 All right, so next up is Mike Burrow, new Alabama fan after his last week, but he's going to talk about Ockham versus Ockham. All right, good morning, everybody. Thanks for having us this morning. We're really excited to be here. So I'm going to talk about a case in neuro-ophthalmology. When I was in med school, I had an attending who I just happened to rotate with several times over the course of a couple years, our clinical years. And he loved to, anytime someone new came on, they hadn't rotated him with him before, he loved to somehow bait them into talking about Ockham's razor and this thought of the simplest explanation, yada, yada. And he was really good at it, no matter what the diagnosis was at the time. He just would try and kind of do those pimp questions over and over again until finally he said, well, why do you want to keep everything in one button? Just spell them now for him. And finally they'd say, well, Ockham's razor, it's parsimony. And that's when he'd dive in and grab him and be like, no, but have you ever heard of this Dr. Hickham? And I never had until he loved doing it. And I'll never forget now, because I probably went through this spiel six or seven times. So I think most of us are familiar with Ockham, but maybe not so many of us are familiar with Dr. John Hickham and what's known as Hickham's dictum. It's not quite so eloquent, but I think it's equally as important to remember. And I hope I have a good case here that I'm going to kind of race through and something that'll illustrate the fact that we do have to keep differential diagnosis broad, including multiple diagnoses, and that everything doesn't always fit in a one nice little package. So this starts back in 2012 as a 16-year-old female who is otherwise healthy. And she presented to the children's ED for whooshing in her ears, blurry vision, some neck pain, and dimouts that had occurred over the period of several months. And she's found to have bilateral stage 4 optic disc edema, and then underwent subsequent imaging, as mentioned there. She did get a lumbar puncture, which showed a very high opening pressure of 50 centimeters of water. And I tried to highlight the important things in red. I somehow missed that sort of in bold and flashing or something. But the only real other abnormal thing on her laboratory imaging workup was her LP also showed a white count of 25 with 96% lymphocytes. She had these other laboratory investigations, as mentioned. She started on dimoxin and then sent to neurophthalmology for evaluation. A little bit more about her HPI that was kind of gathered while she was in the neurophthalmology clinic is this neck pain, the whooshing in the ears had been going on since February, so a couple months. And then she did start developing blurred vision later on in that course with these dimouts that she would describe. And it would happen most often, she would notice it when she was kind of transitioning from lying down to standing up. No other medical history, ocular history, and she wasn't on any other medications and had any changes in her medications recently. And no recent travel, exposure to pets, a lot of the things that we just kind of went over with Becca that are important to really investigate. And then the only other thing on review symptoms, she had a recent URI and then she had some knee pain as well. Her exam is noted here, actually a pretty normal exam at this point. And then on dilated exams, she did have some stage one discodema, so it improved since she'd been in the ED from a reportedly stage four bilaterally to stage one, which you can just see more nasally than temporally right there. And then, oh, good, actually shows up better than I was expecting. So she did have in her macula more on the right eye than the left eye, but this presence of a, let's see, macular star right here. So you can see it shows up a little bit better on hopefully this next screen. And then a little bit of just in the way of some hard exudates that you can see around the macula over here as well, so it shows up just a little bit better. As really usually things don't show up very well on the screen, but that is actually OK. She did have a Humphrey visual field, which showed mild enlargement of both her blind spots. And then some subsequent OCT studies showed ISOS disruption, more notable on the right eye with some small exudates, but also some involvement of the left eye as well that you can see, especially right here. So just a short differential, certainly not all-encompassing, but later on I'll kind of talk about that. The thought was that she obviously had signs of elevated intracranial pressure, but she also had this abnormal CSF study of the elevated white count, so you couldn't call it IIH, but really weren't sure what the etiology could be. She also had signs, this macular star pointing to a neural retinitis, and then the CSF with elevated white count, but also unclear of what the etiology was. And also just something that was being heavily considered at that time was an optic neuritis. So it had a pretty good, took a lot of blood from this girl and sent it out to the lab and then referred her to the EVitis clinic and just continued her on the diamox for the time being. She came back to neuro-ophthalmology a month later before she had a chance to be seen in UVitis because she had some worsen blurry vision and her stiff neck had kind of returned. The laboratory workup that I mentioned, it was all within normal limits. The only abnormal thing was that she had some EVV titers that were showing evidence of prior infection. And then the exam was unchanged except for a rare vitreous cell and then some fullness of the optic nerves, but no edema. It actually improved a little bit. It had a repeat OCT at that time and showed kind of the same thing, this macular star that shows up really well right here and then that same ISOS disruption and photoreceptor loss and then some exudates. And then the left eye was similar to what we had already talked about before. So continued on the diamox. There was a discussion, keep on saying we, I wasn't here at that time, but there was a discussion with infectious disease and about this EVV titer and they had recommended, well, why don't you go ahead and repeat the LP and check for EVV PCR. And so that was planned. She then, you know, a few months later ended up in UVitis for follow-up. That repeat lumbar puncture showed that the EVV PCR was negative, it was just consistent with previous exposure and then she had a normal opening pressure at that time and a normal cell count. Her vision still seemed blurry and then her baseline vision exam really unchanged. Guess, more pictures here. So you can see that partial macular star nasally just a little bit right there, but otherwise really normal and then no evidence macular star there. So things had even improved on her dilated exam. She had a fundus onoflorescence, which was normal in both eyes. And then she did undergo an FA, of course, right? I don't know, Rebecca, what? And she had a normal armed eye and AV transup. She did have some patchy coroial feeling, which I feel like was illustrated well in this snapshot. And then along the superior arcade, she had some of these punctate hyperfluorescence areas that you can see right here. And then finally just some very mild staining of the optic nerves, but nothing to write home about. So otherwise, there was no leakage in the periphobeal capillary network, no leakage or staining of the rental vessels and the left eye was otherwise within all the limits as well. Had UVitis fall up two months later, her vision was normal. She still had some mild blurriness, but that was it. The remainder of her exam was really unchanged, including they repeat an OCT, a fundosodal fluorescence, a visual field. And then she did undergo a multifocal ERG, which was with normal limits in both eyes as well. She had had a couple follow-ups over the next six months, but they were normal, and then she subsequently lost a follow-up until, so five years later, so this last July, she showed up again in her ophthalmology clinic with complaints of five days blurry vision in her left eye as well as pain with eye movements. I've just kind of marked the, like I said, the notable findings here, so a decreased visual acuity in the left eye, she had a trace APD in the left eye, and then her color vision was also decreased in that same eye. Really the only notable thing on CELAM or dilated exam is she had some just irregularity with those pigmentary changes, which you can imagine as we looked at, were kind of the remaining findings from the macular star. She did have a fundus, excuse me, a Humphry visual field done again, a 30-2. And then her left eye, so there were quite a few fixation losses in our can see it, but five out of 15, but still obviously she has a new deficit here in the left eye. OCT was repeated and just showed evidence of those pigmentary changes from the macular star, the same ISOS disruption photoreceptor loss, and the left eye was pretty unchanged. She did have an MRI which showed enhancement to the left optic nerve, sorry, right here, that you can also see pretty well on coronal section right here, suggestive of an optic neuritis, and then her, sorry, I don't know what I'm doing here. And then on her brain, an MRI imaging, she also had a T2 flare white matter lesion right here concerning for multiple sclerosis. So she's diagnosed with optic neuritis, there was concern for multiple sclerosis. So she had, she received, she was admitted to the hospital and received IV cell medrawl for the three days and then was started on a prednisone taper. Symptoms had improved and completely resolved by the end of that steroid taper. And the only real update to her medical history in that time was she had, she had served an LDS mission, so she's living in central Mexico for 18 months, and then she, over that period of time, she gained about 15 pounds, but she still was, her BMI was within normal limits. She came back three months later, and her symptoms had resolved, vision was normal, she just had that small APD in the left eye still, but she had this stage two optic dyscadema in both eyes, even though her visual function was intact. So given this history of optic neuritis, neuro-redonitis, demyelinating lesions on MRI, and then now she has this bilateral painless dyscadema with preserved visual function, really the differential diagnosis, in fact, Dr. Warner had in the room and said, hey, what do you think? I had no idea, and it was just highly embarrassing, and so I looked it up and looked at all these MS mimickers, and really it's quite a broad differential, and I looked up several papers in preparation for this talk, which I'll go over later, and there is quite an extensive differential. But we also had to consider diagnoses that included more than one entity in her case, so thank you, Dr. Hickam. We ordered the lab workup show in there, and then she had already had an MRI C and T spine planned, a CTV to check for venous sinus thrombosis. Her LP did show elevation of opening pressure at 26, and then she also had oligoclonal bands, otherwise her CSF studies were normal. Oops, sorry. And then really her exam, at that point, had returned to normal. So final diagnosis, and just kind of cut into the chase so I can get into kind of what I hope is a learning point for my talk here, is that she had a diagnosis of multiple sclerosis based on the imaging findings and her symptoms, but then she also had symptoms suggestive idiopathic intracranial hypertension. But what about the neuroretinitis? So it was something that we just couldn't quite fit everything in a one nice neat box, but it fits a little better than maybe I thought quite at first. So looking back, there are several papers that have a nice review of a differential diagnosis for optic dyscadema with a macular star. And on each of them, so papillodema is one of the things that needs to be considered. So it is known that papillodema can cause a macular star, and particularly when it is papillodema, then they tend to be bilateral, and then there are obviously other signs and symptoms of increased intracranial pressure. Also it should be known that idiopathic is, it's the most common diagnosis of neuroretinitis or disc swelling with associated macular star. And then again, like I said, papillodema is always mentioned. But you do, of course, need to rule out other possible ideologies, especially infectious causes that need to be treated immediately. So while parsimony is nice, we do need to keep our differential broad. I just thought this is an interesting paper that DR had mentioned to me is we were discussing this case that back in 1987, there was this study done by a group where they followed about 50 patients, or rather they followed 10, and then there was a retrospective review of 40 patients that had developed neuroretinitis, and at some point had developed a macular star. And their hope was to say, well, if people do develop neuroretinitis, is this something we can look at to say they're very unlikely to develop MS in the future? And their findings based on these 50 patients that they either followed prospectively or retrospectively actually did. I mean, what they said is such a star, a macular star, and as present suggests papillitis of vascular cause and militates strongly against the subsequent development of multiple sclerosis. So this was something that had been published, it had been vetted, and presumably was of the thought process at that time. But since then there have been several studies. I just picked out a couple where they've done studies and followed people prospectively again that have developed multiple sclerosis and either looked back and seen if they've had a macular star or vice versa, followed people that have had macular star and followed them prospectively. There's actually quite high percentages of people to do. So just in this particular study that I pulled of three of 35 patients, so not a big cohort but a large percentage of this particular group that had a macular star but still went on to develop multiple sclerosis. So important to keep our minds open. As I mentioned, the differential diagnosis for mimics or chameleons of octonaritis is really bright or broad, but the important thing and something that I think, or at least I hope to continue learning it, especially neuro ophthalmology clinic is just the importance of taking a really good history because this is so broad but a lot of it can be narrowed down based off of that history. You get a clinical history where you can rule out several things and then don't have to throw every single lab test, every single imaging test at the patient and can save them a lot of headache and expense and time. But these are just a few that I pulled out that the list was actually much longer but it would have taken several slides of just copying. So I just pulled out a few that I thought were interesting. So I want to end there. So we have plenty of time for the last presentation but I think that the important thing to remember in all of medicine, certainly ophthalmology isn't excluded in this is that while we try and fit everything into a nice little parsimonious box as often as possible, that it doesn't always happen and that especially in, you know, I think that neuro ophthalmology, uveitis, some of these other very complex subspecialties, it's really important to remember this. And I really, I just like this quote that everything should be made as simple as possible but not simpler. So to try and make everything make sense but at the same time keeping your mind open to other possibilities that may include different diagnoses for one patient presenting with certain symptoms. I think that's it. Just as update, this patient has followed up with her neuro ophthalmology clinic since that time and the last visit she had has been just, she's been doing okay. Hasn't had any visual complaints. So she's doing well at this point but take any questions or are you happy to entertain any comments?