 Okay, so I'll be talking about the infernuclear causes of Diplopia, and again, just to reiterate, we're talking about binocular Diplopia for those that weren't here at the very beginning. So first let me talk about intraaxial or fascicular, so that's anywhere inside the brainstem, but not the actual nucleus itself. Usually when you get these fascicular lesions, there's multiple cranial nerves involved because you're talking about the brainstem and very tight real estate there, so you get multiple deficits. And so when we look at intraaxial involvement of the third, there's basically four syndromes that are tested on OCAPs, and I assume the boards as well. And they all cause kind of a third nerve, an ipsilateral third, plus something else. So Weber syndrome causes a contralateral hemiparesis, that's the only one to really cause that hemiparesis. Then the other three cause some sort of contralateral ataxia with or without an additional finding. So Benedict syndrome can cause this contralateral ataxia with or without a tremor. Claude syndrome can cause just a contralateral ataxia, and this last one can actually cause a super nuclear eye movement dysfunction. Nothmagle. What's that? Nothmagle. Nothmagle, yeah. Sorry, I was avoiding the pronunciation. You caught me, Dr. DeGree. And those are all from different areas, and so I've put in parentheses the spot that the pathology is most likely to occur. I don't know that that's tested as much, but it's at least good to know, and so that'll be here in the PowerPoint slides if you want to see that later. Penial involvement of the fourth, so fascicular lesions of the fourth, it's fairly uncommon, and it's usually due to some sort of compression on the tectum, and that's usually due to a pineal tumor that actually causes a bilateral fourth fascicular lesion. In that kind of context, you can also get basically obstruction of the cilbian aqueduct so then you get elevated ICP, and so you get some other obvious findings with elevated ICP, but that's actually fairly uncommon. Then interaction of involvement of the sixth, so a lot of times it will actually include a seventh nerve just due to location, and so there's two syndromes that kind of come to mind that combine the sixth and a seventh. So phovial syndrome, you get an ipsilateral ABduction deficit, and then facial weakness and loss of taste, so they enter two-thirds of the tongue, and facial hypostesia. Then Miller-Gubbler syndrome is a contralateral hemiplegia with ipsilateral facial nerve palsy, and of course the ABduction deficit from the sixth nerve. Then if we look at kind of the next portion of the nerve, so if we move out of the brainstem into the kind of subarachnoid segment, this is where most people actually hypothesize that ischemic nerve palsies occur, and so they, in this specific location for the cranial nerves that are typically in isolation, so it's usually the cranial nerve three or cranial nerve four or cranial nerve six without other cranial nerves involved. The big things to consider in ischemic nerve palsy, so you should have the maximal deficit at presentation or at least over the next seven to ten days. They may or may not have pain, so I know we always try to figure out was their pain involved, but honestly that isn't real predictive of whether it was ischemic or not. Then this is not necessarily a diagnosis of exclusion, but you should at least rule out other more significant pathology prior to this. They usually improve over three to six months, so if you notice that a lesion is progressing over two weeks or is failing to improve over a three to six month timeframe, you should reconsider an ischemic event and look at more maybe compressive lesions or other issues. Then usually this occurs in the setting of known risk factors, sometimes you're the one that identify those risk factors of diabetes, hypertension, hyperlipidemia. Then the word of warning that the BCSC likes to give is just because something recovers, so when we look at ischemic cranial nerve palsy and they recover in three to six months, that doesn't necessarily mean that it was a benign process, so you can actually get a spontaneous recovery and then a repeat cranial nerve palsy in tumors. The CNS is not an unheard of phenomenon, so that's just something to be mindful of. Then if we look at the actual third, fourth, and sixth nerve palsies, so we've talked or I even just recently talked on third nerve palsies two or three months ago, so I'm going to be a little quick on third nerve palsies, but the big question anytime you see a third nerve palsy is whether it's pupil involving and I've shown all of these kind of repeat drawings that Ashley has already shown just so when you guys were looking back through these slides if you want you can see the actual nerve itself. So when we either identify pupil sparing versus pupil involving, pupil sparing is more consistent with ischemic etiology. It can be associated with pain, usually resolves in three to six months, kind of like the ischemic cranial nerve that I was giving a basic outline on just a second ago. This usually happens in the setting of patients that have known risk factors and then at least what the BCSC recommends that they have known risk factors, it's pupil sparing and they have no history of cancer that you don't necessarily have to neuro image. I would say that a lot of that's kind of controversial at this point due to the ease of imaging, but you can at least, at least from the BCSC do that. Then if it's not in the setting of known risk factors you should at least further work this up and obviously keeping in mind that GCA can do things just like this and that's something you want to be very mindful of. When pupil involving you should basically always assume it's an aneurysm until proven otherwise. The BCSC will actually say that you do an emergent MRA, CTA. If that doesn't identify an aneurysm then you may even want to proceed with a brain angiogram, the gold standard. However imaging is getting much much better so a lot of these very small aneurysms are being picked up on imaging. However that comes with the caveat that 20% of pupil involving third nerve palsies can be vasculopathic in origin so you may not ever identify an aneurysm or more significant pathology it may just be vasculopathic. However that's a diagnosis of exclusion. Then you start getting into more complex issues of the third nerve so relative pupil sparing and all that really means is that people reacts normally but you only have minimal impairment of the levator or and or extra ocular muscle function so you may have some muscles that are still functioning it doesn't really fit a divisional third so in that kind of context you're thinking of more compressive lesions that may then subsequently evolve and to include the pupil. Then divisional just think of kind of the anatomy of the superior and inferior divisions of the third and you can get basically kind of a split not a full third because you're getting either just the superior inferior division affected that's usually pathology into your cavernous sinus. Then the thing that it kind of can skew things after third nerve palsies and this isn't usually in the setting of ischemic thirds is aberrant regeneration and so this is just misrouting of fibers to produce co-contraction of muscles not normally affected or activated at the same time so for example that's eyelid retraction with a with adduction or pupillary meiosis with elevation. Dr. Green. Can I just add two things? Of course. So relative pupil sparing this means that the pupil is actually larger it partially reacts that's where you really get into trouble because you you look at it it's a little bit bigger it works sort of sort of sphere because it works but it's bigger and these these are present in like a third of people involving partially involving third nerve palsy so this is relative pupil sparing is the thing that really gets you into trouble. Do you image every single one of these relative pupil sparing? Do you know how many nights of sleep I lost before? I just said yes. So I just image those and then aberrant regeneration if you see somebody who's got primary aberrant regeneration think they ask patients to be involved in some kind of compression because that if you see primary aberrant regeneration it usually is related to it. Right and like I said usually does not occur so I think this is kind of like I know one of those board questions the person's live goes up with a ad duct type of thing and it's aberrant regeneration and it's usually a two. And just to connect aberrant regeneration to our lecture on pupils what was the sign that's possible to do the aberrant regeneration of pupils? What happens to the third aberrant regeneration of this? What signs of pupils show up? Well no I gave you a diagram last week and asked you to name causes of like near dissociation so you have to kind of first you have to think about that. I've been going to the sorry am I interrupting you? No no please do at any point interrupt Dr. DeGruyne. Fourth nerve palsies so usually you'll get duplopia that worsens and down gaze so usually the patient will come in complaining of double vision while reading. The ocular motility is usually normal and then we basically identify a fourth nerve at least a unilateral fourth off of the three step test for some of the PGY2s that haven't dealt with this or even just a reminder for myself. You try to identify the hypertropia which side it's on which side is it worse in so either left or right gaze and is it worse in right or left head tilt. So for example a fourth a right fourth would have a right hyper that worsens in left gaze and right head tilt. Then just remember any of these closed headed traumas that we're seeing in the ER. It's not uncommon to get a fourth nerve palsy due to closed headed trauma and that's due to the crossing nature of the actual nerve itself. Then the six nerve palsies so it's the most frequently affected isolated ocular motor palsy causes this horizontal binocular duplopia causes adduction deficits that with horizontal duplopia that worsens in gaze to that same side and then you can also get an ipsilateral isa deviation. Most common cause at least in the right age setting is ischemic you can get all sorts of sixth nerves though but that's at least the most common cause. Then I've already given you kind of the guidelines of an isolated mono neuropathy so if it's kind of fits that profile then you can call it ischemic otherwise you probably or at least do a medical work up if you don't have known risk factors otherwise you need to start looking into other things besides ischemic. Then in at least what the BCSC advises anyone under 50 so they don't really fit that ischemic profile you should consider imaging because so few of those are ischemic in origin and so you're looking at other causes of a sixth nerve palsy. Then combinations of cranial nerves and this is kind of a complex thing and I think actually Dr. DeGray is talking about the cavernous sinus and maybe Friday. Okay so 3D cavernous sinus this Friday. That's right so I won't steal too much of her thunder but when you start getting combinations of cranial nerves you're either looking at the cavernous sinus well I guess we can back up and say the brain stem then back into the cavernous sinus or into the superior orbital fissure it's very hard to actually dissect superior orbital fissure and a cavernous sinus so be thinking any of these contiguous nerves three four five six and then sympathetic nerves if you have involvement of multiple of those start thinking cavernous sinus. The neuro exam is critical especially cranial nerve exam in this setting because you need to identify that fifth palsy then this requires pretty extensive work up probably at least starting with imaging and then depending on what imaging shows you may need to go to a lumbar puncture depending on what you think the etiology is in the imaging suggesting then just two kind of things to look out for that are tested fairly frequently so tulosa hunt that's an idiopathic inflammatory event of the cavernous sinus and then cc fistulas and I've given some kind of findings with the cc fistula I'm not really going to hound on that at this point because we'll run into it at other dates so okay