 Center is Ricky Chen. He's one of the senior residents in neurology and he's going on to fellowship in neuro-oncology. He's going to talk about papillodema. So thanks for having me here. I'm going to share with you a interesting case of papillodema that I saw in neuro-ophthalology when I rotated last month. So this guy was a young man from the Marines in Washington DC. He presented to us two weeks after having developed binocular dyplopia and he recently had been discharged from a military hospital in Washington back to Utah to recuperate from viral meningitis. But he was very nonchalant about it. Just said, you know, I had a lot of headache and that all got better and they gave me some symptomatic treatments and I was doing really well but then developed a dyplopia and he didn't really even come in until he leaked some ice pack fluid over his eye because he had some headache and eye pain and he was rubbing it too hard and so he ended up going to the ED for that and then eventually referred to ophthalmology outpatient who diagnosed cranial nerve four and six palsies and some dyskidema so it was referred to neuro ophthalmology at the time but really didn't have much other complaints. So we had to dig a little deeper and talking specifically more about his kind of presenting illness. He was healthy until March, really no medical problems and then in early March he went to a wedding in Hawaii. He did some deep snuba which is like snorkeling going down under and had some sushi and salad. Nothing really remarkable but actually important to the history. He then later, two weeks later developed otitis media presumed and was treated for it with antibiotics. Just basically had some earache and fevers that all went away completely. Until the end of March he redeveloped fevers. He started having headache and neck pain and no visual symptoms. He ended up presenting to Virginia Hospital Center in Washington D.C. where he spent three days. He had a CT head that was normal. He had a lumbar puncture which showed 270 whites, 85% monos and 12% eosinophils interestingly. They didn't really comment on this. The only test they did was EBV and HSV PCRs and those were negative. Otherwise they didn't do glucose or protein per the records that we found and culture was negative. He also had some peripheral eosinophilia, only 4%, mild leukocytosis and they checked influenza which was negative. They gave him a diagnosis of presumptive viral meningitis. Gave him some tramadol and Zofran centum on his way back to Utah to recuperate. He was getting better over a week until he developed this dyplopia which he described as both vertical and horizontal images. It was binocular and rotated relative to each other worst on lateral gaze. His vision was otherwise crisp and good color and depth perception. His headaches and eye pain overall, like I said, had improved. He no longer was having fevers and no other significant past history or medications. On examination we found that he was 20 on the right and 20-25 on the left. His pupils, aside from mild and isochoric which is slightly greater on the left, no RAPD was found, both briskly reactive. His visual fields were full. His extracular movements, motility was pretty abnormal. He had bilateral abducens, palsies worse on the left gaze. Then he had significant isotropy up to 30 diopters and also the left hypertropia of two diopters, mild right head tilt. The remainder of his exam and chocolate pressures, anterior and posterior chambers were normal. The remainder of no exam were normal, including reflexes, sensation, no weakness. His visual fields showed a large blind spot and some scattered kind of subtle deficits, but overall not too bad. On the fundoscopic exam, he had pretty severe papillodema, grade three to four, with cotton wool spots and micro hemorrhages. Then we were pretty concerned. This guy just recently had viral meningitis. They didn't really do a full workup. We sent off to repeat the LP expecting, could this be a worsening condition? His headaches weren't that severe. They weren't even really that positional, but he did end up having increased ICP. He also had increased white count of 500 with 61% eosinophils, which is markedly abnormal. His MRV, which we did to rule out venous clots, was normal. In the MR brain, I'll show you had some pretty significant findings. His flare showed these abnormal regions of hyperintensity near the perivascular spaces. These were nodular enhancing. You can see on the gadolinium, kind of multifocal spots, also included in a little bit in the midbrain, more subtle. Then he had optic nerve T2 signal, as well as some enhancement. There was no stroke or other hemorrhagic findings. He later underwent also a CT scan that showed some peripheral ground glass. The radiologist read it as possible aspergillus or some other fungal infection. This was pretty concerning. Obviously, he ended up spending more than a day in neurophthalmology. He ended up going to neurology for two weeks and with an ID consult. I won't bore you with all the details because this is a short talk. He had everything drawn. He had serial LPs. His pressures would range between 28 to 40s. His white count was between 2 to 400s with persistent eosinophilia, again up to 61%. This really persisted throughout his course, except the pressures would get better after a drain. Then the next day, he'd build up more headache again. Then his pressures would go up again and they drain it. This went on for a long time. ID really didn't recommend any treatment for this, but we had suspicions of what this could be. The differential also was cardiac vegetations, possible vasculitis. They did have other imaging modalities, CTA head and neck, ECHO, abdominal ultrasound were all normal, really on the vasculitis. Also, hepatic infection was ruled out and no evidence of vegetations. The CT chest, as I mentioned, and then finally, because we don't have the test to really do the confirmatory testing for this parasite, we ended up sending it to CDC. This is the actual culprit. It's the number on cause of eosinophilic meningoencephalitis in the world. It's anemotode, worm, actually was discovered in my hometown in Canton, province, China. In 1935, Chen found that this was a worm that was seen in the pulmonary arteries of rats. The first infection was diagnosed in 1945 in Taiwan. It's a worm that can usually live definitively in rat and then do fecal transmission and goes into mollusks and snails. There are a lot of places in the world, including my hometown, we eat snails and sometimes the undercooked snail meat is not such a delicacy. You can get transmission through that as well as through leafy greens that are contaminated by snails and then they can also go into other hosts and seafood. Basically, by human ingestion, you get into the pulmonary, you get into the portal system and then venously go into the pulmonary system and then through the left heart and to the rest of the body. Specifically, mainly only causes disease in the brain and then the majority of cases which are over a thousand now in the world since the 1930s, you get a eosinophilic gradylometis inflammation when the worm travels to the brain and lodges in the perivascular spaces and gets killed. Alternatively, a seprous syndrome develops in rare cases in the eye and that can be presented as eye pain and people have found worms in the eye. This was extracted from a 22-year-old Vietnamese woman, this 22-millimeter worm and they found cases of optic discidema, some prolonged visual evoked potentials and gave a diagnosis of optic neuritis to some people. But those are pretty rare and so the majority, you know, transmission is through these routes and so in our case, our patient had history of ingestion. He also had symptoms consistent with meningitis. So this would be one of the top differentials if you have eosinophilia in the periphery as well as in the CSF greater than 10%. So you met that criteria and then you usually confirm it by Eliza or PCR confirmation. The number one alternative if someone has a similar kind of story is neuronactostomiasis, which is another worm that can live in snails and seafood and then alternatively other causes the eosinophilic meningitis if the patient has risk factors, neurocystercosis, TB, toxo, crypto and others. But by far this particular disease is more common. And most cases actually resolve spontaneously. The severe cases could lead to coma and death but those are very occasional. Treatment can be with supportive measures like draining fluid to reduce ICP. Steroids appears beneficial in some studies. But there's really not that much studied about it. And in general infectious disease recommends avoiding albendazole and mobendazole because of potential for killing the worms and causing increased inflammation, which could worsen the condition. Surgical removal of the worms endoscopically is can prevent further vision loss, but unfortunately the recovery of vision is limited in most cases. This is more of the delicacies. Lots of vegetables out in the open and then some seafood and some street stalls. So our patient had a pretty good outcome. Diplopia improved with some diamox and prednisone. He was down to two doctors of esotropia down from 30 and his visual fields were fully normalized. His headaches pretty much resolved. He's been seeing several times now. It's been a month since he's been in the hospital. So take home points from this case is that it's really important when you have a case of papillodema to look for alternative causes and you might find something special in the CSF that's something to take home from this case and really digging deeper into the history. And as they say, beauty rests in the eye of the beholder or there could be parasites there as well. Any questions?