Great, thanks very much, Caroline. So as Caroline mentioned, this presentation is looking at neurology and first opinion practise and sort of primarily focusing on what to do if you're unable to refer your patients to a centre with an MRI scanner and or a neurologist. And And in terms of how we'll go through the presentation, there's a bit of an introduction, just briefly going through your neurological exam.
And then I thought the best way to probably go forward would be to, to look at a few cases. I think we've got 6 cases, . With different neurological disorders, some are more common than others, and we'll, we'll look at each of them and try to localise their problem from a neuroanatomical point of view, try to come up with a few differential diagnoses and, and the most likely of those, what we would do in a referral setting with regards to diagnostics and treatment, but also what you might be able to do, in your own clinics from a diagnostic and treatment point of view, and then maybe go through a bit about what we'd expect prognostically, and, and then go from there.
So I guess when a lot of you saw the title of this. Webinar, what to do when you can't refer. Maybe the first thing that most of you thought when you have a neuro case, that you can't refer, maybe to try them on some prednisolone.
And, and if that works, maybe go for the next option of, of potentially you to. I'm hoping to persuade you over the next sort of 50 minutes or so, that there are potentially some other options rather than, rather than steroids. So when you have a patient present to you that you think is showing neurological signs, I guess the first and obvious question to try to answer is whether the patient is neurologically normal or abnormal.
In an emergency setting, that's normally quite obvious. Those patients that are either, you know, paralysed or seizuring or showing overt neurological signs, that's quite an easy question to answer. Those patients that are more chronic and more subtle, that can be challenging, and I think that's the first thing to, to try to ascertain.
Once you've done that and you're pretty convinced your patient is neurologically abnormal, the next step is to try to localise the problem a bit further, whether it's the brain, spinal cord or the neuromuscular system, and If it's the brain, try to ascertain whether it's the forebrain, brain stem, or cerebellum. If it's the spinal cord, if it's a, a C1, C5, C6, T2, T3, L3, or L4S3 myelopathy. And, and if you think it's a, a neuromuscular problem, potentially even trying to say whether it's a, a neuropathy, or a myopathy, or even a, a junctionopathy, but I think the, the latter of those obviously will be, be quite difficult.
And in terms of when we do our neurological exam, I tend to try to split it into two sections. You've got your hands off and, and then a minute you'll see your hands-on component. And with your hands off, I tend to have the patient either wander around the consult room, maybe go for a walk outside or walk up and down a corridor, if it's a dog and, and see what abnormalities you can see without having to, to touch them.
And normally, you can get quite a good idea of a patient's mentation, you know, if it's appropriate or inappropriate, and if it's inappropriate, whether they are. Otunded or stuporous, or in a comatose state. Often, I think as well, when you get your history of these patients, normally owners are pretty good at telling you whether they think their animal has an abnormal mentation.
And I think it's almost easier sometimes for them to, to realise slight differences compared to looking at these patients in the consult room. Obviously, as well, you'll be able to ascertain their posture. So things that you might be looking for would be either a head tilt, a head turn, maybe a low head carriage, maybe a degree of lodosis or kyphosis, or even scoliosis, and that might make you a bit more suspicious of a problem in a particular area.
And then obviously, ascertaining or looking at their gait, first question to answer is whether they're ambulatory or non-ambulatory, whether there's any ataxia, and if there's ataxia, whether it's a, a propriceptive cerebellar or vestibular ataxia. But hopefully, you can also ascertain whether these patients are heretic or even plegic, depending on whether they've got any, voluntary movement or not. And then when it comes to your hands-on component, obviously, you're checking their posture responses, and so your poor placement, but also your hopping responses.
Looking at their spinal reflexes are often in these patients, I check their withdrawal reflex and all for immbs, their patella reflexes in both pelvic limbs, and then obviously, their cutaneous trunchi reflex as well. Checking their cranial nerves, so there's lots of nerves that you can check in their, in and around their head and their face and see if you can find any abnormalities. And then finally, and this is the bit I always need to last is to see whether you can get any pain on spinal palpation.
So palpating their neck and their back and just seeing if they've got a normal range of movement of their neck as well, I think is is quite important. I just put this slide in and it's basically just a template of, of how I tend to write my neurological exam down in, in my notes, and this is obviously a patient with a normal neurological exam, but can be altered depending on what abnormalities you find. And I think it's quite useful to, to have, not only when you're discussing the case with colleagues, to have quite a nice succinct neuro exam, but also if you're doing rechecks of dogs that you think or cats that are neurological, you can compare to, to previous notes to see how things are, things are changing, obviously.
And the idea is once you've managed to localise the problem from a neur anatomical point of view, by combining that with these sort of 5 other factors, the idea is then that you can come up with quite a nice succinct list of differential diagnoses as to what could be going on with that patient. And so the obvious one obviously is signalling. So if you have a chondrodystrophic breed or breeds that are predisposed to certain neurological conditions, that might give you a, a hint towards something in particular.
But also knowing the onset of the signs, you know, with these, are these chronic? Is it acute? Is it per acute?
The progression? Are things getting worse? Are they getting better or staying relatively static?
Symmetry is quite important in, in neurology, so are the signs much worse on, on one side of the body? Obviously, if it's pain or not, so do you get any spinal palpation or does it only report that the dog seems in pain? And then combining that with your, localization, we'll try to help.
And the idea was sort of published, in the record back in 2015, and they found that by combining those different factors for each of your cases, particularly in dogs, and this sort of schematic as a dog, for dogs with, spinal cord disorders, you can then come up with relatively, specific differential diagnoses, if you're able to assign each of those factors to, to your patients, which is then really useful, because if you have a, a patient in a first opinion setting that you're Able to say he's more likely to have a disc extrusion versus SRMA versus an intrinsic myelopathy, then the options you're able to give to the owner, in terms of whether they're able to refer or not will be, be a lot better than than if you're not able to do that. So if we start with our first case, and like I say, we've got 6 of these, and we'll just go through each of them and see if we can can localise their problem to begin with. So this is Jasper.
He's an 8 year old man and cocker spaniel. He came to me with a, a 3-day history of progressive weakness in his pelvic limbs. His owner and referring vet thought he was painful, and he was placed on a, on non-steroidal, but didn't seem to respond, and progressively worsened over those preceding 3 days.
And there's no real significant history of any trauma, just that he was getting, worse with regards to, to his back legs. And so when he came to me, this was, how he presented. And so he obviously doesn't look like the happiest of spaniels, but his mentation was relatively appropriate.
He seemed quite alert. You can see his thoracic limbs are looking quite normal, but his pelvic limbs are pretty paralysed. He needs a sling to, to be supported.
You get the impression there's a little bit of movement in that right pelvicly, maybe flicking slightly forward. And so I class him as being non-ambulatory parayretic. If there was no movement there at all, then obviously we'd be saying that he was paraplegic, but I think there is a tiny bit of voluntary movement.
When we checked his poor placement and his pelvic limbs, it was pretty, pretty absent. And then, in the thoracic limbs, it was, as you would expect, quite, quite normal pool placement. When we check his his reflexes, he had an intact patella reflex, so quite a normal patella reflex in the pelvic limb.
And his his withdrawal reflex was also normal as well. And his, cranial nerves were, were quite normal, and he did have some spinal pain when you palpated along his back, and, and his reflexes and his thoracic limbs were, were obviously normal as well. And so, I guess the first question for you guys to have a little think about is where you might localise his problem.
Now, giving you sort of four options, I think it's fair to say, given his normal mentation and normal cranial nerves, that it's likely he's got, a spinal cord disorder. So, out of these four, I don't know which you think is more likely, but for me, he had a T3, L3 myelopathy. So his thoracic limbs were normal, but obviously, his pelvic limbs were paralysed, and so straight away, you think he either has a T3 L3 myelopathy or an L4S3 myelopathy, but because he had, intact reflexes, then it's most likely a T3, L3 myelopathy.
And so then if we were to put him into our, our six-finger rule category, then he's a, a cocker spaniel, slightly older cocker spaniel, with an acute, progressive, painful, relatively symmetrical T3, L3 myopathy. And so in terms of what we might think as This potential differential diagnosis. I put like a different list of neurological conditions, and, and for me, there's two of these are potential options for Jasper, and one is much more likely than the other.
And so I put some, some random options for you to choose from, whether it's a neoplastic process, a spinal fracture, an acute non-compressive physical post extrusion, a disc extrusion, SRMA or discospondylitis, or a fibrocastitis embolism. And out of all of those, For me, certainly the most, likely to would be, an interfetebral disc intrusion being way out in front. But because he's a slightly older dog, and we're just wondering if there's a possibility of it being something near plastic.
But given it was a, you know, an acute, progressive, painful, quite symmetrical, paralysis, then that would be the most likely, particularly given he is a cocker spaniel, and we know, they have a, a chondrodystrophic, breed, and so more likely to get, compressive disc extrusions. So we went ahead and did an MRI scan, and you can see on the left is a, a transverse image of of his spine. And this white or slightly hyper intense slither up here is the spinal cord, and this darker hyper intense, quite round lesion is the, the slipped disc.
On the saggitical view, you can see your spinal cord being relatively normal along here till you get to this point. This is where the disc extruded out, causing the spinal cord to be compressed dorsally before going back to to normal further quarterly. And then this, I just put in a, it's not actually just the surgery, it's a, a different dog, but this is what we tend to do from a surgical point of view to, to decompress these dogs.
So we do a hemilaminectomy to remove a, a window or bone from the vertebral column. And then you can just see left here is the periosteum covering the spinal canal. And just behind that perostem, you see the sort of dark blue, dark red material, that's haemorrhage and disc that's compressing the spinal cord.
So the next stage of that surgery is then to pierce the periosteum and then remove all the haemorrhage and the and the extruded disc material to try to get that spinal cord back to its normal position. And that's what we do in the referral setting for a dog like Jasper. But, and, and this is what we did, and you can see, this is about 2 days following his surgery.
So now, obviously, he's ambulatory without support. He's still a bit erratic and has, a mild degree of ataxia still, but certainly much improved. Still looks pretty, pretty depressed, but otherwise, seems, to be doing well.
. But obviously, the title of this talk was to, to see what you can potentially do if you weren't able to refer a dog such as Jasper, and Certainly, for a dog that you suspect has a compressive disc extrusion, particularly with the paralysis of as Jaspers, the gold standard is to have an MRI scan and and decompressive surgery, because we know that about 95% of those dogs that have a grade 1 to 4 paralysis will get back to walking following surgery. But if for whatever reason, they can't have an MRI. Decompressive surgery, then I guess it doesn't mean that you should give up on these dogs, because a good proportion will still get back to being able to walk.
It might take slightly longer, but certainly have, a relatively good chance. And we think about 60 to 80% of these dogs without, surgical decompression, will get back to being able to ambulate if they're given, given the right treatment and time. The main 4 things to do would be to obviously provide pain relief.
So often, hospitalising these dogs and starting on methadone, and then transition to buprenorphine over the coming days. I often start them on a non-steroidal, if possible, but if not, because of either gastrointestinal or, or renal issues, then paracetamol will be fine as well. And then, depending on how painful, maybe some gabapentin, in addition to, to that.
The most important thing for these dogs is for them to get really quite strict cage rests. So, often just 4 weeks of, of, of strict cage rest, certainly no stairs or, or jumping on furniture. And if they're taken out to, to go to the grass or go to the toilet, and they need it, then certainly providing sling support for, for them is, is really important.
In those dogs that are non-ambulatory, parayretic or paraplegic, then it's likely they're unable to urinate for themselves. And so either placing a catheter and making sure that they're manually expressed either once or twice a day, it's really important to make sure we're not gonna get any complications with regards to the gallbladder itself. And then, in terms of What else you can do?
I think getting a physiotherapist on board, maybe not straight away, but, after they become more comfortable and less reliant on pain relief, then certainly, physiotherapy will benefit these dogs, and then maybe even some hydrotherapy slightly further down the line. When I do hydrotherapy for dogs with compressive disc extrusions, I always suggest starting with underwater treadmill work before, before doing free swimming just to have a bit more control. And like I say, with these dogs that have a grade 1 to 4 paralysis, so that's basically all the grades where they retain.
No deception, then you've got about a 60 to 80% chance. Getting these dogs back to, back to walking. It does change quite drastically when you get a dog that loses feeling in their pelvic limbs.
And even if we have those dogs that come to our referral centre and they are deep pain negative, we often say to the owners that even with surgery, they, There's only a 50% chance of them getting back to, back to walking. And if these dogs are conservatively or medically managed, we don't know for sure, but we think about less than 10% will, will get back to walking. And so, I think if you obviously are unable to do an MRI and, and surgery, and these dogs continue to progress to, to losing feeling in their back legs, then, then obviously, it's important to, to say to the owners that the prognosis to get them.
Back to walking independently is, is much less. But if they retain no deception and stabilise, and you can get them comfortable, then there's a reasonable good chance that you'll get them, get them back to them. Right.
And then if we go on to case number 2. So this is, Kira. She's an 11 year old female neutered Labrador, and she presented to me with this acute onset of difficulty walking and stumbling.
Only reported that she looked very drunken looking. She vomited on the morning of presentation, and, and this was how she presented to us. So you can see that she is able to ambulate for herself, but is markedly attaxic.
And when we talk about dogs and cats, even that are attaxic, there's 3 different types of ataxia. So you've got your prick receptive cerebellar and vestibular ataxia. And for, for her, I'd say she's got a, a vestibular ataxia, given the way she's always drifting more towards that right-hand side and crossing over of her legs, and that wide base starts in her pelvic limbs.
She's obviously very disorientated, but her mentation was otherwise relatively appropriate, given her degree of ataxia. She was, you know, able to respond and relatively alert, but, but you can see obviously quite disorientated. And while she's got quite a severe ataxia, I wouldn't say that she is in any way potic.
There's no weakness in those limbs. It is just a, a quite a marked in coordination. And obviously, when you look at her posture from, from the front, you get the impression that she's got quite a severe head tilt with her towards the right-hand side.
You look at her cranial nerves in more detail, you see this horizontal and the stagmus with the fast face to the left. And when then we sort of elevate her head, you then get the idea that on the right hand side, you have this ventrilateral strabismus in the, in the right eye as well. But her how people reflex was intact in, in both sides.
And her, her menace response was present as well. And the rest of her cranial nerve exam was, was quite normal. She had a normal gag reflex and no other cranial nerve abnormalities.
And when we were checking poor placement with her, she had a sort of normal poor placement in all four limbs when she was being being supported. And so with a dog like that, I think it's fair to say that most people would know that she has vestibular syndrome, she has a head tilt, she's got the vestibular ataxia, she's got the nystagmus, and she has the strabismus. Two main questions we want to try and answer when we have a dog with vestibular.
Disease is which side it is? Is it, you know, left or right-sided? Given her head here was to the right, she was drifting over towards the right, and her strabismus was in the right eye.
But the nystagmus was horizontal with a fast face to the left. That's all very suggestive of a, of a right-sided vestibular syndrome. And the next question we want to try to answer is whether this is a peripheral or central vestibular disease.
And the way we try to do that, once we have those 4 obvious signs of vestibular syndrome. The 3 things to, to double check would be the poor placement, any other cranial nerve deficits, and the dog's mentation, because if you have any abnormalities in these three things, then it suggests that you have more of an essential vestibular syndrome. Whereas if all these 3 things appear normal, whilst you can't rule out essential disease, it potentially suggests that peripheral vestibular system, is the one that's affected.
There are a few exceptions to that, in that if you have a dog with Horner syndrome or facial nerve paralysis, because of the pathways and their proximity to your, vestibular nerve, then it's certainly possible that those dogs are still going to have a peripheral vestibular syndrome, potentially even more likely that they've got peripheral vestibular syndrome. And obviously, if you've got a dog with otitis externa, then maybe your index of suspicion of, peripheral vestibule disease will be slightly higher as well. Of People ask about nystagmus too.
Whether the nature of the nystagmus can indicate whether it's a peripheral versus central problem. So you can see the pug on the left has a, has a vertical nystagmus, and the stay on the right has a horizontal nystagmus. And often we say, if you've got a vertical, maybe on a rotatory nystagmus, it's more suggestive of a central problem, and that pug had a central brain stem lesion.
Whereas if you've got a horizontal nystagmus with an obvious fast phase, then that makes it more likely peripheral with the fast phase being away from the side that's, that's affected. And so for Labrador, she was obviously a geriatric patient. She had an acute, relatively static, obviously non-painful, obviously asymmetrical right-sided vestibular syndrome.
And in terms of coming up then with differential diagnoses, I guess I want you to have a little think as to what you would have on the list of possibilities as to what would be causing her, vestibular. Disease. And for a dog, like Kira, because of her age and because of the fact that there were no obvious central signs, I think this list is, is reasonable, and, and certainly, Way out in front would be acute idiopathic vestibular syndrome, primarily because of her age, primarily because it was an acute onset and relatively static in terms of its, nature.
But obviously, it's possible she has noitis media internal, and then these other three things are, are possible, but I think probably less likely. And so in terms of how we tend to work these up, obviously we would do an nooscopic examination, a full haematology and biochemistry, and then, check her thyroid function. And I would tend to do that in all cases, like Kira that present with, with her signs.
And if they all came back normal, then I would be saying to them is that I we, certainly the most likely is that she has, idiopathic vestibular syndrome. You can never be 100%. And I would always say to owners that if you wanted me to 100% rule out there being a neoplastic process going on in the brain, then certainly we could do an MRI and spinal fluid tap.
But the index of suspicion or finding a problem, in the brain would be really quite low. But that's the only way you could obviously completely rule it out. What I tend to say to, to those people is that what we can do once you've done these three things is to hospitalise the dog and see if the signs do remain static, potentially even improving.
And if they are, then it makes us less likely, needing to do an MRI and spinal fluid tap. But if the signs are staying the same, or maybe even getting worse, then that's when we might do the, the MRI scan. And so in C's case, that's what we, we diagnosed.
With idiopathic vestibular syndrome, it can affect both dogs and cats. It is more common in dogs, but occasionally we do see it in cats, and as the name suggests, normally geriatric patients. It is a diagnosis of exclusion, so we tend to do the blood work and the thyroid function.
Profile and everything else to, to rule out any other underlying conditions. You tend to see an improvement, sort of 1 to 3 weeks following the onset of signs. And whilst there's no known treatment for it, I often give these dogs either moreoppo or Daron if they're nauseous or inappetent, just to try to improve their appetite.
The other thing I always want owners is that even if we see an improvement, there is a chance that we might see a recurrence of their signs in the future. They'd be unlucky, but occasionally we see dogs get, recurrent, idiopathic vestibular syndrome. And often I say to owners as well that you would expect over the coming days and weeks for the ataxia, the strabismus and the stagmus to improve.
But if there's one of these signs that persists long term, it's normally, normally the head tilt, but otherwise, most of the signs resolve. Perfect. So these first two cases were quite sort of common cases that I'm sure many of you have seen in, in a clinical first opinion setting, and that's just an idea as to what you, obviously can do for those, .
And then for our third case, this is little Toby. He is a 10-year-old male, neutered Yorkshire terrier. And he presented with an acute onset of progressive weakness, affecting all four of his limbs.
It sort of happened about 2 or 3 days prior to coming to me, and his owners also noticed a slight change in the tone of his, of his bark. And so this is his examination. So implementation is, is relatively normal.
He's an alert and and responsive dog, but he is unable to ambulate without support. Quite a short strided gait. It's more of a poetic gait.
You can't see any obvious ataxia, but without support, you'll see that he can't really do much for himself, and, and is unable to ambulate without having a, a helping hand. But when you do support him and you check his pull placement, you can see he's got normal pull placement in all four limbs and also normal hopping as well. He, I didn't get any pain in his neck or his back, and all his cranial nerves when they were tested were, were quite normal.
And when we were checking his reflexes, you can see he has a pretty reduced, if not absent, patellar reflex. And his withdrawal reflex in his pelvic limb was also . Absence.
When we check in his front leg, he was less keen on this, but again, not a good withdrawal reflex. But he could feel his limbs, just not, he was just unable to, to withdraw them. And so we have a, a dog that is non-ambulatory tetraporetic, no obvious ataxia, and reduced reflexes in all four limbs.
And so if you were to choose where you would neuroatomically localised, again, I've given you a few options here. But for me, the most likely is a neuromuscular system disorder, primarily because if it was a, a C1, C5 myopathy or C6 T2 myopathy, his reflexes in his pelvic limb should be normal. And if it was a brain stone problem, then there's reflexes in all four limbs should be normal.
So having absent reflexes in both your thoracic and pelvic limbs, coupled with the fact you're, you've got a tetraporetic patient rather than an anottaxic patient makes it more likely a a neuromuscular problem. And when we have a dog with neuromuscular disease, when we put him into the six-finger category, obviously he's an older Yorkshire terrier with an acute, progressive, non-painful, quite symmetrical, neuromuscular disease. From that, to try to come up with a list of differential diagnoses I guess is the, the question.
And this is something that maybe is less commonly seen in practise. But certainly, for me, the most common reason I see dogs with your muscular disease would be either because of an acute idiopathic polyradicular neuritis, or because of a massenia gravis. Very, very rarely do we see dogs with botulism, and in this country, at least, tend not to see dogs with, tick-borne paralysis.
But you do sometimes see neuromuscular disease with, paraoplastic, syndromes, that's always worth considering. So in these dogs with neuromuscular disease, I guess the most important thing to realise is that there's no reason to perform an MRI scan, because we think it's the peripheral nerves, the muscles, or the junctions in between the two, the MRI scan isn't gonna tell us what or, or where the problem is. With these cases, I tend to do a full haematology and biochemistry and a thyroid function profile.
I tend to do thoracic, radiographs, looking for a neoplastic process, but also looking to see if they've got a, a megaesophagus or not. And also an abdominal ultrasound, again, just trying to rule out a tumour going. Somewhere.
I send blood for acetylcholine receptor antibodies. And in, Toby's case, you'll see that actually they were all relatively normal. So nothing on imaging, nothing on blood work, and, and a negative, acetylcholine receptor antibodies, which is the test you would do to check to see if, he had myasthenia gravis.
And for the majority of dogs, I'd probably leave it there in terms of the diagnostics that I do. If the owners wanted me to do more, or to try to be a bit more definitive with maybe we localise, then you could certainly do electrodiagnostics, and that's normally in the form of EMG and nerve conduction studies. You have to wait about 5 to 7 days before you can do electric.
Diagnostics in these dogs before you start to see the changes. And on EMG, you might see some fibrillation potentials and some positive sharp waves. In your nerve conduction studies, you might see a reduction in the conduction velocity.
If you were to do CSF in these dogs, you would see a normal cell count, but you might see a slightly elevated, protein level. And occasionally we might discuss about doing, muscle and nerve biopsies, but again, it's not gonna really probably give you a definitive answer, it's just to try to increase your index of suspicion. And so with Toy, given these results, he was certainly one that we would consider to have acute idiopathic polyradicular neuritis.
And this is typically a, a diagnosis of exclusion. Once you can rule out them having myasthenia gravis, rule out them having a, a neoplastic process, or anything else that can give, give them a neuromuscular disease, and this is probably what you're left with. Typically, it affects the pelvic climbs first before then progressing to the thoracic limbs.
The cranial nerves are normally quite normal, but it is relatively common to hear that they have a change in tone of their bark or become a bit dysphonic, . Interestingly, mega oesophagus isn't a feature of polygradi neuritis, whereas in Marsthenia gravis, commonly you do see them have megaesophagus. Again, it's important to counsel these owners that even if we get these dogs back to walking, it is possible that they might have a, have a recurrence, although again, they'd be quite unlucky.
And there's a few papers that I put on this slides, that look Get risks factors for dogs developing this condition. There's may be a predisposition for Jack Russell, terrorism and Westies to, to get polyradicular uritis, potentially a seasonal, difference, and that we might maybe see this condition more in autumn and wintertime. And there's maybe even a link with, Campylobacter.
So those dogs with polyradicular neuritis, were almost 10 times more likely to have Campylobacter cultured from their faeces compared to a control group. And also in another paper, a real risk factor for developing poly rejective neuritis was dogs that were fed raw chickens, so potentially a link with with Campylobacter. In terms of how you treat these patients, there's no real effective treatment.
There is one paper, again, I've included it on the slide, that treated these dogs with human IV immunoglobulin. And in those cases that were treated with the immunoglobulin, they tended to improve within about 28 days, versus about 75 days in those dogs that didn't receive it. So that's the only treatment.
That we know at the moment to be slightly more effective. It wasn't a statistical difference, but obviously it was trending towards that. In reality, it's very expensive and difficult to, to get, so we don't tend to treat these dogs, with it.
We just give them supportive care. Again, physiotherapy, again, bladder management, and, and time. And normally, you'd expect these dogs to have a Good prognosis.
It does take a few weeks for them to start to show an improvement. It's not, not a quick process. And, normally you would expect to see them improve in about 6 weeks' time, but occasionally, I've had dogs that it's been a few months before we get them back to, back to walking.
But I've never had a dog with polyradicular neuritis not get back to walking. Unless they progress past the tetraplegic stage to, to respiratory arrest. And I guess that's the most important part of this condition is that these dogs often start to be poetic in their pelvic climbs and then progress to their thoracic limbs.
They then become non-ambulatory tetrayretic. And potentially go on to become tetraplegic. And that's where we hope they then plateau and their signs stabilise.
Occasionally, in the severe form of the disease, these dogs will continue to progress to then have a respiratory arrest and unless you mechanically ventilate them, then then they're not gonna do. But the hope is that they will stabilise before they get to the point where they respiratory arrest. And if they do plateau at that stage of either being non-ambulatory, tetraporetic, or, or tetraplegic, and not get any worse, then giving them time and supportive care, and, and managing them, and like I said, I've never had a job, not get back to walking once they, once they get to that level.
Right. And, and like I was saying, with the dogs with polyradicular neuritis, a lot of all those diagnostics that I showed you in terms of the blood work, in terms of the thoracic and abdominal imaging, the blood work for the acetylcholine receptor antibodies can be done in a first opinion setting. Like I said, they don't need an MRI scan because we've localised them to the neuromuscular system.
If they wanted electrodiagnostics and if they wanted nerve muscle biopsy, then obviously that's different, but the majority of cases, it's probably not gonna massively change how we treat them or or what we do, it's just try to increase our index of suspicion. And so if you're able to localise to the neuromuscular system, in these dogs, then it's a lot of that you can do in a first opinion setting and and not need to, not need to refer them. So our 4th case is a dog called Mia.
She is a 3 year old female entire mastiff. And she was referred to me, the vet thought she might have some neck pain. Initially, her owner said that she had quite a high stepping, almost hypermetric gait, before she progressed to being unable to ambulate or, or walk for herself.
She was quite a healthy dog, other than a history of having chronic diarrhoea, and she was on antibiotics for that, but otherwise, no previous health concerns. And this is how she presented, so she's obviously quite a big dog, so difficult to, to lug around, but unable to ambulate it for herself and really not a great deal of of movement here at all. She obviously looks very worried, but her mentation was relatively appropriate for her.
She wasn't abunded or or stuporous. Trying to do poor placement in her was tricky, given her, her weight, and, and difficult to accurately assess. But, but you sometimes got the impression that she had a delayed poor placement.
In a minute, you'll see, particularly in the, in the pelvic climbs. I couldn't get a great withdrawal reflex in her thoracic limbs, but I'm not sure again how, how real that was. And then the pelvic limb is not, not able to, to place her.
Her poor back, but a much better withdrawal reflex in her. Pelvic limb. For me, the most significant thing with Mia's exam was actually in regard to her cranial nerves, and it was difficult to get it on, on video, but occasionally, when you were looking at her eyes, you got the impression there was some nystagmus, and it tends to be like a rotatory, almost vertical nystagmus, particularly when when you And her head.
I'm not sure, but when you, when I was examining her, you definitely got the impression there was, certainly some, some vertical nystagmus going on. But the rest of her cranial nerves were, were quite normal. She had a normal menace response, in both eyes.
And her her people reflex was also quite normal. So she's a much more tricky one to to neuroanatomically localise. Again, I've given you some, some options here, .
Like I was saying before, as soon as I see nystagmus in, in a dog, then straight away, you know, you have to have a problem affecting the vestibular system. And when we, the owners were saying about potentially her having a slightly high stepping, hypermetric gait, then you may be thinking more of like a vestibulo cerebellar disorder. And I think because she was so Unable to ambulate, you weren't really getting an idea as to how ataxic or if there was any ataxia going on.
But for me, I would have localised her to the vestibulo cerebellar centre. And once we've done that, to come up with, a good list of differential diagnoses, I again, I've given you a random list of, of different things here, MUA, metronidazole toxicity, and acute idiopathic polyrejective neuritis, a cervical disc or oplastic process. But given her history and given the nystagmus and maybe potentially the cerebellar, Disease, then for me, most likely was metronidazole toxicity.
And so as soon as you suspect that, I tend to do a full haematology and biochemistry, which in Mia's case was all quite normal. And then the next question is, how do you treat a dog with metroninazole toxicity? And again, there was a paper a few years back now.
And that again found that if you give these dogs diazepam, then then their rate of improvement is much quicker than than not giving it. And in that paper, it showed the most common. Neurological signs in dogs with me or toxicity, and, and the vertical nystagmus was highest on the list.
Then you get the cerebellar vestibular taxi, which obviously was difficult to appreciate and Mia, given the severity of her, her signs. You get this upper motor neuronparesis, which again, I think we could see quite nicely in her. This issue of being hypermetric in quarter of dogs, this rigidity in all limbs in a quarter of dogs, and then a few have intention tremors or, or a head tilt.
And to maybe treat them maybe to do some fluid therapy. And to give them Diazepam, and normally give them half a make per kg every 8 hours. You can do IV or orally, depending on how severe the dog is, and, and giving them a 3-day course, and that's what we did in Mia's case.
And this was her about 24 hours after presentation, so she'd received. Three doses of diazepam by this point, and was maintained on fluid therapy. And already you can see, obviously, much improved.
And this was 2 days later, and you can see much more willing to ambulate, much better core placement and, and reflexes in her, in her limbs. And she still wasn't 100%, but certainly, getting much better and back to normal and, and hoping to confirm our suspicion that she had, had menidazo toxicity. You just do 3 days' worth of Diazepam and supportive care, and then the majority will be back to normal.
And so we know from that paper that dogs treated with Diazepam had a, an average recovery. Of about just over a day and a half. Whereas those dogs that were just given fluids and no other treatment, it took a lot longer, just over 11 days for them to, to show a significant improvement.
And so, if you're suspicious of a dog having metrozole toxicity as the, as a cause of their neurological signs, it's certainly worth giving them their AA, and seeing if you see, see an improvement. The exact mechanism as to why merazole causes these neurological signs is still pretty unknown. There's a suspicion or a thought that it might be due to a modulation of the GABA receptors in your cerebellar and vestibular system, but again, it's, it's not, by no means definitive.
And I also put this paper in at the bottom of the slide. It's a much more recent paper, I think it was 2018 that this was published and it looked at dogs with metron toxicity and looked at how long they were treated and also their dose and you can see the median. Time was 35 days, with an average dose of about 20m per kg twice a day.
But I guess it's important to note that some dogs only had treatment for 5 days, before they developed signs, and some dogs were only on just over 10 ms per kick twice a day. And so it does appear that some dogs are more sensitive to metronidazole than others, and they don't have to be on a, a stokingly high dose to, to have neurological signs. It can be with, with relatively normal doses of metronidazole, and sometimes quite shorter.
Short number of days for treatment. But again, like I say, that's something that doesn't need an MRI scan, that's something that basically just needs a potentially haematology and biochemistry, although that is even debatable, and with time and support and, and diaspora, you might start to see, yeah. A good improvement.
Right, our 5th case is, little Royal. He is a 6 year old male, neutered spring spaniel. He came with me with an acute onset, progressive, initially spinal pain that then progressed to him becoming, weaker and more etaxic in his pelvic limbs.
He was on non-steroidals before he came to me, but again, no, significant improvements. He had a temperature, he was of about 39.9, so he was pyorexic, and his blood work was quite normal, other than a neutrophilia.
. And this was him when he came. So again, relatively normal mentation and I'd say his thoracic limbs are, are quite normal, but when you come to the pelvic limbs, he, he's paralysed, you. Get the impression there's quite good movement in that left pelvic limb occasionally I'm placing it and he's a dog that I classed as non-ambulatory paraytic.
He's got absent poor placement in in his pelvic limbs. But quite normal in his thoracic limb. And when we were checking his, his reflexes, he's got a, a good withdrawal reflex in, in his pelvic limb.
Eventually. And his patellar reflex was intact as well. And his cranial nerves were all, all quite normal.
And and it's probably not too obvious in this video, but you did get the impression that he did have some pain, in his thorac a lumbar region. And so again, similar to, I guess, the first dog in, in terms of where we localise. So because he is non-ambulatory paraytic, we know he's gonna be either a T3, L3 or L4F3 myelopathy.
And because his reflexes were intact, certainly most likely a a T3, L3 myelopathy for me. And then in terms of differential diagnosis, when we summarise his case, he's obviously a springer spaniel with an acute, progressive, painful, symmetrical T3 L3 myelopathy, which is very similar to our cocker spaniel, at the beginning of the, the webinar. The main difference for me between these two dogs is that with Raoul, he was pyreexic and had a neutrophilia.
And so straight to way, I think that slightly changes what you might have as the most likely differential diagnosis. So, again, I've given you a random selection here, and out of those, I don't know what you think is the more likely. But for me, out of all of these, it's much more likely a, a discospodylitis.
And that's primarily because of the pyrexia and the neutrophilia. And so he went ahead and had an MRI scan, and you can see on this top left image, this is a TT weighted sagittool view. So this is where our infected disc is, and you can see the end plates are sort of hyper intense, and you've got quite this bright, really irregular looking disc on a dorsal stern.
So this is where you remove your fat from your sequence. You can see the changes to the muscle either side of the disc, but again, also the disc looking quite bright and abnormal. And on our T1 weighted post-contrast, transverse images of the, the spine.
This is our spinal cord here. But this material on to the side of the spinal cord is quite enhancing, and it's likely, a progression of the infection into the canal where the spinal cord runs. So probably a degree of emyema, compressing the spinal cord.
And Tui is a dog that we diagnosed with disco spondylitis that had progressed into the spinal cord itself. The most common, bacteria that we culture from these dogs are normally Staph aureus or intermedius, or Streptococcus, sometimes brucella and E. Coli, but they're the, the four most common.
We often see this more commonly in male, large, or giant breed dogs. Very rare to see it in cats. I don't think I've ever seen, a cat with disco spondylitis, but it has been reported.
We think it's likely a hematogenous spread, so normally a urinary tract infection or an infection in their mouth or prostate that then. Tracks to their spine. Most of these dogs, to be honest, present with just spinal pain without any neurological signs, and normally able to ambulate and normally quite normal.
But with this history of spinal pain that's waxing and waning, but overall progressive, and then maybe pyrexia and and potentially a neutrophilia. But if that infection's allowed to progress, and it goes into the canal, then they'll start to show neurological signs. The most common sites affected are your T13, L1 and L7, S1 into the teal discs.
And I guess the other important thing to know about it is that the radiographic changes that we see can often lag 10 to 14 days after the onset of the infection. And in terms of the imaging that we can do, obviously, in Raul's case, we did an MRI scan, and certainly MRI is, is thought to be the most sensitive way to pick up a dog with discospondylitis. But again, if you're unable to refer a dog for an MRI, then certainly one thing you could do in a patient similar to him would be to do other forms of imaging.
And so, with radiographs, you get the changes to the vertebral implates, so you get some osteolysis, and then just to the layer adjacent to it, you get some sclerotic changes to the bone. And on a CT again, it's a bit more sensitive than your X-rays, but again, you get the impression that you get some osteolytic emblates and then adjacent sclerosis and osteo proliferation potentially. And so you might be able to diagnose a dog with discos spondylitis on, on those two imaging forms.
In terms of how we treat these dogs, we often do antibiotics. Normally you start them on a broad spectrum, so either creamoxicab or, or cephalosporin. In all these dogs, once I've diagnosed them with discospodylitis, I tend to take blood samples and urine samples to send off for culture to see if we can grow any particular bacteria, which then might change your antibiotic.
In the majority of cases, and in Royal's case, the, cultures came back negative, and so I'd keep them on these broad spectrum antibiotics for, a long time. Often providing them analgesia, normally in the form of a non-steroidal and gabapentin is enough. And then depending on how severe the neurological signs are, if there are changes to the vertebral bodies and these dogs are showing a parasis or plegia, then I often suggest strict cage rest, just to make sure we're not gonna get any significant deterioration.
The big question with these dogs is how long you keep them on antibiotics. And that really does vary, I think, between clinicians. Some do just a couple of months, and some do 10 to 12 months.
You'll see when you read about Disco, that a lot of people do follow-up imaging. So you might, ideally prefer to do maybe 3 months, 6 months. 9-month imaging of what was done initially.
So, if you did an MRI, ideally, you would do subsequent MRI scans to, to compare. But obviously, if you did radiographs or CTs, and then that would be fine to do. And you're looking to see if you see autis proliferation and sclerosis, suggesting that the infection's been cleared.
I think in reality, it's very difficult from looking at those images to know whether the infection's completely cleared. And so sometimes I don't tend to do the, the, the imaging further down the line. And tend to keep these dogs on a, a long course of antibiotics, maybe sort of 8 to 10 months, and if they're clinically doing well at that point, and stopping and and seeing how they get on.
But again, that's a, a case you could potentially do in, in your first opinion practise setting. And this is all about, I think, 2 days after starting antibiotics and, and being on pain relief, and he's much better, much better in both, pelvic limbs, now placing them and, and a little bit happier. And, and when we check his core placement in a minute, you'll see that's, that's improved as well.
But still not, not 100%, but certainly going in the, in the right direction. So again, if you can't refer those sorts of cases, but have a, a relatively strong index of suspicion that there's a discopondylitis, then certainly doing radiographs in that case is, is perfectly acceptable. If you've got access to a CT scanner, then that would be better.
And then if you've got evidence of fatebral M plate lysis, then I think your index of suspicion of disco politis will be really quite high. And then, you know, to treat them with antibiotics and pain relief and hopefully start to see them improve. Well, hopefully you've got time to do our sort of final case.
Case number 6. This is Rai. She's a 3 year old female neutered Bernese mountain dog, and she had a, a really perute onset inability to, to walk whilst out with, her owners.
And they said that she was just walking out in the fields, no obvious trauma, and then just suddenly. Collapsed and was unable to ambulate for herself. And this is how she presented.
So you can see she is non-ambulatory, and I'd say she's tetrauretic, much, much worse on that left-hand side. She's placing her paws on the right, but nothing really going on on the left side. When we check her paw placement on the, the left side, you can see it's absent, in both her pelvic and thoracic limbs.
But on the right side, actually really quite good. Her mentation for me was, was relatively appropriate. She seemed quite alert, quite responsive, and all her, she seemed to be responding well to her environment.
Let me check her cranial nerve, she had a good menace response bilaterally. I get pal people reflex. And the rest of her cranial nerve exam was was relatively no.
And when we checked reflexes, she had a a good patellar reflex in her pelvic limbs. And a, a good withdrawal reflex in, in both her pelvic limb, but also in a minute, you'll see that her reflex in her thoracic limb was normal as well. And when I checked for any spinal pain or or neck pain, she seemed quite comfortable and you can see even just here, she doesn't look like a dog that's in a bit pain.
And in terms of when you, where you localise, I've given you a few options here. A C1, C5 myopathy, a C6 T2 myopathy, a brain stem disorder, or or neuromuscular disease. For me, given that she was non-ambulatory tetrayretic, with good reflexes in all four limbs, and normal mentation and normal cranial nerves, it was most suggestive of a C1, C5 myelopathy.
And so we pop her into our six-finger rule, she's obviously a Bernese mountain dog with a pair of cut. Relatively non-progressive, quite static, non-painful, markedly lateralizing C1, C5, myelopathy. And so in terms of our of these options, I don't know what your most likely differential diagnosis is from this list.
For me, there's two that would make sense and are are way out in front, and they are a fibrocartilagous embolism or an acute non-compressive nucleus proposis extrusion. And so when we MRI Rai, you can see that this is a TT rated sagal view of a spinal cord. You have this intramodullary, linear hyperintensity that you can see on both sequences.
And the disc is normal volume, and there's no real extradural compression. And so this is most likely a, an FCE based on, on the MRI. You can never 100% rule out an ANPE, but, but given the MRI that we're seeing, most likely an FCU.
And we suspect it's the nucleus proposis of the disc. That's the source of the embolism, but to be honest, the pathophysiology is still relatively unclear. We know that miniature schnauzers are predisposed, as are young Irish wolfhounds, but it can affect, any breed.
The only thing to know is that we think of this as a non-painful condition, but occasionally you do hear reports of these dogs being a little bit uncomfortable in the 1st 24 hours. And often people Asking you, why do you get lateralization of the signs, and it's to do with the, the vasculature that supplies the, the blood, the spinal cord. And, and it's normally the, the ventral spinal artery as it branches off, normally gets the embolism and causes the, the ischemia affecting the spinal cord.
And in terms of how you treat it, it's important to have excellent nursing care. Again, bladder management, again, getting physiotherapy involved. With these dogs, you don't have to worry about sort of strictly cage resting them because it's a non-compressive lesion.
The most important thing is to start some physio, maybe even some hydrotherapy, and giving them time to hopefully start to see them improve. If they've got low motor neuron signs, symmetrical deficits, and certainly if they've got loss of nooception, and the prognosis is supposed to be worse. But the majority of these dogs will start to improve in the first two weeks following diagnosis.
And often, about 70 to 90% of these dogs will have a successful outcome and get back to walking for themselves. The only thing that I do warn owners is that there's a chance they might have some long-term face slight deficits, normally on the side that was worse to, to begin with. I met Ronnie.
She had some physiotherapy and And also some hydrotherapy and started her on the underwater treadmill. And she stayed with us for about 2 weeks, and I think this was towards the end of her 2-week stay. You can see she's, much improved.
Still, obviously, nowhere near normal, particularly that left thoracic limb is her worst, and, and it still has some slight deficits there. But she has, managed to go back to being ambulatory and, and pain-free, and, and functioning, and being able to walk quite, quite normally. And I guess the most important thing with these dogs that present with these per acute, asymmetrical, non-painful, and relatively static, if not improving.
Paralysis is that your most likely differential diagnosis is either an FCE or an ANMPE. In reality, it doesn't matter which of those it is, even on an MRI scan, you won't know for sure. But the most important thing to know is that Those are both non-surgical conditions.
The main reason we do an MRI scan is to completely rule out a, a compressive disc extrusion, but the index of suspicion of finding, that's normally quite low. So if I have people come to me that have limited funds, I often sometimes say to reserve their Money for the physio and the hydro, rather than performing an MRI scan, that might not massively change things. And so, if you have dogs presenting with these 4 signs, then, like I say, it's non-surgical.
With time and, and nursing care and physiotherapy, we'll get a good response to, to these dogs. And so, I guess to summarise, when we started, we obviously tried to, to localise our problem to the brain, spinal cord or neuromuscular system. We had a couple of dogs with brain, a few with spinal cord, and one with a very muscular condition.
I think that, I guess the big take home message is that with a lot of these conditions that we've seen. In these 6 cases, with time and supportive care, you'll start to see them improve without much intervention. If you have specific things that you can do that might improve their prognosis, but none of them required any steroid treatment, and most, like I say, we, we'll get back to normal if they're given, given the right sort of care and, and support.
I think that's pretty much it. Like I said, it was only a, a few cases and ones that you might be able to manage in your first opinion setting, and, and yeah, I think that's pretty much it. Thank you very much, Alex, that was really interesting and I hope it gives everyone who's been listening tonight some, some other ideas to, to use in practise for any of these neurology patients that are presenting to practise that are not, are not able to be referred.
So we've got a couple of questions that have come through, if anyone does have any questions, if they would like to send it through to the question and answer box at the bottom of your screen, just type it in there and then we can put them questions to Alex. So the first two that we've got, someone is asking about gabapentin for idiopathic vestibular syndrome. They've just heard about it being used, but do you have any ideas about using that?
Yeah, so I, I don't use it and . Like I say, there's no real great evidence to, to use it in these cases. Often we don't think of them as being painful, and, and I, I would be surprised if it makes a huge difference in terms of how things progress.
I think the most important thing in those dogs is because they normal, normally feel quite nauseous. I to give them either more often or a dance toron and just supportive care. But at the moment, yeah, no, nothing definitive in terms of, of what we can use to treat them.
OK, thank you. And then they were asking about disco spondylitis. What dose of the antibiotics would you use?
Would you use a normal routine doses, or would you increase them doses? I, I tend to go quite high, so with oxab, that's normally the, the antibiotic I go for start IV antibiotics, so normally 20 mix a cake every 8 hours of curmoxicab. And once I've done that for a few days and they're improving.
And then transition them to oral tablets, and then normally go down to 20 mix a cake twice a day rather than 3 times a day, and then obviously do it for quite a few months. Excellent. OK.
And then the last question so far is with fibro cartilaginous embolism, especially with Ronnie, would you advise osteoarthritis management to start directly as well? Yeah, potentially, I think when you've got such a big dog and they're placing so much weight on their other limbs, it's gonna put those. Much more strain and certainly going forward is to have a a good physiotherapist involved, not just in the short term but also long term to make sure that we're getting as good an outcome as possible, but then also keeping an eye on those other joints to see if we are getting any changes or degenerative changes to the joints that might need treating a bit more appropriately.
Absolutely. We have, I have, we have access to a physiotherapist as well, and they've been absolutely, they've just been absolutely wonderful for our, our neurology patients. So, yeah, if they, if practises are able to link him with a veterinary physiotherapist or someone around, that would be absolutely great, really helps out our patients as well.
So yeah, we've had a couple of comments saying that they've had they've really enjoyed that seminar and thank you very much. And there are lots of lots of useful, useful tips that they can take away to use in practise. So that's all the questions we've had for this evening.
So I would just like to thank Peter from the webinar that here in the background, sorting out all the the background tech technical stuff for us. And again, I'd like to thank Alex for a really interesting presentation this evening and thank you to everyone who has attended. Have a good evening.
Good night.