 I have the remainder of the filter in the next 2-3 minutes probably. This is a very effective room. Well, you could spread out in it. Yeah, that's true. I know! For my trial of the first few times, I'm working on it. It'll still be confusing. No, this is great. I think we're reaching critical mass here, Chris. Yes. Everybody knows Dr. Chris Davidson from Neuro Radiology. We really want to thank you for coming every year and giving us an update on neuroimaging because it's so important to all of us in ophthalmology. My pleasure. So, this morning, in addition to an imaging primer that's focused on neuroophthalmology, we've added facial nerve as an extension of the kind of things that you see in your criminal nerves, and the part of diseases that you see. I'm going to sit down because you don't need to look at me. I can see my screen, and I'll take this off so you can hear me. All right. So, we'll start with a brief reminder of our protocol strategy. And I call this imaging in the skull base because it really is pretty much anywhere in the skull base that we're looking at. Not just dormant in the central skull base, but the protocol is transferable to most any place in the head and neck, really. We'll talk about the anatomy of the upper and mid-cranial nerves and we're going to extend this as before to the facial nerve, but when you get facial, you get vestibular costers as a freebie because they're really right in the same neighborhood. And then we'll talk about CT and mRNA appearance of pathology. And for that, what we're going to have is... we're going to have just a very quick list of the differential, but most of the cases are actually going to be part of the quiz. So, we're going to put you on your game to see how many of these things you might recognize. And you're still doing quiz competition, is that right? Well, this year has been kind of a bit different. So, it's just bragging rights this year. Right, bragging rights. But that's still worth something. Okay, so for mRNA imaging, which is kind of the mainstay for most pathology, I mean, for trauma, for simple cellulitis, CT has its roles as a primary imaging approach and for some things likely for calcification, but for the most part for advanced imaging of neurophthalmological conditions, we're really thinking about MRI. Now, this is what I call the six-pack of skull-based imaging. And what you have is you have two planes, actually a coronal, and you do three different sequences. You do a T1 pre... you do a T2 fat-sat. Now, T2 fat-sat can be done one of two ways. The T2 fat-sat, as labeled there, is just to spin echo sequence. The stir sequence for all practical purposes is the same thing, but done in a different way. And you don't really have to know how to do these. For the most part, I don't go up to the machine and turn the knob myself anyway. But the stir is a little bit more reliable in terms of fat suppression, but it doesn't have quite as good of a spatial resolution. So we do one plane in one, another plane in the other one. When you see T2 fat-sat and stir from a perspective of what they look like, they're pretty much the same thing. And then we do a T1 post contrast band-sat. Axial and coronal. If you do these six sequences, you will see pretty much all pathology that you need to see. Now, we had a couple of things on top of that. There's a sequence called a case or a space which is very high resolution, very heavily T2-weighted. What we mean by that is the CSF is very bright and pretty much all the neural structures on the skull base are all dark. So you can't really see soft tissue differentiation on the right, but what you see exquisitely is the CSF in anything running through them, i.e. cranial nerves and vessels. And you don't have some of the flow artifact that you get in the CSF of the other sequences. We call that pulsation artifact when the bright T2 turns dark because there's some CSF motion. And then throw in, you see a whole brain sequence depending on what you're looking for. So these are your six pack. On the upper left, this is a T2, fat to press, and on the T2, this is where the CSF is bright, fat is dark, and then the bottom one, that's going to be a stir. You can flip those, whichever one has one stir that has a T2. And then we have our T1 pre-axial and coronal, and then on the right, you have the T1 post-axial and coronal. These are your money shots. This is at KISS, one of the T2 space sequence. You'll notice that you don't see the brain at Prankma, all that distinctly. Everything's kind of black. What you do see is every single vessel, these nerves, you can see them very, very nicely. These are ultra-thin. These are sub-millimeter things and give you excellent resolution. Okay, so anatomy of the region. It helps to divide up the skull base in these four areas. It's kind of weighted to chunk it and engage your arms around it. And orient these around like the cranial nerves. In this discussion, we're especially interested in the central skull base, the upper and mid-cranial nerves. That is the most complex area in terms of foramina, and mostly really where ophthalmology lives is in the central skull base. What we're going to extend our discussion today is to include the temporal bone, which is the discussion that focuses around cranial nerve 7 and 8. In the central skull base, the CDI bone is the anatomic foundation here with its component parts. A lot of complex foramina. We'll review those on CT. Especially, it's easier to see the foramina on CT, but you need to know where they are on CT so that you can then, when you look at MR, know where they're supposed to be. Temporal bone. It has also a fairly complex anatomy. The components of the temporal bone, the peters where, immediately, where the anterior sits, the mastoid and the squamous bone, which is part of the cauterium, and it houses the 7th and 8th cranial nerves and, of course, the carotid artery. If we look at this series of CT images from top left, superior to the bottom right and inferiorly, let's look at some of the component foramina. These two right there, that's the optic canals. Sometimes, optic canal versus superior orbital fissure can be a little bit easy to mistake. One thing to remember is, these should be crossing. You've got a chiasm that's coming up there. The optic canals are going to be on their way to form an X. That's an easy way to keep that apart. Plus, it's a little higher and more medial. Compare that to these two. Those are the superior fissures. When you're first looking at an image, you may think it was a mistake or for one another, but actually, if you look at the morphology and the level, they are very clearly identifiable. That right there marks the course of the Framon Rotonum. Framon Rotonum back here, it comes forward, and Rotonum is directly in line with the infororbital canal. You can think of the primary component of V2 through Rotonum going into the infororbital canal. You'll see them right in line here on an axial sequence. Down below, this is Framon Rotonum Valley. That is housing V3. It goes straight down where all the other components of V are going forward. Right in front of that is the Vidian canal. The Vidian canal is a distinctive canal. It's kind of easy to identify because it's got that sort of long sickle shape. It's usually visually distinctive and because of that, people sometimes mistake it for Rotonum because it's easier to see and it shows up more and more distinctly as a canal, but you want to not make that mistake. There's the carotid canal. It has a kind of a complex course. Further inferiorly, this is the horizontal portion, kind of coming at 45 degrees here, and then the vertical portion of the peatress segment of the canal right there. The IAC is pretty easy to identify there. And then just pointing out right there, those are the mathoid segments of the facial nerve, and they come straight down and exit at the base of the skull into the stylo-mathoid frame. Can you remind us what goes through the video? It's got bovidian nerve, which is mostly autonomic. It's got components of the GSB, the greater superficial patrol. So let's go into lacrimal salivary. And Dr. Gray, you're going to have to tell me why it causes headaches. Well, because, I mean, the skull-base anatomy is complicated all by itself, right? Yeah. And then the nerve itself is complicated because we don't study it very often. And who's doing anatomy? Somebody? Are you going to cover this? The vidian canal. Yeah. I'm not going to talk about it a little bit, but... The vidian nerve. So, yeah. I mean, we just don't think about it in our terminology that much. I just heard vidian headaches is maybe a thing, but I don't know a lot about how it might be related to what's in there. But it's mostly autonomic. I think GSB is kind of a primary component. Right. It's coming off of... So we'll look at that with facial nerve. Nervous intermediates coming through the temporal bone, and then it enters with facial nerve and goes through the GSB individual. We'll look at that when we get to the facial nerve. Okay. I'm going to just go through each of them again and... Meet the arrows? What was that? You want to look at the arrows again? Yeah. I'll just go through each one and just count. Okay. So, that's optic canal right there. That's actually one you got to know. Vidian one, that's kind of down the line, but optic canal is... Yeah. It's muscle. Optic canal there. Superior fissure here and here. Rotundum. Rotundum is a little short thing, so you can miss it. If you're slicing is all right, you might not even see it. But right in front of rotundum is this little pocket here. That pocket is the pterogarpallin fossa, and we'll see that on the coronal. That's kind of a crossroads where a lot of stuff is coming in and out, so that can help you find rotundum. Go right behind that and you'll see rotundum. Here is pterogarpallin fossa again. Here, bottom part of rotundum. That's coronal canal here and here. Down a little further. So vidding is going to be inferior. It's got this kind of long, sickly shape. It's a small canal, so you could also miss it as well, but it's quite distinctive. You see how it's coming close to the carotid, the horizontal portion of the pteroscarotid canal right there? This is how I think of it. The carotid canal, the carotid artery has sympathetic plexus that's kind of following it up right here. That's why you get horners when you have scoliosis fracture right there, because you're hitting the sympathetics. So think of it this way. The fibers from the sympathetic plexus right here are hooking up with fibers of GSP to make the vidding canal. So the vidding canal connects to the horizontal carotid canal. That's why we don't remember it there. So that would be the other thing that the vidding is made up of. GSP plus fibers from the carotid plexus. This is Ovali right here. Ovali goes straight down. So you'll see the whole pan up like this. This is spacial nerve. Your hand is the ganglion. I'm trying not to show it. Your hand is the ganglion. One and two go forward. Three goes down. So the v3 goes straight down like that. That goes through Ovali right there. Let's see. What else have we got here? So the vidding. Carotid. IEC. We'll look at that a little more closely when we look at the temporal bone. Okay. So same thing, coronal. This big space right here, that is the terabopalatine fossa. You can see why we call it the crossroads because it interfaces with the informal contents through the inferior fissure. It gets into the deep face through the terabopalatine fissure right there. It gets into the nasal cavity through the senile palatine frame. So there's all this connection right here. So we often, when we're kind of orienting ourselves, we'll find the terabopalatine fossa and then you can move from there into all the adjacent structures. Going a little bit further back to this. This is the most flowing from forward to back. Going back a little bit. So this is kind of a classic look of the central skull-based foramina. So in the senile sinus, there are some climate processes and right there, those are the optic canals. Now because the optic canals are at an angle, they're not going to be perfect circles when you look at them in a straight coronal. They're going to be oval and it may even be an incomplete circle in terms of bone because it is an angle. But they're very recognizable here and they're on the upper inner margin from the optic strata. So this is one that connects the climate process to the wall of the senile. So this is the optic strata here. This is the optic canal and right below that, that's the superior orbital fissure. The strata separates the canal from the fissure. That right there is foramen rotatum. And again, it's a short canal so you may only see it on one slice but it's pretty distinctive right here. Just at the lateral margin of the senile sinus and then below and medial to that right there. Now, this piece of bone that houses the rotatum and midian is the pteribod bone. And depending on how much aeration the person's senoids or sinuses are, you can have air that goes all the way down into this. So you have to be ready for this now to get a little distorted if you get an air recess from the senoid sinus into there. So that is the midian right there. That is Ovali. And Ovali is having these two go straight down. Now, right there is kind of a big open chasm when you look at that. This person isn't perfectly even the scanner so if they're not perfectly even then from side to side it might look asymmetric. That is foramen lacerum. Now, lacerum is something that mostly we learn in medical school when we're doing, you know, it doesn't really have much in it. It is a cartilage filled plane that separates the brain from the deep face. But because it's cartilage it shows up as kind of an empty spot on the CT. So just recognize that when you see that it's going to be kind of medial to where Ovali would be. That's not a pathology. That's not something eating the bone. That's foramen lacerum. There's the carotid canal at the horizontal segment. And then there's the IAC. Again, this person is not perfectly even the scanner so you might see one IAC on one side and the other on the other side because they're a little bit tilted. And then that right there that's the matric segment coming straight down out of the temporal bone. And then kind of ground out the other foramen that we see here. The jugular bulb is kind of, it's got a lot of directions to the way things come in. The sigmoid sinus feeds the jugular bulb and then the jugular goes down from that. So it's kind of a big open space but it usually has this contour along the top that we can recognize as the jugular bulb. So in 3D looking at from the top, this is your clinoid. This is the optic nerve coming out of the canal. In the fish we have 3, 4, 6 and all going into the superior fissure. We have V2 coming straight forward into rotundum. V3 going straight down. And then here are 7 and 8 in the IAC. And then 9 to 11 and 12 down further. You've heard of the high hill footprint mark? That's one way to recognize O Valley and spinosal doesn't have a lot going. It does have the middle energy artery and the landmark even. We call it the high hill footprint because it's recognizable as that on CT. From below, the close relationship between the chiasm and the stalk of the pituitary, the ocular motor, the third nerve coming out above the pons and the intrapericular cistern. 4 coming out of the sides. 5 this great big beefy thing coming from the lateral margins of the pons giving it three branches. 6 coming out underneath the pons and ascending near the midline. 7 and 8 coming out at the cervical apontine angle and then 9 to 11 and 12 below. So the anatomic considerations of course they begin at the brain of the nuclear cortical origins. The extra axilla course we can often see it in its cisterns and it goes through the scolese foramina and then ultimately extra cranials through the orbit and deep face and temporal bone. Finally to the end organ. So on imaging then cranular nerve 2 is pretty easy to see obviously for orbital. In the coronal plane again we already talked about this. Here are your optic canals. Notice that there are ovals here. Optic strut superior picture there. It's much easier to see this on CT but you may have to be able to recognize it on MR. So you fix this in your mind and then look at the MR and there they are. So optic nerve here and here. So once you get used to that you can recognize the pattern. The client processes a little harder to see because the bone is dark on MR. The sinuses turn dark. All the bones are a little hard to see here. So just you recognize that morphology and then you can see it every time. The optic chiasm and the tuotering and then back toward the optic tracts. So if you get a slice at an angle you can actually see the chiasm in its proper form there as an X. But that orientation is not usually seen. The chiasm is at an angle about 50-20 degrees like that. So if you want to get that picture you have to do it a special way. We don't normally get it that way but we do that. Midline anatomy important to recognize your landmarks here. This is the optic chiasm right there. Its relationship right for the infodigalum and the best way to see this on MR is actually with a T2. We don't do a lot of T2 midlines but if you're looking specifically for pathology at midline this can be useful. This is the third ventricle into your commissure. To me this looks like the head of a bird. That's the beak. These two little CSF recesses this is the chiasmatic recess and this is the infodigal recess because as you're forming the infodigalum there's a little pocket of fluid right there. And if you get a slice through that you have to see those recesses as little holes. And just to remind you of the anatomy here, we kind of orient ourselves around the third ventricle. And one rookie mistake is to call that third ventricle. It's not. That's the second palusinum that's right below the corpus callus. The third ventricle is this thing right there. And again that's the head of that bird. Okay, third nerve nuclei in the midbrain right in front of the aqueduct. The nerve is coming forward. Exit in the intracurricular cistern, cross between the P1 segment and the superior cerebellum are already forward in the cistern into the cavernous sinus and finally into the superior fissure. Looking at some of the side so here's your origin of the nucleus of three. It comes out exits at the intracurricular cistern kind of dies down a little bit underneath the P1 segment of the PCA into the cavernous sinus and then into the superior fissure and orbit. So remember that relationship right here of the nerve two, these vessels, this is how you get aneurysms that can affect it right there. It's kind of caught in this little pocket of the vessels right there. You know that the four is also close by but it's not quite as kind of trapped right now. So imaging here you can see the nerves come out. Because they descend as they exit the intracurricular cistern, you may not see them as aligned but these are the two nerves as they're just coming out coming forward. You can track it as it comes forward into the cavernous sinus and then finally as it enters into the apex of the orbit. You see there's a little sleeve of the CSF around it. That's the ocular motor cistern and you can actually see that as an imaging feature on these high resolution T2 sequences. So the coronal plane, here you have the basilar artery here's the SCA right and left, here's the P1 segment there's the nerve right between the two. And then as you're coming forward here's the third nerve in that pocket of the CSF that's the ocular motor cistern. And again just reminding us of the relationship of the third nerve to the heart. With regard to possible compression of that nerve from an aneurysm we remember that the third nerve has the ocular motor components centrally, the little dot is the vessel and then on the outside you have the parasympathetic secret fibers which is why when you have extrinsic compression you get a pupil of X. Four, so four has it's very close to three, a little further down near the accurate. They exit around the back and they can say it's coming forward. They have a fairly long course here in the perimes and cephalic cistern. They also course between the SCA and the P1 and follow pretty close to three as they go forward. Because of this long course and it's a relatively smaller artery it is somewhat more susceptible to injury and trauma. From the side again here we see the fourth nucleus that exits in the back comes all the way around the side, perimes and cephalic cistern between this gap between the arteries in the capricinus and superior fissure. So this is a small nerve and you don't all necessarily see it but you can sometimes get lucky and catch it if it's coming around here. It's as much as important to know where it lives because if you can't see it normally there is sometimes you can see pathology in it and you know that it's going to come that this is going to be its course. You might even get lucky and see it in its location that's coming forward between the two arteries but again it's a small nerve and hard to see. This might get over there. Okay, trigeminal nerve this is a big nerve it exits at the lateral mid ponds and it's very easily identifiable the ganglion sits in the trigeminal cistern or a meccalus cave and gives off one, two and three components. It's very easy to see even on routine brain imaging you'll see it's a big fat tree trunk of vessel coming forward and this is a meccalus cave with a trigeminal cistern you'll almost always see a little CSF pocket right there if it's gone then you might be a master for a trigeminal abnormality. You notice that the nerve fiber starts to spread out here so you'll often see instead of a thick trunk you'll start to see some individual fibers in meccalus cave right there. Six, so six has its nuclei at the dorsal kind of mid ponds back here at the anterior margin in the fourth ventricle and we know there's this relationship between the nucleus of six and then the fibers of seven that have to come around it causing the facial colliculus at the surface of the ventricle. So six comes forward through the mid ponds and it kind of exits at the bottom of the ponds right here. It ascends into the pre-pondking cistern goes through this little dural reflection called a duralis canal and then into the cavernous sinus and ultimately through the superior fissure. So here's the nucleus of six. It exits under the ponds and then ascends here in the pre-pondking cistern through the duralis canal and then into the cavernous sinus and ultimately to the superior fissure. Now this is a small nerve but you can usually see it because there's almost nothing else that lives right where it is. So it exits the bottom of the ponds and the lower slice is a little bit lower. So those two right there that's six, it's right where it lives it comes forward and then as it enters into that duralis canal you often see a little kind of a diva right there. Again it's not so important to see it every time necessarily but to know where it lives so you can identify pathology there. And this shows the course of the six coming under the belly of the ponds ascending up toward duralis canal. So these are all of your mid cranial nerves coming through the cavernous sinus. You've got three up here and four V1, V2 lower down lotterly. It's described that six is the one that is the most kind of floating inside the cavernous sinus if you will and therefore it might be perhaps the most sensitive to cavernous sinus pathology like thrombosis. But usually if you have a cavernous sinus process it's going to be getting more than just one cranial nerve but some people say that six is the first one selected for a cavernous sinus process. Okay so now we're going to extend our discussion to seven and eight and if you're going to talk about 70 minutes I'll talk about eight because it comes along with that discussion. So again that's the same picture of the nuclei here of six, seven and eight. The seven nucleus and the fibers pass around the six nerve and into the lateral ponds, the Cp angle, into the IC and the cochlear fibers along with nervous intermedious. That's the parasympathetic and autonomic stuff that's coming along with seven are all going to exit together and these two nerves are going to really be right next to each other the whole way in the cistern and IAC and distract from the front. So here at the potomage of the re-junction here's six ascending right there seven and eight coming out laterally in the cerebellar potting angle into the IAC. So seven and eight, there's a lot going on in the temporal bone. We've drawn them here as four different components so the facial nerve is the biggest one right here. Eight has cochlear and then the two vestibular components so we've kind of drawn them together here but they all course to the IAC and then once you get into the inner ear then a lot starts to happen. So the facial nerve has a very interesting and complex course this kind of outlines what it does in the temporal bone right there maybe we'll do it one more time. So there it is right there it has the interchangelicular segment and then right here as it enters the inner ear this little short bit is the lab routine segment and that has a ganglion right there that's the geniculate ganglion and you see how there's a nerve coming off the front of that, that's the GSP the greater superficial patrols nerve that's your autonomic fibers, they're going to hook up with carotid plexus fibers and together form the vivian canal the facial nerve then makes a hairpin turn and goes straight back almost in a horizontal plane into the middle of the ear and it's going to go back here and eventually imagine a segment that's going to make a 90 degree turn and go straight down so it's a very complex nerve and you wonder why Mother Evolution decided to put it there but it is a really complex set of confidence to keep track of. So in imaging this is a CT space, you will see usually two component nerves the facial and the stupider cochlear will usually show up as a single trunk here but as it goes further into the IEC we can see it split apart if you're going to have a diagnostic quality image of this type you really want to see those two, in fact the identification of those two nerve components is how we have QA is to make sure that it's a good enough scan to be diagnostic. You also get a good fluid signal and you actually see the components of the inner ear and this is more on ontology as well but you can even see the components of the cochlea the scala tip and the scala vestigal inside the cochlea on this sequence. So this is a diagram showing what it looks like from the imagine that you're on the brain side looking into the IEC and you're looking at a very lateral tip of the fundus of the IEC so anterior to the left this is your inner ear the components of the vestibule and the canals and at that very end the tip of fundus of the IEC you have four component nerves. This one here is the facial nerve now if this drawing were more accurate the facial nerve should be bigger it's the biggest nerve here by far. The cochlear nerve is below it and in front and then behind are these two small components of the vestibular nerve so we have facial nerve here cochlear nerve here and the two vestibular components right there. Now this may seem like micro-native and it kind of is but on imaging you can actually see those things you've got the facial nerve here so anterior is on the left plus you're on the right and you're looking straight lateral not quite a true satchel but it's essentially a satchel plane that's the orientation right there that's a slice and you can see these four components facial, cochlear and vestibular components the two vestibular components may kind of join it up a little bit and this relationship is really very predictable and when you're looking for facial or cochlear abnormalities this image helps us get really a good look at things in there. So seven the cochlear of age and then one thing you've heard people say is remember these, seven up, cope down, so the facial nerve is the one on top and the cochlear nerve is the one down at the bottom here and then the superior and inferior divisions of the vestibular nerve so those four nerves are the component parts of the cranial nerves in the IAC. On CT we've got these two canals right there are components of the facial nerve so again the funnest of the IAC this is the loud breathing segment of the facial nerve you've got the ganglion sitting right here, usually the ganglion kind of has a little gap in the bone right there if we could see GSP it would be coming off right there and then it turns back and there is the horizontal or the tympanic segment of the facial nerve. It runs right underneath the semi-circular canal and it has this characteristic angle about 50 degrees right here very identifiable, it may not be a perfect horizontal plane so you may not see the entire thing in one slice but it's nearly horizontal right there now the math by segment is something that would be hard to see so here is a two inches from an MRI in the actual plane and if you were to say, well show me what the math by segment of the facial nerve is it would be hard to say this is kind of like when we were talking about the optic canal you learn the anatomy on CT so this is the math by segment of the facial canal right there, it comes straight down from the posterior part of the tympanic segment and exits at the stylo-mastered frame it's got a lot of aerosols around about CT well if you have fluid in the master it can be a little confusing but it's a soft tissue filled canal that exits right there at the stylo-mastered frame you can usually see the styloid process as it's coming out so now that you know where that is you go back to MR and you can identify it the reason why that's important is because when you have disease from the deep face, especially the parotid that is ascending and affecting the facial nerve you need to be able to identify the stylo-mastered frame that's sort of the first place where you can see like a mass or perineural tumor facing the fabric there and then the facial nerve enters the parotid and then splits up and then it gets this very complex relationship with the deep face of the parotid and all of its component branches and if we look at one more anatomic drawing of the facial nerve so these represent the nuclei in the brain stem so you've got the primary motor components of the facial nerve here in orange coming through this kind of shows you what it's doing is it's coming through the labyrinthine, tympanic and matted segments exiting the stylo-mastered frame and then these are the branches of the facial nerve they're the primary motor components the ones that really get the most attention but you've got these autonomic components you've got a special sensation for taste that's coming through and giving this little branch the core activity that has this very bizarre course lazing through the the ossicles and then also these are autonomic fibers giving off the this is the nervous intermediate there's this nerve we talk about the four nerves in the IAC technically there's a fifth one I don't know where we're going to really see it distinctly so technically there's a fifth nerve in there the nervous intermediates but usually it's such a small nerve you don't really see it but if you saw you could there have been times when we've seen it we think that's the nervous intermediates the nervous intermediates but technically that is passing through the IAC that's giving these components to the GSB so there's a lot of stuff going on here which is why sometimes you have these overlapping neurological findings affecting diseases that are involved in the facial nerve and then one more complexity is the relationship between the third branch of the trigeminal nerve there's the mandibular nerve there there's actually this connection between the mandibular nerve and the facial nerve the trigeminal temporal nerve and so you can have perineural tumors that hop from 5 to 7, 7 to 5 and when that happens this is the culprit right there okay so let's talk about some pathology first I'll give you just the longer list we'll start with the the optic nerve and visual disturbance you have intrinsic tumors of the optic nerve you have the nerve sheath any kind of orbital you know plasma can affect the nerve any kind of intracranial intratuitary a very common neoplasm affecting vision on the inflammatory side you can have demyelination you can have a pseudo tumor you can have granulomus inflammation and then on the vascular side you can have good old fashioned ischemia either a microvascular affecting the nerve or stroke affecting the brain okay so now we get into some quizzes so do you need to keep the score for themselves or yeah we can keep their own score if you want we can just kind of all those are always in the end but we have about 20 questions we're going to go through so question number one what is diagnosis we'll say this is an older child who has a mild vision parent on the left is a T2 fat sat on the right is a T1 post contrast and I will tell you that on the pre-contrast this was not right so this is enhancement T2 T1 so we'll go back overall and we can get the answers okay do you want them to answer if you want to write it down if you're not going to keep score we can just do this informally at the end but I want to go through them all once and then we'll get the answers and go through them all again okay this is still question one maybe the same different patient but maybe the same history older child with mild vision impairment this is a post contrast T1 not that but it is post contrast so same diagnosis as the first okay question two this is a CT on the left and a T1 post contrast on the right and the history of this might be a middle-aged woman with slowly progressive painless vision loss okay question three this is let's say it's a similar history slowly progressive vision loss this is a T1 post contrast fat suppressed in this case we had a follow up two years later and Dr. this is your patient two years later and some steroids we do remember scans these are like our children we remember their face so what's the diagnosis in this case okay question four this is a middle-aged woman with known metastatic breast cancer and she has bilateral decreased visual acuity so what's the diagnosis and that could be as specific as possible in terms of what kind of this diagnosis is not a generic word but it could be a little bit more specific in describing what kind this is and this is a T1 post contrast coronal with fat suppress okay question five this is a younger middle-aged patient with acute painful vision loss on the right what we have is a a stir on the top T2 fat sat T1 fat sat on the bottom and as a bonus on this one I'm going to give you one more picture to help you with the diagnosis the differential is pretty broad here but when you add this it makes the diagnosis more if not have them on maybe close okay this is a patient who has a history of medically treated hyperprolactinemia but presented with sudden acute vision loss we want to know what the diagnosis is including the secondary diagnosis with the sudden onset this is a coronal and importantly is a coronal T1 without contrast it's important no contrast here this is a this is a very tragic case this is a younger middle-aged male who went an extensive skull based surgery for a neurosurgical prolineasm an angioma a short time woke up totally blind bilaterally this is an axial diffusion sequence what's the diagnosis here okay let's talk ocular motor pathology so again we have inflammation, pseudo tumor, granulomus thyroid eye disease demyelination because essentially you can affect motor function tumors lymphoma, lachymelanthymorbis angioma, schwannoma meds, perineural tumor and then vascular aneurysm especially with certain ocular motor nerves they still throw them involved to use it again, anything to cranny on could affect the nerves as well okay question 8 this is a patient with limited extra ocular motor function on the left at least the patient knows what's on the left in Europe you might have found something on the right as well but left is really what the patient was and what the referring provider noticed but you might find them wrong okay this is a patient I should have said that this is a T1 post-contrast with fat suppression okay both of these are T1 post-contrast with fat suppression action on the top and coronal on the bottom this is a patient with painful acute ophthalmoplegia on the right involving multiple cranial nerves okay and if you give us an eponym for this we don't do that but this is a kind of a cute one okay this is a patient who has somewhat similar ophthalmoplegia on the left I'm sorry on the right it's painless and slowly progressive last patient was acute and painless painless and progressive ophthalmoplegia this is an axial T1 post-contrast and a coronal T1 post-contrast both with fat suppression and as a bonus there's an ancillary finding here but that would be kind of both that's good okay this is a patient who presented with painless proptosis and limited extra ocular motor function and a pair of mass effect on the right and interestingly and partly this was painless and you can maybe think yourself would the diagnosis be different or painful instead but this one was painless and did not appear inflammatory this is an axial diffusion sequence through the midbrain I'd love the pons actually and this is a patient with hypertension and microvascular disease presented with an acute classic gaze disturbance so the question is what is the gaze disturbance and maybe for bonus what is what is the Fiber Tractor that seems to be doing this okay so this is these are two T1 post-contrast this is a patient with chronic painless diplobia related to a nerve malfunction on the left and I'm not going to tell you which nerve because you're going to tell me that but the question is what's the diagnosis and maybe another ancillary finding here this is a coronal T1 published through the orbit question 15 this is a 3D reconstruction from an angiogram an internal chronic injection basically laterally the question is what is the artery shown here at the base of which is this aneurysm so what is this artery and for question 16 is the pupil spared or involved in this person's nerve dysfunction question 17 this is a patient with severe chronic kind of injection following a significant head injury I think this is my patient too is your patient too here's a coronal injection here this is the angiogram from the side and this is the pulocontrast CT okay facial nerve pathology we have some congenital things epidermoid, lymphoma, intercranial any number of temporal bone abnormalities tumors especially schwannoma parygernal malignancy coming from the parot especially inflammatory conditions neuritis either infectious or non-infectious otitis when you have otomathritis paratitis then vascular you can have lupin pinchments intercranially there's something called a hemangioma which you probably are familiar with unless you've done an ontology rotation or some work there the nature of thrombovascular disease in the brain okay so this is a patient with slowly progressive hearing loss and mild facial weakness on the left let's say there are probably maybe a younger adult or middle aged adult this is a TTC once on the left and then a diffusion on the right another patient with hypertension diabetes, microvascular disease we could re-infarct this is a diffusion image and the question is in this location which cranial nerve or nerves are going to be affected question 20 so here we have an axial T1 post-contrast and then a sagittal T2 of the cervical spine these are the same patients so the question is well kind of implied in the question is that you know what the diagnosis is but what are the three tumor types related with this syndrome and as a bonus we'll give you the acronym that we use for remembering the syndrome that miss me question 21 this is a patient with acute facial palsy on the left the question is what kind of doctor was Sir Charles Bell question 22 this is a patient who presents with hearing loss on the right relatively rapid onset but consistent after presentation question is what is the most common nerve of origin for this fairly common tumor here's a patient with facial palsy on the left we have a CT scan on the left and on the right we have a T1 post-contrast with fat depression and the question is what segment of the facial nerve is involved and as a double bonus if you recognize this tumor this is a hard one there are some characters features of this that tell us what it is but it's an unusual tumor but it seems if you have to know what it is and question 24 this is the last one here we have a patient with a facial palsy and a big old mass in the product the question is what primary salivary and actually it's not commonly salivary in lacrimal tumors they have a lot of the same epithelial kinds of malignancies in the current time what a salivary tumor is infamous for causing perineural tumor and when you have it in the product or the lacrimal you really worry about about perineural tumor we're about with anything but especially this one and mass for primary is squamous perineural tumor primary epithelial tumor here so I know we're fine because we've got two hours and we have the seventh nerve afterwards that you think residents are going to do so you're fine for time oh by the way this is what it looks like in a good year I don't think we're there yet this is going to be pining for what could be that was it anybody recognize that that's Wolverine Surk up above Brighton okay so what's the diagnosis these can have a wide range of appearances this big fat sausage tubular thing it's not going to get kind of kinged in it brought in T1 but it kind of matters maybe enhancement can be quite variable this is one of those you know CNS tumors that breaks the rules of enhancement they can enhance and not be so there's quite a bit of variability and you know as an example of that here's a patient with bilateral optic chiasm pathway glioma that has almost no enhancements and interestingly you obviously know this but these can build really big and bizarre and have relatively minor impact on vision so that there's a lot of variability but bilateral unilateral any part of the optic path okay what's the diagnosis here shout it out so the tram tracking of the calcium that right there is kind of that's kind of the epitome of an optic nerve meningioma optic nerve sheath meningioma and on the MREOC it enhancing they tend to be sort of differential around the nerve but they could be eccentric it could be bigger on one side so man perfect two lines of tram tracking but the point is that it's on the periphery we call it optic nerve meningioma but it's more probably optic nerve sheath meningioma and you know not uncommon if you get a lesion on MR and you're not sure you can go back and get the CT after the fact to look for the calcification because that will really nail it for you and this patient this is many years ago Dr. Degrees patient when we first saw this the history wasn't really clear and we thought well maybe this is a big old meningioma but then with some steroids and time this thing disappeared so what is it what's the story Mark pseudo tumor is what we ended up concluding this was but it could have been something else that was mass like and inflammatory that would respond to the story it's like maybe a sarcoid Dr. Degrees have you ever seen a sarcoid disappear to this completely I guess I can I don't think she had sarcoid I think it was a pseudo tumor I think it's inflammatory but it really looked like a tumor it's just going to show you why pseudo tumor is well named because it can sure fool you depending on the presentation this is our patient with the metastatic breast cancer the abnormality of course being that you have these abnormal enhancement surrounding the entire nerve now if you had a different history you might have called that an optic nerve meningioma that could look just like that but in her case by the time I'm going to attack breast cancer so what do we call this yeah leptomanageal carcinoma telsis because the metastasis is in the leptomanageal spaces and you can imagine how devastating this would be and how much impact it's going to have on vision this is our patient with acute right optic neuritis and dysfining so they have it's the kind of classic presentation for NS this is our patient who is being treated medically for a prolactinoma and they presented with sudden vision loss so the diagnosis is prolactinoma but what's the secondary diagnosis here Dr. Kennedy just had a case of this apoplexy pituitary apoplexy is one of the few neuro-imaging emergencies because they have to be the second you find this they have to be compressed right away so that you can spare their vision so these are the ones you never ever sit on these and whatever time of the year night it is you call somebody we call somebody and then we go to bed and you fix it and the guy we saw went for weeks was diagnosed and he's probably got a permanent by-temperal and the key here is this is a T1 pre-contrast this is haemorrhage so when we have acute vision loss in the coronal plane we look at the haemorrhage on T2 we will also do a gradient sequence in the coronal plane to see if we can find blood inside the tumor so it's basically haemorrhage into a pre-existing tumor that's causing the apoplexy and you can see that the problem was that they kept thinking that it was enhancing an enhancing adenoma but that was an unenhanced T1 scan so it was a thinking error on the part of the people who had this guy you can imagine how much the opticisum is being affected great over this haemorrhage right there on T1 is the blood as obvious as acute bleed or is this just obvious because it's I mean usually by the time several hours have passed the blood starts to go from a state where it's very hyper acute blood it may be statistically bright but usually by the time we get the imaging there's going to be some bright signal to it but that's also why we throw in the gradient because the gradient will show blood while the signal voyages it and between the T1 and T2 the irregularity of the signal and the gradient you can usually tell that it's blood but it can be a little tricky depending on how old it is you're just saying like as it was it was like CT I remember Rob telling us if it's bright on T1 then it's sub-acute so I was wondering if it's like a hyper acute you believe would be hard to differentiate but it sounds like very early on and it comes bright on T1 very early on it won't be bright just yet I mean it's the metahemoglobin the term that it's really bright so you need several hours for that to happen so it could be that it's super acute you might not see it but usually with the other sequences and the suspicion you'll be able to figure it out this is that tragic case of the patient who woke up blind after an extended surgery what do we call this yeah this is posterior semen optic neuropathy really a devastating outcome and I'm on a surgeon so I don't deal with it but when you have extended surgery do you routinely consent patients for this even though it's very very rare it's a so we don't do the surgeries that cause this it's back surgery and these prolonged surgeries that people get into where there could be blood loss I hate this diagnosis it's horrible I get this big head and neck stuff skull-based stuff, upper spine it may have to do with positioning of the patient upright venous congestion, things like that yeah but you have back surgery and then trauma, post bad trauma with a lot of blood loss so this is very uncommon you'll almost never see this distinguishes from anterior semen optic neuropathy where you won't see this, you might see nothing on AION you might see a little dot on the hand side of the back of the globe but maybe that's it but the abnormal enhancement is the nerves what's that? is the nerves and then this is actually diffusion restriction in the nerves themselves and when you see this you kind of panic well this is a nerve that is very unhappy the nerve itself and then is there anything we've also posted to that in just the region right behind it like this right here there's a lot of noise in the skull-based mucus in the semenoid sinus can look bright on diffusion so we actually care a lot to get distracted by extra cranial things that have diffusion like secretions in the sinuses in the parotid like warthans tumors will be very accurate, we'll have some diffusion cysts and things if they have certain material in them, blood will have diffusion restriction so sometimes stuff that's not neural you have to kind of do a double take and say is that diffusion restriction for some other reason we'll talk about neural structure diffusion equals semenoid yeah, if it's bonafide PION and you get a diffusion you should see positivity at the end of your stroke and what are you going to see if you get called to see somebody who claims they're blind, what are you going to see on exam that's going to tell you what's going on it may look normal it may look normal yeah, the nerve may look normal and the retina may look normal I mean it may look completely normal but the key will be that the pupils will work right the pupils are going to be more fixed they're going to have no or little response to light but they'll have a good near response but when you look at it acutely you may see nothing that could be normal that's where it's such a hard diagnosis okay, moving on to ocular motor pathology question 8 what is the diagnosis because the distribution of disease is so characteristic we talk about imslow, imslo as the preferential involvement of the ocular muscles inferior, medial especially then superior ims, those really are the three most common lateral and oblique muscles common certainly if you have an isolated lateral muscle it's not going to be thyroiditis but this is a pretty common characteristic and even if we don't see it on both sides most of the time pathologically the others have to be involved as well so even though they can be asymmetric on imaging you can easily have bilateral findings and when they get in clinic and they get a proper eye exam you'll notice that there's right symptoms as well left symptoms but in this case the left is clearly abnormal, the right maybe that inferior right is a little bit fat okay so this is our patient with acute painful ophthalmoplegia on the right involved in multiple cranial nerves so what's this? yeah, tolucahan basically a variation of pseudo tumor these can be really subtle and you know we've seen this before you have enhancement of the cavernous sinus and you can imagine that maybe the patient is a little asymmetric in the scanner and you look at that and you go oh that's just some cavernous sinus and in fact there are patients with a finding that might look like this don't have anything, it just happens to be or there's a venous prominence right there that looks like pathology so the pathology the symptoms drive this the patient has acute ophthalmoplegia and clinically looks like tolucahan and is finding in this case it's pretty characteristic but you have in the anterior cavernous sinus headed toward the secure fissure you have this asymmetric enhancement so that's tolucahan can we still have an accident with you too but under all circumstances yeah that's it right there it's subtle, it's easy to miss and again you've loads of multiple slices and convince yourself that it's a little more compelling right there notice how if we use our anatomy there's the clientoid, there's the optic strut optic nerve you right here it's a smack in the middle of the superior fissure this is the other patient with a kind of similar presentation in that they have ophthalmoplegia on the right but there's this painless and progressive and then this is a great appearance of the cavernous meningioma pretty common place to see them too you can see it along the margin of the sinus the meningioma enhances maybe a little less than the pituitary and less than the venous blood of the cavernous sinus but it is pretty intensely enhancing in a prime position here to affect multiple cranial nerves okay so this is a patient with a painless poptosis and a limited EOM and some of the differential in a specific diagnosis the fact that it's painless maybe helps a little bit here any guesses there aren't many wrong guesses here so in this case Pseudotumor would be a great option Pseudotumor sarcoid especially with the intracranial component here sarcoid Pseudotumor ITG4 in this case I use the history of pain less which makes it more likely to be lymphoma there's a lot between lymphoma and granulomatous Pseudotumor from an MD point of view but clinically you can probably tell the part but this one's lymphoma but with a different history this could have been sarcoid could have been Pseudotumor could have been ITG4 okay so this is a patient with a microvascular infarct of the brain stem what's the classic gaze disturbance I know and what lives right there this is kind of a cute case you don't normally get a liquefied infarct it just happens to pick off the NLF but this is one with a classic presentation if we're a little bit bigger you could get a gaze palsy right because if you involve the six nerve nucleus you're going to see MPPRF you're going to see a gaze palsy okay this is a patient with chronic painless diplopia and if you want me to start with the ancillary finding what's the ancillary finding yeah check it out superior ligature this muscle is really small what lives right here yeah that's exactly what the fourth lives so this is going to be a presumptive diagnosis of any yeah schwannoma what did you say I was thinking oh so the history was chronic painless trochlear palsy this is a presumptive diagnosis of a fourth schwannoma we don't get a lot of path on these because you can't possibly make it any better by operating on it but we've seen any number of these and they all kind of occur right here or in this location so a fourth schwannoma is a presumptive diagnosis I suppose you could find that but these are small they last for years and years they don't grow much and so this is a presumptive diagnosis of a fourth schwannoma you get a fourth nerve palsy with these but they usually don't grow they just kind of stay small like this if a surgeon goes after this he could do nothing but harm the patient because this is a very difficult place to get to and it's not going to fix the fourth nerve you're better off to instrument surgery down the line fixing and aligning the eyes with muscle surgery but usually we tell the patient that no matter what we'll probably sell some of this to a business surgeon because they'll overtake you probably get a scan in a few years to make sure at case we see schwannomas that do weird things and get big and cause mass effect but mostly these are little tiny things okay so what is this artery yeah it's a PCA now in this case the aneurysm is associated with a huge PCOM in fact the PCOM is so big we call spetal origins it's a little bit of a misnomer when we call these you know posterior surgery aneurysm because the aneurysm is actually coming off of the carotid it's coming off of the base of the PCOM the PCOM aneurysm so technically it's an ICA aneurysm but they're right there at the origin of the PCOM and when you have a PCOM that is so big it becomes a feel or PCA they have a flow related phenomenon and often times these things are associated with that because it's a flow related effect but the PCOM aneurysm is at the IAC at the origin of the PCOM and then the PCA is coming off so this is the PCA this is a kind of a classic big PCOM aneurysm people is this is the patient with a severe contract type of injection after a head injury what is this CZ Fichterlem and more specifically a direct but here you can see on the carotid injection you're very filling out the branches of the MCA here and you're already filling up the cavernositis and you're pushing contrast into this huge structure right there what is this yeah so the SOV is just it's got retrograde flow it's filling up faster than the Cervarters so this is a direct CZ Fichterlem Facial nerve pathology this will make a little bit more out of your comfort zone but you ask for it so we do it now this is kind of an imaging classic this patient has slowly progressive hearing loss and facial weakness and you have an almost imperceptible mass here it's a mass effect as far as anything else it's causing the appearance on the T2 what's characteristic is this here diffusion restriction in a cistern based mass I'll tell you this also did not enhance anybody recognize this if it were a schwannoma it would enhance now schwannomas can have bright signal they tend to be darker than CSF this thing is bright bright bright and there's zero enhancement CT it might be invisible also the diffusion is what gives this away this is an epidermal tumor this is a congenital rest of athelial tissue and since they're congenital it takes many many years for them to grow they often present as a person is an adult depending on how big they are but they have this characteristic diffusion restriction they grow very very slowly and eventually they'll start to compress what's around them in this location this patient got seven and eight affected and this could be besides facial weakness you could also have a facial spasm if it hits the the root exit salt a good point this is a diffusion sequence this is a T2 bright CSF so this is a plain old T2 spenico but you're seeing that you can't even see it it's the same color as CSF which is why they're really deceptive and on CT they're almost the same density as CSF so they almost look like this almost looks like an arachnoid if you didn't have a diffusion you probably call this an arachnoid cyst so if it were sarcoid it would enhance if it were asthma or metastases or something any other kind of a neoplastic process would enhance plus it wouldn't be this white on T2 almost everything that's going to be masked is going to have some T2 darkness to it cellular things have a lot darker on T2 but before we had diffusion imaging this was confusing we couldn't tell the difference between an arachnoid cyst and an epidermal other than the fact that they grow okay and this is kind of what Dr. DeGrio is referring to earlier here's another patient with a microvascular infarct in a strategic location so what cranial nerve or nerves could be affected here so if you remember our neuroanotomical drawing the nucleus of 6 is right here and what loops around 6 the facial loop so this patient presented with both 6 and 7 because it was just very classically located in that location okay so this patient with a multiple tumor syndrome which one yeah so this is 2 and what does misky stand for multiple inherited meningiomas or schwannomas meningiomas and penoms yeah so we had bilateral schwannomas and then the penoma so this is the classic misky we have to have a meningioma and the hatchery is complete so Dr. Charles was a late 1700s physician so back then nobody specialized he was an anatomist and a physiologist and a theologian and an artist and a neurologist so back then a doctor was just a doctor but he's famous for identifying Bell's palsy this is a classic appearance of Bell's palsy this is a tumor post contrast you see the entire facial nerve is enhancing pretty brightly now the facial nerve has some normal enhancement at the genicula there's usually a little bit of a faint enhancement and the tympanic segment can enhance a little bit too so it can be tricky what should not enhance though is the labyrinthine segment and the IAC segment of the facial nerve should not enhance so when you see this enhancing then it's going to be a facial neuritis now Bell's palsy doesn't usually need imaging unless it's atypical but if you get it this is what we're let's say you're trying to exclude something else this is a typical appearance at the tip of the fund is the IAC for Bell's okay this is a classic appearance of an acoustic neuroma which we shouldn't call it that because they don't usually involve that nerve what is the most common nerve of origin of these of these schwannomas yeah they're usually vestibular so vestibular schwannoma is the most common proper pathologic identity of this for a long time we thought there were almost no cochlear schwannomas but they found a couple of them that on the path they could identify as being coming from the cochlear nerve but by far the most common is the vestibular so we really shouldn't call these acoustic neuromas we should call them vestibular schwannomas now one possible thing to be aware of is that a facial schwannoma can look an awful lot like a vestibular schwannoma they're running in the same place for example now what you look for with a facial schwannoma is the facial nerve is going to be coming right off here remember we said there's a labyrinthine segment the facial nerve right there that's the geniculate ganglion that's normal to have a little bit of enhancement of the geniculate and maybe a little bit along the math way segment here but if this is where a facial schwannoma what you look for is a tail of enhancement following the facial nerve bump here facial nerve schwannoma is going to be tricky because the facial nerve is such a robust nerve sometimes the hearing loss will happen before the facial palsy even though the nerve is even though the nerve of origin is the facial nerve the hearing loss happens first because of compression so for us for imagers we have to be on our game we see a schwannoma we look for that facial tail to make sure it's not a facial schwannoma because the last thing you want to have is your tolerance to go in thinking that it's a the facial schwannoma and the facial winks up with the face of the palsy that question is that different from the dural tail that's talked about with the meningioma so a dural tail is a way to identify it so if you have an extra actual mass it looks like it's plastered against the dural surface and you're trying to decide is it coming from the nerve like a schwannoma which will be more like a ball whereas the meningioma it's coming from the dural and the tail is what the mass kind of blends into the dural surface so the dural tail is a way of saying it's coming from the dural the tail I'm talking about here is it's still in the nerve think of the schwannoma as a tube of tumor but the tube in this case is going into the facial nerve and allowing for the same so it's still a tube in the direction of where the facial nerve goes these are uncommon and because they're uncommon that's why you see an occasional misses unless you're in the otology or we don't really pay attention to it but it's a bad miss to miss that so that's why it's part of our facial nerve evaluation we are aware of that so here's the patient with facial palsy and the abnormality is right here and here this is the post contrast it's enhancing this is much much more enhanced than you should have at the geniculate ganglion so I kind of gave away the answer here but what is the what's the facial nerve segment right here here that's the larynthine segment and then this is the geniculate segment right there the geniculate ganglion and then the master segment comes back from here this is an uncommon tumor, it's kind of a tricky one we know what this is based on this appearance here do you have this kind of little speckled bone right there the bone that kind of wrote it there's little speculations in it and then this mass is sent right smack in the geniculate anybody even heard of this one this is the facial nerve hemangioma it's not a very common tumor but it's got this character's iconic home appearance of the bone is the telltale side of it did that person have pain I don't know I think it was mostly this is originating from the facial nerve proper so I think it's mostly facial nerve symptoms but I don't know but they may have had some pain related to like the GSB and how they get exacted out I guess I guess the epicenter or the center of this mass is the geniculate ganglion the geniculate band in the nerve and then finally what primary epithelial tumor is famous for perineural tumor spread I'm curious I don't know the one that we think is most common is adenocystic it has such an incredibly high rate of perineural tumor that whenever we see it you're going to get worried a lot about it mucoapse will do it squamous will certainly do it if you have a malignant transformation about benign mixed but they call it carcinoma those will also do it if this were lymphoma you certainly get perineural with lymphoma too okay well that's it good job thank you good job for all of you you did a pretty good job of answering I hope you all got them right take very much time so this is covering the facial nerve anatomy getting a doctor degree is joining us today and we both come from the northern woods of minnesota slash wisconsin this is a view of the north shore which leads up into the boundary waters which is a series of lakes that are all how many of you have done it the boundary waters it's highly recommended there are series of lakes that you can portage between and just get lost in the northern woods and lakes of minnesota so as a brief overview of the facial nerve as many of you know it's a mixed sensory nerve a lot of this will be redone and see from our prior talk but maybe have a little more clinical context hopefully the motor root will have a facial expression whereas the sensory root supply and taste the anterior two thirds of the tongue the external auditory neatus and the retro auricular skin and then the facial nerve also transmits the pre anglionic parasympathetic innervation from the senopalatine and subventibular ganglion to the lacrimal sub-maxillary and sublacral glands there is a really good video covering the virtual anatomy in three dimensions that L. Severe puts on but even then we had such a good three-dimensional evaluation of the facial nerve course with our radiology portion I think we can skip that so this will focus kind of what our BCSC focuses on as far as anatomy so here we have two diagrams the one on screen left and the one on screen right both showing the predominantly the motor nucleus of seven which is a cigar shaped column that is about four millimeters long located near the cauldron of the pons you can see it here and then this is more of a three-dimensional representation versus a two-dimensional representation of the facial nucleus in the motors portion highlighted in this orange color you can see that it's ventral lateral to the sixth nerve nucleus and ventral medial to the spinal nucleus of five and dorsal to the superior on our column you can see that the facial nucleus here on this screen left wraps around the abducens nerve cranial nerve six and forming the genu of cranial nerve seven and it has a close approximation to the medial longitudinal fasciculus and then it also does have a close approximation to the vestibular nuclei so you can see that a lesion anywhere along this course can be localized based on involvement of other cranial nerves and other structures and then it joins the here's another good diagram showing the motor course of the facial nerve so including the super nuclear nuclear and infant nuclear course so that the signal for facial facial movements starts within a primary motor cortex and a pre-central gyrus the cortical bulbar fibers travel through the internal capsule down into the medial one-third of the cortical spinal tracts and the cerebellar P-uncles within the mid-brain the pathways as you see here for the other one-third of the facial function including the brow and obicularis run parallel but distinct from the pathways for the lower two-thirds the cortical bulbar fibers travel in the basis pontis but those that control the lower sorry the lower facial muscles décusate at the level of the pons to synapse in the contralateral cranial nerve six nucleus whereas the cortical bulbar fibers that control the upper facial muscles décusate and synapse on the contralateral cranial nerve six nucleus some of those fibers don't cross reaching the ipsilateral cranial nerve six nucleus so you can see the color coordination blue with the blue fibers here intervening the lower two-thirds and green intervening the lower two-thirds and then the upper portion of the face being a mixture and that's clinically relevant which we can talk about here's another good diagram showing the facial nerve peromally its motor function so again the nucleus the motor nucleus of the facial nerve is located in the collar portion of the pons it courses dorsal muley and circles the nucleus of the cranial nerve six after bending around six forming the genu of cranial nerve seven it exits the pons at the cerebellum cerebellum and also combines with five six and near close to five six and eight as we talk about in previous slides so the motor root of seven cranial nerve eight and then the nervous intermediates which is the parasympathetics enter into the internal auditory myatus some of those fibers as depicted here pass through the geniculate ganglion and continue on as the cordae tipini nerve which carries for example taste to the anterior two-thirds of the tongue in this blue picture and also transmits parasympathetics to the sub-indegular and sub-lingual gland so you can follow essentially the motor nucleus in green wrap around six enter the internal auditory canal and then travels through the geniculate ganglion and so hopping off to form the muscle to innervate the muscles facial expression in the lower picture compare that to the red fibers which are the nucleus the superior salivatory nerve which also pass through the geniculate ganglion palatine ganglion and then traveling forward to stimulate or stimulate the lacrimal gland also the other fibers traverse inferior leaf joining the cordae tipini nerve or helping to form it to innervate the sub-lingual and sub-maxillary glands and then the nucleus of the facial salteris also joins the internal auditory canal to innervate the anterior two-thirds of the tongue for taste here is this was pulled more from the oculoplastics perspective of specifically when we think about the branches of the motor component of the facial nerve to Zanzibar by motor car so the temporal zygomatic buccal, mandibular and cervical branches were commonly tested on the course of the temporal nerve specifically in its relation to the smas of the temporal parietal fascia does anyone remember the distinction is the zygomatic arch does the temporal nerve is it superficial or deep to the smas above the zygomatic arch correct yeah so and then below the zygomatic arch would be deep and so that is often tested and is clinically relevant there are a lot of anatomical correlates to those but we won't cover those and then I think when thinking about the facial nerve and how it's both tested and how it presents and how we can localize this is a great diagram that covers kind of the eight most common but eight common presentations based on lesion location so number one here you have a super nuclear facial nerve palsy and based on its anatomy how would a super nuclear facial nerve palsy typically present yep exactly and then how about and that's because of the anatomy we covered previously so then we have a nuclear granular or a facial nerve palsy that involves the nucleus how would that present and what are some other accompanying features based on the size of the lesion that it could present with 6 or 4 yeah exactly so we talked about involving a sixth palsy but also the gaze preference involving the PPRF if it's large enough and then also frequently it's associated with the taxia and occasionally a horn or syndrome on that if it's lateral side and then if we think about a lesion involving three here the cerebellum pontine angle what are some distinguishing features of a lesion there autonomic symptoms yeah so you can have vertigo, ataxia nystagmus involvement of arachnid taste in the anterior two-thirds of the tongue you can have decreased hearing from involvement of cranial nerve H and then you think about a lesion involving the genitidulate ganglion of four and four here also known as a disaster or Ramsey Hunt syndrome how would that typically present or I should say how can you differentiate a lesion at four from that at three and you can see here based on the cerebellum pontine angle having multiple cranial nerve in that location versus the genitidulate ganglion really the distinguishing factor is that other cranial nerves are commonly not involved if it's involved in the genitidulate ganglion or they would be if it's involved in the cerebellum pontine angle so then five so so geniculate involvement would give what so it would give the same as above as a cerebellum pontine angle lesion but it would involve the other person with cranial nerve H or nystagmus or anything like that but you could get geniculate neuralgia can also occur and so you can see ear pain and then because there's some parasympathetic stuff going through there as well then you could have dry eyes and other problems on that side right and then so this is where a lesion of the avidian nerve comes into play you can have in this case an ipsilateral tear deficiency due to involvement of the avidian nerve as we talked about with the genitidulate ganglion it's mainly the lacrimal gland so then a lesion at six in the fallopian canal it can involve the the nerve to the stapedius muscle so presenting with changes in hearing involvement of the chordate timpani involving loss of taste to the anterior two thirds of the tongue and impaired salivation if we go down to seven this is where the distal chordate timpani chorda timpani so that would be involvement of just isolated paralysis of the facial muscles and then here down in eight you can have it a lesion as the facial nerve exits the silomastoid foramen you can have isolated involvement of any one of those branches and or all of them at the same time silomastoid foramen so I think this is a good diagram to review what how can we localize a facial nerve with a lesion based on what we did we'll watch this is a good short video and now I'll how to Hi, I'm Kathleen DeGree, I'm a professor of neurology and ophthalmology at the University of Utah and the Moran Eye Center and today we're going to talk about examining the facial nerve examination because the facial nerve has autonomic features et cetera but what can you do quickly to look at the facial nerve the first thing that I always do is look at the subject straight on and notice if there's any asymmetry in the facial muscles then I might ask the person to close their eyes as tight as they can and here I'm looking at to make sure that the folding of the face is exactly the same on both sides and that they bury their eyelashes about the same as well now open up your eyes really really wide and you notice that you get furrowing of the brow upward and it's symmetric on both sides when it's a peripheral lesion you'll see weakness of the brow elevation and also of the face on the same side if it's central they'll be able to raise their eyebrows equally but the lower face will be weak the other way to look at the facial nerve is also just ask them to smile and then I always say do you know a joke to get a real smile because sometimes emotional subjects or emotional content can be observed differently in the face so sometimes we do that and then sometimes I'll ask them to just blow out their cheeks like this excellent and you can feel how much they care is there and they've got good facial strength and that's the basic evaluation of the facial nerve so I think one thing that came up in clinic the other day is patients are out in worry masks so having their mask over in this situation and you're assessing the facial nerve and then I have just two brief questions that are commonly tested so the first one a patient presents with continuous unilateral undulating contraption of the particular's oculi and most of the facial muscles what is the most common cause of these symptoms anyone have a guess how old is it um this is OCAPS they didn't tell you yeah correct it's Pontine Guillema this is the most common cause if it's just the obicularis I mean everybody gets a little bit of myokymia once in a while if you drink too much starbucks but um but this Pontine Guillema if you see myokymia going on in the face that's what you have to be thinking of no no and myokymia is kind of like a little nitty-bitty jerk and myokymia is more of an undulation going on continuously absolutely but you know frequently people have a hard time describing what they're having and then you need to know what you're looking for injury to the facial nerve can occur during what surgical maneuver dissection of the smas inferior to the zygoma and eyelid presensiton dissection deep to the temporal parietal fascia above the zygoma or dissection superficial to the periosteum over the zygoma bone oh ms wasn't on there but is that more typical in adults versus Pontine Guillema I get that like a thing can you say that again most of the time they say ms is like the most common in adults like facial myokymia oh facial myokymia is not common and ms multiple sclerosis causing it I haven't seen that before but I've seen Pontine Guillema's cause it there's some really nice videos on a novel if you've never seen facial myokymia and you know how to differentiate myokymia from hemifacial spasm right if you all seen hemifacial spasm so you know what that is uh yeah we get to see just comments that Pontine Guillema is the most common but demyelinated lesions such as ms can also cause it but it doesn't specify whether that is I don't think I've ever seen myokymia from an ms lesion I mean I see lots of trigeminal dysfunction with ms and uh facial weakness with ms you know because six nerve palsy with facial weakness with ms because you can get demyelination right by the facial myoklius so good job