 So this is actually based on what Brian Stagg saw originally, and I might point out, immediately diagnosed something. This is the first person diagnosed this week, and then I followed up with him over at the shovel. So it was an eight-year-old boy who, I'll kind of give you his, sort of, HPI. He originally had double, he was cheeky with double vision and diabetic cheekbones. His history on the 16th of December, he had some fever and vomiting. He went to see a primary care doctor a few days later and said, In some people just the medicine. Two days later, what mattress used to be, was he'd woken up with bilateral dilated eyes and had a bunch of hives. So he started fentanyl to try to help with the hives, which did help with the hives. The next day started to have copia, and so went into the ER with the copia, as well as bilateral dilated eyes. The ER saw him and he told him that he thought of most likely an emergency reaction, stopping all of his medications. On the 26th, nothing had improved by that point. So while he was driving back in, still with bilateral dilated eyes, still with bilateral dilated vision, and then also having some non-IPI movements. And he had some vomiting after talking, and was also having a little bit of unsteadyness on his feet. He passed up on history, he was carrying all the pins, met all of his early milestones, he was up to millions of vaccinations, and never had critical surgery, no ocular history. He had a sister who was through business, his mother, and he looked at the health of his mom and her three siblings. And all of his siblings were also sick. He was similar on the rest of the story. Symptoms with the exception of the island of people. Medications, he was at the time of being a senior in the ER. By us, he was on Benadol. I bring about four to six hours to the past four days. He was learned to orientate, his vision was 20-30. He had a bilateral dilated view of most eight millimeters. He had a non-IPI life, he was there on the combination. I had full complication of fields, and then limitation of his extra hand movements. Most notably, he looked most profoundly in AB induction, because his right eye, AB induction, and his left eye, and then also with the most preservation. So this is pictures taken from a video, so they don't totally track how far you're actually about, but it gives you sort of a good idea. His right eye, you can see, has very limited to AB induction, but his AB induction was very good. He was able to do that kind of thing. And then similar over here again, he did very well with his left eye, and then the rest of his ocular exam was probably remarkable. So he had a normal period over chamber. Obviously his iris was dilated. His neurologic exam, this was mostly actually, this was partially done by us, but then also rechecked by the neurologist, and he also saw the patient. He had no anti-absorption. He had normal strain, normal sensation. They thought that his coordination was appropriate for his age, but he didn't have a problem, where he was sort of falling back into an unassessed place. And with this nice place as well. Would you like me to do it? No. I don't know if anyone has some people. No, no, I agree. I think a different don't be a great thing. Do any of you have any suggestions? So work up the things that this patient had done in normal, this very laboratory work, this laboratory work of this patient, including fibroids, ESR, CRP, he had a perinatal plastic pain, and I was sent off with his new year anti-GT-1B, which we'll talk about later. He had a CT that showed maxillary sinus disease, but no cabinet sinus problems or intracranial issues. He had a little barculture to sort of look at infectious ideologies, which was negative for all PCRs, or EBV, HSD, ECV, and normal ACE, and all kind of things in that present. And then besides the perinatal sinus disease, he was ill. His hospital course, so, and then we would see, initially, the 1926, on the 28th, he ended up in Toronto, sort of, California. Pedrology was concerned that he would have this worsening instability, and he seemed to be interested in his new classification, and he was discharged on the 31st. He had slight improvement. His balance was so persistent. And his, sort of, running diagnosis at that point was that he was probably a minority of the CRISPR-type syndrome that we discussed earlier, which is if you want to hear it. A follow-up, he's a follow-up of Dr. Fnard, and basically a month after his on-site is we're going to do the same thing, but we still have to dial on, and we want to dial in people so I know that a lot of information. His motility exam had improved. His anti-GTOB had probably come back positive to the napkin failure and so on and so forth. And then, interestingly, one of the things that Dr. Fnard has read up about and he thinks it best enough was a lot of times his patient lost his sense of community primal heartbeat. So you can see, he's still fairly dilating with white, linear reactions, but very profound reactions have been done in five or ten minutes. This was taken in three minutes at a substantial change in his treatment. His pupils were bothering him because he was positive and like-sensitive to these other things. He talked about this, you know, he was having a lot of issues. That's the type of thing. I have a follow-up again. After that, he still had somewhat persistent by the pupils that were beginning to react slightly. And the equipment and his extra-output movements would continue the limitation of the reduction of vaccination of all other extra-outputs. And at this point, subjectively, there's double vision of most of these are all probably the sort of training of something like this. So the clinical questions that sort of came up for me was, hey, what is this? And these were also questions that parents would have more about. There was double vision about the pupils and crew, how long will it have in each of those settings and what is happening here. So sort of looking at things, no official syndrome. So it's a variant of the young beret. It's sort of classically associated with these three planes, a taxia, an angus, a caesia, an external ophthalmophilia. You can kind of see the sort of these ones. A taxia and external ophthalmophilia typically come around about the same time. So, and they sort of recover around the same time. So typically, you'll have recovery within a six month period, often within the first three to four months. A-reflexion is sort of the longest to stick around and sometimes maybe actually in your system where there's no end. Just sort of a quick overview of the time course. In most cases, patients have a preceding URI most critical, looking at all those sort of different case studies in series in order to pay 56% and 76% of patients usually do. They have the classic triad approximately a week after they have their preceding URI and then neurologic symptoms sort of begin to recover about two weeks to recover. These are kind of the three big case studies that I found that were out there. So, Edo's most recent one that has the most numbers on it. As you can see, again, the important thing is all three of these sort of have the classic p-taxia in reflexion and external inclusion and these are just sort of associated things. Of note, you can see that N-C-U-R-I is present about the course of the patients yesterday. I mean, a lot of them actually will have some of the choices associated with it and the charges that's the same. And then internal off-familifusion, which our patients did have, can actually be seen during the course. And then a lot of times there is some other sort of systemic involved on the administration. In terms of looking at internal off-familifusion which our patients had, there are a number of case reports in series with this. And there's been demonstration of paddle-parking super sensitive as soon as three months or three days close to the development of the battery people. The important things for sort of differentiate between the 80s that are associated with tendon tissue and results also should have a lack of anisoporamic and usually in alignment with the diagnostic work of the big thing is the anti- тамata and gq1b andabombie which is a synone which is a long cicada. There are some people on some centers who are sort of tasked for free scope in-democrat that happen in associated And then in a range of percent, I think on the study of that, some people will have an element of protein that they shouldn't be able to have. And they usually won't have any. They shouldn't have any. With regards to treatment, the biggest thing that I took away from it, you know, almost universally, this is a process that people will recover on their own within three to six months period. There's some literature, because this is a variant of young beret and there's been a lot of randomized home studies demonstrating efficacy of IVMG in the young beret, there has been a number of people who have tried to develop fissures in there. Sort of the difference between the fact is that there's no fissure universally available to cover. And so, there's a lot of people who are going to be able to deal with that exposing the irritation of IVMG across the process. Though, there's been a few sort of anecdotal case reports that patients have in quicker treatment than adults. With regards to prognosis, there's been a lot of looking at different risk factors in associations that have never really found anything that hasn't affected the problem. And most patients have little or no just nearly six months. Recurrence was another issue that the mom was asking about. So, there's one study that looked at recurrence in adults. About 28 patients that have had 70% of the episodes. So, most of them have one recurrence, so there's three people who have more and more common recurrences. And again, similarly, usually these were associated with a similar rate against infection, and usually a similar pattern of recovery. And then there was only two case reports of recurrence in children. Sort of a similar age range. They had a pre-seeming to develop on this bulk of them. And actually, both of these were treated with IVMG in a certain way, and they actually had full steroid therapy in one of the very good response to the bulk of them. There's a pathogenesis. So, it's thought to be that this could be related to sort of molecular mimicry, which Brian kind of talked about in the last three months. But this, these angrier sides of leko-spindle lipids are looking on the positive side. And it seems to be sort of universally found more prominently in the premium areas that supply the angrier lipids. Some of these do not have pure musculoskeletal junction, and some of them have sensory malice as well. And some of them are saccharides that are associated with some of these particular infections seem to have a great deal of benefit in this group. And so there seems to be a cross-reaction between these two. There have been tighter studies that have shown, with clinical presentation in high illness, as the clinical presentation improves the time, you can see these same antibodies in the embryo, that's a lot of screening, up to 95% of the lower-fisher-fisher-stool habit. Acute ophthalmoplasia was actually sort of another thing that was on the differential here, which is basically Miller Fisher without the axiom in the plexiom, which neurology thought he had some borderline axioms in the Fischer Center. There's unknown prevalence of it. So my sort of conclusion is that these antibodies can cause sort of a spectrum of syndromes, but in particular, you have a patient that has a combination of taxiophthalmoplasia and a plexiome, which is considered a differential for both kids and adults. It's typically self-resolving. So to finish our triple-threatener ophthalmology, this is a patient that presented to Dr. Cassie's general ophthalmology clinic. And I saw the current general ophthalmology study. He went over the history of blurred vision, eye strain, and kind of vision. So he did a question. He had recently gone through some treatment, but he learned that this might have caused some cataracts. He had a history of monobusin lacyl in 2002. Some of those dry eyes. And it was previously been healthy. I haven't dealt with diagnosis of small cell lung cancer. Cassie's sister-in-law had a brain, and there's a small, non-satellite region that's been cell-developed. He had been treated with chemotherapy and radiation, as I mentioned, and had also been treated for the past year with this medication called Cifliluminae. Only a year ago. He came in with visual lacyl, a little bit of cataract that it was. He's got a scopic exam, showed some bilateral viscidemia. Got some photos here that you can see. The Cifliluminae viscidemia is fairly symmetric. There's considerable field testing shown that was done with that. What differential at this point in cancer patients with metastatic disease to... So based on, I mean, a brief look at what you've spread to... It's not too commonly... It usually presented more general ICMS and reported that only 7% had a diagnosed congenitalitis. It's a little bit difficult because it's hard to detect very early on. Perhaps a better way to pressure the psychology is something important to look at. So, cytology only populated 76% on initial cytology, directly related to tumor. CSF will be adverse infectious and I think it's secondary to that. I used to show it a lot of the trial. There are sequence and you can see that there is something. So, we thought it was most likely drug use.