All right. Welcome everyone. Today we're gonna be talking about canine and feline vestibular disease.
One of the main reasons that I like to talk about this is due to the fact that unfortunately, it can be a little confusing and a little daunting, really any neuro case can. And so I definitely want to try to take away that neuro mo ph ob ia that everyone can have. So we're gonna go through this and hopefully you guys will be more comfortable at the end.
So to give an overview, we're gonna go through the components of the peripheral and central vestibular system. We're gonna go through how to differentiate peripheral from central vestibular disease based on your neurologic evaluation. We're gonna go through the peripheral and central vestibular disease differentials, the most common differentials, we, of course, can't do a complete exhaustive list here, but we'll go through the most common.
And then we'll go through the recommended diagnostics and treatment options for the most common scenarios that we have for our vestibular patients or most common differentials. So one of the main things just to remember is that if there is a head tilt present, vestibular disease is present. You don't have to try to make it any more complicated than that.
You see a head tilt, you immediately know that there's vestibular disease. And what we have to do is to determine if it's central or peripheral. So I like to think of any neurologist, any GP out there that we're basically little detectives, and we gotta figure out which is which.
So when we look at our vestibular system, it's broken up into the peripheral vestibular system and the central vestibular system. So our peripheral vestibular system includes anything that's going on outside the brain stem. So it's basically anything within the peters temporal bone.
So our middle and inner ear. And when you think of that specifically, this is a T2 weighted axial image. Here is our middle ears that I'm using my mouse for, and these cute little ducks are our Internal ears, basically, I like our cute little tucks on the MRI so that's your inner ear, here's your middle ear, and what we're talking about in this area is everything you remember from that school or kind of have put out the window, right?
So you've got your utercles, your saccules, and then of course your cochlear duct, your circular ducts. That's what is a component of that peripheral vestibular system. And then we have our central vestibular system, which is basically anything that's found within the brain stem.
So there's different parts of the vestibular system, whether it's the vestibular nuclei, locations in the thalamus, different parts that are located within the brain stem. There's also components that are in the cerebellum as well, and then in particular, a component of central vestibular system that we can have. It's what we call paradoxical, and that can include our flocular nodular lobe, which is our associated with our cerebellum, and then also the caudal cerebellar pe uncle.
Excuse me. So when we take a closer look at our vestibular system, this is a T2 weighted sagittal image with on the left side of the screen, here is our olfactory lobe, and then here is our cute cerebellum at the caudal aspect. And so what we're seeing is all those components.
And so MLF stands for our basically fasciculus, which is gonna include all of our eye movements. And so we have cranial nerves 34, and 6 that's located in our brain stem. We have our vestibular nuclei, we have our vestibulo cerebellum centre within that cerebellum.
And then this is the area where we have that caudal cerebellar peduncle, and then our vestibulo spinal tracts that go down to our spinal cord. So, basically, anything within this caudal aspect here could potentially cause central vestibular disease. So how do we figure out if it's peripheral versus central?
Well, the only way we can do that is with our neurologic examination. And so when we're doing a neuro exam, we have two key questions that we want to answer. Number one is, is the patient neurologic?
And if yes, where do they neuro localise? So our path to get there is our hands off neurologic exam and our hands-on neuro exam. We're not gonna go through the details of the neuro exam, but just know that you can get a lot of information from your patients just by evaluating them, walking around in the room, getting the history from the owner.
I personally think the hands-off neurologic exam, I would say 95% of the time you can neuro localise your patients, and then the hands. On just kind of gives you that fine tuning, that reassurance that you're on the right path. And so remember when we're doing that exam, we then want to neuro localise our patients.
And so our main areas that we're looking to neuro localise is our brain, C1, C5, C6, T2, T3L3, or L4S3. And then in particular, when we're talking about our vestibular system, once we say, OK, we have something going on, whether it is the brain or whether it is peripheral, we need to say, OK, I have a vestibular patient now, using that exam, is my patient peripheral or are they central vestibular? And so the way that we can look at doing that is looking at the abnormalities that we might find on our neuro exam they're gonna help us differentiate between the two.
So first, starting with our peripheral vestibular system, so the mentation of these patients, they should be alert, they might be a little disoriented, but they shouldn't be dull. They should know what's going on. They should have a head tilt, and that head tilt is going to be on the same side of the lesion, so it ipsilateral head tilt.
They can have nystagmus in any direction, but by far, a horizontal or rotary is more common with a peripheral vestibular condition. I have seen vertical nystagmus in peripheral, so that's why we just can't hands down say that it can't be, but it's not common. So with our nystagmus as well, if you try to check the nystagmus in a different position, whether or not that means pointing the patient's head up to the ceiling or kind of doing a nice extension and looking to see if their nystagmus changes at all, putting them on their.
Side, putting them on their back. That nystagmus, it shouldn't change the direction. It won't change its position.
It's going to basically stay exactly as it is. If it has a fast phase left, it's gonna stay going fast phase left. It's not gonna change.
In regards to the gates, they can definitely have a vestibular ataxia. So what do we mean? Of course, they are, they don't know which way is up, down, left, right, you know, it's just when you get off the roller coaster.
And so they can have a hard time ambulating. They can be very dizzy, they can be very toxic, but what you want to know is that they do have good strength. They may not be able to put things together, but their limbs should seem like they have very good strength.
Now, when we have a peripheral vestibular, especially if it's something going on with that middle or inner ear, or facial nerve can be involved. We can have Horner syndrome. So remember that Horner syndrome, you're gonna have meiosis and ophthalamus.
You're gonna have that elevated third eyelid, and then you can have ptosis as well. So kind of that up those lids coming down and making them look like they're squinting a little bit. And then in regards to other cranial nerve abnormalities, there shouldn't be any.
And so that's one of your main differential or one of your main kind of helpful clues to know is that there should not be other cranial nerve abnormalities and one of the biggest things too is looking for any conscious proprio. Deficits. If there are conscious proprioceptive deficits, it can, it's not peripheral.
So that's one of the main things that you're gonna be looking for when you're looking for that peripheral. And to give you guys an example of what a peripheral, a very classic peripheral kitty looks like this kitty what you're about to see is classically has a left head tilt, has a horizontal nystagmus with fast face to the right, has corners in the left eye, and then also does have facial nerve paralysis, and this poor kitty is an upper respiratory situation, then secondary developed in otitis media, so we're gonna go ahead and watch this video. So you can see horizontal nystagmus with that fast face to the right, the left head tilts, and the horners in the left eye.
So this is a very, very classic peripheral vestibular kitty. Now, with our peripheral vestibular conditions, when it's bilateral, it can get a little confusing, but these cases kind of have a classic appearance to them. So what you're gonna be looking at when you have these patients is that if you think about it, if both sides of the vestibular system are effective, They can't start balancing out the information that's coming.
So they have no way of knowing, OK, my body needs to be a little more to the left, a little more to the right, because it's just, they're both not working appropriately. So there's no imbalance of inputs. Basically, everything is just kind of at zero is the best way to think about it.
These animals are gonna have a crouched posture because they have a loss of their extensor input. So they don't have that ability to extend those limbs. They don't usually have a nystagmus, a head tilt, or a roll.
They're very disoriented and apprehensive, but they should be alert. They often will have a wide-based stance. They can have what we call wandering eye movements, where it just seems like the eyes aren't moving with the body itself.
And then there's no physiologic nystagmus. So this is one of the keys if you have a bilateral peripheral vestibular. So evaluating for that physiologic nystagmus to see, OK, as I move my patient's head, are their eyes moving appropriately like we would expect, and it will be absent in these quote unquote classic cases.
So here's a video that you guys are gonna be able to watch of this kitty, who has bilateral peripheral vestibular or I should say was neuro localised bilateral peripheral vestibular, and then we found that he had otitis media internal bilaterally. So you'll notice this kitty swings his head from left to right. So at times it almost looks like he has a left or a right head tilt, but he's swinging it left and right.
He's staying very low to the ground cause he can't extend upwards. So they just kind of swing that head around because they unfortunately, they, they don't know where they're supposed to be going. He's gonna stay low, and some people only say, well, it's a cat in the hospital, but at some point, he should at least get up a little higher, especially in those front legs, and he does not do so.
So the main thing you wanna look for is how he is swinging those that head from side to side and has that crouched posture. Now we're looking at the central vestibular system, and of course, be a little different. And then our paradoxical is kind of a subset of that central.
So looking at our central vestibular system for mentation, it can be normal, but it also can be abnormal. So these patients might be obtunded, they might be stuporous, they might be comatose, that's your OSC on the chart here. In regards to the head tilt for a central lesion, a true central, it's going to be ipsilateral.
And the nystagmus can be horizontal, rotary, or vertical, and definitely with the central we commonly will say, you know, yes, we see more commonly vertical nystagmus with these patients over peripheral, but I see horizontal and rotary nystagmus in these central patients all the time. And what's interesting with the nystagmus is that it can change with head position. So if you put these patients on their back or put them on their side, you may notice that that nystagmus will change, and kind of go any way that it wants, and the fast phase for These cases also can go in any direction.
So that's something else to note is that it doesn't have your classic, you know, peripheral vestibular. If I have a left head tilt, my fast phase should then be to the right, cause minus stagmus, my eyes should be running away from the lesion, so we're not gonna get that with central. For our gait, they of course will have a vestibulartaxia, but they also can have weakness.
They can be puretic. And also, you might notice that they maybe have a cerebellar ataxia, that maybe they have a proprioceptive ataxia. So you can definitely see that, but one of the main things too is really that weakness.
Now, for facial nerve and Horners, it may be present. It depends on where our lesion is. But the main thing too is that they can have other Cranial nerve abnormalities.
So if you have any involvement besides your facial nerve and your corners or that sympathetic nerve being involved, any other cranial nerve abnormality, whether it is visual deficits, whether it's involvement of your trigeminal nerve, then none of that fits with the peripheral. So that's how you know it's got to be central. And then CP deficits, they do not have to be present, but if they are present, then you absolutely are going to have a central lesion.
And these are, your CP deficits are gonna be on the side of the lesion. So let's say we have a left brain stem lesion, then your CP deficits will be on the left. And this is important as well to note with our paradoxical.
So when we go through, when we're looking at our paradoxical, this is something everybody probably had to remember for boards, and it's something that can be really tricky to remember. But what kind of puts this a little differently is that your head tilt is gonna be opposite the side of the lesion. So that's first and foremost, and then your nystagmus is actually gonna go towards the lesion, which really doesn't make any sense.
And so the way that you're able to tell the difference is that you have your patient, let's say the patient has a right head tilt, and then you're looking at them and they have CP deficits on the left. That doesn't really make sense because your CP deficits, they don't lie. Like that is always gonna be consistent, that is always gonna be trustworthy.
And so your CP deficits are telling you that you have a lesion on the left, but you have a right head tilt. Well, that doesn't add up. So then you want to start thinking, OK, maybe we do have a paradoxical situation.
And then if you actually end up evaluating, of course, looking at the nystagmus, it's actually gonna be having the fast phase towards the lesion. So in these cases, the fast phase is gonna be actually going towards the left, for the example that we're talking about. So when I have a patience, let's look at this kitty right now, and what you're gonna be noticing with this kitty.
Is that there's a right head tilt and the horizontal nystagmus. With the fast phase to the right. And so immediately when you see that you're thinking this doesn't add up, this doesn't make sense for quote unquote, a classic vestibular case.
As soon as it doesn't make sense, if it's not following the rules, it's gotta be central. So your nystagmus should be running away from the lesion in a peripheral vestibular case, which means your head tilt and nystagmus should be going in those opposite directions. And so when I say that for your classic peripheral cases, if you have a right head tilt, then your nystagmus should be fast phase to the left.
If you have a left head tilt, then your nystagmus should be fast phase to the right. Anything besides this, you immediately know that you have a central lesion. So that's just a little kind of cheat sheet where if you're looking at these vestibular patients, you're already a little confused, and then you see, what the heck, this cat has a right head tilt and it has a fast face to the right.
It's not adding up, you immediately know that you have a central vestibular kitty. So now let's go through some of our differentials that we have. There's not too many degenerative conditions that we're gonna have, that are gonna cause peripheral vestibular.
In regards to anomalous though, we absolutely can have congenital vestibular disease. And so these are gonna be younger dogs that are born and whether or not they are constantly having signs of vestibular disease or potentially they have signs of episodic vestibular disease. And that's not something that you'll see right now with this puppy.
This puppy, you can see the coat colour. Unfortunately, it did not have appropriate developments, of the peripheral vestibular system. And what you're gonna see is as this puppy gets excited, he's all of a sudden going to have evidence of vestibular dysfunction.
So the owner gets him excited, shakes his head, and then all of a sudden we've got These little head bobs with the right head tilt. And a stagmus. Oh, he's so cute.
So you can have congenital vestibular disease. More often it ends up being pretty consistent, but I definitely have these puppies that can have these episodic vestibular episodes with excitement. So then we can have idiopathic vestibular disease, also known as old dog vestibular disease, and I'm sure many of you have seen this.
So it's an acute onset of severe peripheral vestibular disease in older dogs with no underlying cause. These are the cases that are gonna come in acutely vestibular, and they are so dizzy that they are usually rolling. And in these cases, it can be really hard to do a neuro exam when they are rolling like that.
So just know it's not wrong to give them a little bit of time before you fully clarify them as central versus peripheral, cause it can be really difficult when this dog all it wants to do is roll. So give it some supportive care. Give it a little bit of time for the signs to kind of resolve slightly or calm, give the body time to compensate for the vestibular disease, and then oftentimes you'll be able to actually do a more appropriate neurologic evaluation.
It is self resolving and there's no specific treatment except for time and supportive care. So whether or not that means neuroppodin, meclizine, whether or not they need to have IV fluids cause they're not eating. Keeping them in a nice cushy area, making sure they're getting up and going potty, so that's the big thing.
And then normally you're gonna start to see improvement after 2 or 3 days, and the most improvement you're gonna see is within 2 to 4 weeks. Now they can have residual signs and most what that will be, will be a chronic head tilt. And that can be a mild or it can be pretty significant, or sometimes the owners will just say, yeah, when they get excited, we see that little head tilt come back again.
But luckily, this is something that doesn't have a sinister cause and they're gonna get better on their own. Now, hypothyroidism is in our metabolic category, and hypothyroidism actually can cause both peripheral and central vestibular systems. So anytime I have a vestibular patient, it's always a good idea whether they're peripheral or central, of course, to be doing full blood work, but then also to evaluating their thyroid.
So, for the peripheral vestibular dysfunction, the how hypothyroidism causes it is that they can have this mixominous compression of the cranial nerves at the foraminal level, excuse me, and they may have signs of a polyneuropathy. They may have facial nerve paralysis. So there may be other nerves involved due to what's happening at the level of the foramen.
Now switching gears into our central vestibular dysfunction. So what we can have is it can cause an ischemic infarct secondary to atherosclerotic disease. And so these meaning that we're gonna have our cerebral vascular, event that takes place.
And one of the things that you can look for on your blood work that can kinda make you a little more suspicious that this has happened is looking for hypercholesterolemia or hyper triglyceridemia on your blood work. If those are there, then I get a little more suspicious if I truly have a hyperthyroid patient before we do advanced diagnostics that, OK, they could have had a cerebrovascular accident, it could have been ischemic in origin, it could be secondary to that hyperthyroidism. There's also evidence out there that supports that hypothyroidism can cause CNS demyelination, in which case that also can cause vestibular disease.
So basically, just make sure you are evaluating whether you have a peripheral or a central vestibular patient, make sure you're looking at their thyroid status. Now, for neoplastic, they of course can have oral neoplasia. They also can have malignant nerves she tumours at that level.
But unfortunately, if we have oral neoplasia in our kitties, about 85% of the time it's gonna be malignant and approximately 60% of the time in dogs. And whether it's an adenocarcinoma, a squamous cell, and kitties, we always have to have lymphoma on our list, so you definitely want to be evaluating for any evidence of a neoplastic process. Now, when we have inflammatory, the biggest thing that's gonna be causing that goes in this category is our otitis media and turn up.
So, to go through this, we're gonna look at this kitty, who very classically was on evaluation, a peripheral vestibular kitty, but then you're gonna get my little caveat about cats. So this sweet kitty had a left head tilt, horizontal stagmus with fast face to the right. He kind of has a wide base stance, has these serpentine head movements.
They're very subtle, and he does when he gets up and walks, he didn't want it for the video. He did have good strength, but his vestibular ataxia was making it really difficult for him to want to get up and move. So when we had this kitty, he was neuro localised to left peripheral vestibular, but plus or minus bilateral because of those little kind of, they weren't the true big wide head excursions that we'll see in our true bilateral peripheral kitty, but he had these little movements that were suggesting it at time.
And so our differentials, once we neuro localised to left peripheral vestibular, was either a left otitis media and turnout less or minus, involving the right side, or it could be an oral neoplasia. Now, This is a cat, and what you will learn with cats, and which I'm sure you've already learned, is that they can do whatever the heck they. And so even though on my evaluation, if I have a cat and it is slammed on peripheral vestibular disease, I will never exclude that they could be central.
They are able to hide central vestibular disease so well, and I still remember as my first couple of years in practise after my residency that this really kind of sunk in for me cause I kept seeing all of these kitties that were present peripheral, but they actually were central. So here what we're gonna see, this is a T2 weighted sagittal image. These are our ears right here.
So here's our pena that we're having, and then this right here is our otitis media. You can see this hyperintensity within our middle ears, and then you also can see that, see the changes that are occurring. In our little, what should look like a nice little duck, right?
So this is our inner ear. So here's our middle ear, here is our inner ear. And clearly this patient has bilateral otitis media and inda.
But then what we can see is that after we gave a contrast agent, what we have is that we can see. That we have all this hyperintensity, this contrast enhancement that we're dealing with. So, going forward here, we have the same kitty that had the bilateral peripheral vestibular disease, and what we always will do in these cases as well as even if there is an obvious extension into the cranial vault, we always will do contrast to make sure we're not missing anything.
And what you can actually see in this case is that this kitty had a pretty significant What this hyperintensity is, or basically our strong contrast enhancement. So this kitty's middle ear infection had extended into the cranial wall. So it's what we call our intracranial extension.
So this cat basically had an abscess in the brain, but wasn't showing us any signs of that, didn't tell us it had CP deficits, didn't tell us any of that. And so with that, it just always puts me on to let me know that, hey, we have to recognise that even if we have a peripheral vestibular kitty, they absolutely can potentially have intracranial extension. And so going forward with that for otitis media internal with intracranial extension, they do commonly present peripheral.
So they literally can have a brain abscess and yet they'll have no central signs whatsoever. A third of them are gonna have a history of a prior ear infection, but that means that 2/3 of them have no history of a prior ear infection, and 50% of these kitties are gonna have a normal otoscopic examination. Now the common organisms that can cause the otitis medianterna with intracranial extension, you can have your pastorrellis, your staph, strep, ectinomyces, pseudomonas, or even E.
Coli. Now, when we have treatment for these cases, especially when there is an abscess in the brain, it can be medical or it can be surgical treatment. And oftentimes we're always gonna start with medical.
So your medical treatment can be doing, of course, a aryotomy with video otoscopy. Now, we're only ever suctioning these patients, we're not flushing them. Mainly, of course, because we don't want to end up pushing any more of that infection into the brain.
We'll be culturing these patients, and then we'll get them started on oral antibiotics. Usually doing a broad spectrum antibiotic is going to be best based on the most common organisms, so we'll commonly choose amoxicillin clamulinate. And then also doing some prednisolone for these kitties, because not only is there a lot of inflammation going on within the ear, but it's also, of course, in the brain.
And what we have to recognise is that when we start treating these middle or inner ear infections with that intracranial extension, there's gonna be a lot of die-off of those organisms, and we wanna make sure we're controlling that inflammation as best as we can. In regards to our success rate for medical, it has about a 63% success rate, which is pretty good, and oftentimes regardless, we're gonna start with medical management anyway. Now, for surgical management of these cases, like I said, we always start medical and then in regards to the surgical options, they are a ventribola osteotomy, so a VBO if needed.
It's not common that we end up needing to do any sort of craniotomy to evaluate or to Decompress these abscesses. It absolutely has been done and has been reported as being needed in really severe cases. I've personally never had to do one.
I've been very successful with medical management, and then ones that ended up, you know, doing OK, but then they maybe had a reoccurrence, of that otitis media. We just couldn't clear it well enough, then we do a BBO in those cases. And with surgery, there is an 83% success rate for these cases.
Now, other things that you can see within your inflammatory category are nasopharyngeal polyps, so always want to be evaluating these, especially in our younger kitties. I personally have never seen one. I have seen the videos of people removing those, which is pretty impressive.
And then the other category that falls into this is what we call PO, our primary secretory otitis media. This is something very commonly present in our cavaliers. Also our French bulldogs are starting to come up as one of the ones that we'll see commonly as well, and so those are other causes for our peripheral vestibular.
Now, in regards to toxic causes that are gonna be peripheral, it's mainly gonna be your autotoxic drugs. So your aminoglycosides, your diuretics, cisplatin, you also can have florhexidine. So anything that potentially goes in the ear, we always have to know that there could be something that's going on.
Now, in regards to traumatic, you can have inner ear trauma. So whether or not that's something that was done, you know, owner was clearing, cleaning the ear, something happened, something got in the ear, there was a mild, you know, kind of, sometimes we've had it where, you know, the outside and by accident gets hit in the ear. And so anything like that can cause potentially your peripheral vestibular.
And then that last category that you can't really see on the slide, that is vascular and there isn't gonna be anything vascular that's going to cause peripheral vestibular. Now, when we're going through with our central, then what we're going to look at first is our degenerative category. And there's many different degenerative cases, but one of the ones that unfortunately we'll see quite a bit is the category of lysosomal storage diseases.
These patients very commonly are going to show vestibular signs usually kind of towards the end, unfortunately, . Of their life, but things like NCL or neuronal steroid lipofusinosis can do that. And here's a video of how a lot of these patients are going to present, where they have other signs as well, but unfortunately, one of the dominating signs as they progress is going to be, excuse me, central vestibular disease.
This dog will commonly has the right head tilt. You can see he's got a vestibular A. Axia, so that's something that you can see.
Usually, in those cases, you're gonna have, they're not gonna present just with central vestibular. It's gonna be a component of all of their clinical signs. Now, some of the other things in our anomalous category that we can see is arachnoid, what we call cysts or diverticulum, depending on, on what we're calling it.
It really should be called a diverticulum though, cause it's not really a cyst. It doesn't have a nice epithelial lining. But to give you an idea of what we're talking about, these can be present with at the level of surrounding our cerebellum.
So here we have an MRI T2 weighted sagittal image with our Factory lobe and here's our cerebellum, which if you remember from the other images should be nice and round, but then we have this hyperintense structure right here that's causing compression of our cerebellum. And this is what those arachnoid diverticulum or cysts can look like, unfortunately, and they can end up causing pressure on that cerebellum and usually this will be something that becomes an issue more in our, our younger patients is when we're gonna be seeing these. Now, other conditions that we can have is what we call Chiiari malformation or combs or caudal occipital malformation syndrome.
Especially those that also have syringohydromyelia. And so these, let me go back to the slide first. These patients have this crowding of the cerebellum at the caudal aspect.
So here you can see again, remember your cerebellum should be nice and round. Unfortunately, it's having this kind of crowding or pressure on the caudal aspect, which because of what it's doing to the shape of our cerebellum, it's also making it so our spinal fluid cannot flow appropriately out. So we're Having some accumulation of our CSF within our brain, but then also when it's trying to get out, it has a very big turbulent flow.
And that turbulent flow is making it a development of what we call syringohydromyelia, which is this hyperintensity within our spinal cord, which remember, should be nice and grey, as we've seen on the MRI and we've got this hyperintensity letting us know that those vestibulo spinal tracts are gonna be affected as well. And so this is just a reminder of where we have that central vestibular system, and so of course, here we have these vestibulo spinal tracts that are gonna be affected. Our core vestibular cerebellum centre that's going to be right at this level, the cerebellum has this caudal compression or crowding we like to call it, and so that is why we're going to be affected as well and showing vestibular signs in these patients.
Now the other patient that can present with pretty strong vestibular signs are hydrocephalus patients. And so hydrocephalus, which is basically just extra, extra fluid in the brain, is truly what it stands for. But of course we have our obstructive hydrocephalus as well, which we can classically see.
And so we have the congenital versus acquired. So our congenital obstructive hydro. Very classically, we're going to see as these two cuties are showing us how they're going to look classically with our dome-shaped skull, our sunset eyes, they can have behaviour changes, they can have visual deficits, they can develop seizures.
And then in regards to their ataxia, it can be a combination of proprioceptives, cerebellar and vestibular. Now, these younger patients, about 30% of them. They can be greater than 2 years of age, and so that's why I'll always say that yes, they absolutely should be your younger patients.
It should be very classic, but sometimes they don't have that classic appearance. So if you have a 1 or 2 year old patient presenting, it is something to note, though usually they're not only gonna present with vestibular central vestibular signs, they're also gonna have other evidence of neurologic deficits as well. And at this bottom image, this is just to give you an idea.
These two MRI's on the left and on the right are at the same location. And so on our left, this is what a normal brain MRI at our mesencephalon should look like, and then unfortunately here, this is what it looks like in our obstructive hydrocephalic patients. So these are our normal lateral ventricles, these nice thin little hy Hyper intense lines and then this is what we call our mesencephallic aqueduct where spinal fluid flows through and then here is what happens when that CSF can't get out.
And so here's that mesencephalic aqueduct, and here is our very large and obstructed lateral ventricles. Now, we also can have acquired hydrocephalus, and so this can happen in any age patient. Normally they're gonna be middle aged to older, but what happens is we have an obstruction of our CSF flow, and most commonly, unfortunately, it's going to be due to a brain tumour.
It can be those subarachnoid diverticulums or those cysts. You can have severe caudal occipital malformation syndrome, and you can have inflammation, which more commonly we see with FIP. Because of what it will do to our overall CSF.
However, it can be from other inflammatory conditions as well that are causing a severe meningitis encephalitis. And so this MRI is showing us that's in our red circle here, unfortunately, a mass that is likely a choroplexus tumour that is causing an obstructive hydrocephalus for this patient and then you can also see that it's also obstructing our CSF flow out of the brain. Excuse me, out of our cranial vault, and therefore we also have this development of the syrinx, so that's syringo hydromyelia.
Now, when we have these hydrocephalic patients, you just know in regards to diagnostics, you can do ultrasounds. You do need a fontanelle in order to do that. And so most common you're gonna have that in your little dogs and less likely with your larger breeds because they often lack fontanelle.
You can also do CT or MRI. MRI it gives you better detail of all the soft tissue structures and because these patients have a congenital abnormality. It's really nice to be able to evaluate their entire cranial vault, in particular their cranial cervical junction regions to know if they have other potential congenital abnormalities that need to be dealt with.
And so here is just another example of that hydrocephalic patients, and then for medications or treatments for these dogs, medical management for your goals, you want to control inflammation, decrease spinal fluid production, and manage any other clinical signs. So if these patients have seizures, behavioural changes, oftentimes we'll do steroids with prednisone at 0.5 mg per kg once daily to start.
We also can do Prilosec or omeprazole, which will decrease CSF production. Starting dose 0.67 makes per kg once daily.
I usually think of it as a make per keg once daily, can go up to twice daily though, which may actually help, in your really severe cases, giving it BID instead of SID. And then this is more of a management of the condition. It's not gonna be a cure.
So many patients with mild signs and mild MRI findings can do well with medical management. But then, of course, there's many that end up needing surgical management, and this is often preferred for your best long-term outcome. And it's based on the clinical presentation and MRI finding.
So not all patients are good candidates, just cause they have obstructive hydrocephalus, it does not mean that they all are gonna do well with surgical management, especially if the patients have too much brain loss or atrophy. They already have multiple, we find multiple congenital abnormalities that need to be dealt with on the MRI, not just structive. Hydrocephalus and if they have aggressive or other behavioural changes, unfortunately, those commonly are not going to get corrected with surgery.
So you have to have a real heart to heart with these owners in these cases. But if they do wanna do treatment, we do treatment with a ventricular peritoneal shunt placement. So here's a radiograph postoperatively of this patient who has a shunt placed in the left lateral ventricle.
And what happens if we provide this direct path. Going down through the shunts to get that spinal fluid directly into the peritoneal space. So hypothyroidism, we already touched base on, remember, we worry about hypothyroidism causing central vestibular signs if they have potentially caused a cerebrovascular accident.
And then with neoplasia, of course, we can have primary intracranial neoplasia or we can have metastatic. It always has to be on our list. For example, this is a 5 year old golden retriever, and I know everybody's like, OK, you already know what it is, but the doctor presented ambulatory tetraprinic and ataxic with a cerebellar vestibular and proprioceptive ataxia that was more pronounced on the right side.
Had mid-range pupils that are responsive to light, had a right head stilt, and was rolling, falling to the right. And then the big giveaway, of course, is that there was absent CPs on the right limbs and intact in the left limbs. So you read through this, there's CP deficits, so you're gonna be right central vestibular.
And this is the MRI image of this patient. This is from a dorsal view. So these are our mascatory muscles actually on the side.
Here is our cerebellum, and you can see this hyperintense lesion that was present, unfortunately, in the right cerebellum, as well, and this lesion here is the same lesion for unfortunately, our golden retriever who ended up having lymphoma. Now, nutritional, usually we feel like we don't need to worry about nutritional, but definitely in cats, this is something that you wanna have on your list, in particular thiamine deficiency, cause there has recently been kind of an uptake in these patients, with thiamine deficiency due to changes in how patients are, or pets are being fed. And so this is something that I just wanted to touch base on.
So, thiamine deficiency, so the active form of thiamine is thiamine pyrophosphate, and it serves as the coenzyme of three enzyme systems involved in carbohydrate metabolism. So deficiency leads to impaired oxidation of ketoacids. And so we end up having is neuronal loss because we have impaired cerebral energy metabolism, focal lactic acidosis, and then we end up with a cytotoxicity.
And the diets that we commonly see this in are gonna be diets that are deficient in thiamine themselves or ones that have high levels of thiaminese, thiaminease, excuse me, which we'll commonly see in our fish. Fish diets are gonna have higher value. Now, we also can see it higher in regards to our diets that are gonna have lower thiamine is our pate foods because thiamine is a heat label vitamin and during the sterilisation process, our thiamine losses can be, have been reported to be as high as 50% to 90%.
So during that heat process, we unfortunately will lose a lot of that thiamine. And then other diets, home cooked diets, which has become something very popular lately, which, as long as it's done appropriately, it's not a problem, but unfortunately it can be very difficult to do, and we especially see this in raw diets. We had a lot of Young cats that were presenting with thiamine deficiency because they were just being fed the pinky mice, not realising that that wasn't an appropriate diet, unfortunately for them, and so educating those people and getting them on an appropriate diet, we were able to help, help those kitties out.
So definitely wanna make sure you're asking about the diet or any recent change in diet that potentially would raise your suspicion. And just to give you guys an idea of what we're looking for, we can really see that cytotoxicity on the MRI and so here is a T2 weighted axial view of a kitty's, brain, and we have these two hyperintense lesions. So one of the things that we're looking for in an MRI is anytime we have a bilaterally symmetrical lesion, then we usually are gonna be worried about metabolics.
It's not just affecting one focal area that we need to worry about. It's affecting bilaterally two different areas and that's only gonna happen if you have a metabolic component. So what we call a metabolic encephalopathy.
And something just for you guys to take note is in these cases, the thymine deficient kitties are gonna have what we call active ventroflexion. And so of course we have many different diagnos or excuse me, differentials for when we have our ventroflex kitties, most commonly because they are weak and so we have to figure out why. But with diamond deficiency itself, these kitties will present ventroflex, but the difference is that here we have our kitty being held upright and is ventroflexed, and then here what you guys can see is this kitty is then put on its back.
And he stays ventroflexed, so he stays in that flexed position, which is different than any other case of your ventroflexion and cats. And so if they stay in this what we call active ventroflexion when they go on their back. That's kind of classic for your thiamine deficiency versus a cat who just has maybe it's potassium deficient or other causes of weakness, that head is gonna flop down and those other cases.
So this is what we call that active ventral flexion. Now for inflammatory, we category for central, we already talked about our otitis medianterno with intracranial extension, which is huge for kitties. We can also see it in dogs, but less commonly so.
And then our other main category that we're gonna have is what we call our MUOs or NUEs, so our meningoencephalitities of unknown aetiology. So this is our servis, our. Meningitis, our idiopathic tremor syndrome, and then our big MUO is our necrotizing diseases, or granulominous diseases.
And note that this dog is in a purse because any dog that you see that can fit into a purse, non-infectious inflammatory CNS disease should be on your list that MUL. And so looking at these cases, our conditions that fall under this non-infectious meningoencephalomyelitis include our GME, NME, and NLE, but the issue is that we can't categorise our GMEs, our enemies, our NLEs unless we have a histologic diagnosis, which in the majority of times we're not unless it's postmortem. And so when we don't have that histiologic diagnosis, that's why.
We call it that MUO or that MUV because it's just a non-infectious cause of meningoencephalomyelitis. And just to give you guys an idea, here is an example of this dog, and unfortunately, you can see these hyper intense lesions within the brain stem right at the level of where our vestibular nuclei and those cranial nerves 34, and 6 are going to live. So this dog very clearly presented for central vestibular disease.
Now, infectious ideologies as well, of course, are going to be present. And so to give an idea of an infectious aetiology, this is a 2.5 year old hound mix that presented for a complaint of vestibular disease.
This case was interesting because he had had a lymphadenopathy she excused me previously, and had reactive, which were found to be reactive on FNA. The dog also had Horner syndrome. Which was something else to note.
And clindamycin had been started and the clinical signs improved, but when the clindamycin was discontinued, then we had further progression of our vestibular signs. More importantly, noticing involvement of CP deficits with knuckling on the left thoracic limb and then our left head too. So the only major finding was there was a hyperglobu anaemia.
Blasto urine test had been done and was negative. Lymphadenopathy showed us that they were just reactive lymph nodes. 4DX was negative.
And when I looked at this dog, the main thing I saw is that they're definitely, the dog was bright and alert, enlarged left submandibular lymph nodes and left profilial lymph nodes, ambulatory with a vestibular and proprioceptive, ataxia that was most. Pronounced in the left limbs, so they are right away, you know, with that proprioceptive deficit, it's got to be central. Madriasis was OD mid-range OS, and then in regards to our PLRs, it was presently present, excuse me, those slightly diminished on the right, did have intact palpibrile, no pathologic nystagmus, and a left head tilt.
So immediately because we have other cranial nerve deficits as well, we already were knowing it was central because of our appropriate sceptive ataxia. Now we have other cranial nerve deficits besides just a head tilt and possible involvement of cranial nerve seven as well as foreign nerves. So again, confirming that this has to be a central vestibular case.
And then we found those delayed CPS on the left and there was no appreciable spinal hyperesthesia. So this dog for sure was left central vestibular was our Predominant sign, but we're showing us that especially with the changes with the pupils and those things, there is diffuse brain disease as well. And so this dog had an MRI and what the MRI showed was multifocal encephalitis.
And so here at the level of our olfactory lobe, this is after contrast was administered to really just how to show you guys the lesions. We see this hyperintensity, which is our contrast enhancement. We see our contrast enhancement here, we see our contrast enhancement here, so multifocal encephalitis was diagnosed, and the Cryptococcus androgen tighter on this dog, was the highest one I've ever seen.
It was 1 to almost 8200, which is crazy, and I think it's crazy that this dog somehow was still doing OK and had done OK for as long as it did. And so the medications, this dog was started on fluconazole and prednisone, and people always again will say why if there's an infection in the brain, are you putting them on steroid? Remember, inflammation in the brain.
It is not a good thing, and we need to control it and our best way to do so is going to be with steroids to control not only the die-off but then long term inflammation that that organism may be causing. Now, the steroid usually isn't continued, you know, long term, it's just something for the immediate treatment period. And this dog is doing fantastic many, many years later.
Now, other inflammatory causes that we can see, which really stands out in our kitties, of course, is FIP, and this very classically is a paper that came out many years ago now that was showing us those classic findings that we're going to see on MRI with our FIP kitties. And basically they end up with this obstructive hydrocephalus due to the protonacious change to their CSF. And so here we can see this extra CSF accumulation.
That goes on and then it can be a varying, you know, levels, unfortunately, and how it's going to present. So these are the 4 examples of kitties that were diagnosed with FIP, and here's another one where how it can start where you really get this change at the level of the 4th ventricle here, where things will start to accumulate and then you're gonna get changes in the rest of your ventricular system. Now, of course, we used to not have a treatment and we'd always have to say that these kitties had to get euthanized, which was terrible, but now we do.
And so just to, you know, give information on this, of our GS 441524 for our kitties with FIP, what we found is that with Neurologic FIP in particular, it can be cured if sufficient antiviral drug passes the blood brain barrier and the virus has not developed drug resistance yet. So currently right now, what we recommend is the starting dose has been set at 10 mg per kg daily sub-Q. Though more recently we've found that we should actually be using a higher dose, so up to 15 Migs per gig sub Q SID.
It is the 84 day treatment protocol still fits, and the success of treatment is gonna be based on the improvement of clinical signs and any initial abnormal blood works. So looking for things like weight gain, looking for their coat quality, looking for improvement of their vestibular sizes. And you can of course repeat their brain MRI to give you an idea, but so much so is gonna fall on how these kitties are doing clinically.
An improvement in their health and the neurologic signs is usually gonna be present within 24 to 48 hours. So you're usually gonna know pretty quickly if they're going to improve your GS treatment and full recovery with normal, return to normal function is gonna be expected in that 4 to 6 weeks. I personally have had a couple of kitties that have received treatment for this, and they have done very, very well, which is amazing to see.
So toxicity causes, this is something that's really important to make sure you're getting really good history from your owners. So for toxicity, have they been giving or have they been prescribed any recent medications, in particular metronidazole? So metronidazole toxicity is most commonly gonna be seen when doses are administered at 30 makes per cake a day or long-term use.
So you don't necessarily have to be at that 30 makes per cake per day if they've been on it chronically. So I've had some patients that have been on it for months at OK or normal doses, but then the cumulative effect, unfortunately has led to metronidazole toxicity. And the underlying pathology is related to metro metronidazole's effect on our GABA receptors, as well as perinji cell loss and axonal degeneration will occur in our vestibular tracts.
And the treatment is discontinuing metronidazole, and they can never go on metronidazole again, and starting diazepam, actually, because diazepam works by facilitating the effects of our GABA within the vestibular system. And so patients that were treated with diazepam showed improvement within 13 hours, with final resolution of clinical signs at 38 hours, versus those not treated usually show improvement after 4 days, with final resolution after 11 days. So I Definitely expedites the healing of these patients, so it's definitely something that we wanna do, when you have metronidazole toxicity, if you're able to, usually starting with IV treatment in hospital and then switching to oral administration when these patients go home.
And then, of course, these guys need strong supportive care. And it is always possible that they can have residual vestibular signs, but a lot of these dogs will have dramatic improvements. Now other toxicities are lead and another big one unfortunately that we have is bromethyin.
And so this is why when you have your owners, you also wanna make sure are is there any Mouse or wrap it in the house because we'll have owners say there's absolutely no way they could have gotten into that, of course, you know, because it's underneath the fridge or they can't get to it, but cats can always get a way of getting to it and then you also have to understand that if a mouse ends up dropping a piece, or the cats are unfortunately. Eating the mice and those sorts of things, that's something we need to be worried about, but most often when we find a lot of times there's this kind of exposure at lower levels that will lead to these kitties with bromethyin, . Toxicity, but then also, of course, we can see it in dogs as well.
Dogs just normally present more acute, and our kitties will present with more of this chronic presentation, mainly because they're not ingesting large quantities at once, like the dog that gets into the rat be, they're eating the entire thing. These cats are getting small amounts of the vermetholin over time. So bromethyin is a non-anticoagulant rodenoide, and it's metabolised to a more potent metabolite, demethyl bromethyin.
It's lipid-soluble, so therefore, it's gonna readily cross our blood-brain barrier. And how it works is that it uncouples oxidative phosphorylation. So our ATV production drops, which is very important for our brain.
And our sodium potassium pumps are gonna fail. So we end up with this intracellular sodium increase. So our water is gonna come in, we get cytotoxic edoema, and then we have intramyelinic edoema as well.
And then we have the spongy degeneration of the CNS white matter. And unfortunately, that's what this MRI is showing on this kitty. So, this hyperintensity is basically tracking our white matter of these cats.
So you can see as I'm going along. This hyperintensity and it's pretty much a very classic image that you're going to see with your kitties when they have promethyl toxicity. And unfortunately, there is no treatment for those for those guys.
Now, if there's trauma, trauma to the brain stem, it's very, very common. We'll have hit by our dogs that will come in with TBIs and if their brain stem is involved, they absolutely can have evidence of traumatic brain injury that's going to present with central vestibular signs. And then vascular are cerebral vascular accidents.
This is gonna be one too where you have your paradoxical cases. This is one of the main reasons that we'll have paradoxical central vestibular, but your cerebrovascular accidents are gonna be huge, and remember they can be ischemic or they can be hemorrhagic. Most commonly they're going to be ischemic, but you absolutely can have hemorrhagic cerebrovascular accidents as well.
So these are gonna be those cases, those older dogs that present with acute onset of central vestibular signs. And this is an MRI showing an ischemic infarct in this dog at the level of the thalamus, as well as our brain stem here. And here is our T2 weighted axial image to show you what we'll see on MRI.
So it's a very well demarcated hyper intense lesion. So here we're at the level of our thalamus, and then here we kind of, it moved caudally to also involve our midbrain. And so here is a very classic ischemic lesion that we saw, and these patients luckily are going to do great with time and supportive care.
The biggest thing is trying to identify if you can identify why they had a stroke or a vascular event. We're successful about 50% of the time. The 50% of the other times we aren't going to be successful in finding a cause for this, and so then we have to know that they can have another stroke or vascular event down the road.
They also can be hemorrhagic. So here is a patient who has, this is called a GRE or T2 star weighted image, and what we're doing is we're taking advantage of the natural artefacts that are hemorrhagic lesions are going to cause. So these kind of signal voids that we call them, these big black areas, these are all little hemorrhagic strokes that we can see unfortunately as we move through this patient's.
Brain going from cranial to caudal, he unfortunately had multiple hemorrhagic strokes. Now on this kind of whole topic of ischemic encephalopathies are are vascular lesions. I do just want to touch base on cuterebra, what we call feline ischemic encephalopathy, because this is something we see very commonly, and it what happens is that the larva of our cuterebra achieves entry via our mucous membranes of our natural orifice, so we usually think of it as nose to brain.
And vasospasm occurs secondary to toxins from the larva. And so it actually is that vasospasm that is causing that ischemia within the brain. And our classic presentation is that it's gonna be the summer months, we have an indoor outdoor kitty.
They had respiratory signs or were sneezing a couple weeks ago, and now they've developed acute onset neurologic signs that are most often gonna be vestibular. And when we do an MRI on these patients, we can see a distinct tract for where this larva went. And so here is our ischemic lesion that occurred secondary to the tract of this larva moving through the brain.
And again, you can see it right here, these hyperintense lines literally showing us the track that it took through the brain. And again, we have it here as it moved its way caudally through our brain stem. Main treatments are going to be initial treatments that we have is administering diphenhydramine, then giving steroids, sometimes using methylprednisolone versus DexSP and either one is just fine.
And then 2 hours after the first and the second, we're then going to give ivermectin sub-Q. And you're gonna repeat this initial treatment at 24 hours and then 48 hours for a total of 3 doses, and then you do have to warn the owners that they can have an anaphylactic reaction. Now usually his cats will be sent home with it used to be arofloxacin.
I usually use marbafloxacin now, and then going home with steroids as well to help control any of the inflammation that as you can imagine a larva moving through your brain can tends to cause. Also to help with any potential anaphylaxis that's going to occur, but usually if these kitties handles their first dose well, they're going to continue to do well. And overall prognosis is good with treatment.
They can have residual neurologic deficits and usually it's gonna be that head tilt or mild ataxia. So, hopefully, that was a nice quick kind of overview, comprehensive overview for you guys of the peripheral and central vestibular system, how we differentiate between the two, and some common differentials that we have in treatment options for these patients. So again, You want to neuro localise, decide if it's peripheral versus central vestibular, and then you can come up with your list of differentials.
And at any time if you guys have any questions, feel free, you can always reach out to me. You can email me right there at carpenter@mm veterinary neurology.com.