 Alright let's go around this answer. We'll just go group to group. You don't have to have all the answers. We'll just work as a team. So first group, right here. Tony's group. Two? Oh, Tony's group at the event hall and Rufanpeth. Anything else? Oh yeah, if you want, just keep going. Do you want to add two more? Amy Oderon, Zipro, Isla, should we keep going? That's good. Anyone else want to add more? Anything unique that's not on that list? Let's make those more. Two more? Two more? So this is actually from, this isn't even a complete list. This is from our blue book in the neurology or neurology clinic area. So if you're ever like in clinic and you're like, oh what kind of longer list? That doesn't even have all of them. I feel like every time I see a patient I'm worried about toxic. I see like bilateral optic atrophy. The work of every man just affects at their odds to see if there's anything published recently about that. This board has recent publications of just atrophy without swelling. But it's not that well known among patients. Alright, next question. This is a two part question, kind of has like almost four parts. How do you treat NMO and optic dryness acutely and then how do you treat them in the long term? This question. You can think of part B as even like how do you treat that type of stuff. I'm just going to, I'm going to change this too. I'm so good at math. I'm going to currently be able to show you this for those that are tired of me. That's a great idea. Yeah, so a good amount of that might add up. I'm sorry. I'm sorry. I'm sorry. I'm sorry. I'm sorry. I'm sorry. I'm sorry. I'm sorry. I'm sorry. I'm sorry. They can choose to go older. I'm Scott. Any more time? Are you ready? Let's go with Jordan's group. She hasn't answered her part yet. Yeah, so Hyde knows Hyde's steroids to start. So like 12-50 of methyl-frab, P.O. Sterilic, 1-Meg per K, 11-Meg. Which one are both? I thought that you treated both of them with Hyde, which is with Hyde knows steroids at first. You can, exactly. And then what about if NMO, if you don't really, if your vision doesn't improve, you're still like 24-100 or worse after doing steroids. Maybe after doing steroids for a week. Like you can do like IVID or Plex. So yeah, Plex is the next effective treatment usually. Yeah, good job. And then how about Part B? Let's see. Good for Ma. Yeah, is there anything different you would do for NMO patients? That's okay. Anyone else want to add what you could do differently for NMO patients? So there's the other treatments out there. It's kind of hard because they're kind of newer. So like you said, for NMO and acute attack, you'll do IV medical pred three to five days and then you do like a pred taper. You can. If there isn't much improvement, you want to move quickly and try to get them less. You can do a taper while you do the IV medical pred taper while you're on Plex or something like that. Is there a preference between Plex or IVIG? I think Plex seems to be more effective, Dr. Degree. I haven't actually seen NMO patients have been Rax. I don't know if that's changed at all. Plex is what you do next. All right. And then for chronic treatment, I just found this good article to summarize a few things. So as we said, yes, there's even a monster therapy, even for NMO. It's kind of an overlap with MAG. There's some less commonly used treatments here and sit as well. But then there's some more treatments that have been coming out recently. I actually get ads for this on my Instagram. Some of these ads. Great thing what I do. So this was FDA-proof Echolism App in Q 2019. And it was so effective. Like apparently compared to placebo over 49%, like 49% of patients with this treatment for placebo, which only 3% of patients had prevention. They prevented recurrent relapses. So there were fewer relapses essentially. It was very effective. So I just stopped the trial early. And then for phase two and three trials, there's a lot more coming out or already out that are being used. So these are other maps to be aware of. Just be aware that if you're seeing patients at the end of all, and they're on these medications, they might have other autoimmune diseases that are developing as well. And then for MAG, Dr. Chen in Mayo has like become the expert in this and treatment. You do the IV-methyl print, like I mentioned, you can do a long taper. And that's because patients are at risk for relapsing, right? This is a MAG is more of like a can be, and always a more steroid dependent inflammatory condition. So as you're coming off of steroids, sometimes you can have a recurrent attack. So you want to have a long, nice long taper for them. If they don't have much improvement, you can also consider plexor IV-2-HG. And then if they don't have recurrent attacks, you don't have to put them on preventive treatment, essentially for MAG therapy. That's because these patients can just have one attack and not have another one for a long time. So if they have another attack, it's not severe enough to warrant. So you see that they're having recurrent attacks. They're having steroids again and again. You don't want them to be steroid dependent. So then you consider this as the other ITs or IV-HG. But all of these, they had a caveat here that all of these medications have had recurrent attacks, but they seem to decrease like the relapse rate. The difference with NMO is that you are definitely going to have recurrent relapse, essentially, and it's a very severe, progressive, relentless disease, essentially. So you have to put that recurrent attack on some items. You probably want to partner with neurology on this because you're not going to want to manage a society like a family that attacks a map. But you're going to follow the vision. It's actually important. When you're out in practice, even if you're doing cornea, and you happen to take a call for overnight or something like that for hospitals, they come up and you need to make sure these patients are on the right. You've got everybody who knows this. All right, next question. Would you move to work at the patient? So close, close. So C. C. C. Yeah. Yeah. There's going to be a bit of stress. Okay. C. C. C. I love that you're always asking my photographs. Yeah. Yeah. Yeah. Yeah. I think it's storytelling. Yeah. That sounds great, too. Oh, yes. So it's a pretty much... Your case was... Yeah. That's right. Because it was kind of... So controversial. Yeah, and then it was like... It was cancelled. And then she had to... And then she had to... Yeah. Yeah. Alright, you guys want to go with the answers? What about our ex-group? It's partially and then we'll go around and give other people a chance too. We're thinking we're going to... It's causes. You wanted to do a CSF studies. So let's go to the next group. What would you look for? I'm just like... Being there for you or something like that. Sorry. It's just dragging me. What would you guys do to check for what lab you have? Glucose, proteins. What's the function for sugar? What would you look for? It's just... It's good. Any infectious workups you do in the CSF? BDRL. BDRL. One of the infections that we can think about are HSV, VZV, and other viral infections. So you can do an encephalitis panel if that's indicated. So, infection-wise, there's... I'll give you a talk, but I'll also add... The bisarcoid lymphoma, Crohn's... I don't know if that's a problem. But of course, don't forget about that. And then, of course, think about other things that could be other than inflammatory... Just space-occupying plastic condition. Giant cell arthritis. IGU4. IGU4 is always super reliable. So if you can get, like, labs, you have some other site that you feel like is concerning, that's why I'm staying for IGU4. I'm going to check some metastatic disease. Good question. Yeah. Just in general, between serum testing and CSF testing, especially when I'm called, I am confused which ones would be better to do CSF versus serum, especially for infectious labs. You have a couple where you definitely want to do CSF and we're concerned for a CNS infection. So there's actually some limitation to what you're able to test in the CSF and in the serum too. So the encephalitis panel, when I looked it up last recently, there wasn't a serum panel, it looks like a CSF panel. But you can test individual ones of those infections. You can test HSV, VZV, IGM, or the star in the blood as well. I'm not sure that one or the other is particularly important. If you don't have CSF, then you're going to test the blood, right? But you can't always test everything on the encephalitis panel. So sometimes you have to... I would just add cytology. Yeah, I think I have one. CSF cytology. And then the like Bartonella Lyme, I'm not particularly... I don't think those are like other infections like syphilis. I would test both. Because even in the CSF and being in the serum are different things. It changes the diagnosis like neuro-syphilis versus... especially if it helps make the diagnosis you're concerned about ocular syphilis. You can see maybe the URLs positive or something like that. What else on here? So like MOG, CSF testing is not as reliable as serum testing. Even for animal. So serum testing is the most important one. Do you tear this work up? Or do you phase it? Or do you just shock? Or do you just order all this straight up? Like your answer is quite... I know. So sometimes you want to just order everything but you should tailor it. You should tailor it. A lot of it also depends on where is the patient? Are they in the hospital? They're in the hospital. Maybe we should do more extensive work up and just get all this stuff. If they're outpatient there's certain risk factors maybe you'll go for those conditions first. The... I'm trying to get a lot more like CSF and homework. CSF studies can be a little bit harder over your application. So you're going to be doing that and you're concerned enough that they have severe vision loss. Maybe you will hospitalize them and then get all of this testing. So severity of vision loss, severe symptoms, risk factors So this is a little bit longer of a question to answer from time to time. What are the differences in demographics, presentation, object disfeatures, inheritance factors between the labors and... What? It sounds so bad. Well, it sounds so bad. It's true. It's true. It's true. It's true. It's true. It's true. It's true. They're actually... You mean the speech? They're actually... That's probably the defining thing. Labors is the staff. 60 books. Thank you. It's a good idea. It's a good idea. It's a good idea. It's a good idea. It's a good idea. It's a good idea. One more minute. I like that. Let's get started. Abigail, is there ever any answer to this? You can start with whatever you want to go around that. So labors tends to be younger meals maybe in the range of fish. younger, like you're on the age of like 10-ish or so, or younger, the presentation of AOAs, I think they're presenting visions often between 60 and 200, and then laborers, it can be like a sequential vision loss between the two eyes based off of a few days to make something more, and I think their vision ends up being more severe. Um, Rachel, welcome. I'll take this. 2400 seconds. Rachel lowest, but you can get worse than that. Features, um, but hold on, I'm having all the opportunities here. Next group, sorry. Allie, let's cover some of these so far since we have this. So yeah, demographics, first decade, some people say there's like a second wave that shows up, the atrophy, 21 to 30 year olds, maybe when they realize that they can't see as well as they thought. Um, we're being challenged, maybe. I'm not sure. Um, and LHOA, it's definitely more females, sorry, more males than females. We don't know exactly why, even though it's like mitochondrial, sorry, the last one, those mitochondrial inheritance, you would expect it to just be like, you know, genes pass on from the mom to all the kids, but males seem to have a more severe effect of that and show that more than females. Um, so yeah, the onset is 10 to 30 years, but you can see these in patients who are in their, you know, 70s, 80s as well. Presentations are usually slow onset for dominant optic atrophy. Usually vision's better than 2,200. If you just do Ishihara color plates, you might miss the fact that they have color vision loss because Triton or red, I'm sorry, blue, yellow is more commonly missed by these patients. You can try, what's another type of color vision test you can do in these patients? I think this is that. Cool. Yeah, fine, sorry. Um, and then for labors, it's more like you can have sudden or it can be gradual. So some people come in and they're like heavy swollen nerves and sudden onset, but I remember seeing a family in New York last year where three of the kids, three of the boys had labors and they had different stages based on their age of how severe it was. So they just had, they had never been caught with this swelling. They had always just had like gradual atrophy over time. You've seen that too. And it's very variable because you can have labors with sudden onset and it could look just like optic heritis and you think that it's optic heritis and you, like, you can even see an enhancement of the nerve. It's a tricky disease. And you've got to think about it. And then it's like a difference in how the nerves can look. So you have the teleindictages on the nerve and then it's not super swollen, right? You don't have these like hemorrhages coming off the nerve. You don't have like a little spots or anything like that. And talking about these, it's like the most tortuosity or arterial tortuosity too. I'm sorry. Anyway, I'll just go to this side. So autosolid dominant is, is the inheritance binoculars. And the most common gene affected is which one? So OPA1 and then you can see OPA1 to 4. And these are some rare genes that have been identified in either syndromic patients or even just isolated optic atrophy patients. And then the two other things I wanted to go over is just, I don't know if this still comes up in OCAPS, but the most common mutation, the most common one is this 1, 1, 7, 7, 8. And then the one with all the 4s is more fortunate. They have better visual outcomes. And then you have one more condition, 3, 4, 6, 0. And we had a 3, 4, 6, 0 in clinic yesterday. So you're going to see it. And you want to make sure they are evaluated for cardiac conduction defects as well for labors. All right. Last one. What's your differential for dyskidema, unilateral or bilateral with normal? It's for real. Because the one-time context of me last year as a, as a... Can you tell the differential for this again? It seems to be important. Yeah. I think I did. Bialateral. Nice. Bialateral. What's your differential for the cardiac conduction? I'm jumping. Jump on the board. I'm thinking I'm going to jump. What did you say? Spring sports. Spring sports. Spring sports. Spring sports. Spring sports. Spring sports. Spring sports. Do you want me to grab? I can't be with you. I can't run to the restroom. I can't run to the restroom. I can't run to the restroom. Alright, it's for the sake of time. Let's go around and discuss the whole group. I'm going to give you answers. So then going back to your first answer, IIH, or just Papaladema in general. Put another group you guys have anything else to add, any way you can jump in. I bet it's papaladema. Okay, papaladema, yep. I'm going to say schesys and vitro papaladema. What was that? Cruisin, yep. And then anyone else want to add anything else? What's it like Naion? I think it's like incipient Naion, like it hasn't really started. Like QT centrally could be a little bit not too disturbed, but the field loss is a little bit more. Usually they have a QT to loss someone. Oh yeah, I do have that listed here too. So I'll take this and also optic perineuritis because on normal vision, or even like blotchy vision, or some like tunneling of their vision, or even some a little bit of central vision, it works too, but you can have normal vision with optic perineuritis, but they also have some pain with eye movements, which pain behind their eyes in general. So papaloflabitis and impending CRVO, hypertensive retinopathy, don't forget that one. And then vitro papillary attraction, or as someone's developing a PVD, you can sometimes see that interface of the vitreous pulling on the nerve. And then other things you guys said, and then syphilis early on, if you haven't seen other findings in the red now. But this comes up often, like we have, maybe this is the one thing that seems to, you know, put anybody in any sub-specialty on edge, like everything looks fine, but is that just swollen? But the vision's fine. And then you're like, what do I have to think about that? But this is something you can think about. All right, so that's it for that. Next, we're going to do some presentations about you guys. And we'll tell you, so you only have to talk to four minutes, and then we'll talk to you after this. Bring it to your eyes. I'm going wifey. Okay, don't do that. So we'll be on first, we'll talk about a case of pseudo-fidema precision. So kind of busy here, but essentially a six-year-old boy, otherwise healthy, started noticing, sort of looking over things, following what to do with his eyes, check, kind of refract, helped with the vision, but the optometrist also noticed that both the optic nerve were swollen. As a result, they got an MRI. There was a bile to carry male formation that was noticed, referred to neurosurge, looking for anything else on imaging, ECSF, spinal imaging, moving forward. They ended up placing an intracranial pressure monitor. And then they checked the ICP, which was normal, line flat, and then I was in single digits normally, and then it was up to 25. So I started in my own dialogues immediately, and referred to neurophemology. So you can see the no-past-metabastery social history, and history of color vision efficiencies. And then in regards to examination, you can see here, seeing well, no APB, near-full, color plates, all QV, fourth or fourth, a normal anterior segment, posterior segment, and no full chronological deficits. As far as when we initially presented to the neurophemology clinic, some of the examination, we did get just photos, and you can see the optic nerves there. They do look mildly like topocytosis, or like product 0.1 cupid disc ratio dose, has some anomalous vasculature. Notably, you can see like laclopscuration of the blood vessels. It is a pretty hyperremic disc. And there are different sponges as well. You want to get a tarnifle. You see the right eye and the left eye. The left eye, different tones, different swelling. And there it is kind of more nasally. The image computer picks up a little bit of thickening. But notably, you can see kind of the vessels around there are pretty compressive. Can you just look at that? You're just saying there's more vessels around there and on the scan below that. If you go back a slide, you can kind of see that as well. The nasalization of vessels, as well as kind of with the symmetry of the disc, it could look a little, one might say anomalous. As soon as you see a coupless disc, at least ask yourself, could this be an anomalous disc? The other thing here is these blood vessels are a little bit more critical when you're looking at the pad. Exactly. Then lastly, we got an ultrasound with Dr. Harry. The main reason was to look for optic disc intrusions. What? Dr. Harry's done it. I was like, oh, no. I got to give credit to Dr. McKinsey, who's like the ultrasound expert in the hospital. She can see it. I don't know if you're healthy. Basically, we look for it as far as the ultrasound would be optic disc intrusions, so you put the game down. Everybody should be able to do this. Not just Dr. McKinsey. Everybody should be able to do it. I can even do it. No optic disc intrusions, and then other ways that you can check for optic disc intrusions would be in the clinic like an EDI enhancement with folks that you really can't get imaging if they had like a CT before. Because the drusen are classified, you can actually kind of see it. If the slices are thin enough, sometimes you can pick up the result that way as well. So that might be just one non-invasive way to just look at prior imaging. That's honestly great. So as far as this kiddo, I think this is something we'll probably see in clinic a lot as far as kind of referrals for edema, bilateral, people picking it up kind of in the community. Certainly the differential for us would be pseudo-peppal edema with concern for these anomalous looking optic nerves. As Dr. Degui mentioned right now, and then kind of in her lecture, any time that you see kind of a small, couple-less type of edema disc, you just kind of think to yourself, true edema versus pseudo-edema, I'll just kind of have that question in mind while you're kind of getting the work up. As you can see in this case with this kiddo, there's a sense of testing with neurosurgery and neurology and has been through a lot as far as just getting these pressure monitors and at one point was also on dimox. And then certainly for true disc edema, we've kind of talked about in our lecture here, a little bit of ICP, which was everyone's concern when they initially saw that and then all the other things. So as far as the assessment, this was a six-year-old with anomalous appearing, small tilted nerves to bilateral and without, what we thought was true swelling. At that clinic visit, they did stop the dimox and then the client was returning as even in six months, we didn't repeat our NFL and fund this for as of that time. And then as far as counseling, certainly they'll be following up with their sub-specialists here, but it was important to counsel them in terms of kind of the exam findings that we don't think it's true disc swelling. And then let them know so they're aware and certainly communicate with the teams as well so they're aware. Do you use number four, like the congenital tilt and disc syndrome, what is most common and what associated visual field deficits you can get that mimics other problems. So I think it's important. So infrared nasal, right? So you can kind of have the bilateral pine disguise that can kind of mimic the posterior lesions, but you will have crossing the vertical midlines as I can differentiate it. That's a cool pie in the sky lesion. Thanks for working on it. Thanks. And so, the main course of you guys coming up and talking about all of these, that was a good job, is to talk about how you work here differential and what led you towards one thing or the other. And a lot of evidence not leading towards the previous KT-1, especially from the imaging, and then the ICP monitor. He never got an LP. He was on an ICP monitor for like three days. So, George Co. Things in Montana are different. Okay, thanks for your time. Do you want to add anything else starting over here, Carol? Volunteer yourself. That was number two. Can you email it to me? It will be. And you can log me out. It was me, but just kind of work on it. Our plan is, it is just the front. I think so. Yeah, I think so. Yeah, I think so. Yeah, I think so. Yeah, I think so. Yeah, I think so. So we have a ten-year old boy who presented with new seashell-like events and a 10-year-old baby. This was first witnessed while he was playing kind of computer games. And it was observed, video games, and it was observed that he was kind of shaking his arms and his legs for a few minutes, followed by confusion, right-sided facial droop and right arm. In this picture, he was evaluated at the long-distance center in Tenerife. However you say that, Tom. And he tested the baby and he tested positive forward coronavirus and he was started on Capra and Centaur. But at home about four weeks later, he had another episode of that whole body shaking and that was preceded by a slurred speech and some facial stretching. And he returned to an outside hospital. They got a CT and CTL, KG, CBC, CMP that was reportedly all reassuring and he was trying to find a way for children to go further work up. And then he recorded that he had some blurry vision in the right eye, but he is not sure when this started. He didn't have any eye pain. Thanks. Thanks for talking about this. In his past medical history, it's significant for autism, ADHD and asthma. His past ocular history is kind of unclear, but his dad reported that he had some, like a remote history of decreased vision in his right eye that required treatment with idols. But that's all that Ashley was able to find out about that. And his medications, his unsettlingness needed for allergies, not medications. I don't really like checking our email. It became so difficult in the last few weeks. Sorry, keep going. And then in his family history, he has a septum or celiac disease known on history of strabismus and the opium disorders. He lives with his mother, father and two siblings. And then on ocular exam, his visual acuity was 2800, which did not improve with pinhole in the right eye. The left eye was unremarkable. The color vision, he wasn't able to read any of the test plates in the right eye because they all appeared gray. And he had 13 out of 13 plates in the left eye. His pupils were round and sluggishly reactive with a reference of RAPD in the right eye. I always have issues with it. And it was round and brisket in the left eye. He was unable to count fingers in any quadrants in the right eye, but the visual fields were full to computation. Otherwise, extracula movement were normal. There was no pain with extracula movements. The pressure was normal. And on pin-light exam, the anterior sacrum took unremarkable. On dilated fundus exam, the optic nerve on the right eye had diffused pallor with crisp margins, not obscuration of vessels. And then the left eye was unremarkable with a cup to disc of 13 or 14 plates. And macular vessels are very good. Can you repeat the vision again? 2800 in the right eye and 2200 in the left eye. And so he got some imaging on presentation to the hospital. On his MRI brain, he was found to have multifocal areas of patchy enhancement within the left phalamus, the right posterior pudiment, and then the inferior left cerebellum. And you can see some of that enhancement here and over here. And there's another view of it on the sacral part of enhancement there. And then he also had some left omen and gila enhancement as well. But the reason we were consulted is because of these findings, you can see that his right optic nerve was asymmetrically hyper intense and also kind of subtly increased in size compared to the left optic nerve. And this axial view of that as well as a coronal cut. You can see it's more hyper intense compared to the left side. He also had an MRI brain that did not show any vascular abnormalities. And then he had an MRI of his C and T spine that was within normal limits. So to talk about the differential diagnosis a little bit for him, optic neuritis was obviously given that his decreased vision in the right eye and then this appearance of enhancement on imaging and optic neuritis was a major concern. That combined with this multifocal parenchymal enhancement was concerning for something like acute disseminated encephalomyelitis. Particularly because as Lydia mentioned he had had these like intermittent fevers prior to starting these seizures. Another consideration was something like MOG associated disease, neuromyritis, optical although he didn't have any spinal cord involvement on his imaging. Multiple sclerosis was a consideration although it was thought to be probably less likely to be given this age group. And then other considerations that were discussed for things like a CNS vasculitis, a CNS infection or some kind of toxic or metabolic disorder. And to kind of complicate the picture with this kid, it sounded like he had some kind of an unclear history of treatment with drops possibly for an amblyopic eye although the parents were a little unsure of this. But it sounded like he had had kind of a chronic history of poor vision in his right eye which complicated the picture because this wasn't necessarily an acute change. Additionally he didn't have optic nerve edema but he had pallor and maybe some atrophy of that right optic nerve which is also a little bit different from what you might expect to see in someone with acute optic neuritis. So Amblyopia was kind of another consideration for us. And we got labs on him so he got a lumbar puncture. It had normal glucose and protein levels. His white blood cell count was elevated at 57. His RBCs were also elevated at 187. They did a legal clonal band testing on the serum and the CSF both of which were negative. His CSF viral panel was negative and then a CNSD myelanine panel showed negative aquaporn 4 but his MOG antibodies were positive with a tighter of 1 to 160. So ultimately he was diagnosed with MOG-associated disease with clinical imaging findings consistent with ADEM and optic neuritis. We also suspect that Amblyopia was probably contributing to his decreased vision in the right eye on top of what was going on in the central nervous system. And then he was started on IV methyl pred one gram daily for five days followed by an extended oral steroid taper. It's for a good time. Just to go back and talk about that differentially, retrospectively what are some things that kind of made more of a likelihood in him versus some of the other things under differential? Yeah. I think so with MOG having retro orbital optic nerve enhancement like that is something that you can see I think his age Yeah, exactly. I think for his age group MOG is also more likely than maybe something like multiple sclerosis. Because he has these like lesions outside of elsewhere. Yeah. And with the proceeding viral illness I don't know if the virus is positive at the outside of the hospital. I think that also made something like ADEM or MOG-associated disease. And one thing that's sticking out to me is that he had this pallor already. So that's interesting because MOG can sometimes present with pallor because they have like they just can have subclinical episodes of optic heritis where they don't have severe vision loss or decent blurriness. They don't come in for it or get evaluated. And then even without that swelling sometimes they have these episodes where it's just like they're losing some ligament swelling and chronic pelvicness over time. So they have these episodes that may not be caught especially in a child, right? So what if this had been going on with an optic nerve that looks like this and it was thought to be embryopia even though there were signs that there was some objective going on? Yeah. It's time to see you in a week. Okay. So like a paracetamolite review or a child review now. Yeah. Is there anything else you want to add or I'll give you a good job. Good job. Just wondering about my gradual and pathotography. Yeah. But you probably wouldn't have, I'm not sure you'd have enhancement and then of course you can also just rule out other things that would be more common with testing like mod testing and all that. So yeah, hopefully there's other clues and it's not a common condition either. Oh, I see. Oh, you did? I didn't see it. Sorry, do you have other questions too? I had a question. Yeah. Mog, it seems like she comes in with pretty profound vision loss and it's very steroid responsive. But what's the natural history of Mog if it's not treated, if they come in with, do they still tend to improve? Yeah. Actually I don't know that they tend to improve. If you do nothing, like say this kid had these occurrences and just was never treated and never told his mom, whatever. Yeah, would you expect it to improve quite a bit as well? I think you have to treat this. There isn't a publication that I've seen. I did like a review of pediatric optic arthritis last year and I didn't see anything about how an option to not treat these people. Sure, sure. Yeah. More to everyone. We are going to present today a case. Sorry, one more thing. Also just to add onto this. No, it doesn't actually. I'll be enjoying this by your bluster. Jordan, you're back here. Anyway, so also, optic parloritis you should treat. It doesn't just go away. So, even if you have normal vision. Right, sure. I've got an example. So, in some case, August of last year, twenty-two, a 40-year-old woman came to the neuropomology clinic who had noticed, incidentally, vision loss in her right eye and optometrists outside optometrists about eight months before she had tested a 2100 in that right eye, a 220 in the left. Really hadn't had a recent eye exam just a routine eye exam at that optometry office. Before her most recent eye exam was 2020 in both eyes and so this was like a big shocker to her. She was referred outside of Nevada Eye Consultants, I think, about two months later and at that time her vision continued to deteriorate a little bit, around 2140. And then she had MRI done which was suggested of apocalyptic neuritis and possible demyelinating lesions in the right portion. She also had an apocalyptic of her nerve or pallor on that examination and so she was referred out to us a couple of months later. And when she presented us, she had denied really any noticeable symptoms outside of the vision loss. She just was a huge shocker to her. She didn't have any pain. She had no visual distortions or non-dysfunctions, focal neurologic deficits. Really no other optometry that she didn't notice at all. So she presented to us without any noticeable changes outside of her exam that we'll describe in a second. So just from past history her habitable history was really only significant for hypothyroidism, hypertension, OVC, PCOS, breast cardia for shape pacemaker. Otherwise family history was pretty non-contributory, no past popular history, social habits, greaseposing. The only kind of curious thing is about the summer before her initial exam where they found this, she did have an incident where she fell off a horse and hit the right side of her head. She didn't have any loss of consciousness or any other symptoms of TBI or anything like that, but when asking she brought that up. On her exam for visual acuity, she was counting fingers in that right eye, 2020 in the left. She had a pretty pronounced APD in that right eye. Other, and she really had no color perception either. No, didn't get any of these heart traits on the right eye that left was full color. Otherwise, the exam was pretty unremarkable on her undilated fundus exam. They did notice that there was kind of a sealer loop on that. Yes. Oh, sorry. We're going to go through some imaging titles. So, RNFL here, it looks like both eyes have accurate segmentation of the RNFL. The right eye showed generalized thinning compared to the left. The macro CT was for quality and goldmong visual field showed generalized construction of the central scatoma. And fundus photograph demonstrated atrophy and atrophy with an opposite ciliary shunt vessel. MRI brain was re-reviewed with Dr. Warner and showed buzzword, tran-track sign with no positive arrow sign. Oh, yeah. Oh, yeah. Right there. I mean, but it's kind of bilateral. Yeah, right. So, that was a discussion. That's CSF on both sides of the nerve. It's not a slam dunk case, but that was a discussion for sure. I mean, an atrophic optic nerve will give you an atrophic optic nerve. It looks like an atrophic optic nerve. All right. And so that leads us to our differential. So, the incidental vision loss, like you don't go from 2020 to 2100 without likely being a gradual of vision loss. And really the most common cause of gradual vision loss would be glaucoma. Her visual field, I didn't show visual field, but central scatoma. I didn't show glaucoma's pattern to her vision changes. Sorry, just to emphasize, what was unique about it that wasn't glaucoma's? Well, central scatoma in itself can happen. That's really the thing. Right. Yeah. Get evidence of optic nerve for sure. Other things we thought of like an optic nerve picture, but then it doesn't always present that way. And in her pattern of really this gradual vision loss wouldn't really present that kind of pattern. Phenetic questions were asked. She had no family history of sudden vision loss, so the LHON, or Leavers, OPA1 stuff as well. Fairly unlikely for our Wolfram as well. Inflammatory causes were also considered sarcoidosis similar to the paranoid cause we discussed earlier. Typically, again, that would present with pain. So less likely, but still definitely on our differential. Other causes of gradual vision loss, we can just think more interior from refractive changes. She didn't have any issues with her eyes to that. No corneal dystrophy lens abnormalities that we see so often. That's one more thing on the differential. Sorry. I'm going to interrupt you guys a little bit. Just to emphasize differential as part of our discussion. You mentioned she's well off the horse and did you have any changes in her vision at that time? Yeah, that's part of my discussion as well. Trauma was definitely on high on my differential. I just groin in a poor way. She didn't notice any loss of consciousness, no visual changes at that time. Or shortly thereafter. So certainly there, but kind of a obscured picture from that record. 2100 was in February or actually October or December of 2021. And then August of 2022 she was kind of there. And that's what she didn't notice it. She thought her vision was the same when I had talked to her compared to her initial visit with optometry in December 21. So she was out of a really poor historian or truly was having some very subtle visual loss. Other things considered just like chronic retinal diseases that's why we showed you the OCT which is pretty normal outside of the hazy view. Like in post-traumatic like we discussed, CNS tumors although ruled out with our MRIs very unlikely. I should say like an author chief meningioma would be CNS tumor or nerve glioma. So that's still on the differential but other causes of lesion to the optic nerve would be less likely. Eschemic optic neuropathy she's a vascopath. So that's certainly still on the differential as well. You can always consider GCA although she was four years old. So perhaps less likely. She had no B symptoms consistent with that. RD could also be on differential as well but again didn't have any common symptoms or exam findings suggestive of that. Retinal artery vein or venous inclusion or artery inclusion would be also on your differential but once again the fundus exam, her OCT non suggestive of that as well she could have had stroke, she could have used toxins her medication history made toxins less likely or medication-induced pathology less likely. She had no known toxic exposures on questionnaire and stroke again less likely with MRI findings but and lack of any associated deficits as well. Another last one we kind of considered nutritional as well she ended up working on some nutritional defects as well. So we'll get to that. So the plan, we started with the chest x-ray kind of rule out sarcoidosis and and MAG animal we did CT orbits if you were concerned for an optic nursing you could see calcification blinking on the hyperplasia of these you know yeah, that's our hypostosis hypostosis around the canal and so those were things we wanted to explore for her to see if she's meningioma would be more likely seeing her entire picture in this unilateral optic neuropathy gradual vision changes the superior possible vascular looper shunt vessel that we often associate with causes of posterior compression like if there she's meningioma we thought that meningioma would be still fairly high on a differential or definitely should be considered and unfortunately you can't biopsy because of the risk of further vision loss with where it's located so we attacked it by exploring other causes CT ended up being normal we did start a course of steroids for her and she did experience some improvement and so you know it's again a slam dunk but just an interesting case of how to work up the situation and kind of all these things leading you to different ways it's tough, right? sometimes if you see meningioma elsewhere it may be more they all be subtle findings than the lack of another diagnosis sometimes easy with this so that's pretty much it so the main thing we have to focus on with these things is the type of therapy and things like that is there a treatable cause first of all so they target those things supplement nutrition and get rid of a toxin you can treat high pressure things like that we have to worry about the mortality too like morbidity but is there some condition like a vast majority of conditions that can reduce their lifespan so really those out is not just like a part of us figuring out what's going on their eyeball but for their general health this is kind of not great but we have a lot of vision and atrophy still but at least the rest of you is safe she had follicle clonal bands she did not or she did not get an LP she did not get an LP I probably would have done it because of that period ventricular lesion that she has is more typical for demyelinating disease and I don't think that meningioma might be surprising the loop you showed let's go back to that it could be an obtus ciliary loop but most of the time those loops are on the edge and they're in a swollen nerve the two things you think about with those loops meningioma is really good and then chronic retinal vein occlusions can really give you those retinal vascular loops because that's what it is it's a retinal artery to carotid vascular sometimes called obtus ciliary but retinal collateral retinal carotid collateral it's not skeptical but it really allows good things so the word you diagnosed was meningioma I think it's on the last note it was still the working diagnosis but the improvement with steroids where did they find the meningioma well I guess they're not in a biopsy I know what but do you have an MR with gato oh no because that picture I can't diagnose a meningioma it looks like an atrophic optic nerve with CSF and that's not a typical tram track site because that spinal fluid going along the nerve you could see it prominently when you've got atrophy of the nerve so you'd need an MR with gato, fat sat to see a meningioma or a CT scan sometimes CT in this situation is more helpful you did get a CT? yes that was normal the CT is normal so I think I do a spell tap and look for oligoclubans it's a one time one and done maybe it was your trauma from whatever oligoclubans is no small deal no, that's not right is there any significance of the little bulb that you see it's a eyeball you have one more group, right? look at the insertion alright guys we gotta go a little bit faster this last one focus on the differential you don't have to do a I was trying to save you guys the painstaking effort of writing a whole case report but of course I guess it's so thorough I know I didn't want that for you you guys can stick to the 4 minutes that would be awesome I don't think I'm so good I know I said I cut you guys off but I think I can't do it it's too awkward that's great I want to point out that the genealogy in the genealogy that's how you're supposed to hold the mic everybody so this is a 54 year old female she has a past medical history significant for diabetic and stage renal disease she's talking about dialysis she has hypertension, paroxysmal, aphids, sarcoid seizures and actually a prior CDA comprising a right MCA in part with a significant right ICA diagnosis in 2020 which actually is sustained during a COVID admission and she's had subsequent frequent TIA is over the last few months year or two before this presentation where she's now presenting with acute worsening of crime bilateral blurry vision that was difficult for her to localize but this was all in the context of the whole process at high intensive with a measured map in the 60s and requiring one round of CPR prior to Ross one week before her presentation she really knows that she woke up from the CPR event and distinctly had a worse vision even though her baseline was already poor and in addition to this she does have a complicated past of history comprising severe bilateral diabetic retinopathy she's getting anti-dieterative care she does have prior ARDs with bubble repair and lots of ads for valodone for microbalol, perosatin, capra, insulat, tachrylimus, microfenylate, prednisone, totem, gums, etc and every no time she gets exposures or alcohol drugs or anything like that and family history on exam she's 2400 in her right eye hand motion in the left eye with biologically normal pressures she does have an RAPD in the left eye particularly noted by reverse and her visual fields to bigger confrontations show a nasal deficit in the right eye and generalized depression in the left eye UMS are full, she's got some cataracts but notably on her posterior exam she has pale optic nerves biolaterally with attenuated vessels 360 PRP both eyes and some foveal x-stakes in the left eye but there was no diabetic neobascularization seen so after that event they had a neck and I don't have the images for those but overall I didn't show any new stroke they just noted this right eye cesanosis that was from the cause of previous strokes that Jordan just talked about and so they also got MRI and so we're just going to walk that real quick so the MRI also again didn't show any new strokes it showed some old cerebral strokes sorry some bone strokes that you can see over here it was kind of hard for us to find we weren't very sure but these weren't the biggest abnormalities we saw but they showed gliosis also the parietal areas and encephalomalacia and then just some white matter small white matter infarcts here but again no new strokes that could explain her current vision loss and so after that they consulped with us we took a look and consulped to neurology and neurology actually actually reviewed the old CTAs and found that in addition to the right eye cesanosis that was there a long time ago there looks to be new left eye cesanosis that was not caught by the neurologist and so their thought was could this be like a cerebral hypotensive event from the event that she had that required her to go into the ICU and get observed and so they recommended further imaging with neurosurgery looking at this like this cerebral angiogram seeing if we need to do any setting and so they went ahead with this looking at the left eye CA and this here shows this segment that is the nose and the ophthalmic artery I believe comes out right here so this nose just comes distal to the ophthalmic artery not before and so this was a big question we were having is this contributing to a vision loss of this stenosis here and it turns out perhaps not this stenosis here but we I'm going to move forward this is the MRI orbit so I'm going to talk about our differentials real quick here so given this whole picture I'm just going to review this is a woman with severe diabetic right now the vasylopathic risk factors a room of history of sarcoid who's now immunosuppressed and that have this eye-state stenosis and she lost vision acuiaptor had tens of events so on the differential acuia we have posterior stemic optic neuropathy from this had a tens of events it could also be affecting the posterior occipital lobes but we decided that there wasn't any stroke based on the imaging that we got it could also be macular edema worsening from her diabetic retinopathy that's something that I could not tell just based on my bedside exam CRIO was considered but again I did not really show the classic findings of a cherry red spot OIS given the bilateral acenosis considered to could be something that was heavy going on for a long time but again the exam did not show obvious findings of that there could be infiltration given the history of sarcoid and that's also one of the reasons why we got this MRI orbits and lastly infection given that she's even suppressed so there was multiple layers multiple things going on and we decided to go with this scan and we did not see anything of no enhancement of the nerves but and also this is again of the nerves here we did not see any enhancement but they did find amnesioma that was also encasing the left optic nerve small and 270 degrees around the nerve and so now our differential also includes his amnesioma contributing to a vision loss can you trace it out for a moment oh yes, it is right there so multiple layers going on with this patient but in the end we believe that her acute vision loss happening right after this hypertensive event was most likely due to hypo-perfusion given her already multiple risk factors of being a basketball path of likely having some kind of decreased flow to the nerves and also having this amnesioma there all might be contributing to this vision loss but we think that the primary etiology is the posterior ischemic optic neuropathy and so just for following up after this patient what we did was we wanted to bring her over to the brand for further imaging but she was too sick and not stable enough to be moved and so I think we were just following but they discharged her before we could bring her over so I think just a default would be the best thing to do this morning it's one that I'm alright after this after this event where I'm not as low as all of that was there a diffusion restriction in our immunology? it wasn't called officially on the screen but on both of them are just one I think it was I think it was just one, it was just the left side at some point I saw how it was called by then glad that you saw that because we always review those things and we find things that are maybe not seen right away by the neurologists the nerves are really hard to tell actually on DWI and ADC sometimes if there is a fusion restriction or not we correlate to ADC so it's really important to look at that and also history is such an important factor in this case right kind of tell what happened based on the history of the situation and then her past medical history especially. Do you guys have any questions? Beware of making the diagnosis so a PIO on because it's a slippery slope the hypertension is a risk factor and then blood loss especially after back surgeries you won't see a swelling of the disc the nerve could be normal and how would you tell the difference between PIO and an occipital nerve stroke? What's going to be your most important exam at bed site that you can make the diagnosis? Pupils they're like bilateral affecting okay so if it's bilateral PIO on what do you expect the pupil to do? Just not react very well. Poor reactive pupil if you have an occipital lobe stroke and no PIO on what do you expect the pupil to do? It's going to be normal so it's something you can do bed site to look I mean somebody like this has got such her nerves already shot from like diabetes it's going to be hard what's our next step here we're going to do our cases when I try to do four faces we'll see if we can get through them we might just do three so that you guys can do the perhaps we work too hard on these presentations but thank you that's great perfect so the first case is an 18 year old woman who presented with monocular vision loss she went to see an optometrist just for her annual local eye exam and when they were testing and she was being tested they noted that she had a central defect in that left eye her visual acuity was 2015 on the right but 2400 on the left and she did have an affront pupillary defect with just this information that's all you get what would you be most concerned about or what would you be kind of worried about and what would you order next 18 an optometrist that's exactly what optometrist was concerned about as well that was kind of the top thing that they considered and so they got an MRI of her orbits and this is what it showed the arrows don't really come out very well the enhancement of that left optic nerve you can kind of see it on the axial as well as the coronal cut there and it was fairly posterior and it did extend quite a bit as well so it was a longer lesion and so after this they also did an MRI of her spine which showed this also extensive lesion kind of around C4 expanding a little bit further and it involved the posterior of her spinal cord which you can see on the axial and so with this presumed optic neuritis she started on the 5 days of IV methylprednisalone 1 gram daily and after day 1 she noticed that she actually had worsening in her right eye but she completed the steroid 5 days and her words mentioned to her doctors that things are getting a little bit worse so she was referred to us so she was able to see I think in a month later and this was her exam at the time she was no light perception in that left eye her right eye was actually in 2015 still she had a very large atron pubular defect no color vision and the right was normal so at this point what other workup would you guys like to do we give all the labs that Dr. McQuintet kind of so many we didn't go directly there but she went and had a lumbar puncture done which was normal she did not have any oligoclonal bands we did check for NMO this was in 2013 so Hogg was not available yet she was incand negative everything else was kind of negative so she was diagnosed with presumed zero negative NMO so she was started on plasma freezes that's your next stop so if you're not steroid responsive and after the plasma freezes she was actually transitioned to acetyprinazone she was stable for about three weeks and then at the end of November woke up with complete vision loss of her right eye and so again she received five days of IV methylpred and saw us afterward after that and then was started on rituximab but our exam after that when she woke up with complete vision loss in the right eye she was light perception only no light perception in the left and now her nerves were just hellerous here's a picture of them so like I mentioned she was started on rituximab dosing as well and then from March 2013 through May 2017 she received additional treatments for this zero negative NMO including more plasma freezes more rituximab, IVIG ACTH injections all without improvement but as we talked about NMO is that entity where you really have to keep trying if that's what you're trying to treat she had repeat acocorn IV and at the time mom became more popular and so that was tested as well and these were all negative she had repeat neuroimaging which also remained unchanged so at this point in time diagnosis changed at all so during this course in time she did have mitochondrial testing as well which was like nothing was found she was still labeled with the zero negative NMO but there was this ongoing work of as to what else could be causing this could it be genetic could it be you know it was the differential was expanded to include more autoimmune more anything really dermatology everyone to kind of see if there was anything else going on but nothing was determined and then an unexpected visitor came to clinic this was her 54 year old father presented with one week of gradual pain this was a muscle left high when he saw his local ophthalmologist he was count fingers in that left he had central scatomas on his Humphrey visual field and so they tested for Moc also negative his toxic vitamin panel was also everything was normal syphilis was normal so he went to see us and when he saw us he was hand motion only and left and two had one foot had the central scatoma and he already had diffuse pallor he got MRI Orbit's brain and C&T spine and he also had this very similar but much more extensive posterior column so cord kind of lesion and it looked very similar to his daughters except that it could see it like extended all the way down into his thoracic cord and so this is when we kind of expanded our genetic testing so as I mentioned the patient herself had had the mitochondrial testing her father when he initially presented had the nuclear mitochondrial panel which was also normal and so we talked to Emily Spoth the genetic counselor and we went with trio hold exome sequencing so that allowed us to test the patient as well as her parent simultaneously and it revealed this eternally inherited auto dominant mis-sense mutation in AFG-3L2 gene which if you remember from Dr. Caguta's comparison table was one of the rare genes associated with did you guys have the the exome dominant instead of the OPA1 gene and so we provided the family with more genetic counseling we offered other family members to be tested as well and hope these patients were referred to the low vision center but it was this is a novel kind of mutation and has been found in the AFG-3L2 and so it is associated with OPA1 processing in the mitochondria which had not been seen before so those cases crazy right? I didn't see specifics of yellow I just saw the color vision was decreased I didn't see like I didn't see a D15 I'd have to go back to the paper chart I'm still waiting for the paper chart yeah but I mean the case is it doesn't respond to anything and it just keeps getting worse do you think about the genetic causes? Do you see how like we were persistent in thinking that maybe it could be something like animal or especially animal because it's like you can have negative serum testing negative CSF testing for that and she had the spinal cord lesion and the optic nerves involved so there's it doesn't always respond to flex or so just to prevent new lesions you try that treatment again and again I want to mention real quick before we move on is when we're treating NMO versus MOG I think one of the reasons it's a little confusing but one of the ways I remember why MOG is more responsive to steroids and less severe than NMO is because of the difference in mechanism so MOG is demyelinating like I stated optic niuregis or MS-related optic erotis and then NMO is like a cytotoxic issue so you have these astrocyte aquaphorine receptors being attacked essentially so you're losing, you're killing these cells astrocyte cells and not just a deep sense demyelase it's a little more severe because of that or a lot more severe that is a prosthetic anticipation do you see that commonly where there's a prosthetic earlier I don't know I don't think so and the father didn't show any other signs previously he presented maybe earlier than him that's a good question maybe in that mutation there's a lot of different ones out there not generally so is it unusual to see spinal cord involvement with autism with optic atrophy I don't think it's like a common thing so I'm not sure about that genus in detail but there are syndromic versions of autism with optic atrophy where you have one more finding is that gene associated with that or it's that I was reading that did have associated T2 hyperintensity as well and even more demyelinating looking lesions but never such an expansion of the cervical lesion I'm really good about expanding that gene testing and the panel genes that she can test based on those findings well we don't have much time to go through these cases but I think this one is a case where just we'll look at history and then you tell me what Brian was losing vision 40 year old truck driver he depends on his vision to drive he has painless visual loss and his left eye he's not sure when it occurred he does have diabetes he's hypertensive, he smokes he had a MRSA infection four years ago then he developed a new MRSA infection and now this year he got one in his foot and he was put on menizolite and he does have decreased vision in the left eye, he's got a little bit of pallor on the right, EPD on the left, he's lost his stereo and here's his fields so he's got extensive visual field loss on the left but some visual field on the right and he does not he hasn't developed thinning yet but he will his brain with orbits is normal and I gave you the clue of to his visual loss in that history medications so the answer is medication menizolite and I won't believe her that he had a big workup and so menizolite and a lot of these things affect the mind and heart area and that's how people lose vision results I did that last four years but you got the answer and the most important thing is that list of drugs that can cause visual loss you just have to think about it when you look at that drug list this is relentless opticritis 28-year-old woman with slowly progressive visual loss in the right eye and she has some headaches she's morbidly obese she's depressed she has no family history of MS so she's got count fingers vision at the beginning 20-20 in the left eye big affirm pupil people are in defect in the right eye and she has dyscadema on the right side her nerve and retina on the left are completely normal and she has a big central scatoma with only a temporal loss of vision here's her MRI scan this is a T1 fat saturated gadolinium enhancement you can see the arrow sign helping you see that her nerve is enhancing and here you can see and I think this is important this is a T2 weighted image and you can see that this nerve is a little bit expanded right here you see that and you can really get a nice view of the nerve all the way back otherwise it looks pretty normal she has a mega laboratory work up with the usual suspects animal etc etc lumbar puncture looking for bands negative so anybody want to venture some ideas about what could be going on here there's pain there was no pain I mean she has headaches so everything hurts and she's morbid no peace so I mean you know what I mean it's not easy to get the pain story but it's not pain with eye movement she was 24? diabetes no wondering could there be a mass like lesion okay good she goes through the usual IV method premise alone nothing improves and I think that's a message here you know when you put people on treatment and they don't get better what else can it be and we've already heard about the genetic side so it's probably not going to be genetic and then she gets another MRI and that T2 expansion is still there but you can see that the white matter is looking like it's expanding backwards a little bit and maybe even more towards a chiasm this is a T1 Gato enhanced so now this nerve is further expanded and it's enhancing more intensely further back so I hear I'm seeing nodding yeah let it rip so I'm going to so what I'm going to show you is she went underwent a biopsy a very careful biopsy to begin with and of course nothing showed except for some cells then they did end block biopsy and she indeed had a very low-growing glioma but they did it resected and had clean margins so you know I think the important thing here is when the person presents you've got to look at the whole picture over time but also when it doesn't respond to the treatment you've tried and optic retus, mod, even animal can respond to the treatments that we have but when it doesn't then be thinking about could it be a glioma or an infiltrating lesion or genetic and I think those are the take-home messages in these two cases is how to be thinking about these but these are tough cases when you're the one on the front line taking care of has a really tough case I'm actually going to skip mine because it's going to take a good time just so you guys can do the OCAP questions and I kind of want to give you guys this presentation maybe in a morning report briefly just to talk because it's kind of important for when you're on call all the PGY4s are here look at this, turn it out he's kind of shy jeez what are you he's lost he's lost Ali he's doing just email out I'm going to ask the curvy guys can you ask his name he's in a session he's my little intern I know your little intern so I think there's an anatomy right now does it age at C so no you may see an embryo on me so you are I'm sorry No, I'm not. I'm not. He's like, settle the things. That's what I was looking for. That's what I was looking for. He's so far. He's very dangerous. Okay. Oh, there it is. He's very dangerous. Yes. You were set up. I feel it's there, but she was like, I want to be the one doing the laundry. No. No. It's pre-work with an E. I see that's what I said. That's how I know it. Pre-work. It's E.W.E.R. You remind her, right? Do we send it to his Google? No, I sent it to your Google. Oh my gosh. I just want to send it because you replied to me. Do you have any advice about OCAPs for our hero? No, honey. I feel like if you can pass that, if you can pass the neuro op test. You're good. You can pass your OCAPs. QB is the test we give you at the end of your rotation. Oh, there you go. There's a lot of different imaging questions that I remember just kind of, it was hard to parse through things. So I think just like, I think our neuro op malnutrition is good for like the morning before clinic starts of just learning how to recognize different imaging modalities and looking at the anatomy in different cross-sections and recognizing things because sometimes you'll get no context that really, you really rely on your ability to interpret images. It's really amazing to be in other programs how often people don't look at images at all like as much as we have the size of this program. So what's great is like even our reads here are better than another program. It's reliable. You can like boost yourself. You can look at a scan and then look what the neuro radiologist has to say too. You are the neuro radiologist. Brandt and also every negative scan where they're going. According to the ONTT, what is the likely benefit of IV seroid treatment in a patient with typical optic neuritis? The risk of progression, five years visual function that will cover more rapidly the final visual acuity and contrast sensitivity or pain resolution. I think just in general, it's really important to know the ONTT kind of forwards and back because it comes up a lot. So this was a randomized central trial and actually three different groups. So it was with IV steroids and then an oral tape or oral. And what they found at the final visual outcome at six months was not different among the three groups, but that those that got the IV steroids had more rapid visual improvement. Number two, after first episode of optic neuritis, what is the best predictor for future risk of MS, which has phenomenon with exercise and very ventricular white matter lesions enhance the optic nerve. And this is just any like one white matter lesion that looks like demyelination is the best predictor. And then this one goes off the other one in the presence of a white matter abnormality and brain MRI, the initial diagnosis of optic neuritis, what is the risk of developing MS at 15 years? 72% compared to those that you did not have. And a white matter lesion, your risk is still 25%. And I give the 10 year question to rather than 15 and then it's 20, 40, 60 rather than 25, 50, 75. Okay, we've talked about this. Yeah, so different. We've already talked about this. I didn't read your answers. Yes, right. But when we don't really talk about that much is 34, 60. I mean, of course, we've talked about these are all made around their mutations for LH when I mean, the difference between the three of them is the disease course of 11, 70, 70 is pretty severe. But the outcome isn't as bad from what I was able to read as compared to 34, 60, even though the disease course isn't as severe, the outcome is poor. And then 11, 70, 70 is the most common mutation and one of the four is this. Or better. And then can I just say on 34, 60, what other tests do you absolutely want to create a condition? WPWA arrhythmias can occur with 34, 60. I think it's kind of the time course of the vision loss. So I mean, like, the breath loss or some sort of prolonged course. And then the final visual outcome. So, I don't really talk about a whole lot. What did you do? Five years of contralateral optic disc, psychoptics. They're not going to be associated with anyone. We've got one side. Insecret cancer, 15% risk of contralateral involvement. So minimizing risk factors as well as, you know, I remember a couple of years ago, there was one patient that we put on Bermuda team. It's something that's commonly not kind of limited in terms of how much it helps, but it's something. Yeah, it seems like neuroprotective, but I don't really that's anything. We do all kinds of things. But none of them have been studied or been worked. I mean, steroids have been used. The Bremonidine and then Contaxifalon. Trentall has been tried. Is that the European drug? Contaxifalon, people have been trying that, but there's no study that shows that all that stuff works. It makes your heart sink when somebody with AI one walks in your office. Because you, the only good news with it is they tend to get better with time. That's the only good news you can say, but it's never back to normal. While they're just falling as worsening, the vision can worsen, but then maybe some improvement after. I don't know what you've talked about. Visual field. What did you expect in a patient with ADOA? Perforal arcuids. Immersed blind spots. Supercentral hypothermia. Depression. Generalized depression. We had a really good case. So what would you think, Albury? I switched it up on you. Yeah, you're correct. So, supercentral central depression. And a lot of things you've already talked about, but earlier presentations compared to LHON and a lot of the family history, the vision is typically not as severe at the end as LHOIN. And they can look like glaucoma. Because they get that excavation that looks like glaucoma. And that can be a nightmare to try to figure out. Could this be low tension glaucoma, normal tension glaucoma versus dominant opti-gatrophy? Do you get nasal displacement? I don't know that. I don't know that. I think that the vessels stay in the center. All right. 32-year-old woman is bilateral elevated. Optic discs. She has had AIDS for the past three years. Spontaneous viscose pulsations are present in both eyes. What tests would best support the diagnosis of this condition? Or the optic nerve voters show them a lot? Nice. Can't trick you guys. The answer is D. Yes, this is just a lot of the test using them. These are sort of the points that are hidden in BCSC. So prevalence ranging from 0.3%, clinical trials to 2%, and autopsy. Gender is roughly equal, more common in whites. It can be sporadic or inherited autosomal dominantly. And then can have several sort of visual manifestations. Some have TBOs. 75 to 87% can have nerve fiber visual field defects, which are typically stable to slowly progressive. And then it can also be associated with increased risk for anatomine, CNBM, acclaimed homerages. We talked about how BCSCAM, the most effective modality, auto fluorescence, is also effective in going with CT versus MRI. CT is the more effective of them. And then OCT, EDI can also help to delineate these a little bit better. Can I go back? Not regarding this, but back to Brandon's question, like the nasalization of the vessels and such. So we try to look at optic nerve features to try to figure out things to help with the diagnosis, right? When there's significant optic atrophy with some cupping, it becomes much more difficult. And Mark and I are working on that, like a protocol to figure out how to work out patients with that kind of nerve appearance, like following the grand round. So we were talking about it. And there was a recent study we came across where there were experts in NROF and glaucoma who were asked to evaluate pictures of patients with glaucoma, ADOA, labors, and norm, and maybe just like physiologic cupping or something like that. And it was really hard for them to distinguish, I don't remember the exact percentages, but there was no general correlation between like what the person specialized and their ability to determine whether someone had ADOA, labors, or glaucoma because the nerves can look so similar across the board. All right, the 67-year-old Filipino man on treatment for a chronic mycobacteria and ABM infection has blurred vision. His visual beauty, color vision are reduced, nerves modeling play pale. What pattern of visual field loss would you expect on parenetry? I don't know. I mean, what can you ask? They know everything. Oh, yeah, I was going to ask you what the drug was, but everyone knows that. Shout it out anyway. There's a deer in the dissertation. There's more than one. There's more than one. There's more than one. There'll be talk. There'll be talk. Okay. Yeah, so we talked a lot about this. This is from some of Flint's slides. And, you know, in these talks, you can acquire optic neuropathies. The papillomaniac, the bundle, is primarily affected. So it results in an early sort of decrease in visual cutie and a sequo-central defect. The drugs we already talked about, you mentioned this easy way to remember that a lot of these are antibiotics and sort of related the structure of mitochondria to bacterium and just that these drugs can have a particular effect on the most mitochondrial-rich neurofibers, which are in the papillomaniac bundle. I'm not sure how true that is, but it's helpful for remembering. And then toxic effects of any of these drugs can be exacerbated by underlying poor nutrition. And specifically, if ambitology screening recommendations are if greater than 25 milligrams per kilogram per day or if there's a kidney function issue, decrease GFR to screen monthly while they're taking it with visual cutie color and visual field. Just curious, where are those recommendations? Those are from PCSC, I believe, but they're specifically from Flint's PowerPoint, so they may be slightly outdated. No, I was just wondering, because there isn't a generally accepted protocol for this. There's different things you'll see published in different organizations. Like maybe you should do this. I think that's a great way to go. Honestly, if I was, maybe even for less than that, I would just keep them, keep a close watch on them. Yeah, I think you did mention that for less than that. There isn't a specific screening recommendation, but maybe sort of above that, it's sort of definitely widely accepted that you do. Remember doing an atambutol baseline exam on conference artsy speaking patient, who was illiterate, so I was trying to do Ishihara plates. I think Brandon actually had the good idea, like she actually just traced the Ishihara letters with her finger. It's great for kids to do that just sometimes. 49-year-old, right-eyed parent-central visual field lost, found on routine exam, got to disc 0.5, pallor of the right optic disc, with an ILP of 24 in both eyes, what would be the next most appropriate step? Surveillance, visual field in six months, test for TB and syphilis, atopical prostaglandin analog in both eyes, or an MRI with GAD. You can tell me that. The MRI of brain organs. Why? What are the buzzwords that made you say go to MRI? Technically, it's really hard, but on these hookup questions, they're just going to give you a few buzzwords. And pallor does not equal cupping. I don't think I knew that until, like, late in turn, or, like, even mid-June. And it's actually the neural retinal rim that you're looking at, not the cup itself. So if you have that, like, nice pink rim, that's a normal glaucoma disappearance with the cupping. And you can have both things, like this patient probably has glaucoma with that cup to disc in that ILP, and some other key differentiators, which are also tough clinically, but they might give you on a question stem, is, you know, color vision, and an APD, which both should be preserved and feel really advanced. Which exam finding is least likely in a four-year-old with a history of alcohol abuse, gastric bypass, who reports gradually progressive pylid or a vision loss over a four-month period? Maybe. So all these toxic metabolic things we've been talking about should not present with this kind of event. These are similar. Some of the common vitamins are there. Again, you may not see an APD if it's symmetric and bilaterally involved. And then these can all present in a similar fashion to the hereditary optic neuropathies. And the reason for that, I remember, is that we're also talking about mitochondrial effects, which, as Sean mentioned, preferentially affect the papillomac to the bundle. So you can see similar yield defects. That's it. So these are a little bit easier than what you'll see on OCAPs. But thanks a lot for that. Thanks a lot.