 Okay, we're gonna start with the imaging strategy, what we call a protocol. So I'm gonna start by having you answer the question. These are the basic kinds of images, the sequence that we use, and identify the six images. What is the pulse sequence? And those categories aren't necessarily all used. Some of them might be used once or twice or more. Okay, that good? All right, so in radiology, we call this orbit MRI. That's because radiologists are ignorant as to the subtleties of your specialty. We don't know about oculoplastics and their ophthalmology quite as much. But when we say orbit, what we mean is it's basically eyes, orbit, skull base, midbrain, the portions of the brain and skull that are involved with vision and ocular motor and the relative neurological findings. So when we say orbit MRI, we kind of need a grab bag of those things. Now, the core of the sequence is that you can use in this and actually any head neck, if you do what we say head neck, we mean stuff that's not brain. And any part of the head neck, including the orbit, is an actual coronal fin section and you do a T2 fat sat or a stir, a T1 pre and a T1 post contract fat sat. And we call this the six back, and I'll show that in just a second. So in addition to those six, we do an ultra thin T2, which is just looking at the cisterns, the nerves and the arteries in the cisterns. We use diffusion of the brain. There is some diffusion used in the orbit and the head neck and then whatever whole brain and angiographic imaging might be appropriate. So these two, this is basically a pair, three pairs of sequences that we call the head neck six back. And this can cover pretty much any part of the skull and just depends on where you're gonna cover and how often the sequences are gonna be. The two on the left, this is actually a coronal, these are the T2, because the vitreous is bright, CSF is bright. The fat is dark. So it's either gonna be a T2 stir. I'm sorry, is either gonna be a T2 fat sat or a stir. Both of those accomplish the same thing. In the middle, these are T1 pre's. CSF is dark, vitreous is dark, fat is bright. We don't fat suppress pre-contrast generally because you wanna have the contrast of the fat to show you what things are. And by contrast, I mean the visual contrast. And then on the right, these are post-catalinium T1s, axial and coronal. The fat is dark, so the fat has been suppressed. This is our basic six sequences you can pretty much cover any part of the head neck with. In addition, we do these heavily T2 weighted, very CSF-bride sequences that emphasize a structure that are in the cisterns. This is not really great for looking at parenchyma. It's just really a fluid, sensitive sequence. And then we throw in whatever vascular imaging is appropriate. Now for the most part, we've gone to CTA for most of our neurological and probably optimal logical evaluations because it's got better spatial resolution. And also you don't have the temporal issues with a patient sitting down in a magnet and moving for five minutes to get a lot of motion with those. But MRA does have its role. You can do time of flight in the head, dynamic contrast imaging in the neck. And with MRA, the one thing you can get in the urogram of CT is these thrombus-sensitive techniques to look for things like intuohematoma or a dissection. So this is a typical post-contrast dynamic neck. And then this is one of those T2, one of these thrombus-sensitive T1 weighted sequences that shows you little bits of dissection as sudden tilohematoma. This is a non-contrast. This is probably the one time that we use fat suppression with T1. Blood is bright on T1. And when you're trying to look for small areas of dissection, you want to see just a little bit of blood in the wall of the vessel. We use a T1 and we fat suppress that so the fat cycle goes away. And all you see, and we don't even have contrast. So all you see is anything that is intrinsically bright on T1, that includes things like blood, melanin, certain types of calcification. And if you fat suppress, then pretty much what you're left behind is what's bright is maybe something that's flowing. Flow can have some intrinsic T1 signal without contour, without gadolinium. And then blood products that are so acute will be often pretty bright. And so the six sequences are these two on the left, one of them is a stir and the other one is a T2 fat set. And this one is a stir. It's got a little less space resolution. This is a T2 fat set, but they both achieve the same purpose. Leagens are bright and fat and other things are darker. This middle one, these are the T1 spinneco non-contrast enhanced. And this is our sequence that shows basically the anatomy really well. You want the fat signal for the most parts. We don't usually fat suppress these. And then on the right we have the axioclonal T1 post-contrast with fat suppression. These show enhancing lesions very brightly. Of course, things like the extra on per muscles and mucosa vessels will also enhance. The pathology that is past the blood-brain barrier or the tumors or inflammation will enhance. And in this case, you want the fat to go dark because it gets in the way of seeing what's enhancing. So this is a T1 post-contrast fat set axioclonal corone. Okay, skull base anatomy. So I'm gonna show you a series of sequences, a series of CT images. And there are six things to identify and not all visible on each one. So I'll show you one at a time. Starting with the coronal. These five parameters match them up on your sheet. Then after this, I'll show you some axial images with the same numbers. So you give you kind of a confirmation or a confirmation depending on if you're either wrong. I'm gonna give you the axials to see if that helps a little bit. And number six is only on one of the images. And there's one answer that is probably a little imprecise, but that's okay. This isn't the standardized test. And actually some of the best questions that you learn from the most are questions that have a little bit of imprecision to them because then you have to understand the subtleties and it gives us a chance to discuss. It did. Anybody want to go back to the other one? All good? Okay. So when addressing the skull base, it helps to divide it into these four big chunks. The anterior, which is basically number one. The central, which is the complex stuff with a lot of frown, that's a little bit of what we're talking about here, is the central skull base. The t-bone, which is actually just another part of the skull base that has to do with the prenatal nerve seven and eight and the carotid and the posterior skull base, nine through 12. And the central is really what we're talking about with a nerve, though, in orbit. We can look at the list of foramina. And again, these three, the optic canal, oracle, fissures, and rotundum are probably where most of the action is with regard to cranial nerves and skull base foramina. From below, we're looking at three, four, five, the big chunk here, and six, optic nerve above in close approximation to the infidibulum, looking from the skull base above, two, three, four, and six, and five. And on axial CT, this roll on the top, going from superior to inferior, this is the optic canal. Notice how they're coming together to make an X, right? Below and lateral to that is the superior fissure, and then a little further down, superior fissure there. Now, I don't really make a distinction much between superior fissure and inferior fissure, because they're the same structure. They're all connected. It's just what level are you at. So it's not really possible to say on imaging where the superior starts and the inferior stops, because it's a gash right there in the back of the orbital apex. The inferior is more in line with V2 and rotundum, so it's a little bit lower, but for purpose of imaging, it's just that open slot in the back of the orbit. And the biggest thing to remember is that the optic canals are close together and they're angling toward each other, and the fissure is kind of pointing straight back here and here, so that's not optic canal. That is optic canal. A little further down, you have foramen rotundum, which leads into this little space here that is the pterigopalatine fossa. And we call that the crossroads of the deep base because there's all kinds of interconnections right there between the oral cavity, the nasal cavity, the masticator space, orbit intracranial. And from a coronal in front, going further back, this is the optic, this is the optic stretch right there, that little piece of bone that connects the cliner process to the central sphenoid. Above that, and medially, is the optic canal here and here, optic canal here and here. The fissure is right below it, so notice how as you're coming into the very back of the orbital apex, the optic canal, and the superior and inferior orbital fissure are all this kind of open space right there. As you go further back, the optic canal separates out, goes medial, here you have what's left of the fissure, going a little further back, the inferior portion of the fissure turns into foramen rotundum right there. Below and medial to that is the vidian canal, so this is foramen rotundum, vidian, your cliner process, and now the optic nerves are starting to come together, a little further back they're gonna join into the chiasm, and then even further back we have the vidian canal here, and that is now turning into Meckles cave as the rotundum goes back into the cranial compartment. We don't really see foramen rotundum valley much, well valley is more of an E and T thing, it doesn't really enter much into what you do, but here it is right there, foramen rotundum valley is this little foramen right there, and if we were to go even a couple of slices further back, we'd see foramen o valley as a hole right here, and right there, so it's pretty distinctive when you see it, but it's a little further back from what we're dealing with here. Okay, so this was optic canal here and here, here and here, this is superior fissure, if you wanted to call either one of these inferior fissure I think it's fine, because again they're more of the same structure, this is rotundum here, vidian rotundum, as you come forward from these foramina into this open space right there, this is the pterigopalatine fossa, I didn't really label this one, but this is the sitting palatine canal, the pterigopalatine fossa has a connection into the oral cavity through this palatine canal right there. So optic nerves, fissure, fissure, rotundum, pterigopalatine fossa here and here, vidian canal and ovale. Okay, identify these cranial nerves. Okay, got them all? Let's start with vision and second cranial nerve. We follow up from obviously the retina and globe intraorbital segment of the canal, intra-candiliculars of the cisternal chiasm and track them back into the intraprancimal pathways. So we aren't gonna talk a whole lot about the intraorbital nerve, but it's important to recognize what it looks like on imaging because the optic canal is at an angle, they're not gonna show up as round dots, they're gonna be either oval, so you might not even see a complete circle around it because depending on how the slice is taken, but you'll see it if it's perfectly aligned as this ovoid canal here, again, it's medial and above the optic strut and the planet process, fish are below, so this is the optic canal. It's easier to see these things on CT, so you kinda get in your mind what looks like on CT and then you remember that and project it onto MR. So now that I've shown you the CT and superimposed the MR, it's really easy to see where it is. Here's your optic nerve here and here, but it can be kinda hard to do that without a little bit of memory of where these things are. And if you follow this back, you're sure optic nerve that are coming out of the canal and further back into the cisternal portion of the optic nerve, they're back to the chiasm, the level of the infideevillum of the pituitary, further back into the tracts and that would be good. In the actual plane, you can see that the optic canal or the optic nerves, if you kind of just ride after you see the X going from the nerves of the chiasm to the tracts. Now at the nailing, you don't see this view very often because that's a different angle. To see that view, you actually have to take a slice that is quite a bit angled from straight up. So you normally don't see that in the standard imaging, but if you really wanted to kinda lay out the chiasm because you had a particular interest in it, you could do this axle at an angle and have it show that way. In the mid-satidol, this is the third ventricle, massager media, anterior commissure. At the front of the third ventricle, these two little recesses, this recess is right above the optic chiasm. That's the chiasmatic recess, and the right behind it is another little recess. It's the infideevillum recess as it's going into the pituitary. So on a saddle teaching, you can see these things. This is the third ventricle, rookie mistake, this is not the third ventricle, that's the between the lateral ventricles. Third ventricle, and I think it kinda looks like the head of a bird, like a water bird, a loon. This is the eye of the bird, and this is the beak. And this part of the beak, that's the chiasmatic recess. There's the chiasm, infideevillum recess, there's the infideevillum of the pituitary. And you're pretty familiar obviously with the pathways and their geometry. Moving on to the motor nerves, we follow them from the central nuclei and neural pathways into the cisternal segments, through the cavernous sinus, the framina and the skull base, through the fissure, and then into the orbit. So three, paired nuclei in the midbrain, they exit at the interperituncular cistern, they dip down and go under this portion of the posterior cerebral artery. From the side, you can see the nucleus that exits the interperituncular cistern comes down, comes underneath this portion of the posterior cerebral, right above the superior cerebral artery, into the cavernous sinus, through the fissure and into the orbit. On imaging, you can see these nerves that are coming out of the cistern. Again, because they're dipping down, they're not gonna show up as a line, you're just gonna see them as they course through the plane. So the two nerves coming out as you go a little bit further down, you can hear the other one, we don't see quite as well, coursing through the cistern. And then when you get, as it's going into the cavernous sinus, there's a little sleeve of CSF right around the nerve here and here, that's the oculomotor cistern, it's the way you can identify it as it's coming forward into the cavernous sinus. In a criminal plane, here is that nerve, remember, it comes down and loops under the posterior cerebrals. This is the basilar artery, anterior inferior cerebellar, superior cerebellar arteries. Here's the P1 segments of the PCAs and the third nerve comes right between that and it's sort of caught between these two arteries, which is why that could be a place where you can get into trouble. And if you come forward, this is again in the criminal plane, I wish if there's a little sleeve of CSF around it, this is that oculomotor cistern right around the third nerve as it's about to enter into the cavernous sinus. And this is a reminder of that relationship between the third nerve, this carotid, PCOM, and the PCAs and how it's between the PCA and the SCA here coming off the basilar. Fourth nerve, they're a little bit lower in the dorsal midbrain, they exit around the back, come around in the perimesincephalic cistern on both sides. They also, of course, right lateral to the thirds in between those two arteries. So underneath PCA and above superior cerebellar coming forward. So very close to just lateral to the third nerve. So from the lateral, we see it exiting around the back in the perimesincephalic cistern. It's a small nerve has a long course, which is why we think of it as being sort of susceptible and exposed to injury. Coming between the two arteries into the cavernous sinus through the fissure and into the orbit. It's a very small nerve, so you don't always see it, but on these really thin kiss images, you can sometimes see it exiting around the back. It's hard to see it in the perimesincephalic cistern. There's a lot of other stuff in there too. There's the basilar, the basal ways of Rosenthal and the PCAs and branches. So there's a lot going on in this perimesincephalic cistern. So it might be hard to actually track the fourth all the way since it is such a small structure. And if you follow it closely, you can sometimes see it in this space between the PCA and the SCA, but that can be difficult to see every single time because it's a small structure. Fifth nerve, pre-ganguinic segment. The gang is sitting in necklace cave and then the three branches. V1 is the one that most often shows up in the neroth and orbit, but the V2 also coming straight forward here in the frame rotundum through the inferior fissure in the orbit. And then V3, which you don't deal with very much, coming straight down through frame rotundum valley. And this would be a coronal slice in this location would show you that V3 frame rotundum valley going straight down. It's a really easy nerve to see. It's a big fat one and you almost always can see it even on routines of brain imaging. Coming right out of the lateral ponds straight forward and it goes into necklace cave, which is going to be a little pocket of CSF and you'll often see the fibers, which look kind of a trunk behind. As they go into necklace cave, the fibers will often sort of separate. I can see like a little individual fibers coming into the ganguin right here in necklace cave. The sixth nerve with its nuclei posterior in the lower mid-brain and the nerves come straight forward. They exit out underneath the ponds and ascend into the preponted cistern. So from the side, you can see, so here's the nucleus of six, the fibers come out and they exit right underneath the belly of the ponds and then they ascend kind of following this lower contour of the ponds and they go into the cavernous sinus through a little, there's a little dural reflection there, a duralus canal that you can sometimes see as a little pocket as the nerve goes. Kind of skimming right over the edge of the temporal bone right there. Now, it's a really small structure, but because nothing else runs in the same direction, you can usually see it. It's ascending and so it's not gonna show up as a single line throughout this whole course, but there's really only one structure that's coming in this direction, kind of straight forward, maybe angling a little lateral and that's the sixth nerve. So you can usually see one structure coming up here like this and that and that's the sixth nerve. From the side, again, there really aren't very many things that are coming out from one of the ponds ascending up in that direction, so you can often see it, even though it's a fairly small structure. In the coronal drawing of the cavernous sinus, there is the second nerve, third, fourth, V1, V2, and sixth. Six is sometimes described as being the most exposed to cavernous sinus disease because it's the most kind of floating identity within the center of the sinus which has a little bit more of a, kind of a durable approximation. So the sixth nerve of the five nerves here, this is five, this is six, this is two because it's, remember, if you think about the little birch beak, that's the chiasmatic recess, there's the chiasm, this is three, and this is four. Okay, let's talk about some pathology, visual pathways first. Question one, which of the following diagnoses is least likely in this young adult with acute vision loss? We have a coronal T2 fat suppressed and a coronal T1 post-contrast. MS, aquaporin, demyelination, MOG, sarcoid, or wagoners, which is least likely. And the next question, question two, we have a post-contrast axial. This one is not bat suppress, but it's post-contrast. You can see that mucosa and vessels are bright. Which of the following is most correct regarding this optic pathway lesion? Most patients with this lesion have NF1. Most patients with NF1 have this lesion. This lesion is associated with mild vision loss. Enhancement indicates higher tumor grade. So which of those is most correct? Just, oh, a third question. Which of the following is the most likely clinical feature in this lesion? Is the axial CT with no contrast? There's also an MR to go with it. Can you go back to the answer? So these are the options. Sudden vision loss, painful vision loss, post-ovane, cafe au lait spots, middle-age female, prior radiation therapy. Okay. All right. So differential diagnosis of visual pathways affected by tumors in the orbit, skull-based cisterns, optic glioma, meningioma. There's other orbital masses, a lot of which we won't have time to talk about. The tumor theory, because of its close proximity to the optic chiasm, and then metastases of a number of varieties. This is an example of an optic pathway glioma. They can have a lot of variability in their signal. They tend to be quite bright on T2, but as you can see here, they can have some heterogeneity. Enhancement can be quite variable. Now, think of a glioma as kind of like an almost like a polycytic astrocytoma. In a lot of ways, they're the same lesion. Of all the central nervous system tumors, this is the one that breaks the rule about enhancement. Enhancement of a polycytic or a glioma does not correlate with, in fact, you can have these can be two grade ones, and they can have quite a bit of enhancement. So enhancement doesn't tell you about degree of malignancy. It can involve any part of the pathway all the way back into the lateral cheniculocent, and you can also have intraperancomal lesions. They can enhance, they can not enhance, they can be bilateral. As in this case, we have big fat optic nerves, optic chiasm, and tracts. This is an example of an optic, intraorbital optic nerve sheath meningioma, and the classic appearance is what we call tram-track calcification, because it's the dural sheath around the nerve. So if you cut it down the length, you get the calcium on both sides, you get the tram-track, and also you get the same picture on post-contrast T1 MRI. You show the meningioma along its length, and you get tram-track enhancement. So this is a classic appearance of an intraorbital nerve sheath meningioma, and the other thing on T2 that's been described as a feature of this is you get a little pocket of CSF collected right behind the optic nerve head due to the mass effect from the intraorbital dural tumor, and that's called an optic, a perioptic cyst. This is an example of metastases affecting the visual pathways. This is a post-contrast coronal T1 with fat suppression. Now, what shouldn't be there is all this signal here. This is a T1, which means the CSF is supposed to be dark. You're not supposed to have any brightness around the optic nerve. This is a patient with extensive leptomine and geocarcinometosis, and the metastatic disease is falling right down the CSF all the way to the orbit down the optic nerves. Macratinoma, it's a cellar mass. When it has supercellar extension, it can affect the optic pathways. It tends to be very intensely enhancing a little depending on what else is going on. You can have some non-encing areas. One thing that we pay really close attention to when there's vision loss and a pituitary mass is any evidence of blood, because if you have an acute hemorrhage into a pituitary gland and you have sudden enlargement, you can have acute impediment of the optic nerves, and that actually is a neurosurgical emergency and needs to be decompressed. So that's pituitary apoplexy. So if you see blood and sudden vision loss in a pituitary mass, so like here, this is a non-contrast scan, all this brightness here, that's all blood products. You can imagine how it's pushing up on the optic chiasm. To us, that is a neurosurgical or neuro-ophthalmological emergency. Inflammatory conditions of the optic nerve, acute optic neuritis. Pseudocomor can affect the optic nerve, but it tends to be more than just the nerve. Infectious repose, infectious optic neuritis, and then granulomas disease can affect the optic nerve. So this is a patient with acute optic neuritis. So we see the T2, we see enlargements and hyperintensity of the nerve. The CSF around it has been effaced because it's swollen, post-contrast T1. You can see that the nerve is enlarged and enhancing compared to the normal cycle. Now when we see acute optic neuritis and we're thinking about this could be demyelinating disease. In addition to optic pathway imaging specifically, it's really important. In fact, in some ways it's almost more important to make sure you do the whole CNS act so you know how much disease. Here's an example of pseudo-tumor affecting the optic nerve. First, this is a lesion that we weren't sure what it was. It kind of looked like a meningioma, but after some steroids and some time it went away. So this was actually pseudo-tumor in a perioptic location. Ischemia of the optic nerve isn't necessarily always an imaging diagnosis, but there are sometimes when it can be useful, anterior and posterior forms. And then brain imaging, sometimes when you're having patients with stroke can present as visual disturbance depending on where the stroke is. If we think about ischemic optic neuropathy, the anterior form, which is gonna be the more common, isn't really an imaging diagnosis, but if you happen to have imaging of an acute optic neuropathy, you can see a little bit of enhancement at the optic nerve head. And that's a distinction to the very rare, thankfully, and very tragic posterior ischemic optic neuropathy, which is the perianesthetic, prolonged, skull-based cervical spine anesthesia surgery. You can see striking dramatic diffusion restriction and after a few days, you can see some enhancement of the optic nerves. That's thankfully a rare thing. Thromoembolic Barsch can show up as a visual disturbance if it affects the visual cortex specifically. And occasionally, if you have a PCA stroke that happens to affect that primary, that may be the main presenting symptoms, and then usual neurological imaging, profusion diffusion, and then angiography, make sure you know what the anatomy is of the vessels. PCA is actually the lower vessels here and the basal veins of Rosenthal are the ones above, and then we'll track those back as they go into the branches of the PCA. Okay, so question one, which of the following is least likely in the second dollar with acute vision loss? What do you think? So I said E, because all the other ones, we've seen show up as just primarily optic neuritis, but I don't think I've ever seen wagons or show up as just optic neuritis. It has a lot of sinus disease and the oral stuff along with it, which is most correct regarding this optic pathway glioma. Now A and B are, they're associations that are important, but they are minor associations. It's only about, I think it's something like 30% of patients who have this actually have NF1 and only like 50% of patients with NF1 actually have this. So it's not most, it's some. There's an association, but it's a minor association. C is true, because this is, this can often be very, very mild vision loss. You can have these really dramatic-looking masses and the vision is not that bad and enhancement does not indicate higher tumor grade, so it seems the answer here. What's that? You can point out the glioma. Oh, it's the fact that these nerves are big and fat and juicy. Think about the optic nerve should be about this size here and the cisternal and the chiasm part is all really significant. Now because this one doesn't enhance very much, it's a little harder to identify it. And because it's bilateral, yeah. So your eyes are looking for asymmetry and that didn't help you here. What's most likely clinical feature in optic nerve she's been in glioma? Well, vision loss tends to be gradual and painless and this is not associated with that category LA spots, but it is classically seen in middle-aged females and usually, I imagine you could have radiation therapy in this instance, but that's not usually the typical history that we see. Okay, pathology, ocular motor and other intraorbital lesions. Question one, which of the following diagnoses is least likely? I do a lot of least likely questions because, again, this isn't standardized testing. They're actually really useful in radiology because a lot of what we see is you don't always have exactly one answer. It's like, I think I know one or two things that this might be, but it's definitely not this. So which of these is least likely? Pseudotumor, Graves disease, ITG4, lymphoma, or sarcoid. That's not a happy page really, not at this point. What is the best diagnosis for this lesion? Axial T2 with fat suppression. Tepegroma, Lymphangeoma, middle-empathic malformation, cavernous hemangioma, type three vascular malformation. You could argue that there might be more than one correct answer, but depending on how you feel about terminology and the use of certain terms, there's probably one better answer. Okay, intraorbital pathology. Flammatory, we have Pseudotumor, sarcoid, thyroid, eye disease, tumors, we have lymphoma, proliferative as well as metastases, vascular, we have both malformations and neoplasms, so we could expand on these lists quite a bit, but we don't want to spend too much time on just orbit. Idiopathic inflammation can have a number of manifestations, and that's kind of one of its chief hallmarks is it can have one or more of these developments. The myocytic form, especially the lateral, you can have lacrimal form, the anterior form, which is especially involving the nerve and intraconal structures, the apical form, which is at the fissure and the apex, aka tulissa hunt, then you can just have diffuse masses all over the place. Here's an example of a myocytic form of a patient who had an enlarged superior oblique, and the patient had a palsy, it got better, with steroids, presumptive diagnosis of Pseudotumor. Do you know what I think is your patient with a VA many years ago? Very possible. You've seen a couple of those over the years. Yes. This is an example of the apical form of a tulissa hunt. You have this enlargement of the cavernous sinus and mass-like enhancement going into the orbital apex, and this would present with multiple painful cranial neuropathies. Grave disease, we see as non-uniform, but kind of symmetric involvement, and it has a very specific involvement of muscles, especially the inferior and medial, we use the mnemonic, I'm slow, inferior and medial, most likely superior, lateral and obliques, less likely. In fact, if you see isolated lateral or oblique disease, that's not gonna be viral-related disease. Typical examples of thyroid eye disease with symmetric involvement of the muscles in a non-uniform fashion. You can't have asymmetry, but if you have involvement of one set of muscles, you almost always have involvement of the other. Even if macroscopic, we can't see it. If you were to look at biopsies, there would be inflammation in the muscles on the other side. Lymphoma shows up with lots of infiltrative, we call this plastic massages. They tend to get into things, kind of wrap around things, get into everything like lacrimal, intraconal, extraconal, skull base, also intracranial, and orbital vascular lesions. We separate these into two broad categories, malformations and neoplasms. Malformations, we have the venal lymphatic. These are the ones that have had a lot of different names over the years, cystic hygroma, lymphangeoma, but really, venal lymphatic malformations is kind of an overarching term we can use. Orbital cavernous hemangioma is actually a malformation, not a neoplasm. We still call them hemangiomas because that's what we've called them for decades, but they're really malformations. And then true AV hematur, which are pretty rare. Neoplasia is really more of a childhood set of diseases. The infantile hemangioma and congenital hemangiomas, we do see these hemangioperatives when we're in adults which are uncommon. A couple of examples of the childhood kind of diseases. This is an example of one of these venal lymphatic malformations. The characteristics of these is multi-loculations and blood fluid levels. They love to hemorrhage, they love to get big, and these multiple levels of hemorrhage is the classic kind of hemorrhage on your arm. This is an example of an infantile hemangioma, these multi-spatial, intra-orbital face, they can even go into a trail, big infiltrative enhancing masses that tend to regress as the child grows. Leading to the adults, this is the classic cavernous hemangioma. Again, these are malformations that we call them. I call them orbital cavernous malformations and then put hemangioma in chords so people know what we're talking about if you're communicating with somebody who wants to call this a hemangioma. We have to know that that's what we're gonna term it, but it really is a malformation. And then ADMs of the orbit are really quite rare. Okay, so which is the least likely? Well, it involves the nerve, it involves the muscle, but there's also intercranial disease, supercellar, and even the third nerve has some disease aligned. So when you have this kind of multi-focal infiltrative process, it's gonna be either a lymphoma or it's gonna be inflammatory granulomas. So, pseudo-tomorubet, ITG4, yeah, lymphoma for sure, sarcoid, yes. This would be a great picture for any of those. This happens to be sarcoid. The one thing it's not gonna be is thyroid eye disease because it really doesn't have the pattern of muscle involvement, and this kind of nerve intercranial involvement will not be seen. What is the best diagnosis? Well, really the best name for this is venolympatic malformation. Cysticaegroma is an old-fashioned term, hemangioma also old-fashioned. Oma implies neoplasm, and so we don't like to use those terms if we're trying to be really pathologically accurate. So, venolympatic malformation is the best term. Cameras, hemangioma, those are the adult circumscribed, really discreet lesions, the ones that surgeons love to operate because they apparently they just come right out and make you feel good. Type 3 vascular malformation, that would be an AVM, that wouldn't be this. Skull-based intercranial pathology. I think in the interest of time, I'm just gonna, we'll go over these quickly at the end. But I will ask you, number six, which of the following is least likely in this patient with multiple cranial neuropathies? This is a T1, post-contrast knock-pads out of the brain showing all this enhancement in the basal cisterns. West Nile, Cryptococcus, Sarcoid lymphoma, tuberculosis, which is least likely. So, we already talked about pituitary adenoma with regard to visual pathways and meningioma as well, meds either in the skull-based or lifted meningiol. And schwannoma, which is interesting, but somewhat rare. So, in addition to going straight up like these pituitary macro-adenomas tend to do, here you can see a little bit of mass effect on the optic isom. If they go sideways into the cavernous sinus, they can invade and affect cranial nerves there, but that's relatively less common than the typical supercellar extension. Here's an example of a cavernous sinus, sort of a typical location for meningioma. Here we see thickening of the dura and enhancement. This looks an awful lot like that case of Toulouse-Hann, doesn't it? The difference is this is not gonna be multiple painful cranial neuropathies. This is gonna be chronic painless cranial neuropathies. This is a classical location. This is a really common location for a central skull-based meningioma. Notice also that the medial rectus is out. When you have diffuse local meningiol disease, you can get, of course, a lot of other neurological symptoms, but cranial neuropathies is one of the things that you will see because they tend to be exposed and react poorly to the infiltration of anything. In this case, it happens to be a primary cranial tumor of PXA, but anything that is diffusely spread throughout the CSF can give you multiple cranial neuropathies. Schwannoma is a somewhat rare condition, but it's interesting and we've seen them occasionally. They can be isolated on three, four, or six. They can be associated with neurofibromatosis, and they show up as a nodular mass in the cistern along the course of where we know the nerve lifts. Here's an example of a patient who has a superior oblique that's out on one side and you look at the imaging. There's this little nodule right there now. It's going to be hard to see the fourth nerve normally, but that's exactly where the nerve lives, and we know that this patient has a superior oblique that's out, so this is a presumed Schwannoma of the fourth nerve. You're never going to operate on this because you're not going to make anything any better, but that would be a pretty, I think, confident diagnosis to make. Vastor lesions that can affect central skull base, venous thrombosis, and then carot-eficial aneurysm. So cavernous sinus thrombosis, as you can see in association with either something inflammatory like sinusitis or osteomyelitis, but also, you can't see it in malignancy that's invading the central skull base. Here's a patient who has chronic sphenotid sinusitis, and the fact that the bone is so reactive tells us that it's been that way for a long time, but at some point they got an acute secondary infection or a super infection. They got into the cavernous sinuses, and I don't know how the sinuses are wide, and it's a little easier to see that on MR. Multiple neuropathies, you're looking for an enlarged cavernous sinus, non-enhancing clot in the cavernous sinus, and usually the superior aphelic vein of the orbit is enlarged. So here we see a T2 on the left, this big, fat cavernous sinus is just chock-full of stuff on the post-contrast. Usually the cavernous sinus just lights up because it's full of gadolinium. Here we have all this thrombus in here. It is widening the cavernous sinus, but it's not a tancy because that's clot. And that's kind of a devastating thing to have to deal with. Internal carotid lesions in the skull base. You'll often see flow effects. For example, here is an aneurysm of the carotid that's going into the cavernous sinus. You can imagine it compressing nerves there. Look for either the flow void, or on some sequences, like contrast, there is, if you've seen what flow looks like on MR, there is a reverberation of signal along one direction, what we call the phase encoding direction, but if you see these little echoes of flow along one direction, that is what we call a phase-ghost or flow artifact. Aneurysms can't thrombose. There's a giant aneurysm of the terminal ICA. In this case, it's mostly full of thrombus, and you would need the CTA to find out what possibly where the neck of this thing is in relationship to the vessel. And then CC fistula, in this case, the example I showed you, really briefly. Angiography is something that is getting less and less common for us mirror mortals to know about. I did angiography when I was a fellow, but I don't do angiography anymore, and it's starting to be something that is now just for only the neuro-interventionalists to do. But it's good to know what the images look like. This is a lateral angiogram carotid injection. All this contrast here is in the cavernous sinus. It shouldn't be there. This is an early arterial phase, so you should only be filling out the arteries. You are filling out the branches of the MCA, but you're also filling the cavernous sinus, the superior ophthalmic vein, and you're also filling this vein right here, the metrososinus, so all these vein structures should not be filling in the early arterial injection, the structure you have a fistula of the carotid, which is least likely. Well, this is a picture of leptomeningial disease. It's either carcinomatosis or leptomeningial infection. Fungal infection, sure. Sarcoid, yeah, any granulomus disease, lymphoma, TB. When you think of lymphoma, or you think of granulomus, those two have a lot of overlap, so granulomus disease, sarcoid, lymphoma, TB, fungal. When you say one, include the other, because you have a lot of them, you've overlapped it. West Nile is accidentally supplied, as I'm going to show up with leptomeningial disease. Okay, we just have time to do some pupillary mythology. Question one, what is the most common location for aneurysm that causes pupillary dysfunction? This is your circle of willis, kind of schematically splayed out. But pick the letter and then name the vessel. Question two, what type, what subtype of neuronal injury is most likely in this trauma patient with Horner syndrome? First order, preganglionic, second order, preganglionics, second order, postganglionic, third order, postganglionic? And bonus points if you identify the ridiculous answer in this. Okay, so parasympathetic innervation comes from an injured Westfall in the midbrain. It courses very closely with the third nerve. You can kind of think of it in the same location. Compressive lesions have to do with the relative location of whether somatic versus autonomic fibers are in the nerve. So is the pupil involved? Well, it's a sphincter function that's impaired. And you get this when you have extrinsic compression. And that's because the motor fibers, somatic fibers are central, but the parasympathetic fibers are on the outside. So if you have extrinsic compression, it's gonna get the pupil first. So we think of the classic lesion as being a sacular aneurysm at the PCOM origin. A vascular lute into the same thing. So here's a classic PCOM aneurysm. It's the carotid artery coming up. And this is a big aneurysm coming off the back of the carotid at the PCOM. We call it a PCOM aneurysm, but technically it's an internal carotid aneurysm at the origin of the PCOM. This is right where the PCOM takes off. It's in close proximity to where that nerve runs and that's why it gets tagged. Here's an example of a branch. Here you can see the third nerve and it's being compressed by this branch of the anterior cervical, let's say A1. It's pushing it and giving the patient a neuropathy of third nerve. Sympathetic, pre-ganglionic. So the pathway starts from the hypothalamus down to the spine, to the superior cervical ganglion. So it starts on the hypothalamus down to the ciliospinal, comes out and then has its synapses in the superior cervical ganglion. Now to get the terminology straight, it helps to know which ganglion and this took me forever when I was learning this to remember but the stele ganglion is not the ganglion we're talking about. That one's down low at the apex of the chest. The ganglion that we're talking about is the superior cervical ganglion. So when we say pre-ganglionic or plus ganglionic, we're talking about the superior cervical ganglion, not the, is it timeout? Or maybe I'll ask then. I lost the screen, I can let it appear. Okay, so we have the first order nerves down to the spinal cord and the second order nerves up to the superior cervical ganglion. Those are the first and second order pre-ganglionic fibers. The post-ganglionic are those after the superior cervical ganglion. So lesions that give you pre-ganglionic are going to be in the brain with spinal cord. Although a brain and spinal cord lesion is rarely going to pick off just these fibers. You're going to have more than just a horners. You're going to have a bunch of other stuff too, especially if it's intracranial or spinal cord. You're going to know you have a brain lesion or spinal cord lesion. You're not going to have an isolated horners. But if you have something that isn't the brachial plexus or paracetamidostinium, it could be in a position to pick off those autonomic nerves and give you a horners without a whole lot of other things. Classic lung apex, the pachyloce tumor affecting the brachial plexus. You would of course expect to see some brachial plexus symptoms as well, but to be more localized. So here's an example of lymphoma involving the spinal column. There's an intra-spinal component. So you wouldn't be surprised to have some spinal cord symptoms as well, but here we see it affecting the area of the brachial plexus and of course those second order preganglionic nerves. Postganglionic, this is from the superior cervical ganglion and it follows the crotted plexus. He's the third order neurons through the skull base and it kind of follows into the orbit right along with, or V2, where V1 runs. So here's your preganglionic fibers. And beyond that, the postganglionic, they follow the crotted all the way up into the skull base and then through the fissure into the orbit. These are gonna be like classically associated with the crotted dissection, arterial plexus, like FMD. Masses that affect the artery, like glomus tumors. Here's an example of FMD. You can see all this very irregular beating of the crotted artery in the distal cervical segment, the classic location for it. Here's a patient with a long segment dissection of the crotted artery, peterous cavernous segments. And again, how we use these T1 pre-contrast images to look for subintimul hematoma as a sign of dissection compared to the normal artery. Okay, so what's the most common location for aneurysms that causes the pupillary dysfunction? B, right, PECOM. And the reason why the B is here and not here is because, again, the origin of the aneurysm is usually at the crotted where the takeoff of the PECOM is. So here we have a trauma patient and they have a fracture right where we know that those second ordinars are coming out. So this is gonna be, at least this lesion is gonna be causing a second order pre-ganglionic. This was the silly answer because there is no such thing as second order post-ganglionic. Okay, that's all we have. Any questions? Thank you. Thank you.