Good evening everybody and welcome to a Thursday night members webinar. My name is Bruce Stevenson and I have the honour and privilege to chair tonight's session. I don't think we have any new people on tonight, but usual rules, if you've got questions, just click on the Q&A box, pop them in there and we will discuss all those questions at the end.

So tonight's speaker is Alex Forward. And after graduating from Liverpool University in 2011, Alex spent two years in a mixed animal practise in Cornwall. He then completed a rotating internship at the Royal Veterinary College and a subsequent residency in neurology and neurosurgery.

He was awarded his diploma of the European College of Veterinary Neurology in 2018, before joining Davies's Veterinary Specialist. His research interests include intracranial surgery and the treatment of brain tumours in dogs. Alex, welcome to the webinar vet, and it's over to you.

Oh, that's great. Thanks very much, Bruce. So, as Bruce was saying, this webinar is, is primarily focusing on feline neurology and and I think with neurology, probably similar to to most of veterinary medicine, cats are, are quite different to to dogs and how we approach them.

And whilst I guess the fundamental principles of the the neurological exam are are similar. The thing that we often find with cats is that the list of differential diagnosis is often quite, quite different. And there are certainly conditions that we see in both dogs and cats, but normally are quite a different prevalence, and there are obviously quite a few conditions that cats get that that dogs don't, and, and it, because of that, we often see or think about different particular types of, of diseases.

And the idea behind this webinar is just to go through a few cases, . Of cats that I've seen in the past year or so, and sort of go through them in quite a systematic way in terms of their neurological exam and where we might localise and, and coming up with some differential diagnoses and then what we might do to investigate and, and treat them. And there's a few sort of questions along the way, so feel free to, to participate.

And, and if you've got any questions at the end, then obviously I'll try my best to, to answer them at that point. So before we dive into the first cases, I guess the first thing I was gonna mention was in terms of feline seizures. So often when we talk about seizures in both dogs and cats, the default neuroanatomical localization is, is the forebrain.

And there's been a few more recent papers on feline seizures, and, one recent paper sort of highlighted some risk factors, for structural epilepsy in cats. So, Particular things like if you've got a pedigree cat, or an older cat at the the seizure onsets are normally greater than 7 years old. Obviously they've got an abnormal neurological exam and slightly surprising, but if they've got it to vocalisation, so if during their seizure, they vocalise.

Then those things are probably more associated with structural epilepsy. And so if you've got one or more of those factors, you might be thinking more about potentially a neoplastic or inflammatory process that could be causing that particular cat's seizures. Different to dogs, that the neoplasia that we often see affecting cats is predominantly lymphoma or meningiomas.

They'd be certainly the most common. And when we talk about meningoencephalitis in cats, and we often think about a more of an infectious aetiology. So cats are very good at getting either.

IP or a bacterial encephalitis, or even toxoplasma. Whereas normally if I've got a meningoencephalitis in dogs, certainly the most common thing I'd be thinking about would be a noninfectious. So normally the, the autoimmune conditions such as GME or or NME or Ely.

There's a couple of other syndromes that we often think about in cats and are a bit more cat specific. So you've got feline audiogenic reflex seizures, and these are geriatric onset seizures. So normally seen in cats greater than 10 years of age, and they tend to manifest itself as myoclonic seizure activity that's stimulated by sound, that can then progress to become more generalised seizures.

And again, there's a relatively recent paper that found that with these feline audiogenic seizures, and they seem to be quite responsive to levetiracetam. And then another type of, of seizure activity that we think of as as predominantly cats rather than dogs are these feline complex partial seizures with or facial involvement, which we'll come on to in a second. And so if we dive straight into, I guess the first of our, our cases.

So, so this is Mary. She is a 3 year female neutered domestic short hair, and that had about a 3 day history of focal facial seizures with hyper salivation. And her owners reported that she's become a lot more aggressive over the preceding few days, as well as the sort of focal seizures themselves.

Her general physics exam was, was unremarkable. And this was when she came to the consultation during sort of her examination, she started to have one of these focal seizures. So you can see her head goes up and she starts to have this sort of uncontrolled motor activity of her face.

. And this hyper salivating that you can see, and you can also see that she's got sort of bilaterally midriatic pupils. And throughout that episode, if you were to call her name or try to distract her, there'd be no way you can stop that sort of episode. And then you can see as it comes to one towards an end, you can see that she starts to regain a a level of consciousness and and starts to go back to, to being relatively normal.

Now, apart from those episodes and apart from her aggression, the rest of her neurological exam was relatively unremarkable. Everything on that was, was perfectly normal. So it's just this seizure activity and the change in behaviour.

And so the first sort of polling. The question that you've got is to see if you can neuroanatomically localise Mary's problems. So you've got 4 options, either forebrain, cerebellum, brain stem, or multifocal.

So I'll see if you can see if you can answer that 1st, 1st question. So guys, you know how this works. Just simply click on the answer that best represents what you feel is correct.

It is anonymous, so, nobody's gonna know what to answer. But it really is important that you partake in these polls because it does help us or help the presenter and Alex gets a good idea of, of where he's at and where people are and what they're thinking. So, what you put in is what you get out.

So let's give us a, a, a click and choose what suits you best. I'm gonna give it another 5 seconds quickly, Alex, and then I'll close it. Right, let's end that poll and share those results.

Can you see those? Yeah, I can see those. And so, so it looks like the majority of people chose forebrain, and, and that's similar to to what I was thinking as well.

That's all based on the fact that we think this cat is having focal seizure activity. And like I was saying before, as soon as you think your patient is having a formal seizure, then the default your anatomical localization is the forebrain. Cerebellum shouldn't cause seizure activity, and neither should the brain stem.

And while you might have a multifocal neurological problem that could also involve the forebrain, for, for Mary, it was just the forebrain for, for us at the moment, at least. And then so I guess the next question is what might be our most likely differential diagnosis? And and again, you've got 4 options.

FIP, idiopathic epilepsy, feline complex partial seizures with or facial involvement, or, or a brain tumour. That could be sort of the diagnosis for, for Mary. Alright folks, thick and fast the questions tonight.

So just click on the one that you feel represents your answer as accurately as you can. And as I say, don't be shy. It is completely anonymous.

Nobody knows what you have answered. But it really is helpful that the speakers are getting feedback on the questions and especially on webinars when they're talking to themselves. This is a, a chance to give a little bit of feedback.

So we'll give you another 5 seconds or so to answer. And let's end that poll and show you what the people said. You got it?

Yeah, perfect. And and again, I, I would also agree with that in that this feline complex partial seizures that we see in these cats, they're quite characteristic in, in the nature of the the seizure activity itself. And so often they hyper salivate, often they have these uncontrolled motor movements of their, their face and their jaw, and often they hyper salivate and they have these quite symmetrically midriatic pupils.

And so yeah, no, I completely, completely agree. . In terms of what we would then do to investigate, so often I would do full blood work in these patients, so a full haematology and biochemistry and often a urinalysis, and you can see with Mary, that was all all quite normal.

And then we would go ahead and do an MRI scan. So I don't know how comfortable people are with with MRI scans, but you can see there's 4 images here. So the first one on the top left is a TT rated sagittal view of the of Mary's brain.

And when we say TT rated, it primarily means that fat and fluid is hyper intense, so quite bright, in contrast to the rest of the the scan. The top right image is again a TT weighted image, but this time a transverse view. So where the green line is, and we've transversed the brain, and that's at the level of the the hippocampus.

And then the bottom two images, we have a T1 weighted image on the left or the bottom left and a T1 weighted post contrast image on the bottom right. And there's nothing too structural going on here, but I guess the most significant finding would be the the brightness of Mary's hippocampus. You can see these sort of bilaterally TT rated hyper intense, almost sort of C shaped intensities affecting her hippocampus.

And you start to get an impression as well with the post contrast images might be a very faint level of contrast in in both those areas as well. When we have an MRI scan such as that, we'd often take a spinal fluid analysis, and that's what we did with Mary as well. And you would look at the number of cells in her CSF, but also the amount of protein.

And you can see both of those are elevated, so 27, then it should be normally be less than 5, and the protein almost 0.5 grammes per litre, and it should be almost half that amount. And it was a mixed cell leocytosis, so different types of white blood cells in her CSF.

And the other thing that we did was to take a blood sample to check to see if she had voltage-gated potassium channel antibodies, which Mary did. So she was positive for these LG one positive antibodies. And that's again significant because that's often what we associate with these feline complex partial seizures, and you'll often see this type of condition also called hippocampal necrosis in cats, and significantly, it's quite an acute onset, and it rapidly progresses to start with either focal seizures, as we saw in Mary.

But if they're left and they're not treated, they would then go on to progress to more generalised seizure activity. And the signs that we often see, as we did with Mary, would be these focal seizures, often coupled with some aggression, some hyper salivation, and this bilateral maiasis. And typically on the MRI scans, we often see this hippocampal and sometimes the perform lobe as well are hyper intense on on TT weight images and also have some, some contrast enhancement.

And this condition is something that we see in cats, but also something that we see in people and often in people you would see it's called as a limbic encephalitis. And again, it's the same sort of sort of pathophysiology and that we think it's the serum antibodies against these voltage gated potassium channel complexes that cause the signs. Again, it's often acute, and they are associated with this sort of confusion or cluster seizures, involving the facial muscles.

So you can see this lady in the bottom right, she has these focal facial seizures that affect her face, but also, her, her right arm as well. And this was the MRI scan that she had, and again, you can see this sort of hippocampal hyperintensity, that we often think are, is due to the antibodies that these people and these, these patients have. And because of the antibodies that they have, the treatment that isn't just antiepileptics.

So it's important to start these cats on antiepileptics. So often they're started on phenobarbital and plus or minus some levetiracetam. But the other thing that we always start these cats on or we often do, is immunotherapy, and that's the same for, for people as well.

And so we'd often start them on relatively high doses of steroids to suppress their immune system. And this condition was one that has been around for, for quite a few years in cats and historically always had quite a poor prognosis. And I guess the thought process is that maybe it was relatively Sort of unresponsive to treatment because not often people would immunosuppress these patients.

But more recently, as we started to add in quite high doses of steroids to these, these patients, sometimes the actual outcome can be better than we might expect. And so often I'll keep these patients in on antiepileptics and You know, relatively high doses of steroids until they're about 48 hours free of, of seizure activity before sending them home on, on both those medications. I've just put a paper in, that you can look up if you wanted to, about this in a bit more detail about how these patients respond to, to treatment.

Perfect. So, if you move on to our next case, this is Mr. Tynx.

He's a 12 year old male neutered, domestic short hair, and he had quite a vague history when he, he came to us. The the main complaint was that he had been a little bit abnormal for the owners. The first few weeks, maybe even a few months prior to coming to us, and he start to do some quite abnormal behaviours at home in that he'd become more vocal.

He started to be a bit more compulsive in the way he was walking and started to pace a bit more and, and wouldn't settle as as he might do normally. You can see when, when I was examining him, actually, from a neurological point of view, his examination was relatively, relatively unremarkable. He, he walked quite well with no obvious ataxia or paresis.

His posture reactions were all quite good. All his cranial nerves, when they were tested, were, were quite appropriate, as were his, his spinal reflexes, and he wasn't a cat that I could find any sort of pain or, or discomfort with. So, on examination, at least, a relatively normal neurological exam.

The thing that I think is important with cats, obviously with all patients, but cats in particular is, is getting quite a detailed history because they're quite good at hiding some neurological signs. And so if there's been a change in mentation or change in behaviour where they become quite compulsive, often that's something obviously that the owner will pick up on much more than we will do in our consult room. And and given his blood work was relatively unremarkable, and no one could find a, you know, an underlying reason for him to be doing those signs, .

So the next thing that we did was to to do further investigations. But based on his age, being almost 1112 year old cat with a change in sort of mentation and behaviour, and the fact that his blood work and all his other examinations were were relatively unremarkable, I just thought I'd put a quick, again, another poll to see what people might be thinking as the most likely differential for for Mr. Tins.

Right, the good news, Alex, is that they've already started voting, so that's fantastic and they are coming in quickly now, so that's really good. Folks, again, these are anonymous, so don't feel like you need to be embarrassed and no reason to sit on the fence. You'll get splinters in the place you don't want them.

So make a decision, click on an answer and let's give Alex some feedback on what we're thinking. Another 5 seconds and we will close this poll. Right, there you go.

OK, interesting. So I think it's one of those questions that obviously will divide opinion because the history is so, so vague for, for Mr. Tins.

In terms of, I guess, the differentials I gave you, obviously it could be, could be any of these things. For me, any plastic process would be quite a strong possibility given he's an older cat and showing sort of a progressive change in his, his behaviour. Idiopathic epilepsy, I wouldn't really have on my list at the moment at least, because we weren't seeing any obvious sort of seizure activity.

But certainly if he was seizuring with a normal neuro exam, then it would be something that I'd consider. And FIP and a and a metabolic encephalopathy, again, not, not always, but I might expect to find some sort of harder findings on my, on my neurological exam and, and based on my exam, like I said, there's nothing there that was too, too, too problematic, but certainly is, is always possible. So we went ahead and did an MRI scan of Mr.

Tinks, and you can see actually here quite a, quite a strong or or large abnormality. So again, this top image is a TT weighted sagittal view of, of his brain. And in the bottom two images are a T1 weighted post contrast, that's a transverse image, and this is a dorsal view.

And quite clearly, you can see this relatively focal, quite large sort of extra axial lesion, right in the the middle of his forebrain that has quite strong homogeneous contrast enhancement. And so certainly that would be causing quite a significant change or you'd expect it to cause quite a significant change in the cat's cat's mentation. And based on those MRI characteristics, and a few other things, certainly when you have an MRI scan such as that, top of your list would be a meningioma as the type of, of neoplastic process that that is going on there.

And the most sort of frequent clinical sign we see in cats with a meningioma is an augmentation. So I put again this sort of table from the paper at the bottom here. But they looked at about 121 cats that had intracranial meningioma, and certainly the most common sign that was reported was just a general behavioural change.

You do see or can see seizure activity, but it's only in sort of between 14 and 33% of cats with meningomass affecting the forebrain. And again, that's quite different to dogs and that we'd normally expect. Probably about 90 to 95% of dogs with meningiomas in their forebrain, giving them seizure activity, where in cats, it's a, it's a lot less.

Other signs we often see or or might be reported to be circling or ataxia or blindness. And the thing to know about, I guess, meningomma in cats, again, compared to dogs, is that often we think of the prognosis as being quite different. And so if we had a dog with a meningioma.

They often tend to get slightly different subtypes of meningiomas, and those can be slightly nastier. And and when we remove those surgically, they can be more difficult to completely remove because they invade the brain parenchyma a little bit more. And so often if I had a dog with a meningioma and the owners wanted me to perform surgery.

I would often be giving them an idea in terms of the prognosis of about a year, maybe 1 to 2 years in terms of how long that dog might live. Whereas in cats, we often think about it as being a much better long term survival. In that paper, the median survival time was about 37 months, but certainly you'd expect with most cats, if the meningian was Come out quite well.

And the majority wouldn't grow back, before that cat dies for another reason. Because often these are geriatric cats. They're normally about 1213 years old if you were to operate, and you'd be surprised to see those mening meningiomas come back within 345 years following surgery.

So often the prognosis is, is much better. And the actual act of performing surgery normally is quite safe. Often we only get about complications and about 5% of, of cats undergoing that sort of, of treatment.

If whatever reason they didn't want to go down the route of, of surgery, obviously there's a palliative option, so good old steroids again, and plus some an epileptics if they are showing seizure activity is certainly a possibility. And obviously, given the, the nature of what's going on, it's not wrong to, to also consider euthanasia for such patients. But for Mr.

Tins, the owners wanted us to go ahead and do surgery. So we did a transfrontal craniotomy. So we basically do a diamond shaped incision through the frontal bone to get into the sinus, where there's a very thin sort of periosteal layer covering the the forebrain.

And then normally the meningioma comes out quite, quite well. It sort of scoops out and, and normally you can get quite good, differentiation between the meningioma and the brain tissue itself. And then with Mr.

Tins at least, I replaced the, the, the bone flap, and suture it back on. You don't always have to do that, but certainly I think it, it helps to reduce any postoperative complications, if you, if you do. And this was him, the, the following day.

So you can see he recovered, you know, pretty well following the surgeries, got quite a, an impressive scar, but otherwise quite happy to, to be stroked and I was eating quite, quite soon afterwards. I often quite strict about hand feeding these patients just because of the risk of aspiration pneumonia, particularly if they have a slightly subdued mentation. But actually, he seemed quite, quite well and quite happy, following the, the surgery.

And this was a little bit later on, but you can see. I'm relatively good from a, a neurological point of view. And I saw him for recheck, I think about 2 months ago now, and that was, about 2 years following his surgery and still seemingly doing very well.

So fingers crossed he'll continue to, to keep on doing well. Right, so our third case is little Bonnie, so a much younger cat. She's only 1 year old, and she presented with some progressive ataxia, and again, a change in mentation.

She was a lot less responsive to her environment. And her owners and sort of first opinion vet were both reporting that she'd started to to lose some weight and was starting to eat a lot less than they would normally expect. And so again, this is her when she first presented, so you can see she's, ataxic, almost looks a bit like a, a vestibular ataxia, sort of drifts over towards her right hand side, and, and it might also have a, I guess a degree of, of propoceptive ataxia as well.

You can see when you're checking her paw placement, it is a bit sluggish in that she's maybe slightly slower to, to place her, her paw back to, to its normal position than I might expect in a, in a, a normal young cat. And also when you are hopping her, you just get the slight impression that, again, her, her hopping responses are slightly slower than you might normally expect for, for a cat of her age as well. But otherwise, the rest of her examination was relatively normal.

She had a bilaterally intact menace response and her vestibular ocular reflex was, was quite normal as well. And so I guess the main findings for her were this sort of reported change in mentation, so this obtundation, and this ataxia, which could be sort of vestibular or perceptive in nature, and maybe they're slightly reduced postural responses. And so based on that, another, another question for you in terms of where you might consider localising to.

So again, I've given you sort of for intracranial localizations either forebrain, cerebellum, brain stem or or multifocal to, to choose from. Thanks, Alex. I think this one is a little more tricky.

The votes are coming in a little bit slower. But still, we are getting them coming in, which is great. I'll just give it another 10 seconds or so.

Come on, folks. Right, let's close that and share it with you. There you go.

Yeah, and, and I agree it's certainly a tricky one in that, again, I think that's the nature of of cats in particular, but her signs again were quite vague and not the most obvious. Certainly, if I've got a cat where the mentation is reported to be abnormal, straight away. As soon as we think that they are tunded or or showing a worse mentation, it either has to be probably the forebrain or the brain stem in terms of where we might localise.

The cerebellum shouldn't really cause much of a change in a patient's mentation, but certainly the forebrain of the brain stem can. In terms of her ataxia, like I said, it's a little bit difficult to characterise for her, but I think either a vestibular or perceptive attacks is probably fair. Certainly you can get a vestibulotaxia, if it's the cerebellum, but, but also the, the brain stem can do that, and the brain stem can give you a proprioceptive ataxia.

And I guess the hardest finding for me as well were her posture responses in terms of her hopping and, and that back right and poor placement, which again, given all of that combined, I'd be thinking potentially more brain stem out of everything, but I admit she's a, she's a tricky one to be, to be certain for. And so, again, given her young age and given where we think that we're localising her signs too and sort of the acute nature of her signs, I've given you four options as to what you might think the the most likely differential diagnosis is. I think the key here is in her age, am I right?

Yeah, that's it. I think as soon as I get a cat that's maybe her age or or slightly older, certainly there would always be one thing that I'd be thinking about or want to rule out before I start to, to consider the others. Yeah, fantastic.

Right, the votes are coming in thick and fast this time, so I think everybody's realised that, or most people have realised what you were getting at. Another 5 seconds on this one and then I'll end the poll. There we go.

Let's share those results with you. Yeah, so again, it's relatively split. For me, I would always have FIP pretty high up for a cat of her age.

So normally we see it in younger cats and certainly can show the sorts of, of neurological signs. The others are certainly possible. Neop plastic is always possible, although it would be slightly more unusual for her age.

Toxoplasma again, is always, on the list for cats. It's, I guess, less. Common in FIP and hence why I would have FIP higher, but certainly still a possibility.

A metabolic encephalopathy, so she had a ported systemic shunt, and we might see some of the signs that we saw in her examination. It might be a bit more waxing and raining, but certainly also possible. But out of all of those, given her age and and how often we see it, I would certainly want to rule out FIP before start looking at those, those other things.

So we went ahead and did an MRI scan. So if you're getting a bit more used to the scans. So the top left again is a TT rated sagittal view.

The top right is a TT rated transverse, and then we have a flare view in the bottom left. So flare is a little bit like the TT weighted images. It sort of suppresses the fluid or the fluid hyperintensity is is removed.

And at the bottom right, we've got a TO mated post contrast view. And this is at the level of the the me and hatic aqueduct, so sort of around this sort of level based on the the sagittal. In terms of her investigation, so her blood work was relatively normal.

She did have sort of exposure to feline enter coronavirus based on her Eliza and on the MRI scan, nothing too exciting, but one thing you get the impression is that she's got this sort of generalised ventricular megaly. So you wouldn't normally expect to see such a large third ventricle in the cap, and even the median phallic aqueduct and the the general fluid in and around her brain is slightly more than you'd expect. But the hardest finding for me on her MRI scan is the change around the mess phallic aqueduct.

So you can see on the flare image. We have this white line going around it and you can see some faint contrast enhancement. You wouldn't normally expect to see either of those things in a normal cat's brain.

And so certainly that seems to be be quite abnormal. Based on that MRI and based on the signs that she was showing, we took a spinal fluid sample, a cisternal sample, and again, you can see really quite abnormal. So, normally a protein in a cat should be less than 30 milligrammes per deciliter, and hers was 703, and the cell count again, normally should be less than 5, and hers was 2000 or just over.

2000. And interestingly and quite importantly, the predominant cell type in her CSF were neutrophils. So it was a neutrophilic pleocytosis.

And so based on that MRI scan and based on that CSF analysis, I'm certainly the most likely diagnosis for her would be this feline infectious peritonitis. And that's certainly the most common infectious disease that we see affecting the central nervous system, in cats and certainly probably the most common inflammatory condition that we see affecting a cat's brain. And normally, as you probably all know already, we normally see it in cats sort of less than 3 years of age and normally from multi-cat households.

And importantly, it affects particular areas of the central nervous system more than others. So often we see the lepto meninges, and the ependyma and the choroid plexus plexuses being affected, and they're all structures that are in and around the ventricular system. So in a normal cat brain, it would be surrounded by three layers of meninges.

And you've got your dura, your ear and your arachnoid membrane, and it's those inner two layers that make up your lepto meninges, and they can certainly be much more inflamed than the, the external layer. But your ependyma, that's the layer or your cell layer that lines the ventricles, and certainly that can be inflamed, and that's what we were seeing with with his case in, in particular. As I'm sure you all know, treatment isn't great for cats with FIP.

You know, we can sometimes try some prednisone and see if that has a, has a slight response, but it's gonna certainly be be short-lived and, and so always with these patients, we give quite a, a poor prognosis. More recently, they've been looking at this new treatment, this nucleoside analogue, GS 441524. And again, I put a paper in at the bottom.

I think it was out a couple of years ago where they had, I think it was 3 cats that they started to, to treat that were all showing neurological signs secondary to, to FIP. And I think from memory with this medication, they give it once a day to these cats for 12 weeks via injection. So it's quite obviously an invasive treatment and they're kept for 12 weeks in the hospital.

But the outcomes were, were relatively good and that quite a few of these cats were still alive at the time of the, the paper, and quite a few were about being neurologically normal. . So maybe some slight hope in regards to, to treatment for FIP.

The problem with this drug is that it's very, not very widely available at all and and from what I know, super expensive and, and certainly not licenced at at the moment from, from what I know either. In terms of the only other thing to know is that there's again another recent paper by by Abby Crawford at the RVC and she just tried to, I guess, characterise the the features and the imaging characteristics of these cats that have FIP and are sharing concurrent neurological signs. And in that paper, they found that there tends to be three sort of distinct syndromes that these cats tend to present with.

So it can sometimes just be spinal, it can just present with a teeth free. L3 myelopathy, or they can just be a central vestibular syndrome signs, or there's a subset of the these cases that come with multifocal central nervous system disease. And it was also quite nice just to characterise the changes that we see on on the MRI scans.

So often you see this meningeal and ependyal contrast enhancement. You see this ventricular megaly and sometimes some syringomyelia and from magnum herniation. And again, all those cats in that paper, they found they had a high cell count, and, and a high protein with the cells being, being neutrophilic.

And this was another cat I had, I had recently, just a short, a short video, but again, you can see slightly ataxic when trying to get back into to her carry case. And this was her MRI scan. Again, just highlighting the, the quite marked ventricular mega you can sometimes see in these cats, much more than you sometimes expect based on their neurological exam.

And often with the contrast, you can see the, the, the brightness to the ependyma of those ventricles really lighting up when you, when you do the MRI scan. Right, so if you go on to case number 4, this is Ebony. She's a 4 year female neuter domestic short hair that came to me with a relatively acute onset weakness in her pelvic limbs, that by the time she got to us was also starting to, to affect her, her thoracic limbs as well.

So gen generally this inability to, to walk for herself, and which was the main reason that she was referred. Otherwise, was eating quite happily and, and no other problems reported. And so on her exam, the very short videos in terms of trying to get her to walk, but she just could not walk more than a step or two without collapsing on her front and back legs.

Every time she tries to move, she just completely collapses down and wasn't able to walk or, or run away as she should do normally. But when you check her hopping and you check her, her posture responses, given that she's unable to, to walk or to ambulate for herself, actually her, her responses are all pretty good. But significantly, when you try to assess her reflexes, so checking her with dual reflex in that thoracic limb, you can see she's not able to pull it back.

And that's the same for her pelvic limb when you try to see if she can pull her leg back by sort of pulling on it, you can see it's just too weak or she's too weak to allow that to, to happen. And that's the same on the, the right hand side as well. Again, just trying to pull on her toe, giving a little pinch, but she's just unable to, to withdraw as you might expect.

And again, similar in the right hind limb. And her patellar reflex, you can see is, is there. It's just again, a bit more reduced than you might normally expect.

And again, maybe slightly better than that back right leg, but again, maybe less than you might normally expect to see. And it's quite unusual for a cat to allow you to do those reflexes, as, as she is. And the main, I guess, way to characterise her as a patient, I think, is generally weak and that she's just too weak to move and her reflexes are weak and, and that's the main thing to to consider with her, I would say.

And so again, a little neur anatomical localization question, a little bit different this time, but whether you localise to the forebrain, C1C5 myelopathy, the brain stem, or the neuromuscular system. Mixing it up to keep it interesting, Alex. Certainly is a very interesting case to watch her, poor thing can't even take a couple of steps.

No, that's it, it's, it's, it's, it's not very nice to see, but, but interesting. Right, the votes are coming in nice and fast this time. Everybody is hanging on your every word.

Right, a couple more seconds and then we will stop this poll. And let's reveal those answers to you. OK, nice.

So yeah, I completely agree. I think certainly the most likely for, for her would be the neuromuscular system. The main thing with the neuromuscular system, when we have a condition affecting that is you often see these patients, or be a dog or a cat, being generally weak.

So generally, they're quite potic, and can just affect the pelvic limbs, but often we see it affecting all four limbs. You can see that with the C1, C5 myelopathy as well. The main difference to try to see which of those it is, is to check their reflexes.

And if you have reduced reflexes in both the back legs and the front legs, a C1, C5 myopathy wouldn't make sense. Because you should have normal reflexes in your back legs if that's the case. Whereas for the new muscular system, to have reduced reflexes in both your thoracic and and pelvic limbs is is certainly possible.

So yeah, I completely agree that the new muscular system would be my choice as well. And so based on that, and based on the fact that we localise to the neuromuscular system, we then straight away don't need to do any fancy advanced imaging. If we know that the brain and the spinal cord are are not affected, there's no point doing an MRI scan.

The question then becomes what is causing this cat's neuromuscular system to be affected. And when we talk about the neuromuscular system, we're basically thinking about three different parts. So you've got your nerves.

So if you've got a polyneuropathy affecting your peripheral nerves, if you've got a junctionopathy, so something affecting the junctions between your nerves and your muscles, or if you have a myopathy, any of those. Three things would be classed as a neuromuscular abnormality. And often what we think of in terms of neuromuscular disease is a trying to rule out any underlying systemic conditions and if it is, or we can rule those out then it hopefully will will start to improve with with time.

But certainly there's things that we want to rule out before we say that. And so often with these patients, I would do a full haematology and biochemistry, which in her case was was quite normal. I would always check in a cap such as this toxoplasma, just to be thorough and again negative as was FALV.

We did an abdominaloxone scan, and that was all quite normal. And then also did some, some chest radiographs, and nothing too much other than obviously this mass in her cranial mediastinum. And that's significant because as soon as you have a neuromuscular cat with a cranial mediastinal mass, and straight away there'd be one primary differential diagnosis that I would be thinking of, and that would be masthenia gravis.

So when I have a mass such as this and the cat, what we'll often do is try and take a sample, ultrasound guided, and that's what we did in her case, and it came back as consistent with a thymoma. And based on this as well, we sent off some blood to check for some antiastolo estrays, receptor antibodies, and and you can see these are much higher than they should be. So she had 16 animals per litre, and it should be less than 0.3.

And so then that basically confirms our suspicion that she had a a myasthenia gravis, and likely secondary to this thymoma in her cranial medialspinal area. Often in dogs with myasthenia gravis, we would see that they have a concurrent megaesophagus. I think we see it in about 80% of dogs.

But again, cats are very different in that we often don't see it in cats at all or very, very rarely, and that's primarily because they've got an increased proportion of smooth muscle in their oesophagus compared to to dogs where it's mainly or mostly skeletal muscle. And then with cats with myasthenia gravis, particularly those that don't have any underlying reason for it, then you can start certainly start them on pyosigmine and again consider some steroid treatment. In terms of myasthenia gravis in cats, there's a few nice papers that have been out in the last few years.

One of the sad things is that often we see it associated with quite a high euthanasia rates, so almost 60% of these cats will be put to sleep. The Abyssinian and Somali cats tend to have an increased incidence. These are the two on the on the right hand side.

But really interestingly, almost half of all cats with myasthenia had a thymoma. And that's why it's really important. As soon as you have a cat showing your muscular signs, and particularly that could be consistent with my senior gravis, it's always worth taking a chest radiograph because that in itself might help you even more certain about what's going on.

And if you can sample it, great, but if not, in the the index of suspicion would still be. Would still be quite high. And when you compare that to dogs, there's a paper looking at almost 1200 dogs, with myasthenia gravis, and only about 3% of those had a thymoma.

You can see it's a much higher instance in cats with this disease compared to compared to dogs. In terms of what you can do about it, it certainly it's something that you can try and surgically remove. The concern is that even once you remove it, a lot of these cats still need long term treatment and so the prognosis for it even after surgical removal, I think is still quite, quite questionable.

In the paper, referenced at the top, about 9% of these cats went into spontaneous remission after treatment. But those cats that did were those ones that didn't have a thymoma. So we do see myasthenia gravis in cats without a cranial mesinal mass.

And in those cats, you know, there's the chance of them going into spontaneous remission once they're treated, but those with a thymoma are, are, are, are less likely to, to do that and, and are prognostically a lot worse. Whereas in dogs that don't have a thymoma and have myasthenia gravis, the actual chance of remission is much higher, almost 90% of the dogs with a straightforward myasthenia gravis, you'd expect to go into remission. The problem with dogs is that about half of those will die before that point because they'll develop an aspiration pneumonia.

So if you've got a dog with myasthenia gravis, and you can get them to about 1 year post diagnosis without succumbing to aspiration pneumonia, there's a really good chance of quite a good long term prognosis. But like I say, about half of them will aspirate and then, and then often get put to sleep or, or die because of that. And in people, it's a lot more varied and again, I think it depends on the underlying reason for the massenia gravis, but it can be sort of 20 to 75% of people having clinical remission from that, from that disease.

There was a more recent paper, I think looking at about 12 cats from, from memory. And the significant thing about this paper was that these were cats with mass, you know gravis that didn't have a cranial mediasinal mass, so no evidence of a thymoma. And as soon as you take that part out of it, all these cats had a really good long term outcome, and with all of them achieving remission within about 6 months.

And, and so it's quite a good example of Knowing, if you get myasthenia gravis as your diagnosis, but it's really worth doing the chest X-rays because if you can rule in or rule out a thymoma as part of the, the condition, it really affects what you might be talking about in terms of, of prognosis, but also gives you an idea as to how likely it is that you're dealing with mysasenia gravis in the, in the first instance. The only other thing to remember with cats is that often cats that are on methimazole for hyperthyroidism, and they can get acquired myasthenia gravis because of that medication. And so that should always be a consideration as well if you have a cat presenting to you with neuromuscular signs that is also being treated for, for hyperthyroidism.

And so we started, this is one on some periodsigmine and some, some steroids as well. And this was about 2 days after treatment. So you can see starting to, to do a few steps, for herself, which is great.

The owners didn't want to put her through surgery for removal of the thymoma. So they just wanted to treat her medically and see how long, she will go for. And, and this was only a few weeks ago and so far, so good.

But, but like I say, you'd have to give her a relatively guarded prognosis based on, based on what we know so far. Fine. Right.

Well, our next case is Elena. She is a 10 year old female neutered domestic long hair that came to me with a, a really quite sudden, so per cut onset, inability to walk on her, on her back legs. There's no obvious trauma, and, and I guess, importantly, she had a bilaterally synchronous femoral pulses.

So this was her when she, she came to us. You can see, unable to ambulate for herself. Her, her thoracic limbs are, are relatively normal, and you can see a very sort of slight movement, particularly in that left pelvic climb, but nothing in the, in the right.

When you check her posture reactions, you can see her, her thoracic limbs are quite normal. But in her pelvic limb you can see absent for placement. I mean check her withdrawal reflex, you can see her reflex in that back left leg is, is good.

And again, an absent posture response in that back right leg. And you can see quite good patella reflexes as well. And so based on that, again, I've given you a few options in terms of where you might neur anatomically localise.

And I guess the key thing with her is that she is non-ambulatory parayretic, so it's just her back legs that are affected, but her reflexes in those back legs are, are intact. And so, yeah, see what you think. Right, we've got some early responders, which is really nice.

And I think this is a little bit more, a little bit more complex. So, taking a little bit longer for folks to make a decision, which is absolutely fine. We give it another 5 seconds or so and then we will end this poll for you as well.

Right, there we go and let's share those results. OK, great. So I think the majority of people said either a T3, L3 myelopathy or an L4S3 myopathy.

And I agree there would certainly be the two most likely based on the fact it's just her back legs that are affected. So straight away, you know, it's not going to be anything more cranial to T3. I guess the way to distinguish between those two would be whether she has normal reflexes or not.

And the fact that she had good withdrawal reflexes and good patellar reflexes, it means that an L4 SD monopathy would be less likely. And so I would probably say or suggest that she has a Has a T3 L3 myelopathy. And so to summarise her, she's a, a domestic long hair cat with a pair of cute, relatively non-progressive, and non-painful, lateralizing, like she was a lot better on the left back leg compared to the right, T3, L3 myelopathy.

And so based on the fact that it's per acute, non-progressive and non-painful and quite lateralizing, again, I've given you a list of, of differential diagnoses to choose from. And, and the key with this one, I think, is the, the history, and the, the way that she presented. So often in these cases that have a per onset, are lateralizing, are non-painful, I guess that'd be One or two things you'd be thinking about more than than the others.

And, and to be honest with you, out of these 5 options, I think 2 of these answers would be, would be correct. And just remember as well, the history from the beginning was that she had quite good bilaterally synchronous sort of femoral pulses as well, which makes, makes one of these less likely as well. I think we had a couple of the votes in before you said that.

It's OK, at least nobody else has voted for it after you said that. So that's always a good thing. People are listening.

This one is a little more tricky, so I'm just going to extend it a little bit longer, Alex, and just give people a, a little bit more time, . Another 5 seconds. And let's share that with you quickly.

There you go. OK, good. Yes, I think that's probably quite a fair representation.

As soon as I have a cat that comes to me that's paralysed, the one thing that I'd always, always check are the femoral pulses because that's certainly the most common reason that we see these cats coming in if they've got an aortic thrombom. She had quite good synchronous pulses. So again, that makes that very unlikely.

In terms of then what we'd be thinking would be something affecting her spinal cord itself between the T3 and L3 spinal cord segments. Any of those top three can do that. .

Often with a fibrocartilaginous embolism, or an acute non-compressive nucleus proposes extrusion, both of those would be consistent with her history in the fact that it was per acute, naturalising and non-painful and relatively static in terms of its progression. And so I think either an ANP or an FCE would certainly be top of my list. And invertebral disc extrusion is certainly possible.

I'd normally expect that to be a bit more gradual in onsets rather than para cut, maybe more acute, happening over maybe a day or two. Normally they're more painful. And I guess the significant thing to remember is that in vertebral disc extrusions in cats are a lot less common compared to dogs.

And so certainly if she was a dog, it'd be much higher up on my list, but in cats, whilst we do see it, it is a lot, lot less common, compared to these other things. And so for me, either an acute non-compressive nucleus proposes extrusion or, or a fibrocarcinoous embolism would be, would be high on the list. And so we did an MRI scan of her thorac a lumbar spine, and again, this is a TT rated sagittal view of her of her spine.

And you can see this is a spinal cord running along here. That white line above and below it is the normal fat and fluid that would normally surround the spinal cord. These are her vertebral bodies, and these are her in vertebral discs that sit.

In between the bones. And you can see here, this sort of quite focal, and relatively well demarcated hyperintensity within the spinal cord, and just above her disc here. And again, you can see that on the TT weighted transverse view.

So again, there's much brighter intensity to her spinal cord on this view. And so this MRI scan and her history would be very consistent with an acute non-compressive nucleus pulposis extrusion. We did CSF just to be thorough.

She had a slightly high cell count and a slightly neutrophilic, but again, we'd normally see that with a, a conttrusive injury to her spinal cord, and so that would be the most likely diagnosis. In terms of the MRI characteristics, we often see this quite focal hyperintensity overlying into vertebral disc, and that disc itself normally has a reduced volume. So you can see this white part of the disc, that's the nucleus pulposis, that's the fluid central part of the disc.

You can see it's quite reduced in volume compared to this disc and this disc. And that's because with our acute noncompressive nucleus propose extrusions. The fluid part of the discs, that central fluid part, shoots out, and it normally shoots up and hits the spinal cord, and it bruises the spinal cord.

But because it's still quite fluidy, it dissipates along it. So you can see maybe a tiny bit of fluid here still, but it doesn't really cause any active compression. So it's mainly in these patients.

The fluid shoots out, it hits the spinal cord, it uses it, but doesn't compress the cord at all. And that's why these conditions aren't really considered to be surgical. So you might have previously heard of this as being a high velocity, low volume disc extrusion.

And like I say, it represents this non-degenerative nuclear roposis causing the spinal cord and bruising. And in terms of how you differentiate that between an FCE, there are a few changes on the MRI scan that you can sometimes look for. But in reality, the way to definitively tell the difference is our histopathology, which we never in reality do because these patients do very well prognostically.

And the way we treat them is basically giving them lots of time, some physiotherapy, lots of excellent nursing care and, and bladder management, and they end up doing really quite well if they're given the time to, to do so. And so you can see she started some physiotherapy. This is Dai, one of our physiotherapists at at Davies's and trying everything to, to stimulate Elena to, to do a little bit more.

We tried on different slings, so this is a theraband, so slightly less support to see if that helps to to get a bit more movement in those back legs. And you can try other different types of slings to see if that, that can help as well. But the main thing is to get these patients moving and to see if we can stimulate as much movement in those back legs as possible.

. And then like I said, she had lots of, of physiotherapy, which we did while she was with us, but then also asked the owner to do whilst she was at home. But while she was with us, you could gradually see her start to improve. She got much better movement and returning in, in both those back legs, always slightly better on the left compared to the, to the right.

And you can see now with a minimal support, just a little help with her, with her tail, you can see she's moving both those back legs. Much better now than she was before. I think this was the stage that we tended to send her home, and the owner sent some videos in a few weeks later and you can see she's now ambulatory without support.

She's still a tactic and she's still poetic, but certainly I'm going in the, in the right direction. And these patients often have a very good prognosis. And so it's worth saying to people, it's worth giving them the time and the effort to To get them back to walking because the majority can do, can do very well.

The only thing I'd say to people is that there's always a chance there might be a slight defect in in one of the limbs, and that they might appear slightly weak in that limb forever, but normally they get a functional walk quite, quite easily. And again, there's a paper that was out relatively recently, and you can see that the prognosis for these cats was really quite good with about 90% returning to ambulation and all of them becoming urinary and faecal fecally continent. And so with an FCE or ANMP, often remember that these present with a para cut, so very sudden, normally asymmetrical, so normally naturalising signs that are often non-painful.

And if you give them time, often quite static if they aren't improving already. The thing to remember is that both those conditions are non-surgical and just need time and, and physio and some support to, to get back to walking. Fine.

And then I know we're a bit short on time, but this is the last case if if you're happy for me to, to continue, it's little tigger. Is that all OK? Absolutely, please go ahead.

So this is the last one. So he's he's an 11.5 year old, male neutered domestic short hair that had been in a catfight about 7 days before, before coming to us, and since then has become progressively more quiet and maybe start to have some some visual deficits.

So again, you can see him when he, when he arrived, he was quite obtunded, and quite compulsive. He wouldn't settle, and you can see circling, in this sort of clockwise direction, and that's something that the owners reported as well, this sort of persistent circling. He looks hypermetric in that left thoracic limb, but I think that's just his catheter more than, more than anything.

But you can see this persistent clockwise circling and this slightly compulsive, and obtunded behaviour. And in terms of his neurological exam, you can see his posture responses and that, that right for limb is quite normal. But on that left thoracic limb, you can start to get maybe an idea that he's maybe slightly reduced when we knuckle over his paw and that left thoracic limb.

And again, he's reasonably OK with hopping in that right thoracic limb, but on that left, not much going on there at all. And then when you check his menace responses, you can see on the right, he's got a very slight menace. He's starting to blink a little bit, but when we check on the, on the left side.

You can see there's nothing there at all, so completely absent menace response on the on the left side. So, again, another question for you, and I guess to summarise his neurological exam, his mentation was inappropriate. He was obtunded and compulsive.

He was constantly circling in a, in a clockwise direction, so always circling to the right. He had left sided partial deficits. And he had an absent left-sided menace response.

And then the rest of his exam was, was quite normal. So based on, on that, I've given you again 4 options to tone anatomically localise, to see, see what you think. Right, we've got a thick and fast boats coming in, so that's always great.

We're just going to give that another 5 seconds quickly. And then let's reveal them for you. There you go.

OK, perfect. And yeah, I, I completely agree. I would probably have the right forebrain as my, my localization as well, often a circle to the same side as the lesions, so that would be on the right hand side.

And because the pathways for the menace response and the partial responses cross over, then that would fit as well with it being. Being the right forebrain. And so, when we did further investigations, I guess, to summarise, he was an 11 year old domestic short hair that had an acute progressive, non-painful and and right sided forebrain problem.

Again, I put a list of, of differential diagnoses, but maybe we, we Quickly see what you guys think. . So I put FIP, intracranial emyema, a compressive skull fracture, or meningoencephalitis of unknown aetiology on there as your, as your options.

And I guess again, given his localization, but also significantly his history, the fact that he was in a catfight about 7 days prior to, to coming to us, and when you put those together, I guess there's one or two things that I'd be thinking more, more than the others. Right, and again, the answers are coming in thick and fast. So we'll just give it another 5 seconds and then I will end this one for you.

Right, let's share those results. There you go. Yeah, and again, I, I, I completely agree.

So I would certainly have an intracranial emymer as top of my list. You can certainly get a compressive skull fracture if you had had a a trauma to the skull that was giving you the secondary infection. Normally with a compressive skull fracture, you'd expect the signs to be maybe at the same time as the, the trauma, whereas with the Mpiema that can be a little bit delayed whilst the infection takes hold.

So certainly I agree, an intraccranial empire would be top of my list as well. And she went ahead and did the MRI scan for for Tiger. And again, you can see the TT rated sagittal and transverse images, and then a T1 rated post contrast dorsal and and transverse.

And quite clearly, most significantly on the, on the post contrast views, you can see this and really quite focal, well demarcated, quite contrast enhancing intraacts. Lesion in, in his, in his brain. Significantly, you get this sort of rim enhancement, which is quite characteristic of a, of an abscess or empyema.

And that's how you tend to differentiate it between that and and the tumour, but also you can see the tract going through the, the bone of the skull and causing the infection and also the, the changes to the muscle outside of the skull. And so based on that, certainly, I'd be thinking that he most likely has a, a, an abscess in his brain, probably secondary to his cat fights. And these owners were quite keen to go ahead and, and, and explore and to see if we can help him surgically.

And so this was a Rotro tenorial craniectomy over the parietal bone. And you can see here, just as we open the skin and the muscle, you can see the defect in the skull. You can see a few little hairs poking out from, from When the trauma and the cat might happen, and you can see the defect in the in the bone.

And what we did was to remove this segment of bone to get down towards the brain perenyma, which you can see just under the dura was full of pus and and abscess. And so often what we would do for that is to to flush it out and remove as much of the the pureent material as as possible. We often take culture from that and, and, and see if we can culture any bacteria.

It's not surprising that we often get no growth, after about 4 to 8 hours, that seems to be, often what we see in, in culture from the surgical sites in these patients. But following that surgery, we'd start them on a few different medications, so often some steroid to reduce any inflammation. Often that's worse when the bacteria dies off, so we only do it for about 2, maximum 3 days, and then quite strong antibiotic cover.

And this was him, I think about 2 days following his, his surgery. So again, it seems a bit brighter. He's sort of circling obviously quite a bit less, and quite keen for, for some food as well, which is, which is always good.

And I guess one of the questions we always have with cats that have an intracranial and secondary to to a cat by abscess is whether to manage these medically or or surgically. And in reality, you can do both. The consensus is always to try to remove as much of the abscess or or pure material as possible surgically, and because whilst they both might have a very similar short term outcome, the long term survival is much better for those cats that have surgery compared to those that that don't.

And that was sort of shown in a in a recent paper. And so if you've got one in practise that you're very suspicious of, it's certainly fine to, to treat them with antibiotics. And if they can't afford an MRI scan or they can't afford surgery, then doing a long course of antibiotics is sometimes enough to get these cats over it.

In terms of which antibiotic, it's always important to choose one that crosses the, the blood brain barrier. So I often go for, for carmoxola, and then either refloxacin or or metronidazole. .

And then in terms of glucocorticoids, again, we often find that when we start treating these patients with antibiotics and the bacteria starts to to die off and you get the bacterial cell wall lysis, that in itself can cause quite a reaction. And so often we do about 2 to 3 days of, of dexamethasone, just anti-inflammatory doses, whilst the antibiotics are taking effect and then just carry on with the antibiotics long term and we normally do a course of, of about 345 months, sometimes longer, depending on on how the patient is doing. And these are pictures you sent us a few months after his surgery he seems to be back to his, his normal self.

But that's the, that's the last case, right? I'm a bit over, over time, and it's a bit of a whirlwind going through all those cases, but hopefully it's a relatively good example of some of the, the cases that we see, that cats get in particular. And if anyone's got any questions, I'll certainly try my best to to answer them.

Alex, that was absolutely fascinating. Thank you so much for your time and I'm sure nobody minded that it ran over. Besides being incredibly jealous that you get to do brain surgery, literally, the, what's fascinating is that there is so much more that can be done for these cats and, you know, I mean, if, if, if, most cases, people, I don't think would even consider brain surgery unless they attended a fantastic webinar like you've just given to us.

So thank you so much for your time. I really appreciate it. No worries, thank you.

Folks, that's all we have time for tonight. I hope you have enjoyed this webinar half as much as I have. And, big thank you once again to Alex for his time.

Dawn has popped into the, ser the chat box, the survey monkey. When you close up tonight, you'll see it'll also pop up. Do yourself and us a favour, click on that link, and complete that survey, monkey.

This is your channel, and, it really is your way of feeding back to us, not only what you thought about tonight, but what you also want to see in the future. And I know my first thing is going to be, get Alex back again, please. So Alex, thank you once again for your time and to everybody, thank you for attending.

To my controller Dawn in the background, as always, thank you for all the help you do in the background to make it possible. And from myself, it's goodnight folks.