Hello. So, my name is Alex. I'm one of the neurologists here at Davies.

And, and this webinar is primarily looking at the vestibular system and, and vestibular syndrome, in, in dogs and cats. And we sort of split it into two parts. So the first part is a bit more theoretical.

And so we'll discuss the anatomy of the vestibular system, the clinical signs, you might expect to be associated with it, and then the underlying causes for its dysfunction. And then the second part, we'll go through some sort of clinical cases. We've got some videos and things to see, if we can put what we've learned in the first half into, into action.

And so in terms of, of what the, the vestibular system actually is, I always think it's one of those systems that you don't really realise. How important it is until, until it all goes wrong. And when you talk to people who have had a problem with their vestibular system, it, it sounds quite awful, and often they describe it as being a, a combination of having sort of motion sickness and vertigo all rolled up into one.

And I guess essentially it functions to coordinate your body posture and ocular position in relation to the position or motion of your head, and hence, it allows us to maintain Our balance and orientation with respect to, to gravity. And so, essentially, it coordinates our movement with balance and allows us as people to do all these sort of extraordinary things, but also allows animals to, to do some quite, quite amazing things as well. And when we talk about our patients with vestibular syndrome, we often try to differentiate between those ones that have peripheral disease or, or central disease.

And the reason that we do that is it really then . It really then discusses or or changes what we do in terms of a diagnostic . Options, but also what we might expect from a prognostic point of view as well.

And so when we talk about the peripheral vestibular system, it's composed of the vestibular division of cranial nerve eight. So that's your vestibular cochlear nerve, together with its receptors. And these are contained within your inner ear, which is composed of your cochlear, your vestibule, and your semicircular canals.

And so these structures form the bony labyrinth of your entrus temporal bone and the vestibule in your semicircular canals subserve vestibular function while the cochlea is involved in an auditory function. And so when we talk about the receptor organ, we're talking about the macular receptors of the saccule and the utricle located in the vestibule, and also the crista and polaris of your semicircular canals, which are these three canals here. And these detect the position and the movement of your head in space while the animal is either standing or at rest or when it's moving, moving its head.

And the information on the position of the head is then converted into these electrical signals which are then sent via your vestibular branch of your vestibular cochlear nerve into your brain. And so then these three semicircular canals are are tubular structures, that project from the vestibule and are approximately orientated at about 90 degrees to each other. And at each end of the individual canals, is dilated into a structure called an amula, which is then connected to your, to your vestibule.

And the sensory receptors, the Crysta apearas are located in the membranous la labyrinth of the apela, and they're responsible for detection of angular movements of the head. And the most important thing is, because these semicircular canals are at 90 degrees to each other, it's really important because it then shows you that if you move your head in one particular direction, each of those canals will pick it up. And, and so then any movement in any particular direction, that 3D point of view is picked up because of these semi-circular canals and the way in which they are orientated.

It's also really important to remember that we've got these canals in in both of our ears. And so your left and your right semicircular canals form this functional pair. And so, for example, your left and right horizontal canals always respond oppositely to any head movement that both then affects them.

And then this leads to that sort of push pull concept of your vestibular function, so that if you've got some directional sensitivity to head movement, it is coded by these opposing sort of receptor signals. And in one side of each ampula are structures called these cristae, and each of these is lined with these neuroepithelial hair cells in here. And the ampula and the crista collectively within the terminal portion of these semicircular canals, they're terminus crista and polaris.

And this neural activity within these hair cells is continuously tonic, so every time you move your head and you get this slight movement or displacement of this endolymphatic fluid, it alters these tiny little hair cells and then has this sort of tonic neural influence of the semicircular ducts. By deflecting these hair cells, on the chronic or the sort of on the corresponding Crista and polaris. And then this sort of deflection of the hair cells then causes these changes in action potential and then this travels down the nerve and gives us the infant input that we're looking for into our, into our brain stem.

And so when we talk about the central vestibular system, we're talking mainly about these four vestibular nuclei, situated in the medulla oblongata. So when we talk about our brain, if you look at the MRI scan on the right, we have our forebrain here, we have our thalamus, and then our brain stem, and this is our cerebellum sitting above our brain stem. Now our brain stem itself is split into three components.

We've got our midbrain, our ponds, and then this orange circle or oval shape is our medulla oblongata. And that's where our vestibular nuclei sits. And so this is basically the balance control centre in the brain stem and it processes the information and sends messages to the rest of the body to keep the animal upright.

And then messages are also sent to the muscles controlling movement of the eyes, so you get pathways coming from this medulla oblonggata, this vestibular centre to, you know, cranial nerves 34, and 6, and so then that changes the position of the eyes according to the position of our head. And also the vestibular nuli, this sort of central, area of, of balance, receives influence from other higher vestibular centres in the thalamus, but also in the cerebellum. And then these basically have a slightly inhibitory effect on this, on these vestibular nuclelide to again, help us maintain our, our balance and, and other forms.

And so when we talk about our vestibular system, when that goes wrong, and there are tends to be 4 main clinical signs that we see that are a manifestation of, of vestibular dysfunction. And if you have a trial of little thinkers to, to what 4 signs you might expect to see in a dog with vestibular dysfunction, 2 are, are quite obvious, and the other two are a little bit more subtle, but ones that you can normally pick up once you do a bit more of an in-depth neurological examination. And so the four are an ataxia, so often we get a vestibular ataxia, and a stagmus, a strabismus, and a, and a head tilt.

And, and what we'll do now is we'll go through each of those clinical signs in a bit more detail. But it's really important to remember that regardless of whether it's peripheral or central, vestibular syndrome, we'd expect to see all four of these signs, in both. So it doesn't help you, straight away to distinguish between the two, but it's sort of the first part in trying to recognise your patient has, vestibular syndrome.

And if we start off with the, the head tilt. It's a fairly obvious one and probably the, the first thing that people will notice when they have a, a patient with vestibular disease. It's a rotation of the median plane of the head along the axis of the body, and it ends up resulting in one ear being lower than the other.

So you can see in this Labrador, it has a right-sided head tilt. And it happens because we have a loss of the anti-gravity muscle tone on that side of the neck. And so then the other side pushes that head down to have the posture that we can see in the picture.

And then the only other thing to be aware of is that sometimes, or occasionally people get confused between a head tilt and a head turn. And so just make sure that you're happy to, to differentiate between, between those two. When we talk about a nystagmus, so nystagmus is an involuntary rhythmic movement of the eyeballs, and we have a physiological nystagmus, and this is something that animals, all animals have and all people have.

But you also get a pathological nystagmus, which is the one that reflects an underlying vestibular disorder. So physiological ness tags can be induced in anyone, human or animal, by rotating the head from side to side, and that's what we call our vestibular ocular reflex. So when you move a cat or dog's head from left to right, you'd expect the eyes to jet towards the side that you're moving the animal's head to, and that is your physiological nystagmus.

Now, this video I put in because it's a cat that's basically got an absent vestibular octave reflex. So you see, when I move the head from side to side, the eyes may stay in exactly the same position without darting. So this cat does not have a, a physiological, nystagmus, and so something just to, to bear in mind.

But normally you'd expect to see the eyes, go in the direction in which you're manipulating the head. In terms of, of nystagmus, in the absence of any particular head movements, nystagonists shouldn't be present in the normal animal. And so often we talk about pathological nystagmus as being one of the main signs we see in patients with, a problem affecting their vestibular system, and then once you've got to think you've got a pathological nystagmus.

It's important then to try to see if you can differentiate between a spontaneous or positional nystagmus. So you can see in this first video, this, little springer spaniel, its head isn't moving, it's, it's lying on the, on the bed. But you can see the nystagmus, this horizontal nystagmus with the fast phase to the left.

And so this would be classed as a spontaneous, nystagmus. Whereas when we look at the video in the bottom right, this patient didn't have any nystagmus until we started to extend its head upwards, and then you get this nystagmus being induced by, the extension of the head. And so this is what we call a, a positional, pathological nystagmus.

So it's something just to birth to bear in mind to, to be able to differentiate between, between the two. And the only other thing just to be aware of is that we also sometimes see patients with what we describe as a a pendulum nystagmus. Now this is different to the jerk nystagmus in where you have like a slow and a fast phase.

So you remember in that springer spaniel, we could see the fast phase of the horizontal nystagmus going towards the left hand side. Whereas with the pendulum nystagmus, this is often characterised as a sort of continuous oscillation of both globes, without a slow or a fast component, hence why we call it this sort of pendular movement. And it's really important to remember as well that this isn't associated with vestibular disease, and actually is probably secondary to a congenital abnormality in, in the visual pathways.

We tend to only see it in cats, and we see it in cats of particular breeds, so Siamese, bourbon, and Himalayan cats, and we've also seen reports of it in Belgian Shepherd dogs. And we think it's a manifestation of a congenital abnormality in the visual pathway, basically, in which a larger percentage than normal of optic nerve axons cross in the chasm. And so that's why we tend to see it.

So, I've got a video here. It's, it's a very quick video and quite a subtle one, but hopefully you'll get the idea that you can see this very subtle pendulum and the stagmus, in this particular patient. And again, it's really, really short little oscillations without a fast or slow phase, quite symmetrical in, in both eyes.

And you wouldn't normally expect to find any other neurological deficits in these patients. And like I say, it's normally just this congenital, disruption that the optic, optic has and. Fine.

And so then the third sign that we often see, which is obviously quite, quite obvious, is, is an ataxia in our, in our vestibular patients. And remember, we tend to try to characterise our patients with ataxia into three different forms. So you have a receptive, ataxia, a cerebellar ataxia, and a vestibular ataxia.

And obviously, as the name suggests, we often see the latter in those patients with a vestibular dysfunction. And this actually is caused by a, a lack of vestibular input to the ipsilateral limb extensor muscles. And it results in a swaying of the trunk and the head, and you sort of lean or fall over to, to one side.

They often have quite a broad-based stance and sometimes have this slightly exaggerated, extensor tone on the contraductial limb. And you can sometimes see this sort of concavity or curved, back, and that often can be towards the, the side of the lesion. Often in these dogs, they tend to try to sort of hug the wall or stay close to the wall, particularly in terms of the side that they're most weak on to try to maintain the balance.

So you can see the springer spaniel again with our, had the previous horizontal nystagmus. You can see it's got a right-sided head tilt, and you can see as it walks, it drifts over towards its It's right-hand side. And that's a relatively typical vestibular ataxia.

You can also see in its back legs, you've got slightly broad-based stance, a slightly wider apart compared to the thoracic limbs. Again, just trying to maintain, its balance, but, but obviously struggling to, to do so. And then the final of our four clinical signs you might expect to see in our patients with vestibular dysfunction, is a strabismus.

And, and often this is a positional strabismus. And so when you, place the head upwards and extend it dorsally, you'll see that there's a, an abnormal position, of the, of the eye. So in this Labrador, On the right-hand side of his face, you can see that the, the globe of the eye is down and towards the, the right.

And often this causes a sort of a ventral ventrilateral strabismus, such as in this Labrador, and it's ipsilateral to the vestibular lesions. So you'd expect, a vestibular problem on the, on the right-hand side of this dog's, head. Again, you can only sometimes see this when you extend the head upwards.

So if you have a, a patient with vestibular disease or you're a little bit unsure, it's always worth extending their head up and seeing if you have a, a position or strabismus, which might put a bit more weight behind what you think is, is going on. And so the main question we try to answer when we have a patient present to us, with vestibular syndrome is whether it's peripheral or, or central. And by correctly identifying central vestibular disease, or peripheral disease, it helps us then come up with a list of different, differential diagnoses.

And so it all really depends on where your lesion is located. And so there's three sort of questions that you need to ask yourself to try to differentiate between peripheral or, or central. The first is whether you're seeing deficits in cranial nerves 5 to 12.

The second is whether you have any evidence of an ipsilateral paresis or partial deficits on that particular side. And the third is whether you have an abnormal mutation. So in the medulla oblongata, you remember we have our brain stem down here, and that orange oval shape is where our medulla oblongata sits.

There were also lots of other cranial nerve nuclei. So you might see abnormalities of your trigeminal, your abducent, your facial, your glossopharyngeal, or any of the more sort of higher up cranial nerves that can then give you deficits that might then put a bit more weight behind you thinking your patient has sensual vestibular syndrome. It's also important to remember that your upper motor neuron pathways course through this area of the brainstem.

And that's why if you have a lesion in that particular part of the brain stem, you might get these ipsilateral postural deficits as well. And then finally, your ascending reticular activation centre is also located in your mola omegata. And so if that's disturbed by a lesion, and often these patients can be obtunded or stuporous or, or comatose.

So the best advice I can give you is if you have a patient that's got those 4 typical vestibular signs of, you know, a head tilt, ataxia, strabismus, and then nystagmus, after you've noticed or recognised those 4 things, you then start to have to look for any other unusual neurological signs. And the first is to check all your other coal nerves, see if you have any deficits. The second is to see if you have got any partial deficits in any of the limbs, and the third is to try to work out whether that patient is obtunded or, or stupor risk.

And it can be really tricky to do the latter, because often these patients are quite disorientated, but there's a slight difference between a disorientated dog and an obtunded dog, so it's worth trying to, to see if you can tell, tell the difference. I've put this table in and it's in your notes as well, just so we try to help you differentiate between a central or or peripheral vestibular case. So just to quickly run through it, in terms of paresis, it's possible in a dog or central vestibular syndrome, but you wouldn't expect it in one with peripheral.

And that's the same for pro receptive deficits as well. Consciousness, like we just said, you'd expect potentially for a central vestibular dog to be obtunded, stuporous, or even comatose, whereas the ones that have peripheral vestibular disease, they might be disorientated, but they should still be relatively alert and, and responsive. If you've got any cranial nerve deficits between cranial nerves 5 and 12, then you might be slightly increased suspicion of a central vestibular problem.

In terms of peripheral, you wouldn't expect any other cranial nerve deficits apart from maybe cranial nerve 7, and we'll come on to that in a second. And that's also interesting in terms of Horner syndrome. So trying to recognise a patient with Horner syndrome might help you differentiate between central or peripheral, because it's certainly possible or might make peripheral slightly more likely, whereas an essential vestibular syndrome dog, it's a lot, a lot rarer.

And then also the same with nystagmus, so you'd expect a horizontal nystagmus and peripheral veil disease, it can be slightly different in in central. And again, we'll come on to that shortly. And so with Horner syndrome, you see this cat on the, the left of the screen.

It's got meiosis, and ophthalmus, a protruded third eyelid, and also a degree of ptosis. So there are four classic signs of a patient with Horner's syndrome. And as soon as you have a Horner's syndrome in conjunction with, vestibular signs, your index or suspicion of maybe a, a more A peripheral disease, is increased because the pathways, or the sympathetic pathway runs very close to your, vestibular branch of your vestibular cochlear nerve, in your inner ear.

And so often we see the sympathetic, and your vestibular nerve dysfunction, coming together. So, it might put more weight between a problem in the inner ear of these patients. And then that's also true, for a patient with, facial nerve, pers or paralysis.

So you can see this cavalier on the right of the screen. When I check it's how people reflex in his left eye, it's absent, but in the right eye, it's present. And that is, well, once you do your menace response, as well, it's very suggestive of a facial nerve, paralysis on his left-hand side.

Now, if you've got a patient that's got vestibular signs and a Facial nerve paralysis. Again, you might be slightly, increased vision of a problem affecting the middle and inner ear. So, the facial nerves runs from your middle ear into your brain stem, and your, obviously your vestibular nerve runs from your inner ear.

So, if you've got a patient with anotitis media, or internal, you can certainly get both nerves affected, and then give you both, signs that we might then see in both vestibular and facial nerve dysfunction. And so in terms of the nystagmus, often we try to, again, see if that helps us to differentiate between peripheral or, or central. You see the pug on the left of the screen has a sort of a vertical, almost slightly rotatory nystagmus, whereas the stay on the, the right of the screen has more of a horizontal nystagmus with the fast phase to the right.

And so often in horizontal nystagmus, it may be just slightly more likely to be peripheral and, and often we expect the fast pace typically to be away from the side of the lesion. If we have a vertical in a stagmus, it might suggest a more central cause of vestimular syndrome, but obviously checking for your posture reactions, a reduced mentation or other cradal nerve deficits is a much more sort of sensitive way to check to see whether you've got, a problem affecting your, central vestibular system. The stagma see with central diseases, it can be horizontal, it can be rotatory or, or vertical, and it can change direction with, when you change the position of the, of the head.

So it's one to, I guess, interpret with a degree of caution because a central vestibular disease dog can have nystagmus in a variety of, of different ways. There's also a bit of evidence to look at the, the speed of nystagmus, and that is thought to maybe help to differentiate between central and peripheral. So the rate of the resting, and positional nystagmus appears to be sort of faster in those patients with, with a central, vestibular disease compared to, to a peripheral.

And so, what Often we expect, a nystagmus rate of greater than 66 sort of oscillations per per minute in those patients with the peripheral, vestibular syndrome compared to ones with central. In reality, I never tend to count the rate of nystagis. I'm not sure how clinically helpful it is, but it's something just to be, to be aware of.

And so I've just put this sort of flow chart just to try to summarise what we've just been discussing. And again, this is in, in your notes. So the first thing is to recognise your patient with vestibular syndrome.

They've got ataxia, have they got a head tilt? Have they gotten sphagmus, have they got strabismus? If they've got those, then you have a dog or cat with a vestibular dysfunction.

The next thing they're going to check is whether they've got any pull placement deficits, whether they've got any cranial nerve deficits, or whether they've got an abnormal mutation. If they've got any of those three, then it's more likely to be essential vestibular dysfunction. If they haven't, and it's just those 1st 4, underlying causes, then it's probably more likely to be peripheral.

The only exceptions to this would be if you've got a patient with Horner syndrome or a patient with a facial nerve paralysis, because that might be suggestive of a, inner or middle ear disease problem. And so if you've got a dog or cat with ear disease as well, and that might also be, quite, quite possible. And so there are obviously a few exceptions to, to the rule as, as always.

So sometimes we see patients with a a paradoxical vestibular syndrome. And so these patients can have lesions in their cerebellum that can often cause a head tilt to the opposite side of the lesion. And often with these patients, if you see a dog with a paradox called vestibular syndrome, they often have evidence of cerebellar disease on their neurological examination.

But the reason we call it paradoxical vestibular disease is because the head tilt and the circling occur contralateral to the lesion. So in the opposite side to the lesion. And if you do get this because of a cerebellar dysfunction, other signs you might expect to see would be like an ipsilateral dysmetria, maybe a head tremor, or a trunkyl sway as well.

And so often, sometimes these patients, when you see them, walk, they often have a slightly hypermetric or dysmetric gait, on the side in which the cerebellar lesion is. And so often they can affect the propriceptive and motor pathways. And so one thing that's always worth checking again, is your posture reactions because if you've got postural reactions opposite to the side of your head tilt, often that will give you an idea as to where the lesion is because they're normally on the same side as the, the lesion itself.

And so the video on the right, sorry, it's not the best of videos or the best of examples, but it's a little cavalier, that we think had a, a paradox called vestibular dysfunction. So it's not the most easy to see, but it's got a very slight head tilt to the left, but you can see the poor placement on the left, is quite good, but you can see it already spontaneously knuckling on, on the right. So this patient had a right cerebellar lesion, in the flocular nodular lobe, and that caused this left-sided head tilt that gave us these right-sided, posure deficits.

And so we know it's on the right-hand side of the cerebellum, because often it's the same side as the posture deficits themselves. And in cavaliers, we often see these dogs get this paradoxical vestiul disease because they're a bit more predisposed, to getting ischemic infarcs. And when they do get these ischemic infarcs, they tend to happen in the cerebellum.

And so often these patients present with quite a per acute onset of, of. A paradoxical vestibular syndrome. If we scan them, we see this quite obvious, well-defined lesion in the floy nodular lobe of their cerebellum, opposite to the side of the, of the head tilt.

And often we expect it to be all look, it often looks like a, an ischemic infart or a stroke-like lesion. With time and the right sort of rehab, often these patients can, can improve and, and get back to being relatively normal, normal looking. But in dogs, particularly in dogs with ischemic infarcs, we expect about 50% of those could be due to an underlying systemic disease.

So often we then start to look for any underlying reason as to why they've had a stroke. So we look for things like renal disease or Cushing's, or, hyperthyroidism or other things that could make them a bit more predisposed to, to getting these. The other thing just to consider is that occasionally with thalamic lesions, that can also sometimes give you, vestibular signs.

And so, a head tilt on the stagmus have been described again in dogs with ischemic influx in the parameian region of the thalamus. I put this paper in at the bottom, it explains it all in a bit more, bit more detail, but we suspect it's due to damage to the adjacent midbrain regions involved in the vestibular function. And the only other thing to bear in mind, again, as a slight exception, is that occasionally we can see a head tilt in patients with a focal, cervical spinal cord lesion that can change the, the muscles asymmetrically, and then often they can have a slight head tilt.

In those patients, we don't often see other signs of the severe dysfunction. It's just the head tilt itself. So it's just something to, to, to bear in mind.

And so in terms of coming up with a list of, of differential diagnoses, it really depends on whether you think your patient has peripheral or, or sensual disease. And occasionally, you know, we, we can't always differentiate between the two based just on our neurological assessment. We just have to go with what we think is most likely, but it does alter what we think of in terms of, of what the most likely inciting causes, but also then give us an idea as to how to investigate or, or to, to treat them.

And so I put this little list of differential diagnoses for patients with peripheral vestibular syndrome. So the first is otitis media or internal. So often we see this more commonly in certain breeds than others.

So, French bulldogs often are very good at getting otitis media or returner. And cavaliers often get this primary secretory otitis media which can start off with a, a facial nerve paresis or paralysis, but then can progress to having vestibular dysfunction as, as well. And often these patients are then treated with either meningotomies or tiers or if they're a cat, maybe a, a VBO.

Then you often see this acute idiopathic vestibular syndrome, sometimes called geriatric, vestibular syndrome. We'll come on to you a little bit later on. Obviously tumours affecting your middle or inner ear can also affect your peripheral vestibular nerve, and so it can also give you peripheral vestibular syndrome.

Ootoxic medications. So aminoglycoside, antibiotics, furosemide, sort of platinum-containing antineoplastic agents, anything like that, that are topically put down into the ear, can, into a patient with a compromised tympanic membrane can certainly, cause peripheral vestibular signs. And we think it's probably due to damage or death of the, those neuroepithelial hair cells in the membranous labyrinth, but it can vary depending on what, what is used.

Hypothyroidism, again, can cause peripheral vestibular syndrome. You might expect those dogs to have other accompanying signs of sort of flaccid limb weakness, or some form of generalised polyneuropathy, but it's certainly worth, putting on your differential list as well in these, in these patients. For those that have signs more suggestive of a central vestibular syndrome, then often a neoplastic process.

So a tumour affecting the brain stem and in particular your medulla oblonga possible. A meningoencephalitis of unknown aetiology. So this autoimmune inflammation of your brain stem can also give you central vestibular signs.

A brain infarct. So if you have, anaschemic. Inar, or even a hemorrhagic infarct affecting your vestibular system, that can also give you central vestibular signs.

So cavaliers, as we already know, are predisposed, but we also often see it in, in greyhounds. So that's also worth, worth thinking about. Metronidazole toxicity, is also a possibility in these dogs with central, vestibular syndrome.

The exact mechanism of this toxicity isn't really known, but there's a few theories about it being modulated by, the GAA receptors in the vestibular cerebellar system. Often, these dogs present with lots of for the signs as well, but they often can have an ostagmus and sometimes a degree of ataxia. Hypothyroidism, can also, present itself as a central, vestibular problem.

It's not the most common, but something worth, worth bearing in mind as well. Right. So based on that, and based on all the information and those differential diagnoses, I thought the next part of the webinar we could then look at would be to go through a few, a few cases and see if we can, put this into, into action.

So, our first case is Kierra. She's, an 11 year old female neutered, Labrador that had a, a very acute onset of, of difficulty walking and, and stumbling. And her own has noted that she vomited on the, on the morning of presentation.

So here she is. You can see that she is ambulatory, but with quite a marked, ataxia. She's got this sort of broad-based stance, particularly in her pelvic limbs, but also in her, her thoracic limbs as well.

She seems relatively alert. She's obviously very disorientated and struggling to walking, but otherwise seems, seems quite alert in herself. And you can see, she tends to drift over towards the, the right-hand side of the room and often hugs the walls or the cabinets on the, on the right hand side to try to, to maintain her stability.

So she certainly has this vestibular ataxia. The other thing that's quite obvious when you look at her is this right-sided head tilt. So you can see her right ear is, is lower than her, her left.

So quite a, an obvious head tilt there as well. When we look at her eyes, she has a, what I would define as a horizontal nystagmus with the fast phase to the left of her head. And also we elevate her head, you can see she has a strabismus in that right eye, so ventrolateral strabismus, on her, on her right eye.

Her vestibular ocular reflex is otherwise present. You can see her palpal reflex is present, we know her facial nerve is working and is intact. And also she's got a menace response bilaterally as well.

And her gag reflex is intact, and when we check for any pa placement deficits, you can see in her right thoracic limb her paw placement's quite, quite normal. And that's also true in her, her left thoracic limb as well. And in her pelvic limbs.

As well. So, the first, I guess, question that, see if you can answer is whether she has a left or right-sided vestibular syndrome. And the second question to answer is whether you think it's more of a peripheral or, or central problem.

So, I guess the first thing is that she had a right-sided head tilt. She had a horizontal nystagmus with the fast phase to the left. She had a right-sided, positional ventrilaal strabismus, and she had a vestibulartai and often drifted over to the, to the right-hand side.

So for me, it's most likely a right-sided vestibular syndrome. Now, based on the fact that she didn't have any partial deficits, she seemed to be quite inappropriate, sort of mentation. She was disorientated, but otherwise, seemed quite alert and, and quite responsive, and didn't have any other cranial nerve deficits.

I would put her down as being a peripheral, vestibular disease. And so for me, she is a right-sided, peripheral vestibular syndrome. So if you were to summarise her as a case, so she's an older sort of geriatric Labrador with an acute, relatively static, non-painful, obviously asymmetrical, right-sided, vestibular disease.

And from our examination, there's no real evidence of any central component to her vestibular disease. And so the next question I've got for you is to see whether you can come up with any differential diagnosis. What's the most likely differential diagnosis in an older Labrador with quite an acute onset, static, non-painful right-sided vestibular disease without any evidence of an obvious sensual involvement?

And so really, we think about that list that we saw earlier. So, possibilities would be in otitis media or internal, an acute idiopathic vestibular syndrome, neoplastic process, ototoxic medications, or, or hypothyroidism. And to be honest, given, her age, given the acute onset, given the static nature of it, then for me, at the moment at least, it's more like she has this acute idiopathic, vestibular syndrome that we see in these older, older dogs.

And so in terms of how I tend to investigate these patients, I start off by examining their ear, see if there's any evidence of otitis externa, which might increase our suspicion of an otitis media or internner giving us our peripheral vestibular signs. If her ears are clear, I think it's always worth doing a full haematology and biochemistry and also just doing a thyroid profile, just to make sure that her, her T4 and TSH are where you would expect them to be. If you've got clear ears and her haematology biochemistry and thyroid don't give you any explanation as to why she could have vacia disease, then the next step would be to maybe consider an MRI scan and a spinal fluid tap.

I think in reality, if you have an older dog that's got these sorts of signs, it's not wrong to hold off doing any advanced imaging and to see how things progress, because like I say, a large portion of them will be this geriatric or idiopathic vestibular syndrome. But if the owners or you want to be as sure as you can that you're not missing something central or there's nothing else going on that could be treated differently, then the next best step would be an MRI scan of the brain that allows you to look at the brain parenchyma, allows you to look at the medulla oblongata, but also the middle and ear disease to see if there's any obvious, underlying pathology that could give you those signs. And depending on the MRI scan, we might also consider doing a spinal fluid tap to check for anything in, in particular.

And so for Kira, she had everything done, and, nothing was found on her MRI scan or her spinal fluid tap. Her blood work was normal, and her ears were normal. So, we diagnosed her with this acute idiopathic, vestibular syndrome, and it's important to really understand that actually, this tends to be a diagnosis of exclusion.

So we try to rely All the other underlying causes of, of vestibular syndrome. It can affect both dogs and cats, and, and we often tend to see it more in our geriatric patients. And in terms of as a disease, it's often quite a perute or acute onset of, of signs, that can be quite static, for the first few days, but then we start to see a gradual improvement in the, in the coming weeks.

And often we thought, think about supportive treatment. So more ants or down to try if they're nauseous or not really eating. And the other thing that I've tend to do a lot more recently is to have these patients have, have physiotherapy.

Often these dogs, as they start to gradually improve the ataxia improves and the stagmus improves, even the strabismus improves. One thing I often more known is, is that something that can persist even if everything else gets better, is this slight head tilt, and I partly think it might be because of the change in the muscle. Contracture on that one side.

And so I find that physiotherapy helps quite a lot in terms of trying to get these dogs back to being ambula and let it toxic a bit quicker, but also it's quite helpful to try to reduce the chance of them having a, a long-term head tilt, which can be quite, quite good as well. Fine. So Kira the Labrador was quite a typical example of dogs with this, idiopathic, vestibular syndrome.

And like I say, I don't often do MRIs or spinal fluid taps in those patients, if they're quite typical in terms of how they present, but only if we see them deteriorate or not improve as you might expect. And so certainly in the first opinion sort of practise setting to, if you've done some blood work and your neurological assessment suggests more peripheral than, than central, to give those dogs time and see how they progress, because if they start to improve by themselves, the, indication to perform an MRI scan becomes less and, and less. So our next case is little Sky, so she's a 5 year female neutered Chihuahua, and she came to me with this 2 to 3 day history of a progressive worsening of her, her vestibular signs.

So here she is, she's a little bit more tricky to examine because she was so visted with it, she was non-ambulatory and had quite a a marked size. So you can see when we check her menace response that's intact in in both sides, as is her pal people reflex. She's got a vestibular ocular reflex present in, in both sides.

You can see there quite clearly, she's got this left-sided ventrolateral strabismus in her, her left eye. And when we elevate her head up, you get a much better idea of her having a nystagmus. And you can see her nystagmus is slightly different.

It's not horizontal, it's more vertical and slightly rotatory as, as well. And then often she has, you can see she's got this like. Left sided head turn, but then also this head tilt as well on her left hand side.

Her postural reaction on that right thoracic limb was, was normal. It's a bit tricky in the left thoracic because of the cannula, but, but it seems to be intact. And when we check to see if it's in her pelvic limbs, you can see her right pelvic climb seems to have quite good poor placement, and we try to knuckle her over.

That seems quite, quite normal. And when we check it in her, her left pelvic limb, you'll see in a minute that actually it's slightly delayed in her, her back left leg. And she's just slightly slower to place it in this position here.

And she's quite a good example of how sometimes it can be really difficult to examine these patients with such marked vestibular signs, because often, their balances are such that they can't stand up for themselves. And even when you lift them or support them, they often want to spin around or, or turn round. They can be quite challenging patients to, to examine as well.

So again, we have, I guess a couple of questions to try to to answer. The first is whether we think she's got a left-sided or or right-sided vestibular syndrome, and the second is whether we think it's peripheral, or, or central. So she had a head tilt on the left-hand side.

She was very toxic to the point of being non-ambulatory. She had this left-sided ventrolateral strabismus, and she had a stagmus, which wasn't overtly horizontal, it's more sort of rotatory or vertical. But given the left-sided head tilt and the strabismus, I would certainly think maybe more likely a left-sided vestibular syndrome for, for Sky.

Whether it's peripheral or, or central. For me, I would probably lean towards more of a central vestibular syndrome, primarily because her nystagmus was a bit rotatory, and not your typical horizontal, but also because she had that poor placement deficit on her, her left pelvic limb. And again, you wouldn't normally expect to see that in a dog with peripheral, vestibular syndrome.

So for me, I would think that sky is most likely a left-sided central vestibular syndrome. So if you were to summarise her as a case, so she's a young chihuahua with an acute progressive. So the last 2 or 3 days, she started to, to get worse.

Not painful, but obviously asymmetrical left-sided, central vestibular disease. And so we think about differential diagnosis for her. Again, it's a similar list to what we saw before.

So, something nearplastics, or a brain tumour affecting her, her brain stem is, is certainly possible. And meningoencephalitis of unknownology, I think for me is, is more likely based on the fact that she's a young dog, and she's a chihuahua, and often we see that particular condition in those dogs more, more commonly. A brain infarct is possible for a central left-sided vestibular disease, but what wouldn't typically fit is the fact that she progressed over the preceding 2 or 3 days.

Normally with brain infarcs, it's quite a per acute onset, but they're normally quite a static, presentation of, of signs. So I wouldn't expect them to, to drastically deteriorate otherwise. Metronisal toxicity is possible, but again, she's not taking that.

So again, lower or not really on the differential, diagnosis list. And, I mean, deficiency, again, is possible, but less likely based on her, her history. So for me, a meningoencephalitis, I know aetiology would be top of the list, but obviously, you couldn't rule out something near plastic or, or something more, more unusual.

So for her, because of the signs suggesting a central vestibular disease, we went ahead and did an MRI scan. So this is the scan of her head. You can see on the left is a TT rated sagittal view of her brain and a TT weighted transverse view here.

When we say TT rated, it's important to remember that fat and fluid is hyper intense, so brighter than you'd expect. And then this is a flare. Transverse view, and a T1 rated post-contrast view.

And so, you can see on these images that she's got this sort of large, really quite focal, slightly irregularly defined, T2 rated and flare, hyper-intense lesion, at the level of the left cerebellar, that uncle extending, sort of ventrally along her, the left side of her, her brain stem. It's sort of hypo intense on T1 rated images and it has a slight heterogeneous moderate contrast enhancement. There's not a huge degree of, of mass effect, and there's no signal void and when we did the gradient echo sequences.

And there's a slight degree of ventricular megaly. You can see here her lateral ventricles are slightly enlarged, but not, not too exciting, and sometimes that can also be breed related. So that is, you know, that's sort of finding of these relatively ill-defined, slightly hyper intense intraparentchimal lesions, is suggestive of a meningoencephalitis of unknown aetiology.

And often to try to help us confirm that, we take a sample of spinal fluid. And now, normally in a sample of spinal fluid we'd expect to find less than 5 nucleated cells, and in her case, there were 30, and the majority of those were lymphocytes, so a lymphocytic, geocytosis. And based on that, based on the MRI findings, based on her CSF, it is most likely that Sky had a meningoencephalos of unknown aetiology.

So it's important to remember that, and that's an umbrella term encompasses like a heterogeneous group of, of what we presume to be an autoimmune disease that can affect, obviously the central nervous system. And we see it in quite young, sometimes middle-aged dogs, and we see it in certain breeds more than others, typically smaller breeds, and, and certainly we do see it in Chihuahuas. And there's different forms of this disease.

You get the granulomati meningoencephalitis, you get a necrotizing form, and sinophilic form, or a necrotizing leukoencephalitis as well. And this is all presumptive based on the MRI findings and the characteristics, but also based on the spinal fluid analysis. In reality, the only way we'd ever get a definitive diagnosis to confirm it's a, an MUA is to do histopathology, but, but often that's not obviously done, unless these patients go for postmortem.

In terms of how we treat it, it's often treated by immunosuppressing these patients. So we start them on quite high doses of corticosteroids. Sometimes we add in cytarabine, and then often add some physiotherapy in as well to try to, to help with an improvement.

And the prognosis can be quite variable. We often expect or hope that if they have a good initial response to treatment, then hopefully that bodes well and they'll start to gradually improve. But there are certainly cases that don't respond to treatment, and it can be one that also has relapses as they, as they go forward.

And so with Sky, we started her on some intravenous, dexamethasone and also some cytarabine. And she started to improve over the, over the subsequent days. So still obviously has a, an obvious head tilt there, but slightly less, ataxic.

She's now ambulatory, . for herself without, without support. Her mentation is slightly better, but still obviously has some quite severe neurological dysfunction.

But we'd expect that to get better and better, hopefully, as the, the treatment starts to become, more and more effective. Fine. And then our, our last case is little Abby.

She's a 10 month old female neutered, Siamese, and she had quite an acute onset of inhabitants and and ataxia when she came. Now it's not the most obvious in the video, but I tried to capture it, but you can see. Abby is a little bit tactic there, stumbling a little bit from the side.

You get a very, sort of, she's quite low to the ground, and occasionally you get this, suggestion that she's got this slightly, swinging head from, from side to side. But like I say, it's not the most obvious. It is quite subtle and can sometimes be harder to, to see, but, but you can sometimes see the slight wobbleness and the slight drifting over from, from side to side.

So the reason I put Abby in was because actually she's a relatively good example of a, a cat with a bilateral vestibular syndrome. And the reason that I think she has that is because she does have this ataxia that does look more like a vestibular ataxia. And then she also has this head swinging from, from side to side.

And the other important thing to remember with bilateral vestibular syndrome is that it's similar to, to unilateral vestibular disease in that the presence of signs that can't be attributed to the peripheral system, so you know, abnormal mental status, postureaction deficits or a different type of ostagmus or the cranial nerve deficits. Can still be used to differentiate between peripheral or or central vestibular disease. So it's still obviously worth checking about the mentation of the cranial nerve deficits and posture reactions because it's still very important to differentiate between peripheral or central in patients with bilateral vestibular syndrome.

And in terms of the differential diagnosis for cats with this, often a bilateral otitis medial or internal is possible. To be honest with you, the majority of them are acute idiopathic bilateral miss. We don't often find an underlying cause for it.

Bilateral polyps is certainly a possibility, although quite, quite unusual, and the only other things I have at the back of your mind, again, because of her being a cat is a, a thiamine deficient cat. And so for Abby, we did an MRI scan. You can see a T1 rated post-contrast, dorsal view on the left, and then a TT rated saggital view, a TT rated transverse view.

And we also did a CT scan to really evaluate her middle and inner ears as well. And you can see all of those images that it's actually quite a normal looking. Structural brain and normal tympanic bulla on the, on the CT.

We also did the spinal fluid analysis, that was again within normal limits. We checked her haematology and biochemistry, that was within normal limits. Her bile acid stem test was, was also normal, and she was on a normal diet, making a thiamine deficiency less likely.

So she is a, a case of, an acute idiopathic bilateral vestibular patient. And so I just put this slide in as well, just because I know Abby wasn't the clearest of videos, but again, just to try to, make you comfortable in terms of looking at patients with bilateral vestibular syndrome. So, it is characterised by these sort of wide head excursions from side to side, this loss of balance on the other side, and there's quite symmetrical attacks, but often they have this quite crouched posture.

They stay quite, quite close to the, to the ground. The other thing to be really conscious of is that in these patients, there was an absence of a head tilt, and also the absence of a pathological, nystagmus. And just like that cat at the beginning, when I showed you that she had an absent physiological nystagmus, you wouldn't, that is what we expect to find in, in cats with this bilateral vestibular syndrome.

So when you do the vestibular ocular reflex, you will see that these cats don't have, normal physiological nystagmus. And so that cat from the very beginning, also had a bilateral, vestibular syndrome. This is a very short video, but again it's quite a good one to to show you primarily the wide head excursions, this sort of crouched posture and this symmetric ataxia, so have a have a quick look.

So you can see his head going from sort of side to side, sort of widehead excursions are slightly taxier, and being maybe slightly, slightly lower down to the, to the ground. But they are a bit challenging to, to get to grips with, but when you see a few, you start to, to recognise it a bit more, a bit more comfortably. And so then other things to bear in mind, obviously we always say it, but cats aren't aren't small dogs.

I put this paper in just, it's quite a nice one to, to show you the different underlying causes for cats with, vestibular disease. Inflammatory conditions were, were way out in front, which is slightly different to dogs. Sort of bacterial inflammation because of noittis, internal infection was, was most common.

FIP was also quite common in these cats, as was, toxoplasma. Neoplasia and, and vascular disease, were also quite high up on the, on the list as well for patients with, central vestibule disease. For those ones with peripheral vestibu dysfunction, most are common was idiopathic, and the second most common was otitis media or internal.

So again, this is a slightly different list of what you might expect in a dog compared to a cat for sensual versus peripheral, underlying differential diagnosis, but worth bearing in mind. So you've got a good idea as to what to expect from, from both. And so that's pretty much it, in terms of the, the vestibular ramina.

And so it's always quite a tricky disease to, to know how best to proceed. My best advice is to obviously, A, make sure you've got, signs consistent with vesimular disease to begin with. The second best thing is to check to see, whether you've got any evidence of central involvement and Based on that examination, you can come up with quite a, a succinct list of differential diagnoses.

And then based on, on how the patient's progressing, based on the age, and based on the, the history, it's then you can decide whether it's worth, investigating further and, and which tests to do, and hopefully give you a bit of an idea as to what to expect, prognostically. Thanks very much.