 All right, so we're going to go ahead and get started. The PGY2 class, we're presenting the afferent anatomy, and then we're also going to go over some relevant clinical diseases. Kind of a brief overview, touch on a little bit of what's in the BCSC, and I think some of the others have brought in some other information as well. Tina is going to join us as soon as she can get here. She's taking care of a procedure this morning. So I'll start out with the visual pathway here. And this just is the brief overview that you can get kind of looking at everything that's involved in the afferent system. Includes everything from the very front of the eye, from the cornea, through the eyeball, to the retina, to the optic nerve, through the apicaeism tract, and into the brain, and into the visual cortex and the occipital lobe. So all of these pieces are susceptible to damage and susceptible to injury, and can cause different types of disease states that we worry about. As far as the retina goes, here's your overall view of the posterior pole here. This is your fovea, this is your macula, optic nerve. We all take a look at this every day. The things to keep in mind here, and these are kind of points that are emphasized in VCSC that will be important for OCAPs, are just these kind of nuanced measurements that you sort of need to memorize. The optic disc, where it's located, creates a physiologic blind spot that's about 17 degrees from the fovea. And the size of that blind spot is about, if you roughly remember, five degrees. That will be close enough approximation. It's actually a little bit larger in the vertical plane than in the horizontal plane. And that's just due to the different shape of the optic nerve in the vertical plane. The fovea itself normally measures about a disc diameter, which is about 1.5 millimeters. And it's located 4 millimeters temporal and 0.8 millimeters inferior to the optic disc. So you can see it's not exactly horizontal straight across. And that's another good point to remember. As far as the orientation of the nerve fiber layer within the retina, you can see that there's radiations here. And that's important to keep in mind that these cells that are coming in temporally here pass through this horizontal graphene. And they're going to course over the macula. And so when you have injury to particular areas of these vessels that are feeding these areas, you're able to correspond the visual deficits to where those nerve fiber layers are injured. And then the other thing to keep in mind is that as you get more nasally here, you're going to have these fibers coming in really steep angle. And that will cause some of these bow tie configurations, which some of the other presenters are going to go over a little bit later. As far as the really super high level, super low level detail of the cellular organization, I'm not going to go over everything today. Dr. Manlis is going to touch on a lot of this in his lectures. But the important thing to remember is that light pathway actually comes, the retinas sort of flipped upside down. So the photoreceptor cells are actually the furthest away from the light pathway as it comes in. There are a few of these ganglion cells that are located right here in the ganglion cell layer that actually do have some light sensing capability. And these are called these internally photosensitive ganglion cells here. And then the light signal passes all the way through here and gets processed in the outer segments of the photoreceptors. There's also a number of other cells in this section that are important to know about. So bipolar cells are important in vertical transmission of information. These other cells here, we have amocrine cells. There are some interplexiform cells that aren't labeled here. And then we also have the horizontal cells, the horizontal cells that stretch across. And those are actually important in signaling between photoreceptors and between ganglion cells, which is important in distinction of contrast and also in determining spatial location of these light signals that we're getting. And then the last sort of anatomical point that I want to point out here is that in the center of the retina, right in the fovea, there's almost a one-to-one ratio and generally is a one-to-one ratio of the photoreceptors to the ganglion cells. And that's important because you want to have your highest sensitivity of picking up those visual signals in that area. In the periphery, when you get further out, the ratio really expands and it gets out to about one to 1,000. So you see this one ganglion cell here. And this is just obviously a cartoon demonstration. But one ganglion cell is supplying hundreds and thousands of photoreceptors, which is important for processing information and being able to synthesize and say, OK, I know that there's an object coming from this way. That's the important piece of information that I need from that signal. Then I can turn and look at it and see the object and make out more details. I'm not going to go over any of these in any great detail, but the BCSC presents a couple of examples. Basically, any type of retinopathy is a problem affecting the afferent pathway of the visual system in terms of the retina. A couple of these important points to know I've highlighted here. Vitamin A deficiency is one that we probably don't think of all that often, but it's one that can cause problems with the photoreceptor signaling. And the key finding here is that if you were to do an ERG on somebody who's low in vitamin A, you would see rod dysfunction. And then a couple other things. We always are screening patients who are taking placonil for lupus and various other rheumatologic diseases. So the important thing to know is that that risk of damage, that bullseye maculopathy that we see with placonil, is increased risk with duration of treatment greater than five years, and then also with a cumulative dose once it exceeds 1,000 grams. And typically, the recommendations are to screen one year into treatment or any time during that year, and then annually once patients have been undergoing five years of treatment. So you don't have to screen patients every year when they're on placonil. And then there are also some perineoplastic syndromes that are associated. So last point I want to make about the retina is that when you have a patient with decreased vision and you're trying to sort of parse out whether this is an optic nerve or a retinal problem, these are just a couple of things that you can consider. They're both going to have vision changes. So that's common to both pathways. But in terms of the other things that you can look at, color vision is going to be slightly different between the two. Typically with retinopathy, the amount of color vision loss, if there is any, it parallels the degree of visual acuity loss. Whereas if there's optic neuropathy, there tends to be a more dramatic change in color vision. So that's a really quick and easy test. You can do it at the bedside. If you're doing a consult, bring your handbook and just go through those color plates. And even the basic most simple test is grab your phenylephrine and hold the cap up and just test color sensitivity between the two eyes. Secondly, I want to point out that metamorphopsias and photopsias are much more common in retinopathy. And particularly, photopsia usually indicates a problem in the outer segments of the retina. You're rare to have an afferent pupillary defect with a retinal problem, whereas you're more commonly going to have one if there's an optic neuropathy. And then lastly, and this is kind of a subtle distinction because there are some conditions where you will have scatoma in the retinopathy. But typically, there's more distortion of the lines in the Amsler grid with retinopathy as compared to just chunks missing when there's an optic neuropathy. All right. All right, so picking up where Becca left off, the kind of next step in the afferent pathway would be the optic nerve. So this is basically the confluence of those axons of the ganglion cell layer. Again, some numbers kind of picked out from BCSC that seem to be very testable on OCAPS. So a confluence of about 1 to 1.2 million ganglion cell axons. And then they exit through the lamina cabrosa, which contains approximately 200 to 300 channels. So that fact that this is a relatively small number of channels for a lot of axons. I'd just like to say, like, you can use the shit. I totally agree. Yeah. Yeah. It seems to be better to use the shit. Yeah. It has nothing to do with taking care of it. Yes. Absolutely. Yeah. A lot of nonclinical information that seems to be tested. We actually brought that up in our, as we were discussing preparing this lecture. So the combination of that fact paired with kind of this unique blood supply, which I'll talk about in a second, is responsible for the particularly sensitivity of the optic nerve to all different types of damage. So whether it's ischemic, inflammatory, compressive, toxic, metabolic, lots of different things. We've touched on it a couple already. And we'll touch on a few more as we go through the lecture. Some of the measurements. So the diameter of the optic disc, it's approximately 1.5 millimeters at the optic disc. And then about 3 millimeters after it acquires its myelin coating. And then if you include the optic nerve sheath, it's about 6 millimeters in diameter after that. So just posterior to the sclera, I kind of mentioned this, the optic nerve requires a dural sheath. Clinically relevant in this point is that it's contiguous with the periorbid of the optic canal and then the arachnoid membrane. So you do get this channel, the sub-arachnoid space, that choruses all the way up to the posterior globe and is contiguous with the rest of the sub-arachnoid space of the cranium. So any elevation, as we've all known, have seen at this point, most likely, elevation in ICP can really be visualized quite well often in the posterior pole. I actually saw a guy in clinic yesterday that looked probably worse than this and is going to get an optic nerve sheath fenestration today. And then it's also just important to note that in the optic nerve, at least in the retro-bulbar space, there is an approximate retinal topographic representation that's maintained, but later we'll kind of see that that can get rotated and changed. As far as the blood supply, so the optic disc and then the bulbar optic nerve before it actually leaves the sclera, receives a blood supply largely from the branches of the posterior ciliary arteries. And I've seen in some places, actually doesn't mention this in BCSC, at least not in the neuro section, but there's this circle of Zinn-Holler that is mentioned in a few of the pictures that I looked up. But then the retro-bulbar, the orbital optic nerve, receives a blood supply largely from small peel branches coming off of the ophthalmic artery, not the central retinal artery itself. The central retinal artery and vein travel within the anterior 10 to 12 millimeters. So they actually travel underneath, but then they'll pierce that optic nerve sheath at about 10 to 12 milliliters posterior to the globe. And then this, I don't really go into this. We'll probably talk about what's in the superior orbital fissure outside and all that stuff. But I wanted to bring this up because it did talk a little bit about the anatomy. So the optic nerve travels posteriorly through the optic canal. And within the optic canal, we have the ophthalmic artery that traverses the optic canal with the optic nerve. And then it is separated from the superior orbital fissure by this optic strut, which terminates superior is the anterior clinoid. And that seems to be a landmark that's talked about not infrequently when we're reviewing MRI and CT images. And then the optic canal is 8 to 10 millimeters long, 5 to 7 millimeters in diameter. And it's anchored tightly within that canal. So that's why a lot of these traumatic injuries can cause some shearing forces to the optic nerve and cause damage right within that canal. Next, we talk about the optic chiasm. So it's the 8 to 12 millimeter intracranial portion of the optic nerve, or where it terminates. And then it measures about 12 millimeters wide, 8 millimeters long, and 4 millimeters thick. Located anterior to the hypothalamus and third ventricle. And then it's blood supply. This comes up over and over again. Blood supply of the various portions of the afferent system is from small branches off the proximal anterior cerebral and anterior communicating arteries. As far as the location of the optic chiasm relative to the cella, we talk about that most are just superior located, about 10 millimeters above the cella. But there are about 17% that are located anteriorly or what we would call prefixed, and 4% that are located posteriorly. So here we're just, so this is normal where the optic nerve comes. The chiasm is just right above the cella and the pituitary. But then there's this prefixed orientation where it's just anterior and then post-fix where it's posterior. On MRI, I pulled up some pictures that you can kind of see this as well. So this is normal with the optic chiasm here, pituitary. And then we've got an example of a prefixed, a little more anterior and then a post-fixed, post-fixed, a little more posterior. Within the chiasm, as we all know, there's crossing of fibers. So it's the nasal retina and it's approximately 53% of those fibers cross the opposite side. So a superior temporal visual field defect contralateral to a central scatoma is helpful in localizing a lesion to the junction of the optic nerve or a junctional scatoma. I'll show a couple examples of visual field deficits like that on the next slide. And then also it mentions that macular fibers tend to cross posteriorly. And so if you get a posterior lesion on the optic chiasm, then you can get this bi-temporal scatomatous field defect. Here are a couple of examples. So lateral chiasmal or junctional lesion can cause this ipsilateral central scatoma. I couldn't find the best representation but contralateral temporal hemianopia. And to some degree, a lot of the visual field examples I brought up, you know, it would be more of just a superior temporal defect and then a central scatoma. But you could get this temporal hemianopia. If it was posterior central chiasm, then because those macular fibers cross posteriorly, then a lot of times you'll get this bilateral hematomous temporal hemianopia. But this again can be in degrees. So it could be just more of a central defect. But if it's a more extensive lesion then it can grow to be almost complete. Some of the common offenders, and that you'll see or at least we'll see as we rotate through neuroclinic or pituitary adenomas, paracellar meningiomas, cranioferringiomas, so on and so forth. But you also have to consider infectious inflammatory and then neoplastic or lymphocliferative. Okay, our questions are numbered a little weird just because I was too lazy and didn't go change the numbers. But so these, I guess we can do them just as we go along if that's okay. It'll mix things up. So here's just a few questions based off what we talked about so far. So if we're keeping track, you can just write down our honor system or whatever. So approximately how many ganglion cell axons contribute to the optic nerve? What's that? Oh yeah. Bonus points for that, so okay. And then true or false, the ratio of photoreceptor cells to ganglion cells is highest in the periphery and lowest of the phobia and which cells participate in signal processing within the rental layers. And that can be multiple answers. I can't remember if the next slide is, oh, I can see. Okay, this is the answer. So if everyone is ready, there's the answers. All right, I think that's it. You're about the second one? Yeah, that was true. Yeah, it's the, no, it's, so it depends on how you read it. So it's photoreceptors to ganglion, so you have more. So the ratio is, oh, I mixed that up, okay. It's true. Yeah, it's true. You have less photoreceptor cells. Yeah, no, I was thinking if it's a smaller ratio, if it's one to 1,000, but I mixed up the wording of the question. Sorry. You guys got it, you get the point. All right. So it's interesting how the optic, from the fibers from the retina rotate about 90 degrees as they travel through the optic tracts and through the lateral geniculate nucleus. So this is a picture, like a cross-section of the lateral geniculate nucleus. And as those fibers come through, the upper retinal fibers actually rotate 90 degrees to lie immediately in the LGN. And the lower retinal fibers rotate to lie laterally. And in the center, it's called the hyalum, we have the macular fibers. And the way I remember this, just lowers lateral retinal fibers. And the optic tracts themselves, they proceed circumferentially around the hypothalamus. And right before they hit the lateral geniculate nucleus, the pupillary pathway fibers branch off and they go to the pre-tectal nucleus here. So the pupillary pathway is separate. These fibers actually correspond to non-visual retinal ganglion cells, SL axons, that are in the retina itself. And then there are also, there's another offshoot of fibers that project onto the suprachiasmatic nucleus itself to regulate our diurnal cycles too. So the LGN, it's shaped like a mushroom. It's located in the posterior thalamus, on the lateral to the midbrain. And it has a dual blood supply. So from the internal carotid artery, the anterior carotid artery corresponds to the blood supply to the macular region. And the posterior cerebral artery has an offshoot, the posterior lateral carotid artery that corresponds to the blood supply in the medial and lateral aspects of the LGN, you'll see a picture of that soon. And the LGN itself is divided, the gray matter is divided into six layers that are tested again. So going from inferior to superior, the inferior levels are the M cell fibers or the magnocellular fibers that have axons from the retina itself again. And these are responsible for motion detection and it's the larger receptive field. The four superior layers are the P cell axons that are part of the cellular. And these have to do with spatial resolution and color perception. These are just mind mnemonics, so M for motion and P for pretty colors. And in between those layers, you have the K cell axons. These are still under investigation, you don't know exactly what they're responsible for, but we know they're somewhat responsible for color vision as well. And also if you notice, one other way to memorize this is going from inferior to superior. It goes in alphabetical order, M to P. And then sometimes these layers are tested as well. So layers one, four, and six receive axons from the contralateral eye here. And two, three, and five receive axons from the ipsilateral eye. So as you can see, each eye has a magnocellular layer and two parvocellular layers that correspond to it. And I'm not this will be useful, but my mnemonic I came up with again for this is that the ipsilateral size has all prime numbers that are in a row, so two, three, and five, not like one, three, and five, but always two, three, and five. So going further back to these, the axons that originate from the retinal ganglion cells actually terminate in the LGN. And then you have the second order neurons that arise from these ganglion cells. So lesions beyond the LGN in the optic radiations and beyond actually have normal pupillary light reflexes because we saw how the light pathway comes off off of the fibers before the LGN is hit. And you actually don't see optic atrophy because the second order neurons are the ones that are affected. And it's also interesting how the optic tract lesions and LGN lesions have their own type of typical visual field defects. So we see that in all retrochiasmal lesions there are contralateral haemonomous haeminopias. But in the optic tract and LGN lesions these are incongruous specifically. So this is thought to be because the nerve fibers of the corresponding points in the retina. So for example, the left eye right upper quadrant and right eye right upper quadrant because of the rotation of the fibers and the difference in the blood supply as well between the lower retinal and the macular fibers, the corresponding fibers don't lie exactly adjacent to one another. So if you have a common lesion like a compressive mass lesion or aneurysm that causes these type of defects, it can affect the fibers of one eye but not the other. Ischemic insoles are less common. I can show you here, this is the kind of defects that these ischemic insoles often form. These are sectoranopias and sector sparing haemonomous haeminopias. So you can see here again the hylum which corresponds to the macular region is supplied by the posterior corridor and that comes from the posterior cerebral. So you see this contralateral haemonomous horizontal sectoranopia and the lower retinal fibers in the lateral region and the upper retinal fibers in the medial region are supplied by the anterior corridor artery and they can form the sector sparing haemonomous haeminopia. So optic tract syndrome is a triad of typical findings that we see in patients who have optic tract lesions. The three things that we usually see are incongruous contralateral haemonomous haeminopia. We actually see an RAPD on the contralateral eye. So this is because the majority of the optic tract is composed of fibers that have already decasated. So they're mostly nasal fibers and so more of the contralateral eye fibers are hit than the ipsilateral eye and you see a contralateral RAPD. You also see a bilateral RNFL atrophy or optic atrophy in this sort of bowtie configuration you can make out here. It's subtle sometimes when you're examining patients but it can be a clued as to where the lesion is. So why does that happen? We actually saw this in a patient during neurology or neurology rotation. So it's a little bit confusing but if you look at this picture it starts to make a little more sense. So you have the optic nerve here and this is the nasal area, nasal retina, nasal to optic nerve and then you have the macula temporal to it but in the nasal half of the macula the fibers enter right here right here at the optic nerve and all the nasal fibers seem to enter in this bowtie configuration and the temporal fibers enter superiorly and inferiorly. So with unilateral bowtie when you see that it's usually because there's a contralateral optic tract lesion because the contralateral eye hasn't corresponds to the nasal fibers and then the bilateral bowtie atrophy that corresponds to chiasmatic lesions because that's where the nasal fibers decasate so both eyes are hit. So this is a better visual description of what's going on there. So in the optic tract lesion you see the unilateral bowtie and you see the sorry, unilateral bowtie on the contralateral side and the ipsilateral side has a temporal pallor to it. So you can see here in the optic tracks the nasal fibers from the contralateral eye make it over and the temporal fibers from the ipsilateral eye travel this way and you can see it why there would be a configuration in that sense and this is an example of a patient with an MS lesion in the optic tracts. So finally the last section here for me the optic radiations. So the second order neurons they connect at the LGN and then project back to the occipital cortex and here there is again a 90 degree rotation but there's a correction of that 90 degree rotation. So the lower retinal fibers that were originally lateral are again lower and the medial retinal fibers are again, or the upper retinal fibers are again upper rather than being medial. So the inferior fibers, they travel a bit anteriorly here through myr's loop and then project posteriorly to the occipital cortex here and the superior retinal fibers in the parietal lobe they project just straight back instead of going anteriorly first. So you see the typical pie in the sky and pie on the floor lesions where you have the peripheral contralateral hematoma superior quadrantinopia and anterior temporal lobe lesions and you have the contralateral inferior hematomous quadrantinopia for the parietal lobe lesions and sometimes we'll actually see that patients who have these lesions end up having almost like a hematomous hematopia but if you look closely you can sometimes see that their defect is denser superiorly for temporal lobe lesions or denser inferiorly for parietal lobe lesions. And usually these lesions are called the ischemic insults in the MCA territory. Sometimes we see the compressive lesions as well of course. All right, are you ready for some more questions? Second set of questions. I'll just read three of these. So why do lesions and the optic radiation show no optic atrophy on exam? Go to the next one. What type of visual field defects do patients with optic tract lesions have? Is it contralateral? Is it ipsilateral? Is it congruous? Is it incongruous? And this third one hopefully my nemonic maybe helps somebody. Fibers from the right cell, parvocellular, right eye sorry right eye parvocellular ganglion cells will terminate in which level of the left LGN. So right eye, contralateral LGN, which levels are affected? And this is one of those test questions that come up sometimes. Last one, in the triad of optic tract syndrome on which side is the RAPD observed? Ipsilateral to lesion or contralateral to lesion? The answer is here. So the reason why we don't see optic atrophy when we don't examine lesions in optic radiations is that it's posterior to the LGN. So that's second order neurons and we don't have that optic atrophy. The type of lesion that we defect that we usually see on visual fields with optic tract lesions are incongruous, contralateral, hematomus hemiopias. And then fibers from the right eye, parvocellular ganglion cells will terminate on the left LGN correspond to one, four, and six because the ipsilateral eye corresponds to prime numbers in a row, so that's two, three, and five. And the last one, in the topic tract syndrome, we usually see the RAPD on the contralateral side of the lesion because the majority of fibres in the optic tract are decasated fibres that are nasal. Good morning, sorry I'm late guys. We had to do an LPI bi-laterally on a bi-lateral angle closure patient, so I apologize. Last but not least, in our AFRIN pathway, we are finally back to the cortex, primary visual cortex, where we're going to end our journey this morning. So following the lateral geniculate nucleus, our tracts come backwards, as Straff said, both through the temporal lobe and through the parietal lobe to get back to our primary visual cortex. The center of the primary visual cortex is known as broadband area 17, or the striate cortex. And it lies back here, kind of straddling the chalcarin fissure right in the back of the occipital lobe. And that's where all of our fibres will come from the optic tract and terminate here. Kind of as Straff had alluded to, our inferior fibres will travel anterior first, and then lateral all the way around the temporal horn to end up back in our chalcarin fissure here. And like she had said, our superior fibres will come posteriorly through the parietal lobe and end up again back in the chalcarin fissure here. As a reminder, our fibres and the superior retinal quadrants will end up in the inferior visual field, of the inferior visual field will end up superiorly and the contrary is true for the inferior retinal quadrants or the superior visual field. And through all of this, we maintain a retinotropic distribution, meaning that kind of visual field pattern is maintained onto the cortex. Really importantly, remember here, the cortex is very much weighted around the macula. 60% of the cortex is focused on the first central 10 degrees of the macula. And then actually 80% of the cortex is focused around the actual central 30 degrees. So we're very macular heavy in terms of the cortex here. The superior cortex, again, receives information from the inferior visual field and we maintain that retinotropic distribution, which I didn't really know what that meant or had a hard time kind of understanding what that meant, but that just means that the pattern that you see in a retinal visual field is maintained all the way back to the cortex in terms of how we are interpreting that visual information coming to the central part of the brain and the occipital lobe. These areas are important to know. So like I said, we have the broadmen area, which is our primary visual cortex, but then we have V2 through V5, which are also these other more complicated, higher visual functioning cortex regions that I have seen come up in questions before. All of the information will come back here to V1 and then kind of demonstrate forward to these other areas, V2 through V5 for higher cortical visual interpretation. In terms of V3 and V2, we consider these to be contiguous with V1, meaning that this information kind of directly passed to both of those. V4 and V5 are important to remember because V4 is the area that's sensitive to kind of our interpretation of color. And along with that, we consider this to be the area of our interpretation of the what. What are we seeing? What are we interpreting? And that V4 is down below. I just remember it in order. So V4 kind of lower and V5 up above. Cerebral achromatopsia is basically where we aren't able to discern color at all. Patients will describe lesions in this area as seeing the world as dull. They don't see any sort of discernment between color. They will just see various shades of gray. And that means that we've hit somewhere along this pathway from V1 to V4 or the V4 region itself. V5 is important to note up here in the superior temporal sulcus that this is where we sort of discern information in terms of where. So movement and direction of objects, things coming at you being able to discern between stationary and non-stationary and where spatially, visually spatially that information is all kind of here in the V5 area in terms of higher cortical function. So then kind of focusing on occipital lobe lesions themselves. We talk about lesions in the occipital lobe as being either sparing or macular involving depending on how the occipital lobe is being actually affected by the lesion. So why do we get this macular sparing versus non-macular sparing phenomenon? Most people will agree that there is kind of dual innervation of the occipital lobe that allows for this phenomenon. The posterior cerebral artery provides the majority of the blood flow to the occipital lobe. However, there is a small branch of the middle cerebral artery which reaches all the way back and provides some dual supply for the central part of the occipital lobe. Therefore, if you take out your posterior cerebral artery but the middle cerebral artery is maintained, you'll have a homonymous defect that will actually spare the macula usually between five and 10 degrees centrally because that middle cerebral artery is still intact providing that central macula with some blood flow. If you have a situation where you have sort of global ischemia and anoxic brain injury, something like that that hits everything, then certainly we wouldn't expect to see any sort of macular sparing lesion in the cortex. And then briefly going to cortical blindness. If we're hitting the occipital lobe, I think cortical blindness can be a really interesting phenomenon. In terms of acquired cortical blindness that we see in patients who were born with normal cortical function, as far as we know, anoxic brain injury is the most common kind of global injury to this area. Traumatic brain injuries, particularly those that affect the occipital lobe directly. Eclampsia and rarely create clamsia can also cause these phenomenon, CJD, an infection. And then I also was reading about anti-epileptic drugs and there's a variety of anti-epileptic drugs that will create sort of a intermittent or non-permanent cortical blindness that can be acquired. And if you stop the AED, it can actually resolve. In terms of congenital causes of cortical blindness, so traumatic brain injury, birth trauma, occipital lobe malformation, so congenital lesions that way, perinatal ischemia, again, these sort of global ischemic events hitting the occipital lobe. And then meningitis and encephalitis in our newborns can also cause cortical blindness that is irreversible and kind of congenital right from birth. Two phenomenon to know with cortical blindness, so Anton Bobinsky syndrome and Ridduck syndrome. Anton Bobinsky syndrome is where we basically have a patient who's cortically blind, but they are in denial of that loss of visual interpretation. So they will tell you, yes, my vision's fine. I have no difficulty with any sort of vision loss. Why are you asking me that? So that's Anton Bobinsky syndrome. And then Ridduck syndrome is actually where the patient will kind of run into objects because they're not really aware of their lack of visual spatial information coming into them. So both of these are common with cortical blindness. With all of our occipital lobe lesions and cortical injuries, patients in their absent visual fields will often have other light phenomenon, visual phenomenon in those fields. So commonly complaining of circular lights or other things as the brain's trying to come up with information in those areas that are absent, I also read a few studies where if patients had recently had, say, a stroke or some sort of ischemic injury to an area, and they did have some scintillating imagery or visual affects in that area, that that sometimes was an indicative kind of sign that they may actually get some of that vision back. So I'm kind of demonstrating that the retina was trying to still kind of fire away at the cortex and keep that imaging going. I remember these two phenomenon because I remember that Anton, for some reason, he's in denial. And then Ridaq somehow sounds like a sound that I would make if I ran into something. So like, oh, Ridaq, impressive. So I don't know if that's helpful for me, for who it was. So that was kind of the majority of the cortex. It's really important to remember those V1 through V4 areas. And then our macular sparing lesions, why we may or may not have macular sparing vision, and then kind of phenomenon that can create and represent cortical blindness. Can I just say something about Ridaq? Yeah. So George Ridaq was a World War I physician who was in the trenches and saw soldiers whose little lobes had been damaged in the war. But so Ridaq's syndrome is, like you say, the person runs into stationary objects, but what's really peculiar is that anything moving, they can see. So if you were to lift up something and move it, then they can see it. But if it's stationary or just static, they can't. So it's kind of a dissociation between something moving and something stationary. One more question. I think we do this one. Yeah, so these were just actually repeat to over here. Oh, okay. What, oh, did my not, three questions on the computer. Maybe this wasn't the most up to date. But that's okay. Do you want me to just, I think, I suppose, so my first question was just, is it, so if you have, you take out your PCA on the right-hand side, where and what do you expect to see in terms of your lesion? So you would expect to see a contralateral monomest effect that would be macular sparing, given that your posterior cerebral artery was compromised, but your MCI, you would assume, would be still intact unless there was a global scheme you can dream. I think I did a true or false on areas four and five. Do you guys remember area four and area five? Wearing what? Perfect. Color vision is wear.