Good evening everybody and welcome to a Thursday night members webinar. My name is Bruce Stevenson and I have the privilege and honour of chairing tonight's session with a very special guest talking about a subject that I think a lot of us need constant reassurance and, and clarity on neurology and I have no doubt that we're in for a special treat tonight. I don't think we've got any new members, so no need for housekeeping, usual applies.
Pop the questions into the question and answer box, we'll hold them over to the end. So tonight's speaker. Qualified from the University of Cardinal Hea in Valencia, Spain in June 2003.
After that, Elsa spent two years in general practise. She completed a general internship at the University of Autonoma de Barcelona before starting a neurology internship at the Animal Health Trust. Following the internship, she undertook a residency in neurology and neurosurgery at the Animal Health Trust, and she obtained a diploma of the European College of Veterinary Neurology in 2011.
She became a senior clinician in that neurology and neurosurgery at the Animal Health Trust. And then in October of 2014, Elsa joined the Royal Veterinary College, University of London, and she is now lecturing in neurology and neurosurgery. Since October 2015, she has been the chairperson of the ECVN Education Committee.
Elsa is interested in all aspects of veterinary neurology and neurosurgery, but she has a particular interest in understanding neurological sequels in dogs following trauma brain injury. Elsa, welcome to the webinar, vet. And without further ado from me, it's over to you.
OK, good, good evening, everyone. Wherever you are located in the world, we are gonna try to talk the next hour about understanding the dizziness. So what we're gonna talk is about the vestibular system, and we are gonna cover.
Two things, and I mean it's very important and I know that sometimes neuroanatomy when you go back to school and say, oh no, neuroanatomy, but it's so, so important to try to understand the normal function where those anatomical structures are located prior to, to try to understand a vestibular dog, a vestibular cat that comes through your consoles and say, oh, what's going on and, and to Should I be worried to try to answer that question it's very important that we understand the normal function. And then we will see why those clinical signs appear. Why do I have a dog with a head tail, why they have these rotatory vertical horizontal stagmus, and, and the question, should I be worried?
So we're gonna see some clinical cases and, and we will try to, to, to get to the bottom of them and, and, and overall try to learn from them. So. The first question is, what is the vestibular system, what does the vestibular system do?
And the vestibular system is a pure sensory system, so it doesn't have any motor activity and is responsible of keeping us orientated with respect to the gravity. So it keeps us up. Straight, we are not falling because we know where the gravity is.
We're very, we have our sensory system working. So this is my own dog. She doesn't do that anymore because she's a dachshund and guess what?
She had a sleep disc, so she's not allowed to do that anymore. But what happened when we lose this vestibular system, what happened when we do lose the balance? We have signs of vestibular syndrome, we have signs of balance disturbances, so we can have a dog with a head tail, a dog that is not able to walk because it's so uncoordinated.
So we have a type of uncoordination that in, in neurology, we call it ataxia and in particular, they have this vestibular ataxia. So we are gonna see all these clinical signs together, but going back to, to the anatomy, there are two important areas. Of the vestibular system that we need to know where they are located.
And when we talk about the vestibular system, and as we already said, the vestibular system is a pure sensory system. What does it mean? It means that it, it has to detect, it needs to have some receptors of this balance.
So how, how the body detect this gravity, how the body detect that we are moving, so what, what the vestibular system does is control mainly the, the Movement of the eyes, the movement of the, of the limbs and the tract, respect to the movement of the head. So how does, how it's gonna detect that movement and that little beautiful, amazing apparatus is located in the inner ear. So if you remember The parts of the, of the ear back to the anatomy, we have the external ear, we have the middle ear, and we have the inner ear.
So a lot of people say, oh, this dog has a, a, a head tail it's gonna have a middle ear disease. It can have a middle ear disease, but it needs to have an inner ear disease as well. Otherwise, a pure middle ear disease will not give you vestibular syndrome because the vestibular system is located in the inner ear.
This little tiny thing that is so important to keep us up and not falling is located here. So, this, if we have to magnify it in a very simple way, we have the three semicircular canals, the male, the suckle, and also the hearing system, also the cochlear. So this cochlea will give The cochlear nerve and this vestibular apparatus will give the vestibular nerve.
So together, the vestibular nerve and the cochlear nerve are known as vestibular cochlear nerve that going back to anatomy, you remember this is the cranial nerve number 8. And this is located in a bone, so it's the only cranial nerve that never sees the light. I feel very sorry about this one because it just is here and never exit the skull.
So from here, enter this, the cavity through a little fragment here that is known as internal acoustic meatus. If you remember back to the anatomy, where the tympanic membrane is located, this is the external acoustic meatus, this is the internal acoustic meatus, and from there it's gonna enter the, the intracranial. Cavity and it's gonna reach the central nervous system.
So up to here, we're in the peripheral nervous system and now it's gonna enter the CNS which is the central nervous system. And in the central nervous system, we also have areas that contribute to the vestibular system. One is located in this part, which is known as the medulla.
Blongata, which is the caudal part of the brain stem. And then there is a little, little lobe in the cerebellum, which is called, it's gonna be written later, but it's called the flocular nodular lobe. And this lobe also contribute to the vestibular.
So sometimes we can see cerebellar lesions with the vestibular signs because this little lobe is also affected. OK. So, the vestibular system function very, very close in coordination with the cerebellum.
So when we talk about, you go back to the anatomy and say this is the peripheral vestibular system, we're talking about the vestibular system that is located in the inner ear. So we're talking about lesions that are located here. While if we talk about lesions either in the medulla blongata, which is the caudal part of the brain stem.
So this is all the brainstem, this is the forebrain, this is the brain stem. So, the nuclei of number 8 is located here in the, in the medulalogata and part of the vestibular system is also located in this. Little lobe, which is the ocular loop, and this is known as the central vestibular system.
So if we have a lesion here, either here or here, we are, we are gonna be talking about central vestibular syndrome. If we have a lesion in the inner ear, we are gonna talk about peripheral vestibular syndrome. So, if we talk about Other nerves that goes as well through the internal acoustic meatus, this is the facial nerve and it's important because sometimes we have diseases that affect this area and present with vestibular and facial together dysfunction.
Are we surprised? No, because they are very, very close. So, the facial also has some sensory functions.
So, once obviously the sensory comes in, the motor which cause the main function of the, of the facial nerve is, is, make us smile, no. So, so works as the motor to the muscles of facial expression. So, it goes in this little drawing here, you can see it goes to the internal acoustic meatus and the other function of the facial is also, you remember, is innervating the lacrimal glands, the salivary glands, and the nasal glands.
So, as soon as they cross the internal acousticmiatus, the, the, the function that innervates the lacrimal glands. Will go rostra. The ones of the motor is gonna go around the bulla and it's gonna exit caudal to the bulla through another foramen that is still salommatoid.
So, just looking, imagine we have a lesion here, which is gonna affect just our motor of the facial and our vestibular, which clinical signs are we expecting? Typical. Do with a head tail and Tropic phase, the facial, and mental status is gonna be normal.
So this is likely a lesion at this level. What happened if we have a lesion here, which means we are gonna have the facial, the vestibular, but also the parasympathetic branch of the facial, which means the one that innervates the lacrimal gland and the nasal gland. So we are gonna have a head tin, so our vestibular is gonna affected, our facial motor is gonna be affected, but our parasympathetic facial is gonna be affected.
If all these signs are together, your lesion is gonna be in the petrosal bone. It cannot be in the middle ear because then you should not have this dry nose and dry eye. And then there's another nerve that goes very close to the vula, which is the sympathetic innervation to the eye.
So, you remember what happened when we have lack of sympathetic innervation to the eye. Clinically, what do we have? Horner's syndrome.
So we have a lesion here, which means middle ear and a little bit of the petrosal. It's typical. We have head tilt, you can have some facial, but you can have a Horner's syndrome.
All these three together, they can only happen in the, in the middle inner ear, assuming that obviously the mental status because that is the most important sign for central is normal. So, hopefully, that's OK, explaining the peripheral, we are gonna go more in depth. But then what happened with the central, so when we can think about central and the most important er about central is the mental status because they share.
a, a function that there are other pathways here that are very important to wake up our forebrain. And if you remember back to the anatomy, it's known as the RAS, which is the ascending reticular activity system. So they activate and then wake up our Forebrain, which means when we are obtunded, when the dog is lethargic, is less reactive, it could have a diffused brain stem lesion, to diffuse forebrain, and this clinically, we see it as an, as an obtundic dog.
So if you have a dog that is obtunded, is lethargic, and on top of that has the vestibular signs, then it's likely we're talking about the vestibular system that is in the central nervous system. But there is another important pathway that also goes through the brain stem. That are the proprioceptive pathways.
So propriceptive pathways, you remember is when we do the pole positioning, so we turn the, the toes and then all the sensory information goes to the peripheral nerve all the way up silateral to the spinal cord, silateral to the brain stem, and then contralateral forebrain. So this is where the area, if you have a lesion at this level. They can have postal reactions plus the vestibular signs.
So you have a dog with postal reaction deficits and epsilateral signs, vestibular signs, then it's gonna be central, OK. So, the, the proposition deficits, they are also always ipsilateral. And then another important thing that we can have with central vestibular system is as well all the cranial, cranial nerve deficits, and there are different cranial nerves that arise in the medulla longata.
And if we have those affected, we can have anaesthetic extratrabismus. We will see some cases. We can have facial nerve paralysis, decreased facial sensation, which is the, the, the function of the trigeminal.
We can have masticatory muscle atrophy. Which is well is function of the trigeminal, and then most caudal to the, to the mara blongata, we have the glossoparyndula and the vagus nerve, and they are very important for the gag reflex. So you have absent gag reflex, obtaining mental status, and vestibular signs, I will not be thinking about middle inner ear disease.
I will be more worried that that dog or that cat may have something affected the, the brain stem. So, Talking a little bit, why the dog or the cat, why, why, why they fall, why they have this nystagmus, why they have this head tilt. So what is the normal function of the vestibular system?
So the vestibular system, this little apparatus that is in the inner ear is constantly, constantly sending positive inputs. So if we have, as I said, if we have, the anatomy that we talked before, so we have the, the, the vestibular apparatus in the inner ear, we have the vestibular nuclei in the medulla blongata, and then we have this flocular nodular loop in the cerebellum, and this communicates to this nuclei by tracks of white matter, and they are known as peduncles, and there are 3 peduncles that join. The cerebellum with the brain stem, the rostra in the middle and the caudal.
So the one that communicates with the vestibular is the caudal. So they are just like motorways. So they are just tracks of white matter that will communicate the floral lobe with the vestibular.
So, what happened during a normal, so as I say, why we are not falling because constantly we receive positive. Electric input from the inner ear and the cerebellum always, always, always sends negative input. This is why when our cerebellum doesn't work, we are hyper, we are hypermetric, we have this tremor, so everything is hyper.
So when the cerebellum works, always sends negative inputs. So we have positive, positive coming from the inner ear and negative, negative coming from the cerebellum. So we have a balance.
So when we have a balance, we are not falling. What happens when we have vestibular signs? So vestibular signs, they always, always towards the side with less electrical activity and this is very important.
So, what happens when we have a dog doesn't matter if the lesion is in the inner ear or your lesion is in the vestibular nuclei. What happened? We get positive, positive, but we cannot get anything positive here.
So we don't get any positive coming from the inner ear or we don't get any positive in the vestibular nuclei. Plus, we get the negative of the cerebellum, which is the area of less electrical activity. This one.
So the dog is gonna be falling, leaning towards the side. That he has the lesion either in the vestibular nuclei or in the inner ear, OK? So there are exceptions from this and this is not as paradoxical.
Have you ever heard about paradoxical vestibular syndrome? We'll explain it later with a case, but in order to understand this, it's very important that we understand the basics. So the basic is that the tiular signs always are towards the site of less electrical activity.
So if we don't get input from this year, we are gonna get signs towards this site. If we don't get input from these vestibular nuclei, we have got signs towards this side, OK? Hope this is clear.
So now what happens if the vestibular system is functioning normal, this Input is going here, this input is going here, and now what? So that information is going to be transmitted to the eye. So we are able to move the eye as we move the head.
So we are able to follow the objects as we move the head, OK? So that is part of the vestibular system controls the movement of the eyes relative to the movement of the head and the same, sends information to the spinal cord. So then what happens if we, for example, have another information.
So when you are about to fall, you are conscious of it. So that information also reached the forebrain, so it's, it's consciously perceived. So those are the three, the three big areas that the information from the inner ear goes.
So it goes to your eyes, it goes to your spine, and it goes to be consciously perceived. So now, what is the normal function when it goes to the spine? So it's very easy.
Silaterally, what it does, and I cannot do it with you, but if you try to fall towards one side, what are you gonna do? You're gonna constrict your extensors and you're gonna inhibit your flexors. So try to fall without thinking, and this is what you're gonna do.
So, and then you inhibit your contralateral extensors. It looks very funny, but when you fall, you do this, OK? So you you put a positive to your extensors and invite your fractures.
You construct your extensor, in your flexors. So what happens when this doesn't work? We fall.
So we are gonna fall towards the side because we are not able to extend our extensors and sometimes you can see contralateral extend contralateral hyperextended extremity because you're not able to invite your, your, your extensors. So this is something that you may see in dogs. It's not very common to see, but you can see, so that can be an explanation.
And then this is what happened when we are not able to constrict our extensors, we are gonna be falling, and this is the typical characteristic of vestibular ataxia. They lean and fall towards the site of the lesion because they are not able to constrict the extensor. So any movement that they do, they fall, OK?
So that will explain our vestibular ataxia. So, what else? What happened if instead of we having both sides affected, so the dog, oh sorry.
The dog or the cat is not gonna be falling towards the side, towards one side or the other. They are cats that they really go very close to the ground and they have this wide excursion of the head. This is nearly pathognomonic or bilateral vestibular.
And this is, this is It doesn't tell you if it's central or peripheral, but it's something very, very important. If you, if you do this in a cat, one thing that should come into your mind straight away is thiamine deficiency. Until otherwise proven, that cat may have thiamine deficiency, and those patients have to be treated straight away with thiamine until otherwise proven because that, if it's thiamine deficiency, they can start with bilateral vestibular but they progress and in a few days, they may die.
So, as we said, this is the normal function to the, to the spinal cord, and then that function also goes to the movement of the eyes. So, I'm not gonna go too much into these details, but what happened Have you done the vestibulocular reflex to some patients, kind of the physiological stagmus. So we move the head and the eyes move rhythmically.
So why they move like that? Because that stimulus from the inner ear, oh sorry, that stimulus from the inner ear goes into the brain stem and communicates bilateral and symmetrically with the three cranial nerves that innervates the extraocular muscles. You remember there are 3 cranial nerves that innervate the extraocular muscles, the 3, the 4, and the 6.
So, bilateral and symmetrically, they are gonna connect to those muscles, and this is why it allows the movement of the eye. So, vestibulocular reflex is a very simple reflex to do. So, we move the movement of the head.
And we see the movement of the eyes. So you see a fast movement, slow movement, fast movement, and slow movement. And this is how the vestibular connects with the extraocular muscles, and this is a normal function of the vestibular nerve and the nerves of the 34, and, and 6.
OK. So, what happens when we have this affected, for instance, if we have a right vestibular syndrome, doesn't matter if it's central or peripheral, you are gonna block this movement. So you will see it's not very easy to videotape this, but you will see when the head of this dog is moved towards the right, the vestibular ocular reflex is very slow.
However, when you move towards the left, that vestibular ocular reflex is better. So look, It really struggles to follow the movement of the head. Can you see the eyes remain behind?
However, when you move that towards the Left, you can see better movement. Yes, did you see that? Obviously, the good thing now is that you can do slow motion videos, so that can be picked up quite well in a slow motion video.
So you can see how really, so this, the only thing that tells you is that you have a lesion. It doesn't tell you anything about centre or peripheral, just tells you that you have a lesion in the right vestibular system. So, In this case, was central, but what are the clinical signs of central vestibular syndrome, as we said before?
Two important signs, mental status, so there are those that are gonna be obtained and silateral postal reaction deficits. So those are the two clinical signs that we need to look at. Don't rely on vestibular signs alone.
Other thing that we can see is pathological nystagmus. So you've lost the connection and you lost the, the balance of those eyeballs. So those eyeballs have lost of balance and they have this rhythmic movement with a fast face and a slow phase.
So the slow phase is like the balance is lost towards the side and the fast phase. Put it back to the centre. So this is why they say that the fast phase is away from the lesion because they fall, they lose the balance toward the slow, towards the site of the lesion and the contralateral quickly put it back.
I don't know why it was always say that like that. I rather prefer the slow phase toward the site of the lesion, but there we are, to make it more complicated. So, again, Other thing that we can see, have you heard about the positional Extravismus?
So Extravismus, what it means is just an abnormal position of the eyeball relative to the orbit. And we can have two types of travisus, static, which means you don't. Touch the head of that dog or that cat, and there is an abnormal position of the eyeball relative to the orbit.
This is nothing to see with the vestibular. This is either a problem with the extraocular muscles, a problem with the muscles itself, or you can have a retrobar mass. So be careful.
That doesn't mean a vestibular bismus, but this one, how is this extratrabismus elicit is that you challenge the position of that eyeball. So as soon as you lift up the head, that eyeball cannot control the movement of the head and it's gonna drop. So it's always ventral and it's always when you lift up that head.
And this is vestibular signs. Again, central or peripheral can be present on both, but when you have a problem with, with a static strabismus, your problem, as we said, it can be in the muscles, in the nerve, or you can have a retrovalb or mass. So, for example, look at this dog.
This dog has a head tail. You look at the dog, it doesn't have any stravismus, but as soon as we lift up the head, two things can happen. One is that you licit an tachmus, and then you have the ventral stravismus, and you licit anisttachmus because this dog just compensated the, the, the nystagmus, and then you challenge.
Position again of that eyeball and the nystagmus star. So if you have either a positional nystachmus or a spontaneous nystagmus doesn't tell you anything, doesn't tell you the central or peripheral only tells you that the vestibular system doesn't work and it's not nice to elicit a nystagmus when the dog has already compensated the stagmus again. So if you see a head tail.
And you see a positional strabismus, you have enough signs to tell you that that dog has a vestibular dysfunction. There is no point to put the dog upside down to try to visit a stagmus because it's not nice for a dog that is already dizzy to make them more, to make that dizziness to be even worse. But when you do this lifting out of the head, you need to put the head in a normal position.
What does it mean? Look at this dog, the same. If I lift up the head without putting the head tilt in a normal position, look, can you see the strabismus?
No, you can't. So, you need to put the head in a normal position and then lift it up. Because then is when you see that the eyeball is not really falling.
Or it's not, it, it kind of follow the head movement. Yes? So we already see all the vestibular signs, so we are already seeing why the dog or the cat can have an ataxia, and it will be the vestibular ataxia, why they lose the balance on the head tail, why they can have positional strabismus, why they have the pathological nystagmus, and you can see decreased vestibular ocular reflex.
I, as I said, Those signs are always ipsilateral to the lesion, with the exception of the paradoxical that we will see some clinical signs now. But the clinical signs, these clinical signs doesn't tell you if it's central or peripheral. If you have a pathological nystagnus that can be according to the movement either horizontal, rotatory or vertical, the three of them can be central.
And the only one that can only be seen in central is the, the, sorry, the, the 3, so vertical rotatory and, and, and horizontal can be seen in central. The only one that can be seen in peripheral is rotatory and horizontal, but do not rely on this to localise if it's central or peripheral. Because some rotatory nystagmus, they can look vertical and the other way around.
Some vertical nystagmus, they may be rotatory. So to localise if it's central or peripheral, rely on the mental status and rely on the postal reactions. So those are the most reliable ones to identify.
If you just follow the vestibular signs, they are gonna be the same. So, what happened? Put that into clinical practise.
It's very important that we know the signal. It's very important that we know the history, how did this start? It's progressing, how long is it going on?
Is it getting better or is it getting worse? Is it, is in pain? I'm sure you are very good in the history, but that's very important for us to, to give a list of differentials and in neurology, what it works very well is the The vitamin D.
So how this started, was very acute onset, but it's getting better. It's likely to be vascular. It's something that works in a waning, maybe metabolic.
It's something that has an insidious onset, but it is getting worse. It may be inflammatory, infectious, neuroplastic, nutritional. So this is very important as well to, obviously, you have to localise if it's central or peripheral, but doesn't mean that, that if it's peripheral has a better prognosis, doesn't mean that if it's central a bad prognosis.
It can be central. It can be a type of an ischemic encephalopathy like a stroke, and in a few days it's back to normal. So be careful, just say, no, it's central, it's a bad prognosis or, or it's peripheral is gonna get better.
No, that's not, that's not how it works. So, let's see some clinical cases. So we have about half an hour to see some clinical cases.
This stuff comes to your practise. So it's a 12 year old female English pointer. That had an acute onset of balance dysfunction.
So it was with the owner and overnight, she woke up in the morning and she found the dog like that. So it was non-ambulatory, so it was very difficult to assess the gay, had a pathological nystagmus with, can you see, with a fast face, can you see the fast face? So in this case, there were different things.
So we have a head tilt. A head tilt towards, towards the left. And then we had a fast phase of the, of the vestibular dysfunction towards the right.
And the dog was not able to walk. And this is a big question sometimes, and this is real life. So we have a few things that we cannot assess.
One are the postal reactions. So, it was very difficult, but one thing, I don't know if you saw that on the video, one thing that the dog did is lift up the, the, the legs. So if you see, it's like, don't even dare to put me on the floor.
So as soon as you lift it up, it's like put it all. All the legs up, so it didn't look like I have a lot of weakness on the legs. So it was more like very strong, like, don't even dare to put me on the floor.
So, what do we have in this dog? And then obviously the mental status, one thing that can happen with vestibular is that they can be very disoriented and sometimes it's difficult to say, oh, is the dog just disoriented or is the dog obtained and sometimes can see why clinically can be very difficult, but this dog had a horrible nystagmus and imagine if you have a stagmus, like everything is spinning around you. You're not gonna be bright, alert and responsive, but it didn't look very obtunded.
It, it didn't look very lethargic. It's like, I don't know where the things are. And the postal reactions is a 50 kg dog.
It's very difficult to assess, but they were, they, they appear normal. So what do we have? Did everybody localise to the left-sided vestibular dysfunction?
And the rest of the neuro exam was normal, so now the question, should I be worried? They happen very per acute onset. We don't have any signs at the moment of central involvement.
But on the other hand, we don't have any signs of, of Peripheral as well, like the facial nerve is normal. So having an otitis internal, it will be very unlikely that only the vestibular nerve is affected. So the facial is like, oh no, don't touch me.
No, it doesn't work like that. If you have a, a very bad inner ear disease, your facial and your vestibular are gonna be affected. And it doesn't look central either because again, the dog didn't have any obvious deficits and to have that degree of vestibular dysfunction, your medula longata should be severely affected, but this dog didn't have any alteration of the very optimisation of the mental status and the postal reaction on the left side.
They appear normal. So things that we need to take into account here is the age of the dog and the paraacute onset that the, the, of the clinical side. And one of the things that can happen in elderly dogs is the geriatric vestibular.
And what is the geriatric vestibular? So the geriatric vestibular, one of the hypotheses is that the, the crystals in the inner ear, suddenly, they lost the function, so they get kind of stuck and they have an acute onset of vestibular dysfunction. So in these dogs, you do an MRI and guess it's gonna be normal because the inner ear, the vestibular apparatus is microscopic.
You cannot see that in an MRI. Well, we don't see, probably in a, in a few years that, that is different, but nowadays, we cannot see it. And it will be good to rule out other things, but based on the clinic, it's very unlikely this dog has any other thing has been per per acute onset and we don't have signs of central involvement.
So, What, what we can do in this, in this case is we can tell to the owner and the owner didn't have any money, she could not afford to doing further tests. So, OK, we can wait. And if it's a geriatrical vestibular, this dog needs a lot of physiotherapy because they need to learn the balance again.
But the, the, if it's a geriatric vestibular, the dog should not get worse. And this is something that we should monitor in the next 3 to 4 days. So this is a thing, OK, if the dog is not getting worse, it's very likely it's a geriatric vestibular.
In the next 2 to 3 days, if the dog is getting worse, it's not gonna be a geriatric vestibular. And sometimes it's something that the owners are keen to wait. They say, OK, we wait.
If in a 34 days, the dog is a little bit better, then we can continue. And this dog, they don't need any steroids, they don't need any anti-inflammatories, they don't need any medication. So she agreed on wait and see.
So these dogs, the following 1 or 2 days, they remain the same. It takes weeks for this dog to get better and obviously there are dogs that need to be hospitalised if, if, if the owners cannot, cannot stand a 50 kg dogs. And this is just 12 days after presentation is when dogs start being able to, to do fewer steps and assisted and at 3 weeks, he went home, still with a little bit of head till.
And, but as I said, clinically, the most important things on this syndrome is that they happen in geriatric dogs or cats. They have an acute onset. So if it's something that you have, oh it's progressive, it has been getting worse in the last 23 days, that is not gonna be geriatric.
So geriatric is for acute onset. And they should not get worse. So if they start getting worse in the next 23 days, it's something else, OK?
So this is very important. And, and again, one of the theories, and because this dog gets better, we don't get a postmortem in these dogs and even if you get postmortem, there are not many pathologies that will look into the inner ear because they have to declassify the petrosal bone to be able To get into the inner ear. So it's not very easy to diagnose these dogs, but again, with time, and if the owner is mentally prepared that it's gonna take 3 to 45 weeks to, to, to be up and walking, some of them are keen to give that time.
They may remain with a little bit of head tail, but come on, this dog is not going to be running a marathon as far as he's happy walking around and recognising the owner, they can have a quality of life. So, another case. So this is the cutest Frenchie ever.
So it had, it's awake, 8 weeks old and presented with 3-day history of progressive balance. So it wasn't over the next, the last 3 days has been getting worse to the point that the dog is not able to stand up. I don't know if you could see, let me put that again, sorry.
So, the dog is leaning towards. The right It's not able to stand up and then when it does it has a little bit of this metria, can you see how it's lifting up the thoracic a little bit higher and then it was falling towards the right, but you can see now. Is also falling towards the left, you will see.
You see, this has some Demetria, and now you will see it was falling towards the right and now when it's trying to stand up, it's falling towards the left as well. And it's very difficult to see as well, but it has some a little tiny of head tremors and then So Pathological nystagmus which appear vertical slash rotatory sometimes as I said it's very difficult to say. So what do we have here?
We have an 8 week old Frenchy with 3 day history of progressive balance dysfunction. First question, where do we localise? Are we talking about central?
Are we talking about peripheral? If it's peripheral, we should be talking about right or left because it doesn't have a tendency to fall towards the right. And if it's peripheral, can we explain this, this metric gate?
Can we explain this fine tremors? So probably we have something central. So we're talking about the mental status again.
It looks disoriented, it's not a happy puppy. The poster reactions were normal, and it had a right side but also towards the left, but they were a little, there was also some cerebellar signs. So if you remember what we said before, there are some vestibular function in the cerebellum.
So together, we can call it a vestibular cerebellar dysfunction in this dog. And now the question, should I be? It, we need to know more about the history and questioning the owner, she said, oh yes, this dog has been on diarrhoea and and we have, we give metronidazole that, that you gave me.
So, oh really? Yeah. And even if you think they may be in the normal dose.
In puppies, they may be more sensitive or in dogs that have been a long time of metronidazole, they may be coping OK with that dose for 23 months, and suddenly those GAA receptors in the cerebellum gets blocked by the metronidazole, and this is known as metronidazole toxicity, and they can have vestibular cerebellar signs, should be worried? No, as I still the metronidazole, if this dog has a history of being on metronidazole, and this is the dog just 3 days. After stopping the metronidazole.
So, again, sometimes they can look. But they can look like not being able to walk. But if we look neuro localised and we listen to the history and we try to understand why the history could be associated with the clinical science, they don't need further investigation.
So shall we look at another one? Hopefully you're all awake. So stay with me with this one, because this one is very important and very nice, and I like it.
So this is a 2 year old female spade, domestic short hair that presented with one week history of balance dysfunction. So look at the cat, you already can see something, isn't it? So there's a little bit of right-sided head tilt.
So we see the right sided head tilt, and then when the cat starts, it's leaning a little bit towards the right. It looks a little bit quiet, but we just thought it was a very nice cat. And then the post reaction on the right are normal, but oh.
Look on the left. Absent on the thoracic, absent on the pelvic. Then when lift up the head, it has ventrolateral positional trabismus on that eye and we can see a little bit, it's not very so some nystagmus can see very slightly nystagmus, which appears rotatory.
OK, now we have to neuro localise. So what do we have here? We have a cat that is leaning towards the right.
We have a right sided head tilt. We have a right positional strabismus, has some pathological nystagmus, and pole position deficits on the left. What is your neuro localization?
You remember what we said before? If there are poor position deficits, we should be thinking about something central. So hopefully you're all with me that we localise central.
And now the question is yes, but you said that the pole position should be epsilateral. To the vestibular signs. So now it's right or left.
And always, always believe the pole position because they, they are not paradoxical poposition deficits, but they are paradoxical head tilt. So this paradoxical vestibular syndrome, so in this case has a left poposition deficit, vestibular signs, this has a left paradoxical vestibular syndrome. Why on earth this is happening?
Because look, you remember the drawing from before. So we have the vestibular system, so it's very important that we just have a quick reminder of this. So we have the floo nodular lobe, we have the caudal err peruncle.
So we have the positive, positive coming in, negative negative from the cerebellum. We have a balance, we don't fall, OK. So we have a lesion here, positive, positive, so either Inner ear of vestibular negative negative.
The vestibular signs are going to be toward the site, towards the site of the lesion, OK? Because we get negative, we don't have a positive, which is the site of less electrical activity if we compare with the contralateral, this one, yes? So we will have signs towards this one, and this is the clinical signs that we have seen before.
But now, imagine we have a lesion either in the floculo nodal lobe or in the cava era. So positive, positive, negative, 00, negative is not coming. Positive, positive.
So which is the site of less electrical activity, this one. So the vestibular signs are gonna be towards the side because the lesion is here, so it doesn't allow any vision on this one. So you have an imbalance, which is the site of less electrical activity.
So this one is paying for the party going on here. Yes? Does it make sense?
So which other pathways goes very close here? The propriceptive pathways. So you have a lesion in this area, which is the caudal era peruncle, your propriceptive pathways goes here.
So you have a dog, a cat, with proposition deficits on this side, but the vestibular signs in the contralateral side, and this is the paradoxical because you would expect the po position on this side, but no, they're here. And if you have a lesion in the cerebellum, you will not have poor position deficit, but you will have hypermetria on this side and head tilt towards the other. Yes.
Hopefully we can localise later to this one. So going back to the cat, now, what would you localise? In the left svera peronol and it's progressive, it's getting worse.
Should I be worried? I would be worried in this cat, it's a two year old cat with progressive signs intracranial. So, the owner agreed to go for further imaging.
We did haematology comprehensive biochemistry. They were pretty remarkable. So the guy went for an MRI and this is what we found.
So this is very abnormal. So these are like a, a type of a mass lesion in the area of the cerebellum and the caudal cerea peruncle. So it's here and this is before the contrast, this is after the contrast.
Again, MRI is beautiful with the pictures, MRI is Very bad giving final names. So which one are our differentials? Neoplasia, inflammatory, so pretty much the same as before starting.
We have a progressive history. If you remember the vitamin D, we have a progressive history getting worse, lateralized, so inflammatory infectious neoplastic, those are the three big because it's getting worse because it's progressive and because it's lateralized. So, But it is, we cannot do a CSF because look, this cat has a very bad herniation through the foramen magnum.
So we do, we do a CSF sorry. Oh no, you found the results. You do, you do a CSF and what is gonna happen?
We are gonna just end up in the cerebellum. And then there is increasing tracranial pressure. You do the CSF, that cat is gonna die.
So we could not get CSF, so this is what we get. And again, differentials, it's quite young to have a meningioma lymphoma we know can happen at any age. So we did an abdominal ultrasound, it was pretty remarkable.
So we discussed with the owner the possibility, although it's very, very rare to have a toxoplasma granuloma. We could do the, we could do the, the toxoplasma titles. And the other thing that we offer and I offered to the owner is to do a brain biopsy.
So it's not too risky, but obviously it's the caudal so here we have more important blood vessels. Go there, take a little sample and see what we are dealing with. So the owner didn't want to do the surgery and she preferred we take some bloods and we do the toxoplasma knowing that will be quite unlikely.
I said, look, it's very unlikely we're gonna have a granuloma because it's not very common, but she wanted to do the toxoplasma titos and, and they were very, very high. So we discussed with the owners to start eight-week course of lindamycin and reassess the cat. So this is the cat 8 weeks later.
Look at the cat. We could not touch the cat anymore. And she said, oh yeah, no, it's quite aggressive.
I forgot to say, yeah, thank you. So we could not really do much of the neuro exam, but she said that the cat was back to normal. It looked like a kitten again.
It was not losing the balance. It was walking normal, it was no leaning or falling towards the right. It didn't have any stagmus, it didn't have any ventrilateral strabismus.
So, We discussed that it was very unlikely that mass would have disappeared, but she wanted to, to follow up and see if we could do another MRI to look at the lesion. We started a tiny dosage of the steroids just because there was a lot of inflammation surrounding the granuloma. So we did repeat the MRI three months later.
Look at that. It was gone just with clindamycin. I could not believe it and I really wanted to take a biopsy because I think it was the best diagnostic test.
So this for me was a learning lesson. Even if it's very, very uncommon and has been only a couple of reports, definitely toxoplasma in cats can cause granulomas in the brain. These ones were diagnosed intracranally because they were suspected to be tumours, so went there and take a sample and retrospectively, they were diagnosed as a.
Neuroma. Nowadays there was not any paper on medical management only without surgery. So it's definitely possible.
So you want to read more about this paper, this on record case report, and it's just medical management of, of intracranial toxoplasma in a, in a, in a cat. So, you see another case. Hopefully you're not fall asleep.
So this is a 6 year old larger that presented with per acute onset of this sign. So what do we have here? We have one thing that we call a rigidity posture, and this rigidity posture in particular is known as disreblate rigidity.
So they have opistotonous, so they have increased on mental status is, is conscious. They have increased on on the all four, but the pelvic lins may be a little bit flex because of the increased tone in the gliosorus. So this posture tells you that there is a lesion in the cerebellum.
That's it. So this dog was running with the owner in the morning in the park and suddenly collapsed on the floor. She didn't have any trauma.
She didn't have anything, and suddenly presented to our hospital like that. So, it was quite disoriented. It had some dis rigidity and it had very bad as well, spontaneous stag.
So imagine if everything is spinning around you, you should be very, very dizzy. So, again, we have A lesion in the cerebellum because we have this cerebellar rigidity and we have vestibular sign. So are we thinking our central, are we thinking our peripheral?
As you said, it's likely this, this, this dog because of the cerebellum, this, this dog is having a central vestibular syndrome and coming from the cerebellum. So should I be worried? We have a per acute onset.
This though was totally, totally normal before this happened. So if we follow our vitamin D, we have a very severe presentation. And that's it because we don't know how this dog is gonna get because obviously this happened just an hour before coming to the hospital.
So it's very important to know how it's going to progress, but if this dog, it was totally normal until an hour ago and now it's so badly affected, it's very, very unlikely you have an inflammatory, it's very unlikely you have a neoplasty. It's very unlikely to have something nutritional that suddenly out of the blue showing severe neurological signs per acute onset. It didn't have any trauma.
The owner said it was just running behind me and suddenly collapsed and became like that. It was not exposed to any toxic. It's not walking and waning.
So what do we have left? Vascular, vascular, vascular. It's very likely this dog had a stroke.
So what happens when you have a stroke, in the meaning one of the, the arteries that are more common to to cause or to get obstructed in, in, in in canine are the rosal cerebral arteries. So you have a thromboembolism, you have decreased cerebral blood flow, you have an area that is ischemic, and this is the area that Probably would cause permanent damage, but that may be very small, and dogs, they don't have to play piano, they don't have to talk, they don't have to do k movements. So this may not be significant for a dog, but when this happened, they have a, a, a quite extensive penumbra.
So this is kind of known as ischemic penumbra, and this is very likely to be reversible. So who is gonna answer if this dog is gonna recover time? And then trying to see why this dog has a potential stroke, how is the blood pressure, how is the kidney, how is the liver, but they are greyhounds.
Sometimes they just have these strokes and we do a lot of tests and we don't find an underlying cause. The owner was very stressed and I can understand if you suddenly are running with your dog and becomes like that, and, and she really wanted to stop and do nothing because she could not deal with the dog like that. We say, OK, let's us 24, 48 hours.
We don't, we, we, we could not do further imaging, so she Said, I don't want to do anything. If you tell me that there is a possibility, I'm happy to wait 55 days and say, OK, that's a plan. So if these dogs get better in the next 2 to 3 days, it's very likely they may have a full recovery.
So she agreed to wait. So this is the dog the following day, and you can see already the dog much better, but look, did you see? Look at the head.
Can you see? What can you see? Has a head tilt towards the left.
And we, where did we localise in the cerebellum. So now think about the paradoxical if only affects the cerebellum. So we have a head tilt towards this side, what is gonna happen to this side?
How is it going to be the gate? Hypermetric. So this dog, when he presented, potentially had an ischemia to all the cerebellum, but now it's getting better and the problem is just mainly on the right cerebellum.
So look, it recovered. This is just 24 hours after the onset. You see a little bit of this metric now?
So, It's definitely much better. So the father that has improved so much in the next 24 hours with no treatment, just look, so, can you see this metric? What do you see?
Yeah. You see that is very this metric on that and then you have the YB stance which is characteristic for cerebellar disease. This is 48 hours after the onset.
Look at the dog much better, still some of these metric on the right, you see? Well But much better, nearly ambulatory, and then this thing it was like 4 or 5 days. Already walk it unassisted.
Look Kahim, thank you so much for giving me a few days. And then he went back to his own kena, very proud. The him And then he came back for a recheck and they only wanted to show me the dog could run again.
I could not believe it. He say, excuse me, your dog just had a stroke 4 weeks ago. But look, I mean, they can do full recovery.
Obviously, the big question here is why did it happen and, and could it happen again? Yes, could it happen again. We didn't find a, an underlying cause of the blood pressure was OK, the thyroid was OK, but clinically, this though doesn't look hypothyroid.
This though doesn't look like I have a kidney or liver disease. It could be so clinical, but the blood didn't supported that. So they need to do normal life.
I mean, it sometimes happens as well in human, you, you have a stroke, they don't find the underlying cause and it may or may not happen again. So trying to sum up everything, so, when we talk about the localization of, of the lesions, are we talking about central or are we talking about peripheral, which means are we talking about the medulla blongata, the, the, the fluon no lobe? Are are we talking about the little apparatus which is in the inner ear.
So, do we have paresis? It's possible with central, you will not have it with a peripheral. What happened with the mental status may be obtunddi.
We don't use depressed anymore. I don't like that, that word because we, we like to say obtunddi because obviously this can have some psychological interpretations, but with the inner ear, they may be disoriented and they may be quite disoriented, OK. So, sometimes it's difficult to say, oh, are they obtunded or are they really disoriented?
They may be quite alert, but if this acute onset of vestibular is alively they will be alert because they are quite dizzy. They can have some cranial nerve deficits and we know close to the number 8, we have from the 5th to the 12th. So any of them can be affected if the lesion extends cranially or the lesion extends caudally and caudally, one of the tests that you could do.
Is the gag reflex and the gag reflex is the 9 and the 10. So you have gag reflex, potentially obtained mental status, think about something potentially going in the medulla longata. Cranial nerve deficits in the inner ear, sure, the one that we said before, the facial, and depending what it is, if it is in the inner ear, we can have dry eye and dry nose if it's just before coming out.
If Its around this level, so this part of the inner ear and a little bit of the middle ear, your parasympathetic function. So your, your gland, lacrimal glands and salivary glands and nasal glands should be working OK. Horne's syndrome is rare in central, but you have some pathways of the sympathetic innervation to the eye that runs through the medullablogata, but it's very rare.
You should, the dog should be quite mentally obtained. And it's possible with, with periphera? Definitely, because the, your post-ganglionic neuron, it goes very close to the bulla around this level.
So you can have middle ear disease that also affect the inner and have vestibular and whole nerve. The stagmus. It's, it's, it's reported that vertical only happen with central, but as I say, be careful because some rotatory, sometimes it's very difficult to differentiate with, with central and peripheral can have either rotatory or or horizontal.
What happened with the differentials? Again, you've seen different cases, but you can have otitis media internal, in, in peripheral neoplasia, polyps, you can have phototoxicity, trauma, it could be idiopathic, the geriatric one that we have seen. What happened with the central?
You have seen dogs with very bad clinical signs, the, the, the French bulldog with the, with the cerebellar and the maternal toxicity, the greyhound or the larger with the potential ischemic encephalopathy. But they do well. So the fact that this a central, it doesn't mean that they have a bad prognosis, but it could be infectious, it could be inflammatory, it could be neoplastic, as we said, the metronidazole, the cat with the thiamine, bilateral vestibular in a cat, look for thiamine and it's not gonna die for extra thiamine.
So if you have any doubt, just give it, or you can have a cererovascular accident or it can be due to trauma. So, Try to sum up I'm going to the conclusions. So vestibular dysfunction is a common disorder and I'm sure you all have seen cases with vestibular dysfunction, but has many, many etiologies.
And how are we gonna narrow our etiologies based on the, on the signal man, based on the history, and based on the onset and overall how it has progressed as well. So the key to say, oh, should I be worried or no, is the neuro exam and the history and the signal, man. So we can do neuro without MRI.
I mean, you don't need it, sometimes the MRI it's true that sometimes it's necessary, but in many cases it's not necessary and sometimes we, we, we think that if we don't have an MRI they, they, they, they, we cannot do a proper neurological assessment and that's not true. And then, as I said, if you read the literature, it said that vestibular disease have a better prognosis than the CNS in general may be true, but there are some central, nervous system conditions that can resolve on the dog and the cat can go back to to normal life as the cat that you have seen with the toxoplasma granuloma and the dogs that you have seen with the, with the metronid and is ischemia. So, we just did one hour, which was perfect.
So if you have any questions, I will be more than happy to answer if I can. Elsa, that was absolutely fabulous. Your lecture was clear and concise and I'm sure you have answered many, many questions and cleared up many, many grey zones if you'll excuse the pun.
Right, we do have some questions coming through. Greg wants to know, nearly all the cases that he has seen have left-sided head tilts. Is there a reason for this or is it supposed to be just fifty-fifty?
I don't know. I can say no. I don't have a, I, I cannot find a scientific explanation for that in the meaning we see right and left.
It's, it's very interesting that you only see left, but no, definitely not the meaning there is not any anatomical predisposition to have a left sided more affected than the right. OK. Greg also wants to know why do geriatric dogs get recurrent episodes of CIVS?
What do you mean with CIVS? Come on, Greg, give us your abbreviation. He's just typed it as CIVS.
If he comes through, I'll let you know. Let's move on to the next one quickly. Is this vascular?
No, OK, well, Greg type it in now. Raquel wants to know, can the geriatric idiopathic peripheral vestibular happen more than once? And if so, is there any medication or exercise that can be done to help prevent it?
Well, there are some manoeuvres, but we don't really have enough scientific and, and if you, if you, if, if you read some human literature, it's so that there are some manoeuvres that they can do and they can, because as we said, one of the theories that is the crystals in the, in the endolympha in the inner ear, they get blocked. So there are some manoeuvres that you can do and potentially kind of alter this, this, this block and this crystal and, and then allow the fluid to go back to normal function. We think they are a little bit dangerous and we don't think they work, like there are no scientific publications that they work in dogs.
We may need further investigation on that and if they can happen again, definitely they can happen again because it's usually associated with the We don't know exactly exactly the pathophysiology, but if those crystals get stuck once, why cannot they get stuck again? And any medication to stop that, no, you, you don't have in a minute, you can, you can use some meropetan so if you want for, for, if they feel very sick and they are nauseous, but otherwise it's just a matter of time and, and allow them. To do physio and, and those dogs, for example, if they feel better on right lateral recumbency, don't try to put them on the left because they usually try to put themselves in the, in the position that they feel less dizzy.
So if sometimes say oh it's very good to change recumbency on, on vestibular dogs, and I mean you put it on the right, you turn around and they are put on the left again so. As I said, I'm not sure if I answered your question, but this is pretty much, as much as I know. Excellent.
Greg has answered the mystery for us. CIVS stands for canine idiopathic vestibular syndrome. OK, so what was the question again?
Sorry. Why do geriatric dogs get recurrences of it? Yeah, again, I think was pretty much the same question as Raquel.
So I think it's because, because, it's associated with the degeneration of, of the, of the function of the vestibular apparatus in the inner ear and, and, and again those crystals that the most stuck. So this type of, of vestibular idiopathic only happen in. Geriatrics and if it happened once, definitely can happen again, but this is not gonna happen in a dog that comes through your door and is 23 years old.
It, it should be elderly, the same with the cats, and it's because of that, because one of the theories is that there is a kind of a stack of the crystals in the endolyfa of the, of the inner ear. Raquel wants to know, what do you think of the use of vitafillin in vestibular peripheral syndrome? I'm not sure where I understand this, what the meaning.
Yeah, I know that like, to be honest, there's nothing as far as it doesn't harm, you can give it, but we don't give anything unless it's just meropitan and some if they feel nauseous. We, we, we, it's not proof nowadays that there is any other medication that proved. Definitely don't give steroids and, and, and there is no point to give even some anti-inflammatories.
Because there are dogs that they may be a little bit distressed because of, of the vestibular syndrome and they may have some gastric ulcers because of this, and then you give more medication, they may have a perforation, they may have a peritonitis for medication that potentially could not have helped for the primary disease. OK, my question. It's.
Yeah, I mean, we don't use it and and as I said, we don't have studies that, that support why we, we should use it. But as I said, if, if, if there is not anything potentially that can harm, it's not, it's not wrong giving it either, but Sometimes you're treating the owner's anxiety by giving the dog medication. That's it, but, but I don't think it's right.
I think we should treat the anxiety of the owner rather than than give medication that is not needed to the dog. Yeah, no, fair enough. Going back to your case of metronidazole, I think this is opening up a huge can of worms.
That dog was given 25 mg per kilogramme. Greg's comment here is he thought that metronidazole's normal dose was 15 milligramme per kilogramme. I've had cases which I've sent to specialists that it's come back, with 7.5 milligramme per kilogramme.
Where, where is the, the, the right answer? I know, and the problem is that sometimes if you give it that dose, I would not, I would never give more than 15 milligrammes per kg, but sometimes they are, if you look at the, even at the BSAVM manual, you can go up to 20, and the problem of those dogs, and, and we see that in puppies that we may get more, be more sensitive to, to. High dosage, but you, you can keep dogs on high dose.
Even sometimes we see dogs on 25, 30 milligrammes per kg for one month, and they may not show any clinical signs at all, and they say, well, I have used it once, I can use it again, but the other dog probably needs 2 months and they may be OK. So sometimes the one that we see, they have been 2 to 3 months on the metonite so because of chronic diarrhoea. And, and then, as I said, it may be just borderline.
So sometimes even with 20 if the dog is more sensitive, it, it may show more clinical signs, but the most important thing of this is recognising the clinical signs because if that dog is on metronidazole and it starts showing vestibular signs, even if you think they are in the, in the normal dose, it could be the cause. So, and usually it's no lateralized, so it's because it's bilateral and symmetrical, you will not have a, a, a very over your right-sided or left-sided signs. The first thing that you should do is to stop the metronidazole.
And I don't want to go through a lot of details, but one thing that you can use as well is stop the metronidazole on two days of IV diazepam, but just very tiny dose about 0.2 milligrammes per k because what the diazepam does is Kick out the metronidazole from the GAA receptors, so you have kind of a faster recovery. But, but sometimes if for whatever reason the dog cannot receive diazepa, just stopping the, the, the metronidazole and put it up on fluids in, in 34 days, you should see a much better improvement and then you already have the answer because if it's something like it's more or, or a different underlying cause and you have to stop the metronidazolele and that dog gets worse, it's not gonna be the metronidazole then.
Excellent Elsa. Folks, we have pretty much run out of time. Elsa, all that's left for me to say is the other comments that I'm sifting through here are amazing.
And if we were in an auditorium, as Anthony always likes to say, you would be hearing thunderous applause. So Mark says thank you for a great lecture. There are more and more comments here saying unbelievable that was a brilliant webinar.
I've learned so much. Say thank you, please. We are very pleased.
So everybody is joining me in saying thank you so much Elsa, and we would love to have you back on the webinar that again with your clear and concise interpretations. Thank you so much. Thank you and folks, that's it for tonight.
We will see you on the next members webinar next week. Good night and thank you to Lewis, my controller in the background.