 So, our next presenter is Reese Feist. He will be talking about Diplopia in the Child. So that was a lot of corny, and I'm sure everybody's kind of bored now, so we'll go to neuro-ophthalmology and everybody will come back up. So this was a case that I saw back when I was on Pete's service. So it's called the ER to evaluate a seven-year-old boy with a complainant double vision. So about 10 days prior to his presentation, he developed mild fever, bilateral leg pain. They didn't really do anything at that point. On the 17th, so like four days later, his mom noticed that his right eye was kind of wandering inwards, mainly at bedtime, and then around that time he started developing symptomatic double vision when he was watching TV. On the 23rd, he started having difficulty kind of walking around, going into walls, and that prompted a visit to the ED. He's got a past medical history of gross and fine motor developmental delay, speech delay, essential tremor, memory issues, ADHD, and then obstructive sleep apnea, which has apparently resolved on his last sleep study. He's had tonsillectomy, adenoinectomy, no past ocular history. He had two siblings with amblyopia and then an ant with some type of congenital blindness, and then he takes Intuna for his ADHD. So when I saw him down in the ED that day, his vision was 20, 20 in year in both eyes. He wasn't able to get a pressure on him, but his visual field were fully confrontation. He had minus one in ABduction in the right eye, and I felt like also, I didn't put this in here, but maybe minus a half in ABduction in the left eye as well. He didn't have any apherapupillary defect, no anisocorrhea. He had full color plates and red desaturation. For his balance, I didn't take my prisms down to the ER, but it felt like he was about roughly 30 diopters of rightisotropia. The remainder of his eye exam was totally normal. He had normal anterior segment, normal posterior segment, so he kind of pertinent things with the ABduction deficits. No evidence of disc swelling. His margins were totally crisp. Given his neurologic history that he was already a patient of neurology, they also came down to evaluate the kid. They called him a cranial nerve six palsy, felt like the remainder of his cranial nerves were intact. He was noted to have full strength throughout, and then good reflexes, normal sensation of attack, a normal tone, no tremor or rest. So while he was still in the ED, they got a CBC, which was essentially normal, just a little bit of lymphocytosis, slightly high use centiphalos, but his CMP was normal and his TSH was normal. I just like to get ACE more than even the uveitis people, and that was also normal. Really the only thing, he had kind of a slightly elevated ANA titer. They weren't able to get the lumbar puncture initially, but the next day, they had a normal opening pressure under one white cell, normal protein. It was a slightly traumatic attack, so a few red cells. He wasn't able to tolerate sedation on the initial day of the emergency visit, so all they could do was a quick CT brain, which was right as normal. The next day, they were able to get an MRI, but it was slightly motion degraded, and so the neuro radiology hedge was solving the radius, maybe under appreciated, but no real evidence of anything on the MRI, so it was essentially normal as well. So he got admitted, and then somehow I didn't see him again during the course of the hospitalization, but at some point he was also given a diagnosis of a cranial nerve for palsy, which I'm not sure where that came from. I didn't see any evidence of that on my initial exam, but they started him on an oral prednisome taper for kind of a presumed, like, post-viral cranial neuropathy. He was discharged home two days later and then had followed with the neuro-ophthalmology on the 26th. So this was, you know, slightly reassuring the top part, at least. His service was examined, which was kind of roughly what I saw down in the ER. So about 30 diopters of righties of tropium primary gaze. Dr. Warner felt like his exams were consistent with bilateral cranial nerve six palsies, but really the only difference here, his vision was still excellent, normal color vision, all that stuff, but when she checked his reflexes, he was found to be hypoereflexic, kind of in his lower extremities, which was a change from his actual neurology admission. So anybody kind of have an idea for the next step of what you'd like to do? Who's on is? You can pick on people. Nico, you're on neuro-ophthalmology now, so. So you got a lumbar puncture, you got some basic labs and an ACE. You got a slightly elevated ANA. Anything you're going to do? I do. Besides some of the Dr. Warner, so. I'm certain for the hypoereflexia. So maybe EMD studies at this point is maybe one thing to look at. Yeah, I think that's a great idea. So what she actually ended up doing was kind of along that same vein of thinking. So you're thinking of something kind of in that Guillain-Barré spectrum. So she actually ordered any ganglia cytina bodies, and then these came back positive. And I'm not sure who this was scanned into this chart, but I can imagine her writing this. But so Guillain-Barré syndrome is an inflammatory polyneuropathy characterized by acute onset, rapid progression, symmetric muscle weakness. So the overall majority of the cases occur one to two weeks after some type of respiratory or GI infection. There's a ton of different subsets of this syndrome. So most cases in North American Europe are acute inflammatory demyelinating polyridiculine neuropathy, AIDP. And then there's more axonal forms. These are kind of distinguished on paper, but can be really difficult to distinguish clinically. In terms of the symptoms that patients have, the electrodiagnostic testing can be less than helpful sometimes. But on pathology, they say the AIDP is characterized by inflammation of the destruction of the myelin sheath over the nerves. And then AMAN is more actual direct damage to the neuron's cell membrane. So this was a table from one of the papers just kind of talking about some of these other subsets. So in addition to these three main ones, there's some other even more rare forms. So Miller-Fishers is one that we're aware of. Acute panisababnomias kind of affects the sympathetic and parasympathetic nerves. Acute sensory attacks of neuropathy and then pharyngeal cervical brachial weakness. And then there's just a whole spectrum of you can even get kind of a brain semencephalopathy that often coexists with kind of encephalopathy features often coexists with some of these other ones. So the clinical features, I'm not going to go through all of these, but we're all familiar with it. So it's kind of typically thought of as an ascending paralysis. The characteristic thing on lumbar puncture is a cytobium and a logical dissociation. So you get a normal cell count, but you have high protein on the CSF. Nerve conduction studies are typically become abnormal after two weeks. You can do MRI, which can show some enhancement of the nerve roots. And then about 50% of patients with just classic Guillain-Barré syndrome can have positive mania ganglisside antibodies. So Miller-Fisher variants, the one that we kind of encounter more here, is characterized by the tritophthalmoparesis, a taxi and a reflexia. You can have just pupillary abnormalities. So anisechloria, slight reactivity, light-mere dissociation, which can indicate an internal ophthalmoparesis. This is classically associated with ADGQ-1B antibody, and it's reported to be present about 80% to 90% of patients with Miller-Fisher variant over a period of weeks. In the first week of study, after presenting with symptoms, about 48% of the patients had positive antibodies, but no CSF. And so this still has a super high sensitivity for the antibody test, but it does become positive towards the end of the disease. So by about three weeks, most of the patients had positive GQ-1B antibodies. There is, like we saw in that sheet a while back that this is the answer on, there's a lot of different ganglisside antibodies that they test for and kind of classically associated with different subtypes of Guillain-Barré. And so this is just a table showing those. So just to finish up quickly, the patient course, so one month he was seen back, he had no change in his trabismus exam. He was still about 30 diapas of esotropia. He was alternately patching and then followed up in the pediatric neurology clinic, and they were weeding him off his steroids. He's coming back, I think, towards the end of this month, and we'll follow up with Dr. Warner again. And then, you know, important to note that for most of these patients, they typically experience a full recovery over a course of months. So hopefully he'll get back to his baseline, but he was pretty esotropic when I saw him. So that was kind of short, but Dr. Warner always skips my neuro-ophthalmology grain rounds, but this is my second neuro-ophthalmology grain rounds. Because she knows you're so good. So any questions on that? Actually, one thing I forgot to mention too that I think I just skipped over, I found this pretty interesting was on the, and actually I don't know where that went. In one study of about 100 patients with just isolated cranial nerve six palsy, so excluding tumors, excluding a high ICP, excluding diabetes, they found 25% of the patients had any GQ1B positivity when they tested them. So 25% of patients might kind of fall into this category, because any ganglia site antibodies aren't particularly associated with just normal people. It's kind of a pathologic association. So it's kind of something that made me wonder, you know, how many of these things have I missed just with a lot of just the, we call it just a normal six nerve palsy, but, Dr. Olson. So a fascinating case and a couple of things are important is that a lot of us have just thought of classical Guillain-Bret, these super sick people and ventilators, and then we've got all these variants, and some of them can be pretty subtle. And so all of us need to be aware, just like you said, I mean the thought that a lot of these odds are sick, so we get better on it, so we get better, a lot of these could indeed be a variant. The second one is, is that due to Zika virus, you know, we're going to see a lot more Guillain-Bret. Guillain-Bret is getting to be quite common down in Brazil in areas where there's a heavy endemic disease. I mean, this is one of the responses that adults have that have a much higher frequency. So we've got all of you a bit more sensitive to the fact that this is what we're dealing with, and that it is immensely more common. You know, the biggest mistake neurology did is they should have taken this to neuropomology, right from the start, so I think our team probably would have picked it up. I'm glad to hear that even the muscle weakness tends to get better. I mean with Guillain-Bret, you just didn't follow it. Do they ever need to have muscle surgery? I mean, essentially at this point, the feeling is, is it almost 100% given time we're going to recover? Some, like anything else, some don't. I think that you have to follow them long enough, and that will vary depending on whether they are in the amyloid jet range or not. You got a young child, we don't wait a year, an adult we wait a long time, and Leonardo is talking, you can also temper us with Fresnel prisms on glasses or something to try to reestablish binocularity, decrease risk of amylobia, loss of binocularity in a child. This child at age seven is right on that customer. You may or may not have issues, so that I wouldn't hesitate if it is just staying the same and not getting better over, you know, three or four months to go ahead and do some eye muscle surgery, get the eye straight. But you're right, most of them get better, and that is a great case. I think the consult king, I think he said records for a number of consults done, certainly times spent doing consults, was just agonized over consults. It was a wonderful job, and this was another one of those cases. It was a lot of hard work and much appreciated. Thank you. Great case, thank you.