 So we have two presentations today. First is going to be one of our chief residents who's joining the private practice world up in Ogden. Bryce Williams, we all know him really well. Hopefully we'll be seeing him again from time to time. So he's going to talk about interesting neural patient. Is that better? OK. Yeah, emphasis on the chief, for sure. After that roast, I don't know if I can catch up with Lloyd on the. I wanted to thank Dr. Warner. I don't know if she's even here yet. But she caught me in the hallway and said, don't you have a neural presentation left? I said, oh, I was hoping you'd forget about that. But she didn't. And we all know that she never forgets anything. So here we are, flashing gray spot. So this was a 37-year-old female right-handed that came in with a chief complaint of dimness in her left eye, which became flashing lights in a gray spot. And the timeline was that on the 30th of April, she noted this grayness. And she thought her contacts were dirty. The glasses didn't seem to help. Then a couple of days later, the gray spot began to flash. And she noticed that it persisted with her eyes closed. She went in and she was referred to a retina specialist outside of the Moran. And he said, quote, you need to see a neuro-optimologist. And there was this question of some discomfort with eye movement, so there's possible optic neuritis. And she noted some growth of the scatoma, that gray spot over the week before she presented to us in the Neuro-Optimology Clinic. Her history was significant for some depression and recurrent cold sores. She didn't have any contributory surgical history. She had been put on a moxa-cylind a few weeks before for some flu-like symptoms. And she was finishing up that course. She had been placed on acyclovir neproxin just for some pain, just as needed, and a multivitamin. She was allergic to betadine. She had obviously refractive air, as I mentioned before. She complained of some scalp itching for 10 months. And it's kind of persisted. And then lately, several months, this persistent nausea, which was bothersome to her, but she was still functional in these flu-like symptoms that I mentioned. On exam, her vision was down in the left eye. She was still 2020, missed a couple letters. No APD, pressure was normal. There was, the color plates were normal. There was no red desaturation. Confrontational visual fields were full. Extractive movements, saccades of pursuits were normal. Flicker fusion was normal. And on exam, anterior segment was normal. The posterior segment showed some punched out white lesions near the optic nerve head and the right eye. Some rare vitreous cell in the right eye and one plus of it cell in the left eye, otherwise normal. And here I have a fundus photo of that, these punched out lesions and some pigmentation near the optic nerve head on both sides, actually. But otherwise, the fundus appeared fairly normal. Visual fields did show some defects in both eyes. There's good reliability. Mean deviation was depressed in both eyes. The gray pattern didn't show much on the right, but on pattern deviation, you start to see this kind of inferior scatoma. The left eye was very much a significantly enlarged blind spot, which persisted in multifocal ERG. You see this area of depression. Here's the raw data. This area of depression here in the left eye and perhaps some also in the right eye here, which corresponded with the visual fields. This is an outside angiogram, which was fairly normal early on. You don't see any blockage or hyperfluorescence and same thing later on. You don't see any real hyperfluorescence to the optic nerve or any areas lighting up, which was significant for the differential that we were thinking on. So fairly normal fluorescein. Autofluorescence also did not show any obvious defects that may correspond to the scatoma that she was complaining of. OCT looks fairly normal. Again, no obvious problems. The inner segment, outer segment junction seems fairly intact. There may be something here which I'll talk about later. They call this the outer segment of the cones, the cone outer segment tips. They see it kind of falls off here. We'll talk about that in a minute. So the differential includes more than this, but these are kind of the big players. On the left, the enlarged blind spot syndrome would be the top on the differential. Mudes would also be high and azore. So those three I'm gonna discuss in more detail. But less likely, things to consider given our history of cold sores, herpetic disease can never be ruled out as Dr. Mamelis likes to remind us when we go to boards, always talk about herpes. It's always there. Ampy, although it didn't really look like ampy. Punctae inner coroiditis, multiflacoriditis and panuviitis, and acute macular neural retinopathy. But these, classically, will show that auto fluorescence defect that corresponds perfectly with the scatoma. So I'll just focus here on this acute idiopathic blind spot enlargement syndrome, which is kind of a mouthful, so they abbreviated AIBSE in the literature. It's been called big blind spot syndrome in the past. And there was a nice study done back in 2001 of 27 cases where they used this flow chart to kind of identify people with AIBSE. First, you identify a group of patients that have enlarged blind spots on visual field testing. If you don't have optic diswelling to explain the blind spot, they move down this arm of the pathway. And then you look and see if there's anything in the retina that may explain it. Multifocalcoroiditis or PIC. And if there's nothing in the retina to explain it, then they identified these patients and diagnosed them with this AIBSE. And then they studied them and here was some of their characteristics. Of the 27 patients, 25 complained of a loss of vision. Of differ, sometimes they explain it differently, but almost everybody had some sort of loss of vision and almost everybody had some sort of positive visual phenomena. Flashes, swirling, colored lights, after-flashbowl kind of thing. But Photopsius was really the majority of their complaint with the positive visual phenomena. If on visual exam or on visual acuity testing, the majority of them were still 2020. Some had lost a little bit of vision, but by and large most everybody retains good vision with these blind spot enlargements. Interestingly enough, they detected a fair number of APDs. We didn't see that in our patient. And the number of degrees of their scatoma was ranged quite a bit. Here are some examples of the visual fields that they found in their study. These patients, these are 30-2s. They looked a lot like ours, but different patients that can show differently and on Goldman testing as well. So it kind of fits with what our patient was looking like. The one thing that our patient didn't have that they found most commonly was some optic nerve had swelling. And so if you go back to their flow chart, they say, well, if there is enough optic nerve swelling to explain the blind spot, we're gonna call it papillodema and attribute it to that. But if there wasn't quite enough to explain all the visual field defects, then we'll call it this AI BSE and here's some photos of what they didn't think was enough swelling to account for the visual field. So it's kind of a judgment call on that. But a lot of their patients did have these punched out lesions, pigment changes. They're pointing out here this little gray line that maybe showed evidence of old edema. And on Floricine angiogram, they do see a late phase hot nerve which our patient did not have. And even sometimes they'll see these little hyperfluorescent spots and they still would call them this AI BSE instead of one of the white dots syndrome. Here's a study that just came out that it was a case report more than anything. A patient that had complained of a blind spot 10 years prior, he came back in with a new onset of symptoms. And so they imaged him again and they found that in the eye that was symptomatic here, this left eye, that he had lost some of this, what they're calling the cone outer segment tip line, which I think if you look at these three heavy lines, I think it's a second line here is what they're talking about. See how it's lost here in this area compared to this side and the other side has it nice and continuous the whole way. And he had on nerve fiber layer, or no, this is retinal thickness that they use for the ETDRS map. He had had some thinning in that area which corresponded to a scatoma. They thought maybe long-term these patients do lose some of their retinal physiology and anatomy, which can be picked up on high definition OCT. And if you go back to our patient, there was a little bit of loss of that area. So it's an interesting theory, but again, it's just a single case report and needs to be shown more out in a case series. So as a summary, these are kinda how these patients do in general, if you're more of a splitter and you wanna talk about AIBSE as a separate entity, you'll say, okay, there's more female, much many more females than males. Photopsies and blind spot enlargement is the classic symptoms and signs. There's usually no flu-like prodrome, which our patient did have this flu-like prodrome. Usually has some mild optic nerve head swelling and peripapillary pigment changes that resolve within two weeks. We didn't really see that, and we did see her fairly quickly after the onset of symptoms. Humphrey visual field and ERG, so areas of dysfunction that persist long after the symptoms resolve. So you can test them months and years after and they still have the defects. However, their symptoms go away. Fulfilled ERG is normal, which we did not have in this patient, but we're going to obtain. And the fluorescein usually shows some hyperfluorescence of the optic nerve head. Now contrast that with this multiple evanescent white dot syndrome or mutes. Typically does have a flu-like prodrome. Again, females more commonly than male. There is a mild vitritus, which our patient did have. It's usually unilateral, but there's some question of, maybe if you talk to Dr. Vitale, if I hope it's here. He will tell you that he thinks it's usually bilateral, but much more pronounced in one eye than the other. There's this granular retinal appearance with small white spots acutely. And the fluorescein angiogram will show hyperfluorescence in this reef-like pattern with late staining of the optic nerve head and lesion. So there's a lot of overlap with what we've discussed with AI BSE. ICG brings these changes out better than fluorescein. And so if you see patients in the future order an ICG and the Humphrey visual field changes will go away versus the blind spot. The other big one on the differentials is Azor, acute zonal occult outer retinopathy. Again, females more than males, usually bilateral, you get the flu-like prodrome. The fundus will appear normal initially and then late you get these pigmentation changes and I'll show you a picture of that. The fulfilled ERG is decreased, which is diagnostic in this setting to help distinguish it from the other entities. Humphrey field changes will correspond to the pigmentation and it's associated with autoimmune diseases, which is important because it can help distinguish between these. So here's an Azor patient. You see some vascular sheathing and some pigmentation changes. And if they're close enough to the macular you'll see these changes on the field, on the Humphrey visual field and you can pick them up with multifocal ERG changes. So the question is, are these all the same disease with just different types of expression based on the sensitivities of the patient and the immune response of that particular patient? And it kind of goes just what we were speaking about last week with the Epstein-Barr virus patient. Is it just, are you a lump or a splitter? Does it really matter anyway because most of these patients just get better on their own? There's no real treatment. And I think that's my next slide. So what we did with this patient was observed and reassured we did do some lab workup, which all came back fairly negative. There was a question of maybe this was histo that had reactivated and just hadn't, you hadn't seen a new lesion but you had those old punched out lesion, that was negative. So the workup was negative and we're gonna follow up with a repeat field and a multifocal ERG and a fulfilled ERG and maybe we'll have the rest of the story. Interesting patient and it's something to keep in mind when you see these fields that come in with the big blind spots, it'll help you give them a diagnosis and perhaps prognosis, which is good, document. Uh-huh, yeah, that's where I'm leaning. Just, yeah. Oh, Dr. Warner is here. I have my thank you card for you, just.