 We'll review the answers, and we'll use the PowerPoint discussion that was on the video, maybe dig a little deeper if we need to. So the first few questions are anatomic-based, understanding how things look on imaging and cross-cutting CT and MRI. So the first five are name these parameters. So these are the choices, and the questions are these. There's only four on this slide, but there'll be a fifth one coming up. So the next several slides are all questions one through five. And you need to pick which of these answers A through G belongs to one, two, three, four, five in a minute. We'll just slice it a little further. So these should confirm your initial impressions or confuse you if you got one wrong. So here's actual views of the same things, and here are the same numbers. And again, these should either confirm your suspicions or confuse you if you weren't quite right. Here's the very first one. Okay, is that enough time? Anybody need more time? Okay. And this one, it's not ABC, it's just two, three, four, five, and six. So there are four images that are based on high T2, high contrast, cisternal imaging. Five nerves to choose from, and images 6, 7, 8, 9, each show one of these cranial nerves. These are the nerves, these are the nerves that we're after. Is that good? Enough time? Okay. Next few questions are about MRI imaging sequences. So what is this sequence? A few more, here's 10, here's 11, it's a little contrasty, what would normally look like, 13, 10. Another MRI protocol question, which of the following techniques is least useful when you're imaging the cisternal segments of the cranial nerves? Cis or something to say, kiss, fiesta, MP rage, T2 spin echo, T2 space, T1 post contrast. Just gets into the alphabet soup of MRI imaging. All right, this is a lateral view of a digital subtraction angiogram. This is a patient with Cc fish jello, a lateral view. So I'm going to show you a bunch of vessels and you're going to tell me which ones are which. So we've got 15 through 90, so we've got five vessels I'd like you to identify and pick from cavernous sinus, inferior patrols of vein, internal crowded artery, middle cerebral artery, superior ophthalic vein, and posterior communicating artery. Sometimes these things don't project as well, it looks okay, it's not a great project. This is a tough one, by the way, because when you have Cc fistula, the blood's going in all kinds of directions, and that confuses things because on an angiogram, this is a planar or a projectional view, so everything is overlapped. You need more time on this one, is that okay? Okay, so this isn't exact cross-sectional imaging, but we use so much anatomic evaluation, so much of what we do in imaging starts with anatomy, so I want to be able to identify things on the CTA, especially our NMRA, the intracranial vessels. So this is an ABC, we just put the name of the vessel into each of those seven things, we have all eight things identified. Okay, is that good? Almost? Okay, so the next question is the same diagram, but I want you to pick the location that is the most common site of aneurysm that causes pupillary dysfunction, and these are all fairly common places for aneurysms and other circle volus to show up. It is a related question, which is the most common overall site for a circle of volus aneurysm, not necessarily causing pupillary dysfunction, but taking all comers, which site is the most likely to be a place where aneurysm shows up? Now let's get into some pathology. This is an axial T1 post-contrast, the arrows are just identifying the pathology. Which of the following is least likely in this patient who presents with multiple cranial neuropathies? This is a spin echo T1 post-contrast, and a lot of times in imaging, we often talk differentials because the one answer is not often pathodynamic, and so knowing when to exclude sometimes is the best you can do. So these five conditions, which one is least likely to present this way? West Nite, barris infection, cocculant infection, sarcoidosis, intracranial sarcoidosis, lymphoma, or tuberculosis. Which of the following in this T1 post-contrast image? Which of the following diagnosis is least likely? Idiopathic orbital inflammatory disease, thyroid orbitopathy, IgG4-related disease, lymphoma, or sarcoid. And again this is a post-contrast T1 with fat suppression. Which of the following diagnosis is least likely in this young adult with acute vision loss? On the top you have a T2 with fat suppression. On the bottom you have a T1 post-contrast with fat suppression. Your choices are multiple sclerosis, acuporn4, NMO, MOG, positive NMO, sarcoid, or GPA, number 33. Which of the following is most correct regarding this optic pathway lesion? This is a T1 without fat suppression. You can see all the fat is still bright. And it's post-contrast because you can see the vessels. And the mucosa is bright. So which of the following is most correct? Most patients with this lesion have NF1. Most patients with NF1 have this lesion. This lesion is associated with mild vision loss. Enhanced it indicates a higher tumor grade. 34, what is the best diagnosis? Maybe you can tell from the imaging features what kind of a sequence this is. Options are cystic hygroma, lymph angioma, medial lymphatic malformation, cavernous hemangioma, type 1 vascular malformation. 35, you have a CT and an MR. What is the most likely clinical feature that would accompany the presentation of this patient's imaging? And your options are sudden vision loss. Painful vision loss. Coast of Maine, capiola spots. Middle-aged female. History of prior radiation therapy. And 36, I think this is the last one. This is a CT image. What subtype of neuronal injury is most likely in this trauma patient who presents with heart syndrome? First order pre-ganglionic. Second order pre-ganglionic. Second order post-ganglionic. Third order post-ganglionic. Okay, should we go over them? All right, let's start at the top. Number one, somebody knows. Optic canal. Two, superior fissure. Three, rotundum. And four. So ovale is actually a little bit harder to see. Ovale goes up and down. Whereas vidian and rotundum come forward. So if you're in a coronal, you're going to see rotundum and vidian coming right at you as circles. And ovale is going to be right about here, a slice or two back. And it's going to show up as basically a gap. It's going to be a vertical gap in the central skull base right there. So I don't actually show ovale on this one. That's vidian. Rotundum is up and out and lateral. Vidian is down and in. In patients who have a very aerated or hyper aerated scionitis, you'll often see the air of the sinus come between these two. So if the pterogoid itself is pneumatized, which is a pretty common variation, you'll actually see a channel of air between separating the frame and rotundum and the vidian canal. So here's the same thing. So optic canal, superfissure. What's the little piece of bone called that separates the optic canal from the superior fissure? The strut. Optic strut. And in fact, if you think about the anatomy of the fissure, the superior fissure and the inferior fissure are really a continuous structure. They're separated by the bone at the top of rotundum. Through rotundum goes what? V2. And everything else that's important pretty much goes through superior fissure. And the inferior fissure and rotundum are kind of right in line. So if you come out of rotundum, it goes right into the inferior fissure. And then above that is the superior fissure through which go 3v1 and 4 and 6. And what's 5? So that's the pteropallic infossa. And in imaging it's a really distinctive structure because it's this little pocket of fat that's right smack in the middle of the deep, deep face. And we sometimes call it the crossroads of the deep face because it has a pathway to almost everything. It's really close to, it's right in front of Vidian. It has a direct connection to rotundum. So you can get from pteropallic infossa, you can get into the central skull base through rotundum back into the intracranial compartment. It gets into the orbit through the fissure. It actually goes down into the oral cavity through the pterogoid canal. It has a medial axis into the nasal cavity through the ptsunopallic inforamen here. It has access into the deep face, the massacred space through the pteromaxillary fissure. So the pteropallic infossa, we often look at that as one of our search points when we're looking for perineural tumor. Because it is a place where so many things cross over. And what you see in CT and MR is just this little pocket of fat. It's not pure fat because there are neural structures and some bastard structures in there. And there may even be some lymphatic tissue. So it's got a little bit of stuff in it. But when you have perineural tumor, what you see is a fat is a phased by something in hands. And then the axial... Sorry, to what is still the optic canal? It's optic canal. Superior fissure. A little superior fissure. And that's rotundum. That's rotundum. Sorry, because I thought you pointed to it and said vidian. Oh, did I? I'm sorry. Mine's still rotundum. Yeah, think of vidian as being immediately behind the bulk of the pteropathic infosum. So if you put your cursor on vidian and then come forward, you should be kind of swiping, smacking in right at the bottom part of the pteropathic infosum. So you can't see vidian on this one? Right. And you'll often see a little depression as rotundum is forming along the lateral margin of the sphenoid sinus. And that acts as a name that the porous trigeminus is that depression as it's going into an actual canal. So vidian medial and down, rotundum up and out. And then the vidian kind of dumps right here into the pteropathic infosum. You can see that as you come forward, the pteropathic infosum is going to pretty much envelop what's coming out of rotundum right into it as well. So both vidian and rotundum dump into that space that becomes the pteropathic infosum. So in the right slice, you can't see the chiasm forming because the optic canal really is coming at a pretty steep angle. So the optic canals do come in angled towards each other like this. And a rookie mistake is to see this and think it's the optic canal. But one thing to remember is the fissure looks like it's kind of, it's a little short thing. It's coming straight back where the optic canals are coming in angled toward each other to make the chiasm. Rotundum is just a little short canal right here. And below it is the vidian. Vidian and rotundum can be a little bit hard to separate on axial, but vidian has this characteristic long kind of sickle shape to it. In fact, in some patients, the vidian is more conspicuous than rotundum. And another rookie mistake is to call, maybe that's the mistake I made, is to call this rotundum. When it's the, because it's the most distinctive little circle that you'll see, but the vidian is a longer canal and sometimes a little more obvious. So the vidian is kind of a long sickle shape, whereas rotundum is a little short thing. They both dump into the pteropathic, this is the upper part of the pteropathic infosum. This is kind of the main bulk part of the pteropathic infosum. You can see the fat inside of it. So this is one of these sequences that is very heavily T2-weighted. The purpose of the sequence is to really show the cisterns and whatever's running in them, vessels and veins in particular. It's not great at looking at parankable detail. So what's this nerve here? So five is the easiest one to see. It's a big fat chunk. As it comes in toward this little CSF space here, it's not until the fibers are separated. So you'll often see little individual fibers kind of floating within the CSF right there. What is this CSF pocket here called? That's Michael's Cave. This is these two on almost any sequence, these are normal findings. And one of the things that we look for like a, maybe a meningioma or a schwannoma that's occupying five and necklace cave. When necklace cave is missing, you'll hear us use the term a winking necklace cave because it's missing on one side. But that's the structure. It's very reliably seen associated with five. This is a sagittale. You can see the belly of the ponds. And there's a structure that's cutting it up at this angle right there. It's really only one thing that does that. What's that? That's six. It can be hard to define, but if you know where it runs, really, there's nothing that's going in that direction. All the veins and arteries are usually kind of coming at oblique or more transverse angles. And it's, even though it's a very small thing, within T2 weighted imaging, you can usually pick it out of a crowd. Eight, three. So three is a pretty big nerve. And you can usually see it quite easily that it runs right between the P1 and the SCA segments right there. Four also runs in the same space. Four runs out lateral here. It's a much smaller nerve, and I think it's really hard to reliably see it on a coronal. So what was this one then on nine? Four, I don't think you would necessarily always see four. If you see something that runs right there, that's sitting on the back, that's probably a pretty good identification. But I find four is not always reliably identified. It's a very small nerve. Okay, so there's just some bread and butter imaging. What's this? Fats bright. Mucosa is not enhancing. Fluid is dark. So this is a T1 spin echo. This is one of your primary non-contrast sequences. So this is a T1 spin echo. Coronal. In this case, we have CSF is dark. Notice how the so fluid is dark. Very brightly enhancing mucosa and muscles. The fat is dark. So what's this one? T1 with fat suppression. Right, so this is a T1 way to spin echo with contrast and fat suppression. This is one of our other core sequences because it brings out pathology, but it suppresses the fat, which has a lot of signals so that pathology becomes more conspicuous. Put an axial image. Vitreous, CSF, very bright. Fat is dark. You actually have two choices on this one and you get credit for either one. So what are the two choices? T2 with fat suppression. So T2 with fat suppression and the other option would be a stir, which stands for short tau inversion recovery. It's a different kind of a pulse sequence. Both of these give you T2 fluid and usually pathology have a signal, but it makes the fat go away. Spin echo T2, if you don't... If you have just a plain old spin echo T2 without fat suppression, the way that T2 is done in order to get it... T2 can be very slow to acquire and the technique allows us to get a lot of T2 slices quickly actually brings out a fair amount of fat signal with it. So if you do a T2 spin echo without fat suppression, all your fat is going to be really, really bright. So if you want to see pathology emphasized, you do a T2 with spin echo, but then you add fat suppression on top of it to make the signal go away. A stir sequence is a different kind of a pulse sequence and it doesn't have any fat excitation at all. So you don't have to suppress it. The issue with fat suppression is it's an additional gradient that takes... If you were to think about it from a point of view of electrical engineering and a celloscope, there's actually a signal spike in the fat when you do T2 acquisition with spin echo. When the tech is doing the scan, they actually pull up a spectrum and they can see a spike of signal that is resonating at fat and they put a suppression pulse right on that spike to make the fat signal go away, but just a very narrow suppression pulse. So the fat signal goes away, but nothing else does. The problem is that that depends on a very homogeneous magnetic field. And when you put metal in there or if you have other factors to get in the way, people have braces or implants, that the magnetic field gets irregular and your suppression pulse is not always perfect at taking out just the fat spike of signal and they can miss the fat spike and suppress other things. So when you have a fat, when you have a T2 sequence with fat suppression, well, it's the same thing applies to any fat suppression, the fat suppression can be inconsistent or it can be wrong and you might get accidental fat signal and something else gets suppressed. So you have to be able to look at these things and know whether the fat suppression is working or not. The stir doesn't have any fat signal to begin with so there's nothing to suppress. So it's a much more reliable sequence in determining what's fat and what's not. So we usually will do one plane in stir and one plane in T2 fat sat with suppression. So we'll do one of these and one of these, usually an axial here and then the coronal fat suppression. You get a little bit better spatial resolution with spatial. So we like to have at least one of these because you get a little bit better detail but we do at least one of them with the stir just in case the fat suppression has a problem. So this is kind of an alphabet soup. Four of these are T2 sequences and two of them are T1 and this probably isn't all that fair. An MP rage is a variation of how to do T1 imaging. And the basic T1 sequence which is a spin echo is the one that was originally developed that's most commonly used. But it has some, the T1 spin echo can have issues with phase artifact. We have all the flowing vessels at 3T especially. And so if you want to have a T1 sequence that doesn't have the same kinds of motion artifact, an MP rage is a T1 sequence that has some advantages. But it is essentially a T1 weighted sequence. Of all of these, the T2s are the most important when you're looking at cisternal cranial nerves. Now three of these, the kiss, the fiesta, and the T2 space. So A, B, and E are all pretty much the same thing these are actually vendor terms. It's kind of unfair that Siemens and GE which are the two main manufacturers we have experience with, they use different acronyms for their imaging sequence. The bottom line is the kiss, the fiesta, and the T2 space are sequences that are heavily, heavily T2. They really emphasize the fluid signal and the parankama kind of is just amorphous black. But they really give you great cisternal lemurs. So the kiss, the fiesta, and the T2 space are of that kind what we call heavily T2 weighted. A plate old spin echo T2 is not bad because you can still see the CSF pretty well. It's more prone to pulsation artifact in the CSF so it can be a little bit harder to see. You can't get quite thin sequences with a spin echo T2 whereas the T2 space and the fiesta, and the kiss gives you really super thin sub millimeter slices. If you have pathology that's enhancing the post-contrast would be useful. But of all these, the MP range without contrast would be the least useful because when you're looking at cisternal structures, the CSF on T1, the CSF is darkish, the NERS are darkish, you're not going to be able to see anything. So of these, the MP range is probably the least useful. An angiogram is performed by putting a catheter in the internal carotid artery in the neck usually. So you put the catheter up into on the right side of the breaker, cephalic in the carotid or the left of the common carotid. And usually when you're doing an internal injection, you like to get the catheter past the bifurcation and the catheters have little angle tips so you move the tip around so that it angles into the internal. Usually it's kind of pointed back and lateral. Slide it into the first couple centimeters of the internal and then do an injection with a power injector and take a series of images over the next 10 seconds. With CT, you can get really nice pictures in cross-section. The problem is that it only takes a couple of seconds to get from the first incident of injection to where you're filling out the arteries and even getting into the veins. The intracranial circulation is very low resistance. You fill up the arteries in the veins very, very quickly. You only have a couple of second window. CT and certainly MR, you don't have enough temporal resolution. You can't image fast enough to see things go. So if you need to see the detail of an early arterial filling, the only way to do that is with an Instagram with a digital subtraction entry. So the contrast is injected into the ICA. So here's your internal carotid right here. Comes up and then right here, usually what you see is a nice pretty siphon. So you see the S-curve of the cavernous sinus coming up to the terminal ICA. But in this case, you have a big blob of contrast filling what structure? What's 16? Cavernous sinus because this patient has a C-C fistula. And in addition to filling the cavernous sinus, you have pressurized now that venous space with arterial flow. So you're filling two things that normally shouldn't fill on an angiogram. One of them is this structure here, which is filling anterograde. What's this? That's the syrups. This is the pyrophilic vein. So this venous contrast is actually going forward this way filling this structure. And it's really big in addition to filling arterial phase. You notice how the arterial phase is still pretty early. Most of the arterial tree is not filled up. You already got the cavernous sinus. And the supra-optalic vein filling. There's one more structure that's filling up normally. That's the thing right here coming off the cavernous sinus. It's actually flowing downward. You know what 17 is? Yeah, that's the inferior protrusal vein. That's one more venous piece of evidence that this thing is a clearly abnormal arterial venous connection. And what does that make? 15? Yeah, I suppose a branch of MCA. Because this is a lateral view, they're coming out at you. And then if I had an arrow on this, what's that right there? This little order right there? That's a PCOM. PCOM comes straight off the back of the terminal. ICA. So I'll just point to it. What's 20? ACOM? 22? A1? 21? 2? ICA? PCOM? Which famous aneurysm causes people involved in their nerve palsy? So yeah, so it's B. We know that PCOM is the classic aneurysm, but what we don't often remember to emphasize is that it's actually not a PCOM aneurysm per se. It's an ICA aneurysm that is arising at the origin of the tumor. This is where you usually see them. So if you had an aneurysm, it would show up right here, usually sticking off the back of the terminal ICA where the PCOM is coming off. So that's the most common place to see it. It's technically, it's an ICA aneurysm, but we call it a PCOM aneurysm. And what's the most common place for aneurysms in general? It's going to be ACOM. I don't have the MCA bifurcation. That would be the other most common place if you had the MCAs. Okay, so this is a T1 post-contrast. Diarromality is lots and lots of enhancement filling the cisternal spaces. Paramesan's phallic, interbranicular, supercellar, going out of the MCA cisterns, all kinds of enhancement filling up everything. This is a pattern that we would term, well, if you were to describe the generic pattern of involvement, what would you, what would you, what term would you use? The leptomeningeal. This is, this is a leptomeningeal process of some kind. It's either leptomeningeal inflammation or it's leptomeningeal tumor. So which of these is least likely to give you leptomeningeal manifestations? And this is a really striking extreme manifestation. Well, certainly fungal meningitis will do this. Sarkarosis and lymphoma. Lymphoma and craniolemus diseases have a lot of imaging overlap. If you hear yourself saying sarcoid or fungal disease or TB, in the same sentence you're probably going to say, in addition to infection, we consider lymphoma. Because those, those have a lot of imaging overlap. So craniolemus diseases, craniolemus infections and lymphoma, these have a lot of imaging overlap. And leptomeningeal manifestations is a common thing for them to do. Whereas West Nile virus is more of an encephalitis. I wouldn't really give you, it's kind of an extreme leptomeningeal enhancing picture. Okay, T1 post-contrast. And this patient has lots of, lots of abnormalities. They have the muscle involved, optic nerve involved. And if you look closely, you even have intracranial disease. They've got a mass in the supracelular region. And there's even some linear enhancement right along. What normally runs right there? That's their nerve. So you've got somebody with lots and lots of multifocal, pretty extreme enhancement. So when you think about things that give you multifocal orbital and possible intracranial disease, which is the least likely. But that, thyroid, yeah. So thyroid has a pretty specific orbital manifestation. And I don't know that I've seen orbit give you this kind of optic nerve or intracranial disease. Certainly, idiopathic disease, IgG4, which in some ways we almost think of like a kind of variation of a pseudotumor. This would be a great look for the VOMA for sure. This would happen to be sarcoid. But any of these inflammatory conditions could run out this way. Okay, so here we have a young adult. We have a T2, T1 post-contrast. On the right, we have nerve enhancement, a little bit of swelling, because it's a-facing the normal cuff of CSF that you see around the optic nerve. Orbit look pretty clean. And then on the post-contrast, you see it's enhancing the swollen nerve, normal on this side. And at least on this picture, the rest of the orbital looks pretty good. So, you know, we're targeting optic neuritis. Which of the following is least likely to present with what appears to be an isolated optic neuritis? So this is where I'm getting getting out of my territory, because now I'm trying to pretend like I'm an ophthalmologist tonight. I know how these things present, but you'll have to tell me if I'm wrong. But I don't think GPA presents this way, does it? Not usually. I mean, you can get the optic neuritis with GPA. But these other ones would all be, certainly the demyelinating conditions would be pretty typical for optic acute optic neuritis. And we've seen Sarkin present with acute optic neuritis as well. So I thought E was the right answer. Judith, is that the best answer? Okay. Plus, I wanted to tell like I knew. Okay. So what's the optic pathway lesion here? You have a T1 post-contrast because we have all the enhancement of the vascular structures and the mucosa, which are these big, fat, bilateral optic nerves, chiasm and tract. So this is a optic pathway glioma. So the question is, which of the statements is the most accurate? So I guess I'd say what percentage of patients with optic pathway glioma end up also having NF1? Well, so this is where you'll probably have to help me out a little bit. But in my reading, most patients, there's definitely an association, but it's a minority of patients. If a patient presents with optic pathway glioma, fewer than half are going to have NF1. Is that right, Judith? You know what? I don't know the numbers. It seems like it's 15, 30%. And the same is true of patients who have NF1, most of them don't have optic glioma, optic pathway glioma. Now, certainly many of them do because there's a clear association, but most don't. So I think that these two are, that A and B are not true. It's an association, but it's not most. These patients often have surprisingly minor vision impairment. They can have these big, huge masses and their vision seems to be not that bad. Again, I'm getting into your realm a little bit since I don't see these patients myself, but in my readings, and when we see the patients who have optic pathway lesions, I'm often amazed at how well the patients are described to be able to see. So C is the right answer. And enhancement, unlike other glial neoplasms, enhancement does not correlate with grade of tumor. You can almost think of these as like pylocytic astrocytoma. So the classic posterior fossa pediatric brain tumor, pylocytic astrocytomas have an intensely enhancing nodule, but that's not a high grade malignancy that is one of the features of that tumor. So optic pathway gliomas are a little bit like, you can think of them as kind of like these grade one glial tumors in that they can have quite a bit of enhancement and not be a great higher grade malignancy. This is kind of a paradox here. All right, so here we have what kind of sequence? So it's T2 and the fat is dark. So it's T2 with fat suppression, either a spin echo or a stir. And you could say that all of these answers are right about one, right? So I use the word best on purpose because I think there's one best answer, maybe two best answers. What's your best answer? Was that D? Unfortunately, that's the one wrong answer. And the reason is because this is multilocular with fluid layers, which means this is a repeated hemorrhage multilocular relation. I would call this a venal lymphatic malformation. It's a malformative lesion and it often presents in kids. It can have these serial events. They will often have sudden vision loss because of hemorrhage and over time you build up these fluid layers. These two terms are kind of falling out of favor because they're old style. They're 20th century terms and they don't reflect the pathology as well as we understand them and they have the OMA in them which makes it sound proliferative or neoplastic, which these are. These are malformations. So we try to get away from cystic hygroma and lymphangeoma. Venal lymphatic malformation is probably the most pathologically accurate term. These are usually type one master malformations because they may or may not have any venous component. There is overlap. They can have venous component or not. Clearly they have some kind of bastard connection because they bleed but they can either type one or type two. Now if they have a varic syndrome and we've seen some of these patients they're pretty uncommon but these dramatic varices where a patient holds their breath and in about 20 seconds they can make their eye pop out by filling this varix up with venous blood. Those will be the type two malformations. They can have a very similar pathology to these originally used to call lymphangeomas because they do have this venous connection but these are malformations and they're distinctly different from a cavernous hymengeoma. This is also a bad, not a great word because they are also malformations and not tumors. But the cavernous hymengeoma is an adult lesion. It's very discreet. It's encapsulated. They don't hemorrhage. They don't have calcification in them and it's a different beast. Okay, so here you have a CT and an MR post-contrast with this varic characteristic what we call tram-track calcification meaning it's something that is casing the optic nerve and it's enhancing on a post-contrast T1. So what is this? Meningeoma. So now this will be again pretending like I'm a clinician and trying to imagine what kind of clinical feature might accompany this. So what's the best answer here? Well, does revision loss happen suddenly? Usually it's a very gradual, right? And unlike acute octandritis it tends to be pain less. This is a complete red herring. What does this come from? There was the last oral conference we showed a patient that you can be keen all right because of me carefully spot those trying to throw you off with maybe some sort of neurofibromatosis idea. This is the typical demographic here. Now this one, Judith, I imagine that radiation could induce a meningioma. We're starting to see the intracranial. It's probably not the most likely but have you seen radiation-induced intraorbital meningiomas? No, not an optic nursing meningioma. I've seen from radiation in general but not from your sheath. So I thought D was the answer I was looking for here. Okay, so this is a trauma patient and they have a fractured transverse process. And by the way, can you recognize the level by the morphology? What's that? I'll give you a hint. The transverse foramen is this little tiny thing that is not being used. That's why it's tiny. One of the cervical vertebra doesn't have the vertebral arteries in its frayment. It's a vestigial frayment. At which level is that? Seven. So you can actually tell seven by its morphology. They have a transverse process fracture here and this patient presented with a hornar syndrome. Now of course with trauma and hornars, we get a CTA and everything. This person's CTA was normal and this was the cause of the hornars. So what kind of hornars is this? And any volunteers? So I did bring a diagram of this. So down here, you're actually getting the second order neurons. So the answer here is the second order first order would be the neurons that come from the hypothalamus down to the cilio spinal center. So the brain, the spinal cord is the first order. The second order are the ones that come out with a brachial plexus and then ascend toward the superior cervical ganglion and the third orders are the ones that take off after that. If you chose C, you have to get a minus point because there is no such thing. The second orders are pre-ganglionic by definition. This one is quite long. I was wondering if you could have some new anatomical structure that I hadn't heard of. No. Okay, so here's the diagram. So for pre-ganglionic, the pathway goes from the hypothalamus down to the cilio spinal center. So it comes down here. Synapses there and then it comes out up to the superior cervical ganglion. And there are two ganglion here to remember that are named. There's the stellate ganglion and there's a superior cervical ganglion. The ganglion part of this term is actually this refers to the superior cervical ganglion not the stellate ganglion which is kind of a combined superior thoracic ganglion with another ganglion. So when we say ganglion we mean this one right here. So you have first-order nerves here that are pre-ganglionic and second-order pre-ganglionic here. And when you have a trauma or something in the lung apex, that's going to be the second order. And the third-order post-ganglionic are after that. So the lesions do this. So the first-order brain and spinal cord, brachial plexus, perispinus, medistinum, lung apex, those are going to be the second-order pre-ganglionic partners. Whereas the post-ganglionic they come from the superior cervical ganglion along the crottin plexus into the skull base and kind of follow V1 into the eye into the orbit. So pre-ganglionic there's the ganglion and then it follows the artery up and into the orbit that way. So for those we see it with dissection are sure opposite like FMD masses, glumus, tumor ocean. Okay.