 All right, I'll introduce the next speaker. It's Don Raphael Nguyen. He is currently rotating through the Neuroophthalmology department right now. He went to medical school at the University of Iowa. He's currently a third year neurology resident, and he aspires to be a neuroophthalmologist. So without further ado, you guys all hear me OK? So I wanted to present a really interesting case that I was able to see both on the neurology service, on the inpatient neurology service, as well as the neuroophthalmology clinic. While I was doing my neuroophthalmology clinic rotation, I was often pulled out around 4 p.m. to go and be back up for the new junior residents and see patients in the emergency department with them and kind of guide and direct them. So this is a patient I got to see. OK, so our patient is a Mr. S. He's 74 years old. And he has a sudden onset of double vision. The timeline for this is at 6 a.m. He wakes up. He's doing fine, no problems. Goes to the bathroom, goes back to bed, lays down. He gets up at 7, and now the room is spinning around him. He feels nauseous and states that everything looks like a Picasso painting. So we asked him, what do you mean looks like a Picasso painting? And he says, well, there's seven. I think we had seven people in the room with several residents and medical students in the small emergency department room. And I just irritated him to have so many people in there. He saw 14 people. And the double image of some of the people was kind of working its way up here, while the other image was working its way down here. And just everything was kind of a jumble. So he just wanted to keep his eyes closed. So more specifically, regarding his depopia, it's there all the time since it started when he woke up at 7. And the images were separated horizontally initially, but later they were separated more obliquely. And it was worse whenever he tried to look to the right. But he wasn't certain if it was worse looking at things in a distance or things up close. And then it was binocular. It resolved when he covered one eye. He preferred to cover his left eye. And there was no pain with eye movement. Although when we were examining him, he started to get a headache at that time. And so there was some confusion as to whether or not he did have some eye pain. But we just more careful questioning and resolved that there was no actual eye pain. Just a mild headache he was getting. So really briefly with his past medical history, he has a history of hypothyroidism. He's had some migraines in his 20s and 30s, but hasn't really experienced anything since. And he doesn't really have any neurologic history or any really profound medical history that we know of. He actually hasn't been to the doctor in a long time. The last position he saw was, I think, a week or two before this, he saw Dr. Katz for a subliminal type of hemorrhage. But besides that, he hadn't been to see anyone. We get a little bit more into his history. And of note, in his late teens, he says he was a trouble child. He was in a gang in LA. And his parents were really worried about him, thought that he might have these behavioral problems because of an underlying endocrine at hypothyroidism. And they did a thyroidectomy. In his mind, this was an unnecessary procedure, kind of like people in the 60s lobotomizing their kids is what he compared it to. And he didn't think it was necessary. And he didn't really think he had a problem with that. And then a year ago, a year before he presented to us, he started taking synthroid when he found that he had hypothyroidism. And then interesting, he was in gangs in LA. And he made his way to become a professor of art history and architecture, hence the Picasso comparison and a lot of other comparisons. And just kind of a side note, he loved the neurooptimology clinic and kept commenting on Leonardo da Vinci when he saw the prisons and culture and lenses. He just thought it was the most amazing clinic. He loved it. And then he didn't really have much more of note with his family history and social history. So neurology is consulted. We go down and we see him. And the main thing on physical exam is he looks like he has this left-sided optosis. On his neuro exam, we notice that he has some left eye closure weakness compared to the right side. It's kind of subtle, but it's there. And other than the cranial nerve exam, which I'll get to, the rest of his neurologic exam was really unremarkable. So as I mentioned, he has that did. And he has subconjunctival hemorrhage in that eye as well, which I think. And then his acuity would be better on that left side. But it's otherwise not too bad, as visual field goes back. The main thing is with his eye movement. So he has this decreased adduction on the left eye. And he has this rotary nystagmus in both eyes in all directions, but it's worse when he tries to look to the right. And it appeared to us that he could not overcome the adduction problem with convergence. And so I'll come back to this later. This is really important. We tried one time, said, look at my finger. OK, follow it with your eye. OK, no, he's not converging in. We were done. And we didn't test it more thoroughly than that. This is a person who had some left hypertrophy and exotropy. I don't know if he saw where the finger was when we tried to test it. So I got this off of Will's Eye Resonant case series online. And this case was really neat to me because it was very similar to our patient in his appearance and also in his MRI findings. And you can see with, let's see if I can get this to work, you can see with this gentleman right here, he has this on this left eye. He has some hypertrophy, exotropy. It's kind of going up in this direction right here. And then he can also see over here that he doesn't have any adduction when he's looking over to the right. So this is almost exactly how our patient presented to us, which was a very bizarre presentation to us. And then in addition to that, just kind of imagine right here that he has a little bit of a proptosis. So we recommend getting an MRI brain. And his brainstem looks clean. I don't have that image here, but we do find these little punctate foci of diffusion restriction. And I don't have that image here either, but we did find it in kind of the end of the cortex, kind of pointing to maybe some kind of embolic shower. And on both sides, so in multiple vascular territories. So then with eyes that strange, we're going to send them to neuroophthalmology clinic next day, for sure. And if we're going to send them to neuroophthalmology clinic, we better give them some imaging that they'd like to work with. So we order an MR of the orbits, and we get this to work. It's read as a normal MRI of the orbits. And so we think, OK, it doesn't look normal. So we go down and talk to him with more detail, and we get one of the neuro-radiology attendings to look at it with us, and we get ourselves an addendum. And so he has that proptosis on the left. It's a little mild, though. And then he has this, and I don't know if this is going to come out too well on this, but he has this diffuse fatty infiltration of his extraocular muscles here. It's in every extraocular muscle that we image, as we scroll up and down. And their overall impression is this could be maybe from a chronic thyroid issue. So we admit him to our service on the inpatient side, and we start doing our work up here. So we do some labs here. And really the only things that come up, he's positive are cannabinoids, and his thyroid proxidase antibodies are elevated. But everything else, inflammatory markers, infectious markers, et cetera, are kind of coming up negative. We do a lumbar puncture. And his cell count is unremarkable. And I'd just like to point out that I did this lumbar puncture. No? No? And then his protein is unremarkable, infectious work up, opening pressure, really nothing to write home about. So then we come to this question, and we're really perplexed about this. And so is this a central process? Is this a peripheral process? Are both co-occurring? That seems highly unlikely. But he is the rotary nystagmus. That's got to be central. He has all these recent embolic-like strokes. So maybe there's a stroke that we're just not seeing? Why didn't it show up on MRI? And then peripheral, so he can't overcome the adduction on our exam. And so, OK, it's probably not an I&O. It's something else. And he has that proptosis. And he appears to have this multiple cranial nerve involvement with the eye closure weakness, with the eye being exotropic and hypertropic. And so we're not really sure what's going on there. It doesn't appear to be any obvious mass on the MR orbits. But is there some autoimmune issue going on? Do we need to start steroids on this guy ASAP? Because in the time he's been in the emergency department, it seems like he's gone from this horizontal diplopia to oblique. And from the initial ED resident who saw him to us, it seems like his eyes have gotten a little worse. So we sent him to our neuro-ophthalmology clinic next day. And he was surprised to see me there. But I didn't examine him alone. So we saw him. And his visual fields are normal. The slit lamp exam is within normal range. He has a few findings there with the injection in that left eye. His optic nerves look completely normal. He has a very slight exothalamus, just 19 to 17. And then he has his conjugate rotary and upbeat misdiagnose. And he has the hypertropia, the exotropia, as we noted. And he has an INO. And so he was able to AD duct with convergence. We just had to coach him. And we had to really get him to focus on the finger so he knew what he was supposed to do. And so once we got that, things kind of fell a little bit more into place. So our impression that we write up and give back to the neurology team is there's a left INO with a skew deviation. And it's probably because of something in the pontometallary junction, like the MLF. And the thyroid disease is kind of a red herring. There is no acute peripheral issue causing proptosis and the findings on the extraocular muscles in the MRI of the orbits. That's simply his old thyroid disease. He really did have some severe thyroid disease that he got his thyroidectomy for. And a recommendation, get another MRI. So we got some repeat- If you know what you're looking for, you often can get a MRI. And so we got a repeat MRI and there it is. And it's exactly where it was predicted by the neuro-ophthalmology team. This punctate focus, the restricted diffusion. And it's just right there in the MLF. This makes sense. It can cause the INO and by disrupting the utricular pathway up to the midbrain, it's also causing a skew deviation. So I looked in this a little bit more. I'd always heard that MRIs of the posterior fossa can sometimes miss a stroke. And so I wanted to look at this literature a little bit more, because I never actually had a case where this happened. And I found this study done in 2000. They had about 140 patients. They did MRs within 24 hours and then they did it within 48 hours after that. They had a large number of people. They found about 3% of the anterior circulation strokes had negative DWIs in the first 24 hours. And then they found 31%, 10 times that in the posterior circulation, posterior fossa, like our patient, had negative DWIs in those first 24 hours. But this is really interesting, is that they should show up after 24 hours, according to the study, every single one did show up. So lessons learned. This was, these were some great lessons for me to learn. One is that if one exam finding is kind of screwing up your whole diagnosis, then repeat it, really make sure it is, be sure of it. And so we had him track our finger really quick. He did an AD duct, okay, no I and no, moving on. And we should have said, no, no, no, wait a minute, let's try that again. And had several people try it, if needed. Two, and this is something that came in, that was really handy with a recent case I had on pediatric neurology, where if you think you have two diagnoses that kind of coexist and they seem like they, if it's like a lesion site, they're separated by a great deal of space or they're just completely different parts of the body and you think that they're happening at the same time. Well, one might be chronic, one might be acute, or you might be just wrong about one of them. And so I had a similar case where I was able to apply this principle recently on pediatric neurology, where we had a six year old kid who had a seizure, came in and we, from an outside hospital and when I examined him, he seemed to have this downbeatness stagmus and ataxia in his right arm and I thought, oh, great, so I think I can localize this. He's got something that's cerebellum and it's affecting his cervical medullary junction and that's why he has the downbeatness stagmus. Then as I examined him further, I found he had a right hemifield defect. And so as I sat down and thought about it, I thought, okay, so I've got something here and I've got something here. What are the odds they both happened at the same time? You remember what happened that last case? Think, think, which one doesn't make sense? Went back and reexamined him. This wasn't ataxia, this was weakness. So you had weakness here, right side of visual defect, that kind of pointed to here. So why has he got downbeatness stagmus? Think, think. Oh, that's right. What did they give him at the outside hospital? Phosphonitone. And that explained his downbeatness stagmus, which resolved, the other symptoms did not and the MRI confirmed his lesion. And then the final note was just imaging, even MRI is not perfect and it's good to know it's limitations. It's helpful for me to do a little literature research and see that kind of the numbers there of 3% to 20% or to 30% in the first 24 hours. Thank you very much. Any questions?