OK. Welcome, everyone. I want to get us started with a medical grand rounds, which today it's doubling as a clinical pathology conference. So welcome to our applicants to the residency program here, today. So to everyone else, they've already been warned, this is a little bit like a dance move that's one beat off for us, since we're not normally interviewing on a Friday. 

But the fun of that, is that we get to have this next 45 minutes of education time together, in which, everyone in the department will get to enjoy one of the things that we enjoy most throughout the season-- right now, I'm just kind of upping the ante, on Dr. Bell here-- and that's clinical pathology conference. 

So CPC, one of our case based teaching conferences, where a chief resident is selecting an unknown case and is presenting it to our faculty, who are taking us through their analysis and reasoning of the case, teaching us along the way. I think they're fairly, heavily invested in getting the right answer. But as with the case records in the New England Journal-- which this is a similar exercise to-- really the fun is seeing a case that was cared for here at UVA by our house staff, and our faculty, and our students. And learning from the process of how we think as physicians and how we solve problems. So that's the rules of the game. And I'll have Dr. Sumner Abraham come up and introduce our faculty discussing. 

Thank you. Again, to our applicants, welcome. We're really glad you're here hopefully, you all get to enjoy some time in Charlottesville this weekend. It really is a privilege for me to get to introduce Dr. Tyson Bell. He is beloved by our department, and the house staff. And was the 2018 inpatient attendee of the year. And really is an excellent teacher in all the different realms that he interacts with the house staff. 

He got a BA from UVA, went on to get as MD from Columbia. Did his residency and chief residency at Massachusetts General Hospital. Got his ID fellowship at the combined Mass General and Brigham Women's Program, and at a critical care fellowship. And as if he's not busy enough, being an ID and critical care attending. He's also in the midst of getting his executive MBA at UVA Darden School of Business. 

So with that introduction, I'll go ahead and present the case for us. Says there's a 39-year-old Hispanic male who presented to his PCP for some prolonged visual impairment. Two to three months ago, he notice some gradual onset of blurry vision in his right eye. And pretty quickly after this, this also started to affect his left visual field, as well. 

He complained kind of in his right eye, more of a complete loss of central vision. And in his left eye, more of a peripheral vision loss. And also, had a severe headache that was associated with this. He said that it originated in his upper back and radiated up into his neck, and was predominantly left sided in nature. 

When he was-- when more history was obtained, it seemed like this was going on for quite some time. 15 years is, kind of, when he said that it started, in terms of his headaches. But just, most recently, with the visual impairment. He did quit smoking and drinking five years ago, thinking that this was triggering his headaches. But noted that his headaches actually got worse at that time and started to have more of a vibrating sensation. 

He takes four Tylenol, ibuprofen and Excedrin. This used to help, but no longer. Downward gaze exacerbates his headache, and lateral gaze exacerbates his blurry vision. On review of systems, he had nausea, especially, when he was working outside with sunlight. He and his wife both noted some intermittent confusion. 

He had some chronic constipation, cold intolerance, a 50 pound weight gain over about the last 30 months. Some dizziness, some tinnitus. And he had some numbness and tingling on his left side, which we'll talk about in a minute. He denied any changes in libido, or erectile dysfunction, breast pain, urinary frequency, change in his appetite, or vomiting, or diarrhea. 

For his past medical history, the stroke that he had in 2017 was difficult to really tease out what was going on. He said that it resolved after he gave himself neurobion injections and had some chronic neck and back pain. No surgeries. He wasn't on any meds at the time that he presented. 

He was born in Guatemala, married with three children. Doesn't have any high risk behaviors. His cessation of alcohol and tobacco use was around the time of he became the Seventh Day Adventist. And he reported that he had been to El Salvador around a year ago, sounds like closer to 13 months than 12. 

His initial physical exam, his vital signs were normal. Generally speaking, his exam was unrevealing until we get to his neurologic exam. He was alert and oriented, there was no issues with his language, or his gates. And his strength exam was normal. 

But his cranial nerve exam was the most interesting. He had a temporal hemianopsia of his left eye. And decreased central vision of his right eye. He had decreased sensation all along his left fifth cranial nerve, that he reported was chronic. And then, also a change in sensation along his whole entire left, upper and lower extremity. Again, that he said was chronic. 

He did not have leukocytosis, and no anemia. His metabolic panel was unreavealing. He had a slight elevation in his aminotransferases. He had a UA and EKG that was unrevealing. And then, it had a whole host of endocrine studies that were [INAUDIBLE]. He had slightly low sex hormone binding globulin, with an associated slightly low total testosterone. But his free testosterone was normal. And all the other lab abnormalities that were checked were within a normal limit. 

Given consultation of his physical exam signs, a CTA head and MRI were both ordered. Briefly from his CTA head, he did have a complex, solid and cystic supercellar mass that was contacting his bilateral A1 anterior cerebral arteries. An MRI characterized it a bit more. A 2 by 2 by 2 solid and cystic complex supercellar mass with market distortion of the optic pathway. And we have a couple of slices that are representative of these findings. The first is the T2 weighted coronal view. 

This is a T2 weighted axial, and T1 images as well. So at this time he, was admitted to the hospital, and a neurosurgery was performed. And the pathology, ultimately, did reveal his diagnosis. So with that, I'll turn it over to Dr. Tyson Bell to walk us through the case. 

Hi, guys. So here we go. The thanks you get. Third year in a row I've done this now. I started a few months after I first started, literally, my first CPC. My white coat wasn't even ready yet. I picked it out that day. I decided to wear it for a little protection. But now, third time, and you start to think, maybe, it'll be a little bit more fair. 

But then, you get a bunch of endocrine labs. Just like this is going to be great. All right. So these are always fun when you learn a little bit of something about the presenters. So I need to disclose something about myself, which I don't know if the Chief knew this or not. But I almost became an endocrinologist. When I applied to residency, I was mentored by a bunch of endocrine people. And I really loved it. But then, during the course of medicine training, discovered I did not like diabetes. 

But this wasn't until, like I had actually started applying to induction programs. So this is what I did. I had actually missed the deadline for the ID program at Mass General and Brigham. I asked them if I could apply anyway, they said yes. I interviewed, and then, I ranked them first. And then, because I didn't want to delay any of my training, I ranked endocrine programs after that. 

Now, don't get me wrong, it seemed like a bad idea at the time. But this is what residency will do to you, it'll twist your mind and twist your logic. And I did not want to spend any extra time getting to where I wanted to go. So, then, of course, what do I do? I do another fellowship after I finish ID. 

So, anyway, I used to know some random endocrine stuff for that reason. But it's all gone now. Let's pretend for a second that this is what had happened. So the ID critical care, that was kind of a stretch when I got a job here. But imagine the endo intents of this. I imagine my slogans would be something like, airways and ACTH. Take tales of paired thyroids, traits and TCH. But this is what I was reduced to, people. Digging through step one. An updated version, which I had to ask for. 

So here we go. I always establish some baseline rules for a CPC. And I realize and embrace what a CPC actually is. And we're going to get exactly to that. Lay out your clinical reasoning, but you also want to make sure you put your number one diagnosis out there. All right? At the same time, you need to undercut yourself, because, as physicians, we want to avoid anchoring. Right? It's all for the purpose of avoiding anchoring. You don't want to do that. 

Remember you can't ever rule out TB, syphilis, and sarcoid. All right. This part's for the applicants. Here, at UVA, we practice medicine in a mutually, reassuring, uplifting environment, where we reinforce each other's values, our differences, and we collectively strive for the greater good and excellence. 99.99% of the time, that's what happens. 

This, my friends, is not what that is. This is the battle. This is war. This is what a CPC actually is. You see, the thing about it is, when it's presented to you, make it seem like you're on the same team. Like, yeah, we're going to go out and get the bad guys. And this will be great. And then, I'm thinking, all right, cool. Like we can do this. Maybe I get to be Chadwick Boseman in the Black Panther. I am the Black Panther. But, no, what I'm actually-- I'm the raccoon. And not the cool raccoon. This used the photo beam gun, but this one. I'm the comic relief. 

So I've been forced, now, to teach you all about things that I have no idea what I'm talking about. And I have no authority to do so. In other words, I've been forced to mansplain to you throughout this CPC. So you might ask yourself, why would you do this and subject yourself to it? 

Well, ultimately, it is a lot of fun. And one of the rules I always established with the two presidents is that, if they're going to put me up here, then, I reserve the right to make them a little uncomfortable too. So I know for a fact that someone tried to peruse my Instagram to find incriminating evidence. But that's highly curated, because I had the social media person at UVA go through it. But let's just see what happens if we Google Sumner Abraham. 

I see drunk history. All right. Right here, director of marketing and media. And let's just start at-- 

[VIDEO PLAYBACK] 

- Ladies and gentlemen. 

I mean, we can start anywhere. But, let's start right here. 

- --and beautiful. To make this life a wonderful adventure. And I'm here to tell you that the next step in this adventure takes us back to 776 BC in Greece. 776 BC was the best of times. A times before the world was saturated with the ideas and the persuasions of sex, drugs, and rock and roll-- [INAUDIBLE] time-- a time when men were men, and boys were boys. 

And there was a man who helped in the process of turning these boys into the said men. He was-- 

So let's just stop there. 

These boys turned to me-- 

I reserve five minutes at the end for Sumner to explain himself. But I have so many questions. So many. 

- Dammit. This man was [INAUDIBLE]. 

So you might ask yourself, why do you do this? Aside from the fun-- 

- And people [INAUDIBLE] in the great state of Mississippi-- 

I can stop this. 

[END PLAYBACK] 

We can keep it going. This is great. You can just derail the whole clinical part. Like the Ole Miss helmet, the turtle. 

All right. All right. So first, CPC. I was told this would be a great way for faculty to get to know you. You're new, this is great. Second, it would be so good to have you back again. And now, this is the first time we're doing a grand rounds CPC. This will be great. It'll be cool. And now, it's just a whole bunch of people looking at me about the fall of my face. 

So like other people who do not take good words of wisdom, I draw some inspiration from Kanye West. He said at the 2017 Coachella, CBC's don't change. It's only the people stupid enough to do them. All right. So I actually got some words of wisdom-- which I do every year-- from some of my trusted mentors. He also said I was stupid to do this. 

But he said, you get four different kinds of presentations. First, are common things I present commonly. Common things that present uncommonly. Then, uncommon things that present commonly. And in the last category, uncommon things that present uncommonly. 

So we can take off this one, because that's boring. Right? That's like your usual sort of medicine mission. You'll have low back pain, but it's from degenerative diseases. Like, we're not going to do that. But then, the last category, uncommon things that present uncommonly. That's just unfair. Like, why would you do that to someone? 

In fact, I've reserved another five minutes at the end of this conference to launch impeachment proceedings-- if the chief residents-- if they actually do this to me, I'm ready to go. All right. So let's jump into some actual clinical reasoning. So the ID sort of a training point of view is to start with epidemiologic triangle, not that this patient necessarily has an infection. But it's a good way to think about things. 

We've got a combination of the patient, their exposures, and risk factors, and the actual pathology that you see. Our patient is young, relatively. He has, essentially, he's got some issues going on, the Bell's palsy, et cetera. But essentially, he's healthy. He doesn't have any chronic organ disease going on. And he's from Guatemala-- which will have to get back to-- because I don't want to anchor on that. 

So now, let's just start with a 50,000 foot view. Broad differential for a solid mass. This would be just absolutely fantastic for me to go through with you all. 

But let's first talk about benign tumors, pituitary adenomas, which will be the most common form of a sellar or suprasellar mass. And then cranial, pharyngeal, and meningeal, we'll talk about all these, followed by malignant tumors that you can see here. 

If the pituitary, actually, you have normal tissue, but it's over-expressing, you can have hyperplasia. And this can be induced from chronic hypothyroidism. You might have thyrotroph hyperplasia et cetera. And then cysts, which we have to consider, because there's a cystic component to the lesion. 

So that breaks down to Rathke's cleft, arachnoid cysts, and dermoid cysts. And then other sort of things, abscesses, apophysitis, carotid AV fistula, which sounds really bad. I'm not sure if I believe that's a thing. 

So, first, pituitary adenomas, these are the most common cellular mass in that they are decade on at around 10%. And they're broken down by two different categories, so microadenomas would be less than a centimeter macro or above. And they can be hormone secreting or not. 

Your hormone-secreting ones will lead to secretion from the active cells. They may grow and compress your other cells and cause hyposecretion by that mechanism as well. Or if you're non-hormone secreting, you can cause decreased secretion just by compression in and of itself. 

Your incidence is 4 in 100,000. But the prevalence is actually pretty high. And I've seen some studies that said it's up to a fourth of patients on autopsy will have evidence of a pituitary adenoma. So that clearly means that a lot of these are asymptomatic and are just discovered incidentally and don't cause problems. But I was surprised to see that. 

So I think the first thing to determine is do we have a hot or cold mass here? This is the optic pathway, which you guys probably know this way better than I do. I just kind of thought that this would go away. But here we are. 

So he has some features-- well, actually, he has some features of a chiasmatic-- or a compression. I don't know if that's a word. And he has a visual field deficit. So he described-- I believe it was left temporal, which would be this guy right here. And then, right, it was kind of central. 

So if he had just central compression, you would expect him to have a bitemporal hemianopia or biperipheral hemianopia. So out here, you wouldn't be able to see. But he's got some additional deficits as well too. 

This is the actual anatomy that we're dealing with right here. And as you can see, this is a very busy area. So right here is your sphenoid sinus. This is your sella. Sella means saddle. 

So the pituitary kind of sits right above that. And if you have a tumor, you can see there's-- it's really easy. You don't to grow that large actually to cause compression in the optic chiasm. And then right here is your cavernous sinus. Here are your internal carotids. 

And you can have issues depending on the nature of the mass of the growth that it's invasive or if it's just kind of growing and causing compression, so a tight area. Let's talk about some hormones, which is great. 

So your pituitary breaks down into two different lobes, the anterior the posterior. Let's deal with the posterior first because that's easier. Your posterior is going to release ADH, which will cause water imbalance, diabetes insipidus, which you don't have symptoms of. 

He's a guy. So we can get that one off the map. Yeah. So we're not dealing with problems here. 

Now let's look at these endocrine labs. Most of them are normal. But, you know, some of them are red, but just by a little bit. So let's go through these. So GnRH leading to LH secretion and FSH secretion. 

We can see that he has normal free values, although his sex hormone binding globulin is, you know, low normal. 10, we can give him-- we can maybe push him over the line a little bit. But his total T is also low, 191. But his free testosterone is actually normal. 

And he has three children. So, clearly, things are working. So maybe having three young children it feels like they're sucking protein from your body anyway. So maybe that's what's going on. 

So we don't have issues there. Going to the thyroid, that's normal, so no issues here. And then prolactin-- so for men-- so for women, it sort of manifests in amennorhea. For men, not necessarily. It would decrease testosterone production. It's very rare that you would actually develop breasts and produce milk. 

But we're not-- he doesn't have symptoms of decreased libido, et cetera. So we don't seem to be dealing with that. His IGF levels were also negative. He doesn't have signs of acromegaly or bossing or anything like that, so unlikely. 

And then adrenal axis, you know, 12:00 at 2:00 PM. I don't really know what that means. But it's essentially in a normal-ish range that I would expect. What was interesting about this case is that he did report some clinical findings that could be suggestive of some endocrine abnormalities. 

Dizziness withstanding. So you're thinking it could be a adrenal problem there, a lot of weight gain. That would be the other direction, or Cushing's, or IGF issues. There's fatigue and cold intolerance. And maybe that's a TSH sort of issue. 

But I lean towards not favoring involvement of the pituitary gland because there's no suggestion of this on imaging. And it looks separate from the pituitary gland itself. And his endocrine profile looks fine. So thank goodness we're done with that. 

So now we can take a few things off, things that involve the pituitary itself. So adenoma, I think, no. Pituicytoma, which is a new finding for me. 

[LAUGHTER] 

But this is a weird thing that it's a part of the pituitary, but it's also not. So I don't get it. So let's just ignore it. Pituitary carcinoma, unlikely. And then the pituitary hyperplasia-- let's just take them off. It doesn't seem to be a pituitary issue. And then a pituitary abscess, probably not. Again, the MRI looks like it's separate from that. 

So then what else stands out about this presentation? Well, a few things. The severe headaches, which have been longstanding and have some-- have some kind of correlation with looking down and the visual disturbance. And then the imaging, the MRI, suggested solid encystic components that were separate from the pituitary, as we mentioned. 

And the solid part was T2 hypointense. I don't know what that means, but it's an interesting avenue to explore. And the cystic part has some small areas of ring enhancement. The head CT shows partially-calcified lesions. There was also a note of other parenchymal lesions. 

But then in the OR, they confirmed it was a mixed, solid, and a cystic component. And they were able to resect it without violating the dura, which is important to note. So in my reading, I found this. Then I thought, man, we're good. Let's just look at this algorithm and then call it a day. 

[LAUGHTER] 

There's a reason I didn't do endocrine. 

[LAUGHTER] 

A version of this is, did they look sick or not. If they look sick, do something. If not, walk away. That's not what we're dealing with here. 

But if we look at this part right here, this is basically based on histopath. But if you're dealing with cystic lesions, there's a few things to consider. So a Rathke's cleft cyst, craniopharyngioma, arachnoic cysts, epidermoid cyst, and et cetera. 

So let's talk a little bit about specifically cystic masses in the sellar region. And I have the honor and privilege of taking you through this sketch right here. So your pituitary develops from two different embryological remnants, so the diencephalon, the base of the brain, and the roof of the mouth. 

So the mouth and brain come together, which sounds really bad from an ID perspective, but fine. I'll leave that alone. Your Rathke's pouch is formed from the meeting of the anterior and the posterior gland. And in a lot of people, there's a cleft that forms that's basically kind of a potential space. 

It's not a part of the interior. It's not a part of the posterior. But it's definitely in the mix, but doesn't participate. So it's kind of like Switzerland unless it becomes an issue. 

So Rathke's cleft cysts are benign cysts that start in this area, has a female to male ratio of 2 to 1, causes a round to ovoid-shaped mass that's either T1 or T2 hyperintense, but doesn't concentrate gadolinium. That would be pituitary tissue concentrates gadolinium. 

Craniopharyngioma is really interesting. They also arise from Rathke's pouch. But they're different. They have a bimodal distribution. So a lot of these will present before the age of 20, so pediatric endocrinologists. And they're all just dealing with this. 

But then the other spike is around 50 to 60-- 50 to 75. And they present classically with highs-- symptoms of high CP, so headache, nausea, vomiting, papilledema. This will be more common in children. But in adults, it will be visual complaints that are very typical. 

And then on imaging, classically, there's a solid and a cystic component. And there's calcification on imaging, which we have some evidence of. So we'll circle back to that. 

The arachnoid cysts are a little different. These are areas of CSF that are actually covered by an arachnoid layer. You'll note that in the OR, they did not violate the dural layer or get to the arachnoid space. So I think this is unlikely. 

And then I would expect CSF to be pretty hyperintense on imaging, which we then see. There was some mentions of that. But it didn't seem to be a prominent sort of-- part of the presentation. Interestingly enough, head trauma can exacerbate this or cause it. 

And he did have a head strike a few years ago. So it's worth just thinking about, but seems less likely. And then a dermoid cyst, I mean, I would hope if there was like teeth and hair going in this thing that somebody would mention it to me. But you never know. 

I want to talk a little bit about MRI, T1 versus T2. This has been-- it was an area of struggle for me when I was a medical student just remembering which lights up what on what sequence. But here's a way to remember it. It's all based on water content. 

So if you have a high water content tissue, this would be fat, edema, blood infection-- or acute blood, I should say. It'll be dark on T1 or dark on T1, bright on T2. If you have low, it's the opposite. And the mnemonic to remember is World War II. Water is white on T2. 

Now none of this actually helped me try to figure out what this was. But we're here for T2. All right, so back to our 50,000-foot view. A few more things we can take off, I think meningioma because we didn't seem to have to deal with dural layers there. There was no dural tail. 

He seems systemically OK. I don't get a picture of a metastatic lesion that's going to the brain. The same for sarcoma. These people tend to be pretty sick. A cordoma is an interesting entity. These will tend to be-- these are glial tumors that are slow growing and don't necessarily respect spaces. 

So they will invade nearby areas, invade into the cell, into the bone, encase the segments of the carotid artery, invade into the cavernous sinus. You know, he doesn't have a good problem. Let's not be mistaken about that. But it seems to be respecting the anatomical boundaries for the most part. So I think that is less likely. 

And then arachnoid cysts, I don't think we're dealing with the contain CSF collection. All right, so we're making some progress. But we got a few to go. Dermoid cysts, I mean, if that's what this is, then meet me after. 

And then AB fistula, I'm still-- I'm not-- I don't even think this is a real thing. 

[LAUGHTER] 

So it sounds bad. Then hypophasitis, so the classic medical school case would be a pregnant woman who's in the course of delivery. Sheehan's syndrome would be associated with this as well too. You would see vestibular stalk thickening and things like that. 

I think that's unlikely in this case. It doesn't seem to be a lot of inflammation. It doesn't seem to be a prominent issue on imaging. 

Now one thing I do want to talk about is neurocysticercosis. And I've been intentionally ignoring this because it's a young man from Guatemala. But we need to talk about it. This is the leading cause of seizures and epilepsy in the developing world. Estimated 50 million people affected. And this is just neurocysticercosis, not the generalized disease. 

And it's a growing problem in the US. We have more immigrants coming in. And I saw some estimates that, for instance, in LA County hospital, UCLA public hospital, about-- they admit one person with neurocysticercosis every two to three days. So it's becoming a larger issue. 

Lesions may be parenchymal or extraparenchymal in different stages. Different stages can coexist at the same time. About over 60% of them will be parenchymal, but the extraparenchymal can be subarachnoid, intraventricular, and et cetera. The treatments is albendazol plus praziquantel. 

Let's go through the lifecycle. So it starts with eggs, or a proglottid, that's excreted from a human ingested by a pig or human. So let's do the pig first. We have oncospheres that attach to the intestinal wall. They penetrate, go through, and then go into the musculature. 

And then we eat the pig. And then the cycle repeats itself, right? If someone then poops out these eggs, or proglottids, and then a human ingests that, so this is a fecal-oral contamination, then you essentially you can become the pig. 

So you will have cysticerci go to your muscles and bone and go to your brain in different areas there. And I've seen essentially this can spread anywhere. Now, what's interesting is that there are four different stages. And depending on what stage you're in will depend on what your symptoms may look like. 

So I'm going from A to D over here. So first would be a vesicular cyst. And you can see right here, there's a cute little scolex right there. See that? Now this is interesting. This is the first stage. 

It is not-- so if you notice, there's not a lot of enhancement around there. It just looks like there's a hole in the brain, but not a lot of else going on around it. This is actually not a really intense immunological reaction. It's thought that the scolex itself has immune-modulating effects and can suppress the immune system. 

And as long as it's intact, it can kind of exist like this. It can even float around in your ventricles. And if you had issues from it, it'll be if it's obstructing your cisterns or CSF flow or things like that. That's when it will cause an issue. When it starts to degrade is when it becomes a problem. 

So first will be your, whoops, colloid cyst, which is B right here. You can start to see some ring enhancement. And this is starting from an intense immune sort of response to this. I mean, that's the classic ring-enhancing lesion that you see. And then once it starts to calcify further, you get to a nodular-glandular. 

And then the last stage is calcification. And this is what will predispose to seizure activity. So interesting in how it can progress through stages. As far as the time course, it can be fairly long. I've seen up to two decades or so. 

So he came from Guatemala in the mid-90s or so. So it's possible that it could be manifesting at this point. Sellar involvement, however, is extremely rare, suprasellar involvement. This was a review done in a Belgian journal. He did a Medline search over the course of 30 years, found 23 patients, mostly case reports. 

But their symptomatology broke down to visual disturbance, endocrinal abnormalities in less than half, 13 underwent surgical resection. But the visual symptoms only improved in two of them. So it seems like it wasn't that great of a therapy. Five received antiparasitics without surgery. And zero of those improved, so not a good prognosis, but it looks like it's fairly rare. 

Now I want to toss this up to cystic trypanococcus, which I think is unlikely. But, you know, we're-- we don't want to anchor, right? So this would be the dog tapeworm and sheep. And this is more common in Eurasia and places where there's a lot of sheep. It's not a real Latin America sort of thing. 

But this would be a common cause of liver lesions, liver cysts, that would metastasize to the brain. I do note he had some mildly-elevated LT. He's complaining of some abdominal pain. I'm covering myself right here. But I think it's unlikely. 

All right, I want to zone out a little bit more on just the differential for a ring-enhancing lesion. It wasn't described in robust sort of terms. But there was some mention of ring enhancement. Three main categories-- infection, toxo, neurocysticercosis, as we mentioned, brain abscess, and tuberculoma. 

I think tuberculoma is interesting. TB infects one third of the world. And CNS manifestations, though not common, are not uncommon. It's up to 10% I've seen in some estimates. And a fair amount of those either manifest with TB meningitis or tuberculomas, et cetera. 

Malignancy is primarily CNS lymphoma. GBM is the classic ring-enhancing lesion and metastases. And we didn't have any imaging evidence of any vascular involvement. But hematomas and thrombosis aneurysms can also cause this. 

Now if you have HIV, and this wasn't reported, but I would want to HIV test, your differential actually narrows quite a bit to three-- toxoplasmosis, CNS lymphoma, and brain abscess. So out of this list, I think neurocysticercosis, and remember the rule, you can never rule out TB. So we're going to keep that as well too. 

So back to our actual words of wisdom, we're taking out these two. And we're left with common things presenting uncommonly and uncommon things presenting commonly. And I'm getting more and more excited about neurocysticercosis. But I have to resolve a few things. 

So one was he re-infected, or does this represent recrudescence of his known infection? Luckily, for me, the American Society of Tropical Medicine is meeting in DC right now. And this is a tweet from none other than [INAUDIBLE] who's an epidemiologists who tweeted out a heat map two days ago showing where the hotspots for neurocysticercosis are. 

As you can see, Guatemala is definitely a hotspot. And El Salvador is right here. So then a year ago, he traveled to this area. Now that would be a short time frame to develop symptomatic neurocysticercosis from re-infection. 

It's also controversial whether re-infection is a thing because I read that you can have immunity, but immunity can wane. So who knows. But that's something to consider. 

Now another inconsistency is the Seventh Day Adventists. Now, we practice cultural competency at UVA as well too. So let's talk a little bit about Seventh Day Adventists. 

This was born of the Millerite Movement in the US established formally in 1863. They observed Saturday as the Sabbath. But most interestingly, they promote holistic lifestyle and a diet. There's actually some epidemiological data suggesting that Seventh Day Adventists have a longer lifespan. And some people think it's connected to this reason. 

But they promote vegetarianism, plus or minus veganism, but certainly not pork, shellfish, and the other sorts of things. So if he was actively practicing Adventist, he would not have gone to El Salvador and ate pork. But pork is a hell of a drug. 

[LAUGHTER] 

So maybe the pull of being back close to the homeland, you reingest some. You get that rush. And then you get neurocysticercosis. 

[LAUGHTER] 

Now, putting this all together, we have a young, essentially healthy man with a sellar mass or suprasellar mass causing visual disturbance and headaches, no hormonal compromise. MRI shows mixed solid and cystic lesion that's T2 hypointense and some REM enhancement. 

CT shows what looks like old neurocysticercosis with the parenchymal calcifications and a new lesion that's partially calcified. It lists over here craniopharyngioma, which looks really interesting, Rathke's cleft cyst, germ cell tumor, and then, as far as infection, neurocysticercosis, tuberculoma versus cold abscess, which is hard to distinguish. And then whenever I see tuberculosis, I just toss in the mycoses as well to just to cover myself, but also clinic-- that's clinically-- that's what you should do. 

So craniopharyngioma would be one of these sort of uncommon things that would be presenting uncommonly in this case because of the bimodal distribution. Remember, it's before age 20, then again, age 50 to 70. So I think that's less likely. 

So I want to go out on a limb here and say neurocysticercosis either chronic or re-infection leading to optic nerve compression and visual deficits. And this is what I've sent to Sumner this morning when I woke up out of bed. 

But see, there's another layer to this. And now we're going to get into the dynamics of being a chief resident because I was one in putting a CPC together. So there are some things that bother me about this. It seems too easy. 

He's got calcifications in the parenchymal areas of his brain already. It seems like a fastball over the plate. Cysticercosis, evidence of it already, and just a new manifestation of it. It's also extremely rare. It's impressive to-- I've done a search over 20, 30 years and find just 20 or so cases or so. And mostly those are case reports. 

And I just get this feeling that I'm being led to my destruction. And then there's some other things about the MRI that still bother me. Now MRI is not a slam dunk for any of these things. 

But my thought is if he was having symptoms from a degenerating neurocysticercosis lesion that was then causing inflammation and more compression and more symptoms, I would expect that to be more active, especially on T2. But the report said that there marked T2 hypointensity, at least in the solid components. And that seemed a little odd to me. 

He's the wrong age where he's got that bimodal distribution. But a lot of the presentation is actually consistent with craniopharyngioma, as far as the location, how it's growing, the symptoms that it's causing. Then over and over again in my reading, it was the mix of solid insistent component with some REM enhancement is consistent with craniopharyngioma. 

And then, lastly, you just can't trust these people. They have just really good smiles. They look fantastic. They take a picture, photogenic, but they can't be trusted. 

So my final, final diagnosis is craniopharyngioma. 

[APPLAUSE] 

Thank you very much. So I am Beatriz Lopes. I am a neuropathologist here. And what I forgot to tell is UVA is one of the world-renowned center of pituitary neuroendocrine disease and pituitary center. So in any other place in this country, you're going to see 300 pituitary cases a year. 

So that is the trick, right? And common things are common things. And I remember one time when I was a fellow, and I had my first time [INAUDIBLE], and I went to the ER. And the chief resident at that time, her last name was Eckel. 

She came to me is, like, oh you're from Brazil. You have tuberculosis. And she went to do an LP. I was, like, wait, wait a minute. I'm a physician. I don't have TB. I know. This is my first surgery. 

So when we got this case, you know, [INAUDIBLE] sent to us. He didn't ask for [INAUDIBLE]. But we could make the diagnosis grossly. It was a cystic lesion. So it was a cyst. 

And what we had was this. There was a very well-organized cyst. And there was some pink material that we normally think it is the cyst content. But we're going to see in details. So the first thing that you do is to analyze the cyst wall. 

This is a high magnification of the cyst wall. And if you go to a higher magnification, you see a few things. First, there was an area of particular area that you can that is very pink, bright material. 

And on the top, you see those little speckles. These weren't cilia. That's called microtrichia. And then you have, below the cuticular area, some what we call middle cellular area that you can see some nuclei. But this is not very normal. It's a little bit degenerated. 

And then you have the inner reticular area. Dr. Bell, what's the diagnosis? 

[LAUGHTER] 

In other areas, we could see that pink-like material was not actually a cyst contents, but was exactly the same histology as the cyst wall. What was that was degenerated. This is cysticercus. So you're right from the first time-- so tricky. It's a tricky one. 

So if you go back-- if we go back here, so you're going to see that this is the cyst of the parasite. And this is the dead areas that we have more to solution. So if we had a growth picture, this is the base of the brain. 

So here you are looking at the base. This is the optic-- the olfactory bulbs. This is the optic chiasma. And you can see in this picture, you have three cysts, one that is more infrachiasmitic and one's more supra. 

So as talked by Dr. Bell, this is extremely rare to occur in this particular location. But subarachnoid cyst is described common to see. And, normally, what we have in the histology if it is a well-prepared type of tissue, and the cyst is still alive, you're going to see the scolex with the suckers that we do didn't have. 

The only thing we have in this particular one was the cyst wall. And the cyst wall had different phases. And when we had this case, the ID team came together because it was partially dead. It was dead. But there was partially still some reaction in normal type of a cyst. 

But we didn't have any CNS tissue around. Dr. Jane took exactly only the cyst in subarachnoid. As discussed before, if you have a dead cyst, you're going to see, in the area of the pathology, more calcified type of lesions. And I was going to go over the same-- [LAUGHTER] the same thing. 

So I don't have to because we've already discussed that. But that would be the phase that we are. So we are in this cyst that is located in the CNS And has some reaction. It doesn't have a reaction to the tissue surrounding. But there was already calcification and partially dead. So this is our final diagnosis for the cysticercosis. 

[APPLAUSE]