syndrome where the patient is blind, but they have a form of um confabulation where they deny their visual loss despite clear evidence of that. Um So we call that visual anal agnosia because they don't um acknowledge their disease or they are unable to acknowledge their disease. Then there are other cortical visual field effects. There's something called Reddox phenomenon which is basically sta statokinetic association where the patient can perceive an object that's moving but not static objects in a visual field that points towards the occipital lobe. There's something called balance syndrome where they get something um a triad of symptoms, one is agnosia. So if you provide them to stimuli within the visual field, they can't perceive both at the same time, they have something called oculomotor apraxia. So they can't voluntarily guide their eye movements. Optic ataxia, they can't move their hands towards an object, using their vision, but they could use it, they could use sensory input to perform that. It tends to be due to bilateral price of occipital lesions, cerebral achromatopsia, which is basically cortical color binder. Um because there's crossed supply. If you have damage to one occipital lobe, they might have half the visual field where they can't see the color, but the other half is normal. Then there's something called color agnosia. So the patient is able to perceive colors, but they can't recognize it. It tends to be a, that's the sort of language, it tends to be a dominant lobe. So if you ask a patient to identify a red bull out of a collection of red and blue balls, they won't be able to tell you which one is the red bull. But if you ask them to sort them based on color, they'll, they're able to separate the different shades of red and blue out. And then there's a kind of a disconnection syndrome which manifests as alexia without agraphia where the patient can't read, but they can write and they can recognize words that are spelled out to them. Um This is due to a problem with the left cipral lobe and being of the corpus callosum. And again, it's related to uh language. OK. So that was a whirlwind tour of the visual pathway. I have a couple of cases just to um integrate that. So I will actually ask if you can participate in this bit. So uh what vi visual field defects might be present with this lesion by temp. He is correct because so this is the optic chiasm being which has been pushed up here. So what kind of lesion is this do you think? Yeah. So it's probably a pituitary macroadenoma. Um It's, well, this is at one post contrast MRI scan, there's a lesion that's probably in the Sellar that's got suprasellar extension which is causing distortional pressure on the visual adopted chiasm. These are the carotid arteries here. There's probably a bit of parasa or cavernous extension um because it's a lesion that's below and pushing the chiasm up. Which portion of the visual field would we expect to be disproportionately affected? Yeah, the superior visual field because remember the fibers from the inferior retina run in the inferior aspect of the chiasm. In contrast, if you had a lesion that was from above pushing down, we'd expect there to be an inferior field field problem. Um The main differential for this lesion would be something like acela or para meningioma, but it's got the characteristic features of a pituitary adenoma um which is like the snowman type shape. How would you operate on this? What's the preferred approach? Yeah, generally transoral surgery is favored for um pituitary lesions like this. The caveats would be, it may not be, it may be difficult to get that suprasellar extension. But most of the time the tumor will fall into the field and also the the cavernous um component, it might be challenging to um evac to uh excise or debunk that. But remember, pituitary tumors tend to be, tend to be slow growing. Um And the priority of treatment in this uh patient would be to decompress the optic apparatus or the optic chiasm. Obviously, if this is something like a prolactinoma, then we tend to try and manage it non operatively with medical treatments. So it's always worth asking for the pituitary profile before you decide that you're going to operate on something like this. This is the bitemporal field defect. OK. What about this? This is two, these are two, this is a preoperative and postoperative uh scan. So what field defect might be present with the lesion? What kind of lesion is? Where is the lesion? And what kind of lesion do you think it is seal lobe? Yeah, it's not a PCA though. What, what's the underlying pathology? Yeah, GBM. So an intrinsic lesion, you can kind of tell it's intrinsic because there's no clear demarcation between the cortex. This is a contrast MRI scan, you can see this patch or this peripheral enhancement with an area of central hypo intensity. Obviously, the differential for ring enhancing lesions includes abscess or metastasis. Um But this the, the pattern of the enhancement in the way that it's kind of diffusely infiltrating. The brain suggests uh a primary glial neoplasm such as a GBM, the patients had a creno and debulking of that lesion. Um So the left occipital lobe is affected. So what visual field defect might they have? Yeah, it's primary, it's the visual cortex, it's retrochiasmatic, it's gonna be crossed. So if you're having a visual visual cortex defect, on the left hand side, it's gonna give you a a right homonymous hemianopia. It does depend on the extent of infiltration or resection and pos possibly there might be a degree of macular sparing. It's not clear because we don't quite understand the mechanism for that final one. So what's this field defect called? And where does it localize to? So it's a monocular field defect. So this this eye is blind and a superior temporal field defect. So this is one of those funny junctional junctional screamers and this is the the junctional scam. Oh It's pointing to a problem at the junction of the optic nerve and the chiasm. It could be caused by some weird skull base lesion like this meningioma. OK. So, so it's a bit of a whirlwind tour. It's always quite hard to do it online when there's no uh kind of uh verbal interaction. But if you want to read anything further about the subjects, the roam collection, which is free to sign up is very good. There's a new ophthalmologist who has a youtube videos called Andrew Lee who goes through a lot of the kind of compressive or structural uh eye or visual problems. My Wikipedia has more detailed information. I think that's mainly for ophthalmologists and this is a very, very good book for medical student level. If you want to read about neurology and neurosurgery, it has incredibly good pictures and breaks things down in a very accessible way. Thank you. OK. Uh Thank you, Mister White for that talk. Um At this point, we, I mean, as it says on his slides, uh we open, we open kind of a panel for any questions that you may have for our speaker. Um I II actually have a question if that's OK. Well, yeah, of course. Well, I was depends on the question. Uh Yeah, I mean, it's a, it's, it's not, it's not very much, it might not be very neuro but I, you, you mentioned how in an extra pon and the central pontine myolysis overcorrection of hypo um hyponatremia can lead, can lead to that. I was I was just curious why. Well, it's a, it's a cat, it's so it's part of that syndrome called osmotic demyelination syndrome. So if you remember if you have um hyponatremia, you have an increased level of um kind of body water essentially or um you know, the sodium is normally dilute as a consequence. You get cerebral edema. Um and also the, you know, obviously the um CSF or the the brain becomes relatively hyponatremic as well. So, if you overcorrect that systemic hyponatremia by giving, you know, hypertonic saline or something, and normally endocrinologist is a bit funny about how quickly you do that. They say less than eight millimoles correction in sodium over um 8 to 12 hours. If you rapidly correct the systemic hyponatremia, you get a big shift of water from the brain into the blood. And as that water moves it, um demyelinate or causes demyelination of the neurons. For some reason, the the pons is disproportionately affected. The patient can develop a thing like locked in syndromes. They're basically only able to move their eyes and blink to communicate, they get ophthalmoplegia. Um It tends to be, it's incredibly rare. So I've seen it once. Um and it tends to be in patients who are high risk. So if you have a very chronic hyponatremia and you correct it very aggressively, these fluid shifts are much quicker and the chance of you having demyelination occur is much higher. Um Similarly, alcoholics or patients with anemia seem to be high risk for it. Um But it's a classic thing that comes up in your final exams. Um Central pontine myelinolysis, um but the geniculate visual manifestations, obviously an incredibly rare manifestation of that. Um And it's just as an aside, an interest point that you can get this kind of bilateral hourglass defect from extrapontine myelinolysis as well. Does that answer your question? No, very much. Thank you. I was, I was, can I ask a follow up to that in, in terms of, in terms of, are there distinct, are there distinct presenting features when they would present with an extra pontine to when they would present with a central Ponti? No, I mean, I think a lot of this, a lot of these focal presentations of systemic neurological illness are um a bit of an oversimplification. The reality of central pontine is in LY is that you have a patient who comes in with a hypernatremia that gets corrected and then a couple of days later, they become uh in stupor or coma and you do an MRI scan, it shows some high signal within the pons itself. And that suggests that you've probably done something like overcorrect the sodium too aggressively. But in terms of clinical symptomology, it tends not to be like a clear clinical progression that you kind of kind of finding out after the fact that something catastrophic has happened, it tends to be an irreversible neurological injury. Um So the endocrinologists are always quite cautious about it. It's why when you do your med school finals, when you talk about managing hyponatremia, you break it down into whether it's chronic or acute based on how long or how severe the hypernatremia is. It guides how aggressive you are with managing the sodium correction. Obviously, a lot of medications cause hyponatremia. And you have these old patients 80 year old who've been in the community for two years with a sodium of 120 if they come into hospital and then you then aggressively resuscitate them or aggressively treat the sodium and get them to the sodium of 140. Over the course of a few hours, they're going to be at high risk of having problems because you've completely disturbed their normal homeostasis. Um So, no, I think what you would see is you'd see a patient with some disorder of consciousness who has high signal in the brain stem and also possibly in the later geniculate body. Who if you were able to do a detailed visual examination on them, they might have this funny um hourglass pattern which you could explain by the manifestation of the sodium er correction. Yeah, thank you. Um Good cats. Uh I have a question. That's OK. Um It's more clinical than like an R did, but I was just wondering how you approach, I guess like clinical discussions probably b before surgery where like the risk of visual deterioration or damage to the visual pathway is quite high. Like how do you approach the kind of consent discussion there? Well, it it depends, obviously, we're quite pessimistic in neurosurgery. So generally when we're consenting patients for who have an existing neurological deficit, we're doing the surgery to prevent them from getting worse we would never say that by doing this, the vision is going to recover. So generally, with things like pituitary tumors, the indication for treatment in the context of visual or visual compromises either they've already got a visual issue, which if you leave it unchecked and the tumor grows, it's normally over the course of months to years, it's likely to result in blindness. If you say we're doing this to stop you from getting worse, or the patient comes in with impending or threatened vision because the chiasm is being touched. And there's a risk that if you did nothing over the over the months to years that the tumor grew, they would get progressive visual deterioration at which point, whatever they've lost, they can't get back. So the first thing is to counsel the patient on the indication for surgery and the likely outcomes, which is basically to prevent the vision from getting worse. Um For pituitary tumors, it's to get a sample of tissue to guide the to further management. Obviously, there's always the option for conservative management. So you need to put that on the table. But we know that the natural history of if you have a tumor that's causing pressure on the optic nerve and the patients who got visual symptoms, we know the natural history of that is it's going to get worse because the tumor is going to grow. Um So if you explain that the natural history is of progression of at an unclear rate and that whatever you're operating on, um, the visual, the vision is not going to get better. Uh, after the surgery, then it becomes a slightly easy consultation because either the patient goes slowly blind over the course of years or they accept the risks of an operation where they could go blind. But actually the chance of having a serious nerve injury is quite low. Um So yeah, that's how you do it. And we have, I mean, it kind of based on, based on kind of the question that you answered pre uh you just answered, we have a question of a similar topic from the newsletter. This is the last question I'll ask, I promise. Um in regards in regards to visual pathways, are there any kind of emerging emer emerging therapies emerging like interventions that can repair damaged, like visual or have are aiming towards repairing uh damaged sections of the visual pathway, damaged section of the visual pathway. I mean that there's not really anything that's in the, it's in the mainstream practice that's been demonstrated to, to repair nerve function. So, you know, the optic nerve, if you cut the optic nerve in surgery and stitch it back together using a microscope, it's not going to, it won't heal. Um There is some evidence that treating compressive pathology. Um can, you know, sometimes the pituitary, the vision gets better after you take the pressure off the nerve, but we never say that it's going to get better. But it makes sense that by reducing the compressive effect, you maximize the chance for it to recover. Um So you do sometimes see the patients who had a preexisting bitemporal hemianopia have it resolve after you take the pressure off the optic nerve. But you can't say that's the likelihood. I mean, obviously it's a, an area of a lot of interest, especially for Twitter, aficionados with Neuralink and Elon Musk and things. I think it's not inconceivable that in the future, some form of, you know, technology will be able to transduce light signals and push, you know, um transmit that to the cortical surface in a way that's interpretable for the brain. But I'm not aware of any uh active treatment that's been shown to reverse or restore damaged optic nerve function. OK. Thank you. That's fine. Um I think, I mean, I don't see any other questions and um I think uh we've hit, we've hit like the limit of our talk. So again, once again, on behalf of the kind of neuro anatomy collaborative, so I'd like to thank you for attending another year giving us this talk. Um It's OK. And to anyone who is to any of our audience still here, I'd just like to remind them that uh another talk is happening next week and with that, thank you for attending. Thanks to our speaker and yeah, thank you. Have a nice evening. Thank you. Thank you for coming, everyone. See you next week.