 Well good morning we get to do neuro radiology for an hour and Judith I did bring a quiz. It's actually a quiz from a couple years ago but I don't think that they would have necessarily remembered the answers or would benefit from having seen it before and repetition is good so. So all right well I was asked to kind of give an overview and focus on you know a broad range of things I have to do with neuro ophthalmology imaging and so I'm kind of including a smattering of orbit, icomotor, visual and even a little bit of autonomic so kind of a little bit of everything for you. Our objectives we're gonna look at imaging strategies we'll review the anatomy particularly of the upper cranial nerves will come up with a develop a differential strategy for how we image both central and peripheral dysfunction that you will see in clinic and then we'll look at appearance of common and common lesions as they are seen on CT and MRI. The imaging strategy that we will use for for really the vast majority of neuro ophthalmology conditions is what we would call the orbit protocol now in the radiology world we don't have as much distinction about the way that you use words like ophthalmologic and orbital but to the radiologist orbit basically means a horizontal slab through the middle of the face that gets the eyes the orbits the central skull base and the cisternal and central pathways of the cranial nerves and that region really covers the vast majority of everything that you need to see. We call this in head and neck imaging the six pack. These six sequences so we do a T2 and a fat set a stir which is basically the same thing as a T2 with a fat set just acquired in a little different way a T1 pre-contrast and then T1 post-contrast with fat set these three sequences done axial and coronal. Thin section through the orbit in midbrain region this covers really the vast majority of everything that you will need to see. In addition we throw in one of these heavily T2 weighted sequences what these do is these give you so much fluid signal that it makes sort of a black and white image where everything is either fluid or it's not fluid and it gives you a nice way to see what's in the cisterns in particular so we use this for looking for the the cranial nerve pathways. There are two sequences that you might see referred to these are vendor specific terms don't really know what they are but you'll often hear us talk about about a kiss or a T2 space sequence this is probably the one the space that we use the most around here with our Siemens equipment. Fiesta if you are in a GE system. The VA does have one GE scanner still so you may see that that term pop up yeah and then of course we always throw in some whole brain sequences because a number of conditions will have other intracranial manifestations and just it's a good idea to see what else is going on. We're surprised often enough by what we see that we weren't expecting that we just make sure that we don't don't miss anything in the rest of the brain. So here's your your six pack of imaging these two are the T2 weighted and they're T2 weighted if you look at your internal control your vitreous and your in your CSF these are T2 weighted but the fat is dark and you can get the fat dark a couple ways you can do a spin it spin echo sequence and then apply a fat suppression pulse that makes this the fat signal go away or you can do a stir which basically never had fat signal ex excited to begin with and so there's nothing to suppress it just it's a little cleaner in different circumstances you have different kinds of artifacts so usually we'll do one of these two with the T2 fats other than with the stir just we get one of each in case there are some technical problems a little bit just hedging your bets you get one good sequence to see everything a T1 without contrast sometimes you'll see some practices will do a T1 pre-contest without with fat suppression but generally you like to see the fat in the orbits the deep face and the skull base because it gives you nice intrinsic contrast and sometimes if you have problems with your post-contrast sequences you can see a lot just by knowing where the fat has been replaced and then the post-contrast sequences or we see basket or physiologic enhancement many of the pathological processes and in this case we do like to suppress the fat because both fat and gadolinium are going to be bright and they want one of those to go away so we suppress the fat signal and this is what one of those heavily T2 weighted kiosk or fiesta or T2 star sequences and these aren't really good for looking at the soft tissues and the neurological structures because everything gets kind of very dark and black what you do see is a very stark contrast between tissue and CSF so the nerves show up really really nicely and this is a sequence specifically to look for this is internal segments of the cranial nerves. Vascular imaging is a big part also of what we do CT is pretty bulletproof in terms of getting it done patients who have a lot of issues maybe can't lie in a scanner maybe have contraindications CT is a very reliable way to get angiographic imaging radiation obviously is a potential risk and then MRA is a little more complicated because the patient is often already in the MR scanner doing angiographic imaging while they're there is often a good idea and you get a little bit different kind of information the pendulum has swung a little bit for before we had really good fast resolution with CT MRA was maybe a little bit preferred and then as CT got very very fast very high resolution we started to prefer CT a little bit for its spatial resolution and in the last couple of years has been maybe a bit more of a swing some of the more advanced MR techniques especially looking for things like plaque characterization now there's a reason to maybe favor MRI MRA a little bit when we do an MR sequence it's a little bit more complicated there's the time of flight technique which is a non-contrast technique that's basically looking for things that move you can also do a contrast technique which you inject gadolinium and dynamically watch it as it does a first pass through the cervical cerebral vessels and then we also have some of these techniques like thrombosensitive techniques looking for plaque hemorrhage these are useful for particularly patients with atherosclerotic disease and we're looking for a chronic occlusive or dissection and things like that the MR images can be very pretty the time of flight sequences and the dynamic sequences because you had so much resolution so much signal from the intravascular contrast or signal that you can get as a traction that shows you a really nice view of what the vessels look like and this is one of those thrombosensitive techniques a way to identify subinterval thrombus or dissection in the setting of a patient with with an underlying disease process that these sequences are particularly good at bringing this out making very obvious that you have a dissection or possibly an occlusion all right let's talk about anatomy before we move on to pathology we approach the anatomy of the skull base by looking at it in these four segments and this is a way to kind of get your arms around the great complexity of the skull base and when we're talking about neuro ophthalmology imaging we're really looking at the central skull base this is this is where the cranial nerves pass there of interest to these disease processes and where we'll focus our attention but you kind of think of of these as ways to segment out kind of going from just if you go down the list of cranial nerves the way to segment out these regions and talk about them individually but we'll spend our time with the central skull base is made up primarily of the student bone especially the greater wing you also have a portion of the basis phenoid and the cell and of all the complex foramina that we're going to deal with here and then the upper to mid cranial nerves pass through them so we can make a long list of a foramina and structures that pass through them of these the two that are the most meaningful to us are going to be optic canal with the second cranial nerve and the superior orbital fissure with the ocular motor as well as some trigeminal these other pathways will come up rotundum with with v2 these become more issues with a valuation of the deep face often more of a E&T kind of evaluation and then sponosum invidium these do have some pathological processes that we may we may visit but as much as anything we need to know what they are so we don't confuse them with maybe the areas that we spend more time so here is a series of images axial from superior to inferior and then we have some some coronal sequences if we look at the axials here starting up the top if you have a slice that's going through the optic canals notice how they're hanging toward each other so that is the X of the chiasm and it's an easy mistake to confuse the optic canal with the foramina right below it which is the superior orbital fissures the way you tell the differences again these are coming in an X and just below that the superior fissures are kind of coming straight back and be surprised how hard it is sometimes to tell these apart but once you get that sort of morphology in your mind it'll it'll be pretty clear if you go a little bit further down you get this little short canal there which is fremen rotundum right in front of that is this little space of terrapalium fossa and if you keep going out further you get this kind of elongated sickle shaped canal which is the vidian canal in the coronal plane at the level of the superior fissure you'll notice that the superior and fissure are continuous there's sort of like this gash right through the back of the orbital apex and then as you go a little further back you can see that superior fissure kind of goes back toward where we're gonna have maybe one other piece of anatomy what we'll talk about first is the client processes are a landmark that you can identify now an MR it's hard to see them on CT so we kind of train our brains to look at the anatomy in CT and then you project that when you get to the MR so the client processes are attached to the Bayesian where the sciences by this little bit of bone the optic strut and the optic strut is it is a distation but provides a kind of a physical barrier between the optic canal and superior fissure so optic canal superior fissure remember the optic canals they're at an angle so when you do a coronal slice you're not going to see the optic canal as a circle you're gonna see it is kind of an oval or maybe just a partially enclosed oval so you have to kind of know where it is because it's not gonna show up as a discrete circle so here's the superior fissure and then below that remember the inferior fissure if you take it straight back it's gonna become Framon rotundum because that's where v2 runs through so rotundum and rotundum superior optic canal as you go back a bit further you can see rotundum more discreetly here and here and then it goes back toward the trigeminal cave or meccalus cave this little dent here is called the porous trigeminus and then we also see another frame that pops up here which is right there this little small one down below that's the vidian canal sometimes the vidian canal is more conspicuous than rotundum so it's easy sometimes people will confuse it confuse those two so the way to remember is rotundum is it's more superior and a little more lateral than the vidian canal so these are the landmarks that we learn on CT and then we remember them and we project them onto under MR when we get to those images drawing of this of the central skull base planard process at the optic strut would be right underneath that second the optic nerve and superior fissure with three four six and v1 going through it inferior fissure of the rotundum here going toward inferior fissure and then if we were to go further down we would see ovale with v3 going through it kind of straight down and then same view from below okay so anatomic considerations with the optic nerve we begin by looking at the globe and the orbit in the interorbital nervous becomes more of an orbit discussion as you go back we get to the optic canal and then the intercalricular portion of the nerve this could be actually relatively hard to see so again you have to know know where it lives to look for subtle abnormalities there further approximately into the cisternal segment of the nerve the chiasm and the tract and then going further back in the lateral geniculate and then once we get into the radiations the cortex becomes more of a brain imaging situation interorbital we won't spend a lot of time about today other than to be aware of the fact that we have a this the second cranial nerve is of course is a central nervous system tract so it has a dural sheath surrounding it and both of those structures can have abnormalities that we'll see within the orbit a close-up here of the optic canal again we see it as an oval here the optic strut and the and the client a process separating the canal from the superficial if you take that image and go to a corresponding MRI this is what it will look like not as conspicuous but now we know where everything is we know that we have the senoid sinus the Bayes's senoid client processes optic strut and so there's your optic nerve right there and there and you find that then you can track it as you go forward and backward through those coronal sequence so here we have the optic nerve here and here planet processes senoid sinus optic nerve going back now in the external portion back toward the chiasm and then chiasm relationship to the cello the pituitary stock and the to their gland further back toward the geniculate and then we're into the brain so that is how we identify it and again this is a one of those kiss or T2 space sequences it lets us see the the structure very very clearly but again use your CT knowledge to project onto the MR so you can find these structures the optic chiasm can be seen as a structure if you get the angle just right now the angle of the chiasm is not true axial it's about 15 to 20 degrees off so usually we won't get a picture that looks like this unless you go out of your way to ask for it so usually we don't need this image per se but there's a particular reason to want to identify these structures in plane you can get a sequence that will they will lay that out for you but this is what they would look like if you were in an off-axial plane like that midline sagittal anatomy is is also something that you want to be familiar with so in this drawing third ventricle along the floor of the third ventricle there are some structures that are going to be really conspicuous so floor of the third ventricle just off the side you have hypothalamus mammary bodies and you can have these two little recesses right here at the front of the third ventricle one of them is going to go down into the infundiblum so make it sort of like a little central channel within the infundiblum partway down toward the pituitary and then right in front of that you're going to have a little pocket that is right above the optic chiasm and that is the the chiasmatic recess and and if you look at this shape to me it looks kind of like the head of a bird there's there's the bird beak and the eye of the bird the beak is that the chiasmatic and the infundibular recesses so if you look at an MRI you can see those things really pretty clarity right so now you see the bird so third ventricle mass intermedia floor of the third ventricle mammary body there is the infundibular recess going down towards pituitary optic chiasm chiasmatic recess so there is the optic chiasm so on a midline you can always find the optic nerve and then you can go track it to side to side and see it as it goes into the optic canal and this is the anterior commissure so the the physiology and pathways and right and left is the things that are all second nature to use so I won't try to teach you anything about this anatomic considerations of the third fourth and sixth motor nerves these begin as central nuclei and we obviously try to understand their neural pathways as they come out into the cisterns and into the skull base of orbit we have these cisternal segments that we can identify and occasionally although it's somewhat uncommon we can actually see disease processes directly affecting the cisternal segments of the nerves and then we track them into the cavernous sinus and the central skull base where we probably have more disease that affect them and then ultimately through the superior fissure and into the orbits a drawing of the third cranial nerve so here we see at the level of the the midbrain the nerves come along come out along the lateral margins of the intracerectal cistern they come forward down a little bit and they pass right between the P1 segment of the posterior cerebral artery and the superior cerebral artery as they pass through the cisternal segment into the cavernous sinus and to the superior fissure into the orbit from the side here we see at the level of the midbrain this nerve comes out into bronchocistern descends a little bit sort of hooks underneath this P1 segment above of the superior cerebral artery through the cistern into the cavernous sinus superior fissure and then into the orbit on these high heavily T2 weighted sequences you can see them coming out again because they're descending a little bit as they come out of this of the of the intracerectal cistern you won't see them as a line necessarily they'll drop a little bit and then as they come forward here to the cistern as they angle toward as they head toward the cavernous sinus you'll see them coming forward and then there are these little pockets of CSF around them that's the ocular motor cistern that you'll see surrounding these nerves as they're heading into the cavernous sinus in coronal plane so here's the third nerves again P1 segments of the PCA SCA and there they are right in between those two arterial branches and then as they come forward here we see that the little pocket of CSF the ocular motor cistern and this is to again remind us of that relationship between the vascular structures of the P1s and the SCAs and the third nerves we have these little bits of the crottin stront and to remind us that there are the posterior communicating arteries and this relationship is what sets up these nerves for a possible problem if you have an aneurysm right there fourth nerve just a little bit below the third nerves and the midbrain these exit around the back cross along the dorsal midbrain through the intracerectal cistern I'm sorry through the pyramids and sphalic cistern and then it has a similar course and that it passes between these two arterial branches as it goes into the cavernous sinus other side the same thing so similar to the third nerve after it comes around the back from the side we see it exiting on the back it decasates around the back into the pyramids and sphalic cistern between the two arterial branches and then into the cavernous sinus and orbit this is a much smaller nerve so it's harder to see but you can often find a linear structure that is a candidate for this nerve and since it has a somewhat unique course you can usually identify it as a discrete structure although it's not as reliable as the third nerve in the coronal plane you may be able to identify it as a small structure coursing around the side because there are venous structures that pass in the same location I think it's a little hard to be too dogmatic about saying I know what that is but sometimes we'll see a lesion that is clearly from the fourth there we'll show you an example of that but as a normal structure it might be inconsistently found the fifth there it doesn't have a lot to do with ocular motor dysfunction but it is such a prominent structure and it does have branches that come into the orbit we want to make sure that we know how it looks as well large ganglion sitting in necklace cave it's got the pre ganglionic segment that comes around the ponds sort of at the mid ponds level and it has components that will go through the superior fissure frame rotundum inferior fissure and then as well as down in the frame and O Valley the fifth there is very easy to see even on routine brain imaging you'll usually see it as this big trunk of fibers coming out the lateral ponds at the level of the mid ponds headed towards meckles cave the sixth nerve has its nuclei and the level of the mid upper ponds just anterior to the fourth ventricle and it has its fibers that come out just below the ponds and then ascend up and into the pre pointing cistern through the little reflection of Dura and drills canal as it's headed toward the cavernous sinus and it has this relationship we understand about the facial loop as it goes around it at the back of the ponds and the side here we see the sixth nucleus the fibers exiting under the belly of the ponds ascending in the pre pointing cistern as they go up to go through this drill canal this drill reflection into the cavernous sinus this is also a small structure but because it runs in a in a course that doesn't really have anything else there to confuse it with it's usually pretty reliable to find this as structure that is running almost straight enter like this a little bit sort of like a shallow v-shape coming forward it's ascending so you won't necessarily see it as a line in the axial but in the sagittal if you do an acquisition you can actually see that the sixth nerve in that very characteristic course and nothing else really runs there so that's usually relatively straightforward to try and identify even though it's quite small and then we're aware of all of these nerves that have a course of the cavernous sinus the third the fourth nerves and then the sixth nerve is described as being the one that is the most suspended internally within the cavernous sinus and given that it has this a lot of exposure around it and it's a relatively small nerve is sometimes said to be the nerve that is the most likely to have an early manifestation of a cranial neuropathy if you do have a cavernous sinus process although ultimately you would expect all of the cavernous sinus nerves to potentially be affected if you had a disease process and then the branches of five as well okay so let's talk pathology right visual pathology tumors of the orbit skull and cisterns in the orbit or cisterns optic glioma and meningioma two of the more common reasons we might see causing visual pathway dysfunction there's any number of orbital masses that we don't have a lot of time to talk about we'll just maybe put a list up and mention them briefly pituitary disease because of its relationship with the chiasm is not an uncommon cause of visual disturbance and metastases of the skull base in particular but also cisternal disease an optic pathway glioma can occur anywhere in the orbit it has an association with NF1 it's minor they have some variable appearance usually brought on t2 enhancement can be a quiet variable and in that it behaves a little bit like pylositic sort of an astrocytoma you can have a lot of enhancement without it being an advanced grade tumor usually a lower grade tumor especially in younger patients it can affect any part of the pathway here we see bilateral optic pathway gliomas relatively no enhancement getting all the way back to the chiasm so this is a condition that you may see in your in your pediatric patients meningioma is a disease of older patients and it has a characteristic appearance of this tram track calcification that is a hallmark and not uncommonly we will get patients who we have a maybe an optic neuropathy we think we see something in MRI we're not sure we'd like to get one more piece of data we might after the MR get a CT to find those calcifications because if you see those calcifications that's that's a pretty passive mnemonic for an optic path an optic nerve meningioma in the orbit but we see that the tram track enhancement of the of the dural mass that's surrounding the nerve and then the corresponding calcification on T2 a sign that's been associated with optic nerve meningioma is a little perioptic cyst that collects the back just behind the globe presumably due to the mass effect from the the dural mass macrodinoma has the the possibility of causing compression of the chiasm because it lives right below that cisternal portion of of the optic pathways on imaging what we see is a cellular mass that doesn't have a discrete gland apart from it so it appears to be coming from the gland the hourglass contrast to do with the fact that there's a dive a little diaphragm of sally that the pituitary sort of squeezes through as it's going upward a generally intense enhancement but i want to be aware of the fact that these things may contain blood or cysts and you may have areas of non enhancement within them one manifestation that we need to be aware of and that you will hopefully get informed of from us if we see it is is hemorrhage within the gland will show up as an area of non enhancement now hemorrhage can be can be quite bright on t1 when it's acute or subacute so we have to be aware of looking at our pre and our post contrast sequences to make sure that we know that you have an area of of blood within it and one reason why this matters is because there aren't that many things that are neuro radiological emergencies we don't live the very fast paced lives that you guys live where you're taking care of patients you have to deal with something right away but there are some things that when we see they get our attention we say we have to deal with this right now tonight this can't wait till tomorrow and apoplexy is one because if these patients show up with a large tumor that has hemorrhage and has sudden mass effect on the chiasm that needs to be decompressed immediately and so we need to be aware of these imaging manifestations of apoplexy that can be an emergency that has to be dealt with right away there's a long list of orbital masses that we won't have time to go through the list is a little different from adults versus kids i'm an adult things like cavernous hemangioma liver proliferative disease tumors of the adnexa metastases in the pediatric population we have different kind of vascular lesions usually malformations sarcomas lingering hand cell disease metastatic tumors and so forth and these generally become over discussions but they can't affect vision maybe just one mention of a kind of a metastatic process it is uncommon but can show up as visual dysfunction this is a patient with leptomeningial carcinomatosis this is a post-contrast T1 notice how you have a ring of enhancement all the way down the interorbital course of the nerve this is not a meningioma this is leptomeningial breast metastatic metastatic disease that is following the csf down the sheets into the orbits and this is an uncommon but a known manifestation of metastatic disease that is something you might see in the orbits inflammatory optic nerve disease acute optic neuritis especially associated with demyelinating disease and then adiopathic inflammation there are other kinds of of optic neuritis that are specific and granulitis disease that we commonly see but there there's a lot of images you overlap between these so we include them in our differential lists here's an appearance of a patient with acute optic neuritis you see a t2 sequence again notice the csf for your internal controls normal csf normal optic nerve on the right you have a swollen optic nerve it's kind of facing all the csf and the nerve itself is is very bright on the post-contrast T1 you can see that the nerve is is enhancing compared to the normal nerve it should have should be nearly black and have almost no enhanced maybe a little bit of normal perioptic enhancement but this is an abnormally enhancing nerve in a patient with acute optic neuritis and in these patients getting the brain imaging is just as important as getting perhaps more important than getting the intra-orbital imaging to identify the very common correlating finding of you know a presentation of demyelinating disease idiopathic inflammation that affects the optic nerve there are any number of manifestations and we can kind of classify how a pseudotomor shows up depending on what part of of the the orbit and skull base it involves the anterior form is the one that may affect the optic nerve in a somewhat isolated fashion generally when you have a lot of disease it's not as as specific to just the visual pathways but occasionally it might be here's an example of a of a lesion that was a patient of doctor degrees many years ago that we initially diagnosed the inflammatory component wasn't as clear on the clinical presentation we even wondered ourselves this kind of looks a little bit like a meningioma but after some time some stories it went away this was an example of an unusual pseudotomor uh this is a patient with sarcoidosis and just to remind us the many manifestations you can get with granulomus disease notice we have this this striking diffuse enhancement enlargement of the optic nerve which also have disease involving the muscles you also have uh this is the third nerve and also even some supercellar disease so you can have a lot of different manifestations of some of these inflammatory conditions. The ischemia of the optic nerve two types that we might see the anterior and the posterior form you can also see ischemic disease showing up as visual dysfunction when you have somewhat localized cortical involvement from thromboembolic disease. Anterior ischemic optic neuropathy which we associate with older patients and micro master kind of disease imaging on that is is often somewhat normal you may see a little bit of enhancement the optic nerve had this is a very distinct entity and much much more common than the dreaded posterior ischemic optic neuropathy which this is from a patient from just a couple of weeks ago that some of you probably saw very unfortunate young man who had a very extensive skull base and a perservative surgery which is associated with this condition and here we see on the diffusion sequence these long segments his case was bilateral and a devastating complication a dreaded but unfortunately not always possible to avoid problem with certain perisurgical perianocetic operative conditions. And then thromboembolic disease showing up as visual dysfunction if you if you have a stroke that picks off visual cortex especially if you've you've got something that's localized to the posterior cervical artery territory you may show up with a primarily visual dysfunction we do perfusion and diffusion imaging to identify this this is again the posterior cervical artery territory now this can come either through the anterior circulation if you have a big PCOM or maybe even a fetal origin PCA a carotid embolus can do this or also of course if you have a vertebral basilar event you can get a PCA stroke. One of the things to be aware of when you're doing posterior cervical artery imaging you have to know the anatomy in the perimesis phallic cistern you actually have two vessels that live in the perimesis phallic cistern to go around the midbrain. One of them is a vein the other is an artery and you know that the vein is on top and the artery is below so that the stroke here is the missing artery right below the vein these are the the basal veins of Rosenthal. Okay moving on to pathology of the oculomotor structures again as with with visual pathways inflammatory disease especially idiopathic inflammation sarcoid can give you manifestations that will it will cause oculomotor dysfunction then of course thyroid over topathy maybe one of the more common conditions that you will see giving you this function and some tumors lymph proliferous disease and and mats which we won't talk a whole lot about same list of the sub types of pseudotumor and the areas that may affect the cranial nerves or the oculomotor functions are going to be in particular the myocytic form and you're going to have pseudotumor that just affects the muscles there's also this this apical form the tulusa hunt disease that will give you multiple painful cranial neuropathies here's an example of a patient to present her with a right-sided trochlear policy and the only imaging finding was a subtle enlargement of the superior oblique compared to the other side this is a presumptive diagnosis because after the patient got steroids it went away and here's an example of a patient with a Toulouse hunt this is a doctor degrees patient from a couple weeks ago who reminded me that I really need to read the history this was we read this at night at first we looked at this and the history was I think painful ophthalmoplegia or something like that and we get so many scans that come through from clinicians who don't necessarily know as much as doctor degree that we sometimes just read the scans and don't necessarily get the finer points and the next morning she comes down and says this patient really worries me can we look at these pictures again and make sure there's not something and sure enough on closer inspection we see that there is this mass-like enhancement in the anterior carpenter sinus heading right into the superior ophthalmic superior orbital fissure a classic presentation of pseudotumor what we would call Toulouse hunt so I'm sure that's what this patient ended up having because it was so yeah so anyway a lesson for us that when it comes from our ophthalmologic colleagues we really need to pay attention to the things that you tell us there's the abnormality thyroid ophthalmopathy grave disease this shows up as generally symmetric non-conform enlargement of the extra the extractor muscles we use that the mnemonic inferior medial superior lateral oblique is a way to think of their commonness of involvement although and I think inferior medial inferior medial and superior in particular but we do have some patients have preferentially superior muscle involvement so this isn't completely followed obliques and lateral is very uncommon though so especially the inferior medial and superior the most commonly involved muscles these is something that can be seen on CT and MRI generally the clinical presentation is seems to be clear enough that we don't often get imaging confirmation but in confusing cases we might be able to help you out and identify the characteristic appearance of muscle involvement it can be symmetric as on this MR the left muscle seem to be more involved in the right but pathologically here's the pathology they're all going to be positive but they may be macroscopically asymmetric in their involvement lymphopriliferous disease is a somewhat common malignancy that can affect the orbit and we won't spend a lot of time with this but just be aware that lymphoma is a very solid mass it doesn't have necrosis doesn't have system shows up as these sheets of infiltrating tissue can occur anywhere in the orbit or skull base it's pliable we sometimes use the word plastic because it tends to get into things it can cause some bone destruction but it can sort of just wrap around and it looks a lot like an inflammatory process in fact one of the one of the common likenesses that we talk about in neuroideology is that lymphoma and granulomas disease have a lot of images you overlook they look a lot like each other so if you see yourself thinking about one you often include the other in the differential here's an example of a patient with orbital lymphoma involving lacrimal gland the rectus muscle a little bit of intraconal disease and also intracranial disease as well this looks an awful lot like that case of sarcoid i showed you several slides ago heading further back now for the ocular motor dysfunction tumors that affect the skull base and cisterns pituitary not so much because the pituitary tends to be more midline well-behaved when it extends it goes up usually but it can go off to the side and get into the cavernous sinus meningioma the petroclival region is a very common location to get meningiomas so to have a meningioma affect cranial nerves is not at all uncommon and then metastatic disease involving the skull base the bones of the skull base or leptomeningial structures involving the nerves and the cisterns schwannoma is a lesion we occasionally see relatively rare in the cranial nerves but we'll show a couple of examples of that here's an example of a pituitary adenoma that did actually go off to the side it's unusual again they usually go up but they can invade the cavernous sinuses and when they do you can get ocular motor symptoms as well as visual symptoms here's a typical appearance of a kind of a cavernous sinus pitroclival region meningioma you see a mass along the lateral margin of the the cella filling up of the cavernous sinus headed toward the superior fissure and again lateral march of the cavernous sinus become a little bit forward this is going to go straight toward the superior fissure and this this looks a little bit like that case of cititum or that tulissa hunt that we saw but in these cases instead of being painful it's going to be chronic progressive symptoms and these are going to have generally a fairly slow growth and a fairly typical imaging appearance from meningioma notice you have the the the chronic denervation atrophy of that medial rectus muscle this is just an example of leptomine angiocarsinomatosis this could be primary gliomal weakness could be lymphoma could be fungal disease could be sarcoid could be any number of leptomine angioprocesses but when you have this much disease you're going to be able you're going to expect to see a lot of multiple cranial nerves involved tb exactly schwannomas of the the mid-deprecranial nerves are relatively uncommon but we do see them here's an example of one that's coming off the bottom of the third nerve when they are isolated they're somewhat rare they can be associated with NF2 when they do show up on imaging they will they will be seen as a nodular mass in the cistern right where we know the nerve lifts so here's an example of a patient who has asymmetric superior obliques in this case it's atrophied on the left and if you look at this patient's paramedicine cistern sure enough there is a nodule right where we know that fourth nerve runs in that paramedicine cistern this is a presumptive schwannoma no one's going to go after this because you can only make things worse but that would be almost certainly what this is and we've seen a number of these over the years and intraorbital schwannomas aren't that common we do see them they tend to be in the cisterns and for the fourth it really likes this location around the side of the midbrain okay Chris on this picture can you sort of show where the tentorium is and emphasize for our oncology residents how vulnerable the fourth nerve is as it sort of parallels the tentorium so the way they identify this entorium an axial is you kind of have to notice the difference between cerebellum and occipital lobes and temporal lobes so cerebellum is going to have the folia in it and because the the tentorium is sort of angled like a like a shallow tent in an axial slice you're going to get both supertentorial and infertentorial in the same picture so this slice shows cerebellum temporal lobe and occipital lobe what that means is the tentorium is between those so whatever is between this and this there's your tentorium there and there you often get a little bit of venous structures that go along the tentorium so that's how you can identify it there and there you can see the tentorium right there there's your your cerebral hemispheres and then the cerebellum below it so there is the tentorium that a little bit of vascularity will on a post-conscious will help you identify it and as Julia points out the proximity of that tentorium to the nerve is one that's just waiting for a reason to get injured and the fact that it is a small nervous it's a very long course means it's a very exposed nerve and has a kind of a fragility to it that makes it um not uncommonly affected this is an example of a sixth cranial nervous schwannoma this has when these schwannomas get big they can get a little bit of cystic degeneration in them not across exactly but they can be heterogeneous in their enhancement this one we know it's right in that area of duralis canal and this patient also had a sixth nerve dysfunction that was chronic and didn't have any other signs of of malignancy and then for the back of the skull basin cisterns talking about infectious disease um skull is infectious this is uncommon to see but sometimes in diabetic patients who may have things like um osteomyelitis we've seen some of these patients over the years that come up with aggressive or chronic persistent skull base infections that can get into the central skull base and there's ambassador conditions thrombosis cavern sinus carotid fistula aneurysms that can affect the structures in the central skull base um gradenigos is a skull base osteomyelitis that's particularly at the petrus apex but can also be getting into the the central skull base the the basis phenoid this is more or less an extension of acutotitis otomastoiditis this is an airspace when it is pneumatized and so it shares the same disease processes as the middle-ear and mastoid in particular the sixth cranial nerve is is at risk here because it has that courses that runs right over the petrus apex going into the cavernous sinus through that little dural reflection of duralis canal makes it particularly susceptible so six is kind of the classic uh neuropathy that we see with with petrus apocytus um and as with other areas of infection we're looking for rim enhancing heterogeneous enhancement often with with dural disease petrus apex fluid in the case of gradenigos um otomastoiditis as well cavernous sinus thrombosis is a dreaded complication um it is associated in the in infectious conditions with with acute or chronic sinusitis in this case this patient has pretty clearly chronic disease look at how much mucoperiostal thickening that that sinus has been inflamed and reactive for a for a long time so this patient is no stranger probably to sinus disease and sinus pain but they presented somewhat acutely with acute multiple cranial neuropathies and if you look kind of closely the cavernous sinus looks way bigger than it should we have the the the dural margins are pushed out and there's a concern that this is going to be a cavernous sinus thrombosis in a previously chronic serotonin sinusitis uh this is going to occur with sinusitis uh head next cellulitis and the the presentation of multiple cranial neuropathies again especially six because of its course through the cavernous sinus an imaging what we're looking for is an enlargement and often bowing of the margin of the cavernous sinus and on contrast imaging you see non-enhancing clot the cavernous sinus should enhance because it's just a venous space and when you see soft tissue that's not enhancing that is what thrombosis is going to look like you can also see an enlarged superior abdomen vein due to pressure effects so here's that same patient on a t2 sequence notice you have this markedly enlarged cavernous sinus with these sort of outwardly bowing margins there's all this stuff in here that's going to be either tumor or it's or it's going to be thrombus on the post-contrast sequences you have these large areas that um if it was just venous space let's say you had a cavernous clot of fistula and the and the cavernous sinus is just full of you know pressurized blood it ought to be very very bright but what you have instead is these large areas of non-enhancing thrombosis especially on on the right side moving on to some other carotid lesions in the skull base when you see either an aneurysm or a fistula complex flow on mr is going to be kind of your tip-off vessels have a lot of signal regularities when they're tortuous and when they're arterial in part because with with MRI there there are competing signal effects that they can get in the way if you give gadolinium gadolinium is bright on t1 but things that move quickly cause blackness of the flow void so if you have both gadolinium signal and flow void competing with each other and then you add to it the tortuosity and turbulence that comes with with flow sometimes it can be hard to see exactly where vessels are on MRIs we look for the complex flow with aneurysm we look for obviously enlargement and they can be partially thrombosed with a fistula we're looking for the secondary effects of the fistula arterialization of the venous pressures enlargement of the superior at thymic vein here's an example of a flow void in an aneurysm one of the things to be careful of is right next door to these these the cavernous segments of the are of the carotids are the clinoid processes and and the an aerated clinoid process can be a dead ringer for an aneurysm so you want to make sure you pay attention to where the clinoids are and if you think it could be a clinoid aeration instead of an aneurysm you can do an angiographic sequence or just a ct will often prove that it's just an aerated space here's an example of a very of a giant aneurysm of the of the cavernous carotid full of thrombus it's obviously in a position to cause the same kind of mass effect that we would see with a meningioma for example and here's an example of a patient with a cc fistula here's a carotid an internal carotid injection what we see is in addition to filling these nice normal cerebral artery branches what you have is a a blush of contrast in the wrong space in that that's filling the cavernous sinus and we know this is wrong because you've just barely injected the carotid and you're just barely starting to fill out the cerebral artery branches the cerebral arteries are low resistance high flow branches so they should fill right up if you start to see venous spaces before you've even filled out the branches of the mca you know you have a fistula's connection in addition you have this retrograde filling of the superior ophthalmic vein and even filling the cavernous sinus standard in the the inferior pretrosal sinus and a corresponding enlarged superior ophthalmic vein superior ophthalmic veins can have some normal variability in some patients they're just big and so you have to be a little careful about over calling it but when you have other suspicions and you're trying to get more information to say do i have something that's affecting the cavernous sinus a really big superior ophthalmic vein can be a useful piece of information then if we keep going further approximately we get into the parankama of the midbrain microvascular stroke can affect upper cranial nerves demyelinating disease and there some other conditions occasionally we've seen these small carotid malformations that are localized enough that they pick off a cranial nerve and don't do much else ischemia that affects affects the midbrain has to do with these vertebral basilar perforators and for that reason isolated midbrain strokes really are not thromboembolic events they're microvascular events so we see them in patients with hypertension diabetes microvascular disease t2 is a little more sensitive than flair so we pay attention to that especially diffusion abnormality and again these are very small lesions so the adc may not always be positive so here's an example of a patient with an acute midbrain microvascular stroke bright on diffusion a little easier to see on the t2 than the flair demyelinating disease no stranger to the midbrain typical symptoms that you will see isolated nerve policies are somewhat rare they have been described as as being a little bit more common in six obviously the imaging task with with demyelinating disease is to find the whole pattern and looking for disease where it occurs and here's an example of patient with a some large demyelinating plaque in the upper midbrain this would be in a good position to affect cranial nerve 3 and then we can occasionally pick up very acute plaques on diffusion sequences of a patient with a small plaque in the region of the of the mlf you would expect them to have maybe some typical symptoms let's see um it is five more minutes i threw in just a a little bit about autonomic pathology because it's part of the discussion we can have with with a neuroideological imaging so maybe just a few slides on this parasympathetic disease um edginger westfall and it's and it's pathways pretty much parallel the third cranial nerve um peripheral nerve fibers and so you can kind of think of anatomically and and in terms of disease processes it's going to be a lot of this overlap between that and an oxidative motor dysfunction compressive lesions now we do get into this interesting discussion about the location of the somatic versus the auto components of three as it exits the midbrain and how that can affect which are affected and it gets into this discussion of pupillary involvement and whether the sphincter dysfunction is is isolated or in conjunction with with third nerve palsy and it has to do with this phenomenon of extrinsic compression from classically an aneurysm so the the somatic fibers or the the the parasympathetic fibers on the are on the exterior and then the somatic fibers are centrally so in theory if you have a massive outcome from the outside you will get the parasympathetic fibers first and that brings us to this phenomenon of the sacular aneurysm typically of the PCOM that presses on the third nerve giving you people are involved or a vascular loop similar to an aneurysm so here's a typical appearance of an aneurysm coming off the origins here's the carotid artery there's the the plastric communicating already going back and the aneurysm usually occurs at the carotid artery origin of the PCOM and in that location we know where the nerve passes it's in a location to cause extrinsic compression here is another vascular condition not an aneurysm per se but here we see a torch was a branch of a one that is causing the third nerve here to be displaced and you can again see how that might cause a mechanical compression of the nerve sympathetic dysfunction gets to be a little bit more complicated because we have to talk about it's pre-ganglionic and post-ganglionic courses if it's pre-ganglionic we have the pathway from the hypothalamus cilia spinal into the superior cervical ganglion and the kind of lesions we see causing disease here are going to be proximal neurological brachial plexus lesions masses of the perispinostasis mediastinum or lesions of the lung apex classically a pancoast tumor so here's a patient with lymphoma affecting the spinal canal brachial plexus in a good location to cause a pre-ganglionic corners another uncommon but known cause of pre-ganglionic corners is trauma this is a patient with a fracture you can see that this is the seventh vertebral body you can tell by the shape of the of the the foramina we have a fracture right there which is right where those those nerves are going to run and this patient did present with the corners and we did dutifully did a full ct angiogram which was negative and that's because the problem was actually pre-ganglionic. Post-ganglionic disease from the superior cervical ganglion they ascend via the carotid plexus these are the third order neurons into the skull basin basically more or less follow the course of the first branch of the trigeminal nerve and these are going to be vascular lesions especially the section of the carotid which we associate with things like you can have atheromodous dissections arteriopathies like fibromuscular dysplasia and some masses like glomus tumors in the neighborhood here's a patient with fmb with a typical appearance of these beading webbing tortuous multiple irregularities these patients are prone to to the dissection a dissection from any number of varieties it can be it can be traumatic and lead to to an arteriopathy and on imaging when we see a non occlusive dissection you'll see these irregular long segmental areas of significant narrowing and as I as we showed before some of your thrombosomes of the sequences can actually show you the subintimal hematoma that is the marker of a dissection and then finally vascular masses like this aglomus vagalli generally these are benign tumors so they don't cause as much carotide plexus disease but in large lesions you can sometimes get post ganglion of corners from these lesions okay so that is everything I do have just a quick summary slide here and to start that I show you a picture of what what life used to be like this is many years ago this is a picture I'm going to show my grandchildren when I say before climate change we used to have snow up in the wastes mountains I don't keep fingers crossed maybe look like this in a few months right hopefully before the mountains close yes all right so we talked about visual and ocular motor dysfunction we talked about a whole variety of intrinsic and extrinsic lesions vascular neoplastic inflammatory isolated multiple neuropathies and we talked a little bit about pathways and we've tracked everything from the orbit the skull-based cisterns all the way back to the brain okay that's it thank you now we're out of time but I did bring the a quiz if we if we if we're still doing that yeah beginning of your talk you use the pronoun we by which you mean university of Utah not neuro radiology right well that my identity is kind of both those things but now it's also the VA which which we the reason I bring it up is because you know most of our residents when they leave here will not be practicing here and they may be practicing a place where they don't even have a neuro radiology so you maybe give some pointers for like the sorts of things you can do if you're working with a general radiologist in a community setting so I think that yeah if you're if you're dealing with a non-specialist radiologist they're probably going to need direction most of the time if the if the the disease process is pretty well targeted and the location of the abnormality is suspect from a clinical examination they can find it these these anatomic and sort of regional findings that are typical that we've seen here most radiologists have been exposed to them and they'll know where these things are and and it was with a little bit of prompting they can find it it's kind of like like the case I had with with Kathleen just last week where even as an as an expert we sort of walked past the important finding because we weren't thinking about it in a very directed way but as soon as we got the good history that said we have this condition and this is the one thing I'm worried about radiologists we get into the weeds pretty easily because we have to look at so many things when we get a brain scan and oftentimes the history we're accustomed to having a medical record systems that don't feed us a very good history so we kind of have to look at everything and there are lots of incidental things that sometimes get our attention so we're a little we have a little bit of the shiny key phenomenon that when something looks meaningful but we don't have a driver to either take us two or away from that sometimes we can we can talk about everything and not talk about the one thing so when the history is good and very specific and if you say I have an abducens palsy and that's the thing I care about then all of a sudden the arachnoid cyst in the temporal lobe doesn't mean anything and the degenerative disease in the cervical spine doesn't mean anything on the other hand if there's a very specific symptom of a cranial neuropathy that is in the setting of maybe a known cancer and you think well this looks like it's somebody that's got multiple neuropathies then maybe we can open up our field of view a little bit and look at more things so I think that if it seems like you've got a real problem that you think that you just smells wrong to you and there's there's something that that you'd like to get another look at don't be afraid to ask him to say and getting a hold of radiologists I don't know if getting a hold of radiologists is as hard as for us to get a hold of you but if you I think if you know where they live and have their phone numbers and at least in column and say this is what again this is what we did with with this patient last week is call them up and say I'm really worried about this one symptom could you look again and see if there's anything there so I think targeting targeting specific clinical questions is the best way to get for us to not miss something