Hi everyone, and thanks for joining me this evening. I'm Jamie Pratton. I'm one of the medicine specialists at Lit Eine Hospital, and having spent some time over at UC Davis, during my residency, I, I got quite used to doing neurological examinations.

So today I'm gonna be talking about the equine neurological examination, going through how to do it. And sort of some, some tips and tricks on that front. And then also looking at some recent outbreaks which in reality in, in the equine world in the UK are fairly limited to herpes, but I'll mention a couple of other little ones as well, just, so they're in your head.

So, when we look at the neurological, sorry, when we talk about Fletcher, I say can do the neuro exam, what diagnostics we can be using in that examination as well. And then particularly I'm gonna to centre around EHV so we're gonna look at the clinical picture, the pathogenesis, the treatment, but significantly what happened in Valencia, in 2021 and how we can take some information from there to make sure that we do the best we can, as vets if we see these cases again. But I think I always sort of use this slide in neurologic lectures to sort of highlight that although the UK we, we have a limited number of disease processes that are going on in neurologic cases, that actually there is quite a broad spectrum of disease processes that could occur.

So sort of highlighted in red at the moment are those that I think I see more frequently than others. So Pyrexia, for example, causes significant neurologic disease, or not, but neurologic clinical symptoms. Trauma, wobbler CVM, cervical osteo osteoarthritis, we see a huge amount of that here at, the lip and we're sort of learning more and more as we do CTs all the way down to about T2 in the vast majority of cases.

EHB and then hyperaminemia, which is either via the liver or gastrointestinal. When we start to look at the slightly more unusual cases, we can talk about sleep deprivation, which, although not truly a neurologic disease, can present as so. Borreliaderi, bogdor, sorry, Lyme disease, THO melanomas in rare cases, meningitis is even rarer, and halocephalivus are the, the worms in even, even rarer cases.

We always have knocking at our door the viral encephalitides whether you know that that's West Nile virus or Borna virus or some of the other more extreme ones which might only occur when a horse is being brought back from a foreign country. We thankfully don't have EPM in the UK, but again, I've seen a few cases since I've been back, in the last 7 years, which are due to normally those horses coming from whether it's America or Argentina or, or other locations that have it. What I'm not going to talk today about is the cases in folds because I think that's a whole different conversation and needs a whole different skill set to be able to interpret the neurological examination appropriately.

So when we look at the examination of a horse for neurologic disease, there are two components to every neurologic examination, the static and the dynamic. And I think when you're first starting, you're first looking at the cranial nerve examination, it's really important to make sure that you really bunch these down into, sorry, into individual cases, into individual nerves, and then as you get more used to them, you can sort of group them into those significant areas, making your examination much, much easier and quicker. So when we look at our ocular examination, I link our optic oculomotor trocular abjucence, and I'm gonna go through all these nerves with some videos in a minute.

We then look at the facial examination, movement and sensation with the trigeminal and facial. We then look at swallowing with the glossoparyngeal vagus and hypoglossal, and then you're left with these sort of odd ones out, the olfactory vestibular cochlear and accessory. And so this has really helped me over time to sort of highlight these abnormalities.

I think if you're in America where EPM is more significant, then yes, you do need to look at each one individually on both sides to make sure you're right. So whenever you're doing any neurological examination, great to have a friend, but always do both sides yourself because you're going to menace in a different way to somebody else. You're also going to touch more aggressively or more gently depending on who you are.

So make sure that you are doing only, you are doing both sides, even if somebody then later repeats what you're doing. When we look at the eye, it's important to remember that the cranial nerve you're testing also has to have the cranial nerve coming out to lead to the blink, for example. So it's always important to remember that you are not testing just one nerve, but you're normally testing two nerves.

So when we look at the optic, you've gotta consider testing in multiple areas because you can have retinal disease that might lead to er to an abnormality, or sorry, yeah, an abnormality where just one location of the retina isn't working, therefore a slight loss of vision in that area. When you're doing this test, it's important not to touch the the eyelashes because if you do so, you're likely gonna lead to a blink, which will be testing your trigeminal rather than your optic nerve. When we look at the ocular motor, there are a couple of things that we want to be doing.

So obviously we're going to look at the PLR, so your pupillary light reflex, which is going to be the constriction of the pupil, as you shine a bright light into the eye. And it's important to note that actually sometimes, although iPhone lights are very bright, they don't actually cause all that much constriction of, of the pupil, so an appropriate light source is essential. But when you also do this, what you want to be looking for is what's called dazzle.

So this is saying, OK, I can actually see that bright light, and it is uncomfortable rather than I'm just, my body is going from the eye through the optic nerve and then coming out straight into the ocular motor via the, the, the nucleus. So what we should see is that slight blink there, which maybe not that great in this horse, but in others is, is pretty profound. Then we're going to look at how the eye moves.

So what we need to be seeing is two things. We want to look at strabismus. So when you lift that horse's head, do the eyes become more horizontal, so they stay, sorry, they stay horizontal as you bring the head up.

And also, which we'll talk about a little bit more with nystagmus, is you can do some consensual nystagmus, physiological, sorry, where you move the head left and right, and you should get that consensual response, so. The eyes should flick fast to the direction you're looking, and then slowly return the other direction, and both of those things should be happening to confirm that the trochlear, is working and the adjacent and the, are working appropriately. The abduccence is the last one to test and that's going to be the easiest ways to use pressure on the eye, and the retractor bulb should pull the eye backwards.

And as long as that's happening equally on both sides, you can be fairly happy that the abduccence is working. So this is what I meant by remembering that you're testing both nerves. So when we talk about the pupillary light reflex, we're looking at the light going inside the optic nerve, and then coming out either the synthetic chain, to dilate the virus or ocular motor cranial nerve number 3, if we're talking about constricting it.

When we're talking about the dazzle response, so my, the brain actually sort of kicking into gear and saying, OK, it's working, we're talking about 2 going into the optic, and then 7 coming out of the facial. Menace is exactly the same, and then palpebril, if you're gonna touch those eyelashes, is gonna be creating a 5, going in and 7 coming out. So just remember that the PLR, although very useful, does not confirm visual acuity.

All it tells you is that that light is going into the eye, it's going to the hillary ganglion, and then coming back out and nothing more. What about swallowing? Swallowing is one of the most slightly difficult ones to to remember all what all of the nerves do.

And I always have to remind myself, but you've got the glossoparyngeal and the hypoglossal all involved in, swallowing and also tongue movement, and then the vagus is looking at the movement of the atenoids in, the, the pharynx. In reality, the only way to definitively check these is to do a swallow tests, so just give them some food. Nothing complex, pretty simple.

You can also look, obviously with an endoscope at the movement of the larynx and the pharynx and see if there's anything else going on that might, might indicate what, what else we need to look at. So when we look at the facial examination, so we're looking at cranial nerve number 5 to start with, so the trigeminal. It's important to remember that the trigeminal not only has sensory, but it also has motor action.

So sensory, we're looking at our three branches, the maxillary, the mandibular, and the ophthalmic. So it's important to test all three, in isolation, so you're using, using your finger, nothing more complex. What's important to note is that as you touch down along the bottom of the jaw that there is an attenuation of those .

Of the response, and that's very, very normal. So if you're genuinely worried about loss of sensation along this area, you're probably going to need to do something a little bit more aggressive than your finger. The other thing to note is that I touched the inside of the nose in this video, and if you touch the inside of the ear, you're actually testing cranial nerve number 7 for sensation as long as you get past those guard heads, which is virtually impossible in a horse.

The motor to the muscle of mastication is the other big function of the trigeminal nerve, and so it's important to assess all three of the main muscle groups, so your masceters, your temporalis, and your terygoids. And so if you lift up the forelock, you should see your temporalis, have a good palpated your mastters, and I think it's important to make sure that you don't have any, temporomandibular joint osteoarthritis that might confuse, the visual, sensation of, of whether or not they're, they're equal. And then your terry boys are sitting sort of in that fossil, so only really noticeable if one of them has massively atrophied rather than than if one's a little bit odd.

When we look at cranial nerve number 7, the facial nerve, this muscle this nerve, sorry, does a lot. The main thing obviously is motor to muscles of expression. So we should, when we're looking at a face, be looking for any ear droop, any ptosis, muscle deviation, remembering that the muzzle will be dragged to the side that's working because the muscles aren't working on the affected side.

But also it does some other things, so it does salivation, it, it creates lachrymation and also tastes the proximal side of the tongue, very hard to assess in the horse. So when you do get facial nerve paralysis and you get an ulcer secondary to that, then part of it is that the eye obviously can't blink, so you, you're getting exposure, but also there's a lack of, tear film production, which is therefore going to make, the, the eye a lot drier. And what about our slightly other, cranial nerves, olfactory, difficult to test in, you know, to be definitive about it, but in reality, the easiest way is just a bit of food in one, in one hand and then not in the other and see if the horse can smell it and and go to that hand.

So that's normally pretty effective, as much as we are aware. The vestibular cochlear, I think, is one of the most interesting cranial nerves. It, it's two parts.

So there's the cochlea that's going to do hearing. And there's no good way of testing this in the UK that I'm aware of. You can do the crack test and see if they respond, but pretty crude.

You can do a brain stem auditory evoked response test, which is an electrical way of sensing if the hearing's actually there. So you put a little bud in the ear, you put sensors on the back of the head, and it will tell you if the horse is deaf or not. And that's really important or really useful in temporal higher osteoarthropathy where there's normally a unilateral deafness unilateral vestibular cochlear disease.

When we look at the vestibular signs, component of this nerve, we're often looking for a few hallmark things. So nystagmus is one of them, and often when you, what you first notice in the horse is they're gonna be blinking every time their eyes flicking. If we're talking about peripheral nystagmus, peripheral lesions, sorry, leading to nystagmus, you're gonna have the fast space running away from the lesions.

So, nice and easy to remember, it always runs away from peripheral lesions. If you're talking about a central vestibular disease, which thankfully horses don't have too often, it can be, vertical, it can be circling, or it can be horizontal, and it can be towards or away from the lesion. So, if you genuinely have a central, that's gonna really mess with your clinical interpretation.

They're also going to circle to the side of the lesion in a peripheral disease and a head tilt to that side of the disease as well. And then finally, the accessory nerve is muscles of the shoulder and neck, so really good to get the horse to stand square with their head straight and assess both the neck muscles and into the shoulder and palpate and look visually as well. The, now that we've done the static examination, which I sometimes do at the beginning or at the end of my dynamic, depending on how wound up the horse is, we move on to the dynamic examination.

And the first thing to make sure that we work out is whether or not the horse is lame at all, because any lameness is going to significantly affect our ability to diagnose, neurologic disease. And so if you're worried about it, it needs to be looked at and maybe treated before giving a definitive diagnostic, diagnosis with neurologic disease. When we first look at this, I start with a straight line walk and drop.

And what I'm looking for are things like the trunkal sway that you can see in this video with the tail really moving from left to right. You're also going to look for any obvious clear abnormalities such as, toe dragging or, or interference in the foetal falling over, pretty obvious things. If at that stage I'm concerned that the horse has er lameness rather than neurologic disease, I will go on to do some lunging both on the hard and the soft to make sure that I haven't missed anything.

Next stage is to do a straight line with a head up, and the idea behind this is that we're going to try and take away the visual ability to assess the landscape and so rely on proprioceptive neurologic signs rather than visual acuity. Now, most of the time this again doesn't cause too many problems unless you have vestibular disease in which case it can be a little bit more exciting, so, so care when doing it. Then my next stage is surface line.

I normally do this in two stages. One is I look at it on one surface, so normally on the heart, and then I normally do another one going on and off surfaces, and if you're lucky and you have a nice curb or something like that, you can do it going on and off the curb. Each one of those is assessing different things, so on the hard alone, what you're, you're doing is just a general neurologic examination, so you're looking for circumduction, you're looking for interference, toe drag, any of those things.

When you start to add the other components, so in this video you're talking about looking at the differences in the the materials. One is assessing the ability to step over that plank and whether or not they slip, they clip it or anything like that. And also if they're having some visual deficits, then sometimes they'll really struggle with the change of light to dark, so it's a good way to assess, some visual deficits.

And then if you've got a curb, it's a really good way to highlight some of the abnormalities of proprioception as well. Next is polls, and I think there are a few things to really note when you talk about polls, and how to set them up. This is sort of how I used to do them, straight line with intermittent or variable gaps between each pole, so they have to adjust their stride length.

I now do it in a far more haphazard way with, with, with theory or, or, or at least ideas behind it. So that we're trying constantly trying to change the strike length, we're also entering at different angles, so I normally have them all at sort of triangular angles, and then going in and out, turning left and right as you as you go through them. I think what's important is, note with these is, is it lame, is it neurologic disease or is it laziness?

So if this is a cult, I'm just gonna say, a breed, that likes to drag its hind limbs, can't really bother to pick them up, and it clips them with its hind limbs, then I'm not particularly worried. If on the other hand, they start to stand on the top of the poles and slip on them backwards and forwards, then we're starting to get interested. And more often than not, that sort of that clipping that we see will just be with the hind limbs rather than with the forelimbs.

So obviously with all neurological examination, there's a a a degree of interpretation, but this is one that I definitely think needs significant interpretation. The tailpo is a really useful technique, and I think what I use it for more often than not is deciding whether your horse is weak or neurologic. So when you pull that tail, I like to do it over a number of strides with good pressure, and I do it 2 or 3 times on each run.

And what you should be seeing is a with weakness, sorry, you should see that the horse will move with you very easily, but that the stride lengths will pretty much stay exactly the same because the horse's rhythm, the reception is appropriate. If on the other hand, when you do this, the stride length changes or they're stumbling or they're falling, then you can start to consider that this is more likely to be neurologic than weakness. Hills are very helpful, we don't have a particularly big one at Lib, but I think what we're looking for is a couple of things.

So on the way up, what I'm assessing is, are the feet stabbing into the surface? So particularly the fore feet, are they hidden in that ground with their toe rather than sort of being placed on them? And then as you go down the hill with the forelimbs, you're looking for that slight hover, before the foot touches the ground to imply some sort of, some degree of appropriate septic deficit.

But also quite often those hocks, if it's neurologic, again, the feet will hover maybe for a second, but if they're really weak, for example, or have a lameness, then those hocks might sink a little bit more than that you would expect. And so we, I will always watch them as they go up, this one's a bit stabby on the way up and then actually pretty good on the way down, and I'll do that a good few times as we go through the examination. This is sort of where we start to get into slightly more interesting things that I think highlight a lot of our diseases in the UK.

Tight circles are probably the best, and it's important that the horses always move forward. I'll show you some examples of, of bad turning that we did on purpose. And what we're looking for is that the horse is not pivoting on the feet, so are they spinning on that foot on the surface?

They should be crossing over. Are they interfering? Are they hitting their feet at all?

Are they toe dragging? Are they circumducting? They're the main things that we're really going to watch for.

And so I, I personally always start to think to the left so that I can always review it back in my head, and making sure they're turning hard so we can see this horse is at induction, unwilling to cross feet, interfering, you know, quite a few of the cardinal sins. What should be noted is that it's quite often important to then go down onto concrete or something like that because they will quite often slip and allow spinning of their feet if they're on a bit of gravel. Proprioceptive testing is quite difficult with horses, and I think there are a lot of different techniques out there and everybody has to have their own.

I'm not a big believer in the Hop test, I think that . It's a very unusual thing for a horse to have to do, so they're going to be a bit weird. Also, if it's truly neurologic, you're asking for, a bit of a beating in one way, shape, or another.

I also think that placing feet on top of others, is always a little bit dodgy because some horses are so well trained they'll, they'll leave their feet where they're told to until they're asked to move. So, I, I don't do that. This is sort of what I learned from Monica Alleman when I was over in America is to take a step.

Is that there's a tight circle and then stop. And what the horse should do, it should always correct its feet, so that it is pretty much ready to go, at all times. And I do that multiple times each way.

The one thing to be aware of is what is the horse thinking and looking at, because as you can see in this video, the horse is staring somewhere else and its feet are in a slightly odd position. So a little bit of, leeway in that case is sensible. Then we look at neck neck flexion, if you go to the left and the right, and it's important that the horse is not twisting the head, when it's doing this.

It should just be able to bend round and reach for the pretty much all the way to its flank. And then obviously we also do it all the way down to the ground and then up as well. The final couple of things, as I mentioned, curves are really helpful just to really highlight some abnormalities it's a really abnormal horse without any question, but they'll often interfere and hit their feet as they go up or jump in an abnormal way to get down because they can't quite work it out.

This horse is the example of bad turning this nurse was requested to do this rather than doing a bad job. And what we can see is that because the horse is not walking forward as it's taking these steps, it looks horrendously neurologic. So be aware that if the person handling the horse is not doing the job very well, your horse will come out as neurologic.

And finally, blindfolding is probably the, the one I don't do that often unless I'm truly worried about vestibular disease. It should worsen most cases of neurologic disease, even if they aren't vestibular. What I normally do is place the, obviously on a good surface, or handler having a helmet on to make sure that a hat on, sorry, to make sure that they're not going to get reduce the risk of injury.

And then I have something that can be removed very, very quickly, if the horse does start to panic. So placing the item, I normally do use in it, just because I find it easy with being able to do a loose knot, but still be able to get it off. And then ideally try and get them to walk forwards or backwards, whichever way they're gonna go.

If it's truly vestibular, even at this stage, it will have fallen over by now, so we know that this horse does not have vestibular disease. The whole point of all of this was to get to neuro localization and therefore plan on next step. The differentiation between upper motor neuron and low motor neuron is, is quite difficult in horses.

Upper is, sort of ataxia and things like that, whereas low motor neuron neuron is weakness. We do see some of those low motor neuron diseases with outflow tract problems, in the lowest cervical, region and the first thoracic vertebrae or in the hind limbs on very occasional cases. So when I get to the end of my workup, I always ask the team that's with me, is there a central lesion?

Is the horse a normal mentation? The answer's normally yes, it's fine. Is there a cranial nerve deficit?

So therefore brain stem, and if we're left with everything else, we start to get into the vertebrae. Obviously if there's forelimb and hind limb, you're probably talking about the cervical vertebrae and then you work through the thoracic lumbar lumbar and coccyal as you work further and further back. Once you have that neuro localization, we can then at least start our diagnostics more appropriately.

Neurologic grading er is quite, but there is an inherent observer difference, so even between specialists you'll have at least one grade difference between the vast majority of people. When we look at the gradings, grade 0 is normal, grade 1 is that it's only visible on repeated testing and by a trained observer, so it's quite intermittent, it's quite hard to see. Grade 2 is visible and seen by most people and consistent throughout all the different techniques.

Grade 3 is clearly visible without seeing you know there's something wrong with that horse as soon as you see it walk past. Grade 4 is that upon testing you can maybe make the horse fall if you push it hard enough, and then grade 5 is recumbent. The diagnostics, there's a lot of them, that we could be doing and some of them are more feasible than others.

So I think, you know, we can do opthalmic examination, usually the power to be of the same with the phynx. CT is hugely helpful, and I think we're using it more and more. We're doing a lot of myelograms, we're doing a lot of, intravenous, contrast studies for masses, now, so we, we are using it to its full potential, I think, at the moment.

MRI would be wonderful, but it's very difficult. The RBC currently at this moment aren't doing it and 3 counts I think are, but trying to ship courses there is always difficult from where we are. Blood work is also very important, and then you can do the others, radiography, CSF sampling, muscle biopsies, it all depends on on the case.

Even in some cases you could do electrodiagnostic examinations, so EMG and EEG, although I'm unaware of anyone in the UK able to do those things. The ophthalmic examination is, is very important. I, I'm adding this beyond just the normal PLR and, and dazzle and menace because I think it's important to highlight a few more points.

So sorry for the picture of the cat, but trying to get a picture of Anna Siroria, in a horse when the eyes are on different sides, the head is surprisingly difficult. But Annasioria can give you a lot of information, whether it is just a local lesion or whether it's more central, where you've got sort of the dilation of one eye and constriction of the other. What's really important though is to work out which is the abnormal eye.

I know that sounds silly. This cat might be a bit more obvious, but in horses it can be difficult. So moving them from light to dark is really important.

Do they dilate appropriately, do they constrict appropriately? Which one is the abnormal one? As I mentioned, always look for strabismus, so does when you lift the horse's head, does it level out?

Antosis can give you a good idea of cranial nerve 7, but also it can give you pain, for example. Is there a protruding mixitating membrane that might lead you down the tetanus route? And although glaucoma, this sort of picture of the house stria is a bit of an unusual one, I've had some weird horses present with glaucoma that they're so painful they can appear neurologic, so hence why I've included that in there.

And then obviously the statements which you mentioned. Pouch endoscopy is pretty important to the examination because there are lots of diseases that can affect the guttural pouch, strangles, for example, strep zoo epidemius, fungal plaques, tympani in the foal, and then THO, that bottom picture as well, where you get that sort of knobbly appearance to the style of hyoid leading to tile hyoid osteoarthropathy and all the clinical signs there. It's very easy to perform obviously, and actually the vast majority of neurologic courses will allow it surprisingly well, .

So yeah, it's, it's to me it's an integral part of a neurological examination where there's any cranial nerve deficits, particularly of either the hypoglossal glossopharyngeal, cranial nerve eight, or even the vagus cos they all run very close by. People's spinal fluid, really important obviously in BPM and things like that where there is a disease process or if you think there's neuroborreliosis, but often in the UK it's not all that integral in the, in the majority of cases. What should be noted is that if you do suspect something like EPM that you look at the different sites.

So atlanto-occipital versus lumbosacral, we know that the cell population can differ surprisingly, by a large amount, even though that's all in one horse. AO does require general anaesthesia, but nowadays we are doing standing C1, C2 ultrasound guided approach, but it is definitely a bit of a. A stressful one, when you're not used to it because you are scanning and sticking a needle right next to the spinal column in an away course.

Both that and LS, obviously I say outstanding procedures. I think it's really important when you talk about these that you talk about how to do them from the point of view of excellent sedation is required. If you don't have that, you're risking both the horse and the handlers.

I pretty much always use those switches just a way to control, a little bit of that excitement if, if you are going through, or when you are going through Madura. Always be aware of the risk of kicking and rearing, so making sure that all handlers are to the side and never behind the horse, and ideally this should always be done in stocks, for, for the safety of everyone, but that's not always possible in a truly neurological course. The CT has become a main thing of our diagnostics here at Lippoke Hospital in neurologic cases, partly because it's quick, it's for a head thing disease, it's very easy, it's standing, and doesn't really is, is, is very quick and easy.

For a neurologic case where we're talking about cervical vertebrae, then we're gonna be doing a general anaesthesia, and normally we start with a plain film, and we only do that if there's no neurologic disease, so if there's a pain-related disease. And then we always do a contrast, myelogram if any neurologic signs are present. And we're now reaching T2 on a regular basis, so we're getting a really good overview of the whole of the, the whole of the cervical spine down to the thoracic.

And it is absolutely excellent imaging and, and pretty well tolerated. We've had a couple of horses have seizures post-myelogram, and due to the contrast, we've now altered our technique, and that's meant we haven't had one, for a very long time, which is, is fantastic. And I think it's important to look for the sort of the slightly weird and wonderful fractures in odd locations.

We've had melanomas sitting behind the guttural pouch that all need to neurologic signs, so well worth doing if we're wondering about it. So we go back to this drawing, and for today, we really are gonna only focus on a couple of things, EHB and a couple of others at at the end. PHD, so we're gonna discuss a typical time, how to diagnose, what the treatment options are, the biosecurity is essential.

I don't think there's much more to say than that, and what happens in Valencia. So a lot of the information from Valencia, I've, I've kindly sort of listened to other lectures. I, I wasn't involved, so I've just taken their information.

So the clinical presentation, it's very difficult for the majority of cases, so we're seeing respiratory signs. It's the early phase, with a pyrexia, we also see late term abortions, neonatal foal death, choorectinopathy, and the most significant that we always worry about is EHM, equine, herpes, myeoencephalopathy. And when we look at the neurologic sign specifically over EHM, we start to look at ataxia, paresis, urinary incontinence, again, fever, and normally it's affecting multiple horses throughout that yard rather than just an individual horse.

It is a highly transmissible disease, with a high morbidity, so morbidity is normally around 40%, and then if we're talking about EHM we're talking about a mortality of about 40, sorry, morbidity 80%, mortality 40%. We have an unknown level of latent carriers, but it's thought to be about 80 to 90% of the population carry EHP1, so it's very much out there. And we don't know what the risk of recrudescence is or why exactly it happens, although we are trying to study that network at the moment.

So what are the risk factors for EHM that we do know? So from a couple of studies a little while ago, we know that horses over the age of 20 are more likely to get EHM if infected with EHV. It's most likely seen in autumn, winter and spring, whether that's due to the airspace that these horses are sharing, rather than it being a truly seasonal thing.

The higher the temperature, the more likely they are to get EHM. Whether there was a new horse in the herd recently, and females were greater than males, to have EHM. All of that information is from the Hennier paper in 2007.

And the potential risk factors, stress that might cause recrudescence, the immune status is of the horse, suppressed in any way. So they're, they're sort of the things that we worry about, and whether or not these horses are going to be pushed over that boundary and into EHM is a very difficult thing to understand or know, and hopefully their immune status will, will try and reduce that risk. So, how does it cause EHM?

How does EHV cause EHM? So primarily the virus rapidly enters the respiratory epithelial cells and is trafficked through the submcules submucosal tissues by directing cell transfer to monocytes and lymphocytes, which leads to this secondary monocyte infection. These cells then move and spread through the body, invading local blood vessels and respiratory tract lymph nodes within 12 hours of infection.

Virus amplification though may occur within the lymph nodes, leading to infected lymphocytes and monocytes, entering the lymphatics and the systemic blood circulation, ably a cell associated viaremia. and then once you've got that viremia, then the, the virus is gonna settle out, into various different other blood vessels, leading to secondary replication within that endothelium of the small blood vessels. And as that happens, that's often within the placenta and spinal cord, and that secondary growth of the viruses in those locations will lead to a secondary phase of pyrexia.

Once those endothelial cells are infected, you're going to get vasculitis and thrombosis in that location. And within the placenta or spinal cord, we're worried about this because this reaction will interrupt the blood supply, in the sensitive to issues resulting in ischemia and death. So that's gonna happen in multiple locations, but why does it have such a big an effect in both the spinal column and the placenta?

The equine microcoilliden is very susceptible to thrombus formations, it's supplied by a single arterial and venule. And the simple epithelial choreo, equine placenta unzips at that stage, resulting in a red bag abortion. Damage to the placenta typically results in EHV infecting the foetus, hence why that we can get the, the answers from the foetus if we were to do a postmortem on those ones.

In EHM the compromise of the spinal blood supply results in swelling of neurons and haemorrhage, . With the extent and location of the neurological lesions completely dependent on the nature, on the, the location of the thrombus, and thus it will detect this clinical signs. So When we talk about what the factors are that are going to affect the the pathogenesis, as I've mentioned, we talked about the the horse's own immune status, but also we're gonna talk about the strain, so we know there are different forms of EHV, the virulence of the strain, the infectious dose, so how much are they exposed to, the level of viremia going through the body, the degree of ischemia within the, the spinal column or the placenta.

I say the hosts immunity, the vaccination status potentially, and . Changes in the single nucleotide polymorphism that might lead to differences in the clinical symptoms. So, how far is EHP spread?

And I think this is, it is quite important when we start considering whether or not how we're going to implement biosecurity changes, sorry. . So there's limited definitive information available on how far EHV one is going to be spread in its aerosolized form.

AAP recommends that there should be about a 10 metre separation between horses, . To reduce the risk of EHP spreading between them. In 2009, Nicola Perula showed that it could be detected 14.5 metres away.

Now, that was a slightly artificial form of the disease in the sense that they nebulized virus particles into a barn and then measured how far they got, but it does show that the aerosolized form of it can spread quite a long way. If we look at bovine herpes virus one, which has a far more definitive number, anything less than 4.4 metres between animals will massively increase the risk of infection.

So somewhere in that region is what we could be talking about separating horses by. But the most productive way is smear infection rather than aerosol or foamite transmission. Therefore, it is utterly critical that horses are not allowed nose to nose contact.

Obviously flumite is a very easy way to transmit the virus as well. So anyone handling these horses or using equipment make sure that they are clean between each of the horses. But most importantly, let's reduce those those contact, which I think everybody would do in any of these cases.

What about testing, testing in the acute phase is very easy. I don't think anyone would, get confused by this. It's PTR is by far and away the easiest one.

And there's some good research by again by Nicola Stern in 2008 showing that nasal swabs are only needed, not nasopharyngeal swabs, they're, they're pretty consistent. And actually, although in this study on the right hand side we see that . There there were some differences in the frequency of false positive and false negatives.

Statistics didn't bear out and they're pretty equivalent for, for use in a clinical case. When you take a nasal swab, ideally you should have that swab in the nose for about 5 to 10 seconds and then transported in viral media. It's also possible to do a PCR or buffy coat.

What I would say it's a very helpful additional parallel diagnostic rather than a, a, a stepwise process. So it's, yeah, it's really useful just to confirm or deny when you have a positive or a negative on a nasopharyngeal swab. Virology is to show conversion, so it has been exposure, but an individual sample is relatively pointless because you don't know if they've had a vaccination or they've been exposed previously and got over it without anybody knowing, so I really wouldn't be using a single serological sample in any of these cases.

Virus isolation, of course, is very useful in research and give you a lot of information as to what's going on out there, but in the vast majority of clinical cases, it's probably not that helpful. And TSF sampling, although interesting to show is that Crimea, is fairly non-specific, and therefore can be actually a little bit difficult to interpret in, in, in some of these cases. More challengingly, is testing to remove restriction.

So I think this is a far more difficult question to decide, and it depends on the context that you're involved in. So in Valencia and, the French team decided that they were going to do two negative swabs each a week apart to prove that the horse was negative. Very interestingly, they had multiple horses test positive on different weeks, so they get a negative and then a positive, then a negative, then a positive.

And so I think in the vast majority of cases you're probably not going to be able to get that involvement from an owner, on a yard, but it's a very good place to start from and then recommend from there. Dealing with a less extreme outbreak than Valencia, then, you could dope serology at 14 days apart with multiple swabs throughout, so every 3 odd days or something along those lines. And that's what we did here at Lipo when, I admitted an EHB by accident, and then we had to shut down and make sure that nobody else got it.

Thankfully, due to our isolation process, we didn't see any other horses have any EHV at all, throughout the the two week period. And then there's a middle of the road sort of process where you do pet serology and maybe a negative swab two weeks after the last case is positive, . The easiest way to expedite all of this is to have good isolation in process.

And I think what's important just to mention about the outbreak that we had here was that the clinical symptoms were not pathonemonic for EHP at all. These were horses with, what appeared to be cere cerebellum disease processes, so intention tremors, very centrally depressed rather than any of the normal things. So it was a very unusual presentation that we were dealing with.

What about vaccination for VHM? So we're talking about trying to reduce the risk of EHM, not about abortion or anything like that. Should we be doing it yes or no?

But I think, you know, the whole COVID stuff has proven to people that there's always contentious issues about vaccination, there's no, no way around that. And actually a decision is not always as easy as it should be. What we do know is that high, the vaccination will result in an increased antibody, titer, and also therefore, stop serological testing being useful.

So, in the outbreak here, we did not vaccinate in the face of an outbreak because we were worried that it would alter our serological testing and therefore our ability to, release the horses from isolation. There is no licence for reducing signs of neurological disease, only abortion, but what we do know is it will reduce the shedding of EHB dramatically and therefore reduce that viral load that other horses are going to experience. There is no real evidence that leads to worsening of the neurology, and I'll sort of discuss that a little bit more in a moment.

And therefore it should reduce the spread of teeth. So we should, I think, really be considering it, and, Lutz Goering was sort of talking about there might be some new vaccines coming out, RNA vaccines, which will, will help with all of this. So, watch this spaces is sort of what I'm mentioning.

But what we need to do is try and increase herd immunity so that we are reducing the, the disease spread as much as is humanly possible, cos that's what we've got to do to reduce EHM. So to get herd immunity, we need to get about 70% of the population vaccinated, and that will reduce the spread. So, does vaccination increase the risk of EHM?

And there have been two studies, there's now the one coming from Valencia, which actually, I'll go into a little bit more, but, it didn't have enough, information in its sadly not enough numbers to get statistical significance. There are only two studies even beginning to get close to discussing it. There's, one in 2013 and one in 2007.

Neither shows evidence of vaccination leads to EHM, but neither shows that they are not associated. So in other words, How do we interpret that? And I think from all the information from those two studies, also from the work in Valencia, that I don't, I personally don't think that the vaccination is going to increase the risk of EHM, there doesn't seem to be enough data out there, but what it's gonna do is significantly the risk of the viremia, the spread of the disease, and therefore at the herd level, is going to be significantly important to reducing further outbreaks of the HM.

There was sort of a roundtable consensus that recently, that was to vaccinate, to reduce the spread of disease. There's some stuff coming out soon, that their, their feeling was the same as well. The one thing to note is that there is a delay in immunological response response, so it may limit the effectiveness of it in the face of a true outbreak, rather than doing it before you go anywhere.

How best to utilise it for obviously high vaccine coverage at both base and event trying to do it before we go away so these horses are ready to be exposed. Always use it as per the manufacturing guidelines, so we're getting the best antibody response. And then how about some testing?

So should we be doing strategic testing at at big events? Should we be doing entry during and then more significantly, probably on arrival back at the home barn, because that's the most common location of the HV outbreaks rather than at the competition itself and improve education for both the owner and the vet so that we know what we're dealing with and how we can help as much as is humanly possible. When we talk about treatment and and the like, what are we, what are we gonna do?

And I think, first of all, the main thing is that we're doing symptomatic and supportive care for the majority of these cases. And so that's gonna include fluid therapy, lifting, turning, urinary catheters, monitoring eyes, all the sort of the intensive nursing that goes along with anything that might be recumbent at all. When we talk about drugs, non-steroidals are integral, and they're used, or sorry, I should say they're they're integral, but they're used but unknown if it has any effect on the disease progression, but common sense has got to imply there's an inflammatory process going on, so reduce some of that.

There's also pain from lying down, etc. So I, I can't see a reason not to use non-steroidals as long as you are looking after the urinary catheter and giving enough fluids to reduce the risk of any renal disease. Corticosteroids are used a lot, so they can reduce the cellular response in EHM, therefore reduce the inflammation within the spinal column or the placenta, reducing vasculitis, thrombosis, and vascular injury.

But does it lead to immunosuppression, so there could be a flip side. I would always use steroids in all of my cases, but there's always gonna be that slight bit in the back of your head of, of making sure it's the right choice. So acyclovir, I'll come ontoval acyclovir in a second at 10 milligrammes per kilogramme every 4 hours.

So, a couple of studies in 2005 and 2008 showed that the bioavailability was pretty poor at sort of 1 to 2.8%, so pretty terrible. So everybody stopped using it.

But then in 2007, Henninger also did his study when he was in an outbreak and found that the serological levels required in humans were achieved with the 10 mes perking every 4 hours. So actually the acyclovine may be having a better effect and a better response, and we were giving credit, . Yeah.

What do they do? What happened in the Valencia outbreak, most of you know these stats, but just, here's a bit of a brief summary, as I say, I wasn't there, so I don't know all the details, but I've got a rough idea. There were 752 horses involved in the tour, and due the HP1 outbreak, the whole tour was cancelled, and the site was locked down with a total of 160 horses from 15 countries still on site rather than those that had already left.

We're talking about a lot of horses in one location. Clinical signs were pretty consistent with the normal AHV outbreak, so we're talking about fevers of 38.6 up to 41.2, lasting 1 to 10 days, pretty normal.

And then when the neurologic signs occurred, ataxia, urinary incontinence, recumbency, everything that you would expect. So what were some of the interesting stats that I sort of pulled out? The mean vaccine time before the outbreak was 1.4 months before, the last vaccine was given before arrival, and all with the equipped vaccine because that's what was available.

Whether we sort of start to crunch numbers of how many horses were vaccinated versus not, we see that 88 were not vaccinated 34 at that time, with the 160 horses of the ones they had data for. And then in the neurologic group, 33 were vaccinated, 27 not vaccinated. So you could say, OK, there's the trend towards the neurologic group having more vaccinated horses than not, but there were not enough numbers to have any statistical significance.

It was too, too variable. What they did find though, consistent with the Henneer paper was that location had a significant effect. So in other words, inside the barn leads to an increased risk.

So airspace, common airspace was a big problem. Sex, stallion and geldings was 6 times more likely to have a fever, but not neurological. And that, as with the Henneer, mayors were far more likely to have EHM than the gelding ortalians were.

Horses over 9, so they reduce the age from 20 to 9 were 6 times more likely to have neurologic signs, but again, there might be a slight sort of bend in each of these papers by, sorry, depending on the population. So it seems unlikely that the horses on this tour were going to be over 20, whereas in the Henneer paper, that was a far more sort of local, outbreak, so far more likely to have older horses. Interestingly, they found that the duration of the Febrile period was not associated with the occurrence of VHM in these horses.

What do they do for treatment wise? Valet cyclovir, they have this sort of set routine of 30 migs per gig for 3 times for 2 days and then down to 20 migs per gig, twice a day for 14 days. And what they felt and saw from the data was that there was a better response to treatment if started before inoculation of the EHV virus, and therefore, if you're an outbreak, probably better to start anyone who's willing to pay the money on vallecycllivib before they get the disease.

They used nin in the febrile periods and then moved to Ferro cogitive afterwards and they used dexamethasone at a varying dose depending on the case and severity of sizes. What they did mention though was that they said make sure you're careful because they did have a couple of these cases have laminitis, and these aren't probably your stereotypical horses that would get laminitis, so a little bit of care there. They did also use heparin in some cases, being that there is a hypercoagulable state during the viremic phase, so by using heparin or a fractionated heparin, such as fragmin, you're gonna reduce the risk of that hypercoagulable state and therefore reduce the risk of thrombus formation.

So there could be a good link with that. And then some horses again went on to aspirin, and they felt there was a positive effect on cases in Valencia. The one thing to notice is the dose ranges range from 5 to 20 Migs per gig every 24 hours.

And should only be used in the pre-viremic and viremic faces. There's no point in the afterwards. So there is a slight concern that there is, if the spinal cord haemorrhage EHM might in HM then aspirin could make it worse.

But my experience of using aspirin in other cases is that it doesn't do all that much, so I, I, I personally wouldn't be all that worried about it causing or leading to increased haemorrhage. They also use some vitamin E, in these cases, remembering that alpha tocool is essential, and try not to get any selenium because to get, if you've got a viti selenium, product, you're probably not gonna have all that much vitamin E and you could, could cause a selenium toxicosis. But there you sort of state, who knows what the effect could be.

So, what were the outcomes in Valencia, and I think this is sort of the significant part of it to, to, to see how these cases went. When we looked at it, there were 53 sites of EHV across the whole of Europe following Valencia. So these are sort of reported EHV outbreaks.

58 of them were directly attributable to Valencia, so horses were transported back there and then had the case. It affected 12 countries across the whole of Europe, a pretty significant area was affected. 20 horses overall were euthanized, .

And amazingly, the FAI imposed mandatory quarantine and testing on 3,836 horses, so it's pretty significant, effect not only on the horses that were euthanized, and the horses that were neurologic, of which and the vast majority are doing very well, following treatment and a bit of a break. But more significantly, it's gonna have a massive effect on any other events, any other things that are going on at that time. And therefore we've really got to consider that actually is vaccination something we should be pushing as a a group to make sure that we don't allow this to happen again.

So they now require a attempt to be put down an FEI website prior to any movement, and also they're now saying that they should be moved into the dedicated separate airspaces if EHB is found at all as an outbreak. The PCR should be readily available for all competitors, and all competition, sorry, because I think there was a slight delay in being able to do that testing, just because of a lack of equipment, on site. So, a lot to learn from them, some really useful stuff on how to treat them, and how it can so quickly spread and so quickly go wrong.

And I've done some really good lectures at Beaver and things like that, that really highlights the real detail that I don't have, on, on that outbreak. I mentioned biosecurity, this is our outbreak, . It is absolutely critical, I think, you know, we genuinely isolated every single horse here at Lit book.

We had a separate equipment for everything, everybody had to change and get changed again, and because of that we didn't have a single horse, get EHV following that primary case that came in. So it just shows that appropriate biosecurity will do everything you need it to do. So, two things I'm just gonna mention, and I, I, they're not through outbreaks, but I think there are things that we see in the UK, rather than anywhere else.

So hepatic encephalopathy is normally a single horse, rather than a herd. I'm not trying to pretend it's anything else, but what I'm saying is that it's normally an outbreak of disease that's going on in the herd, and you'll probably find a sentinel creature. So we see it relatively commonly here at Lippo, I think we just it's a referral situation.

And these horses will present as dull, depressed, hyperactive in some cases. They'll do this manic walking where they just will not stop walking. Whatever you do, you could literally put anything in front of them and they'll they'll try and walk through it.

They'll also often be blind, and they'll often have gastric fractures. We don't really understand why lots of those things happen in these cases, we just know they do. Obviously diagnoses are gonna be via the blood work, potentially biopsy, and the treatments are all the very normal ones that you're going to do for any liver, liver disease cases, so hypertonic, lactulose, steroids, maybe antibiotics, although we really very, very rarely see, infectious causes of hepatopathies in the UK.

In those where there is paralysis of the trachea of the larynx, sorry, you're going to need to do a tracheostomy. The reason, as I say, for the outbreak covered is that when you get this sentinel creature, make sure that you go and test all the other horses on the yard, because I would bet in the vast majority of cases that you're gonna have an elevated GGT in a lot of those horses. So let's get them off the forage, let's get them away from the pasture, whatever we think that is causing these cases.

We need to try and fix that as soon as we possibly can to reduce the the disease outcome. Yes, N, I, I'll keep it short and simple, don't have it at the moment, great news. Horses and humans are the dead end host, and a lot of the horses won't show any symptoms, but when they do, they'll have sonialos, muscle flicks, vesiculations, ataxia, .

I say we don't have it, but whether with environmental changes, and all these sorts of things that are happening in the world at the moment, whether we'll start to see it happening, it is very much, up for debate. We've definitely got the mosquitoes, we've definitely got the birds and the chickens to act as a reservoir, so whether it's gonna come over, who knows, but if, if you ever worry about a case, particularly on the east coast, and that's where the the migratory birds are gonna follow, then make sure we get it tested. I just put this slide in, because I think with all neurologic cases, the question is to ride or not to ride, and I think it's a really difficult question to answer in a lot of cases, and it comes down purely to your acumen and also what you're willing to put your name to.

So I think firstly, what is the grade, there are some clear cut ones here that, you know, pretty much anything from 3 upwards, absolutely not, from a legal standpoint that people ride them, that's their choice. Grade 2. Excuse me.

Grade 2, I also personally wouldn't be pushing them to, to ride it. Grade 1 starts to get a little bit, difficult to know. Diagnosis, obviously, if it's a bit of osteoarthritis that you think's gonna be manageable, then probably they're gonna be able to carry on riding and watch that horse as it progresses.

If it's CVM where you're worried that it could get acutely worse, care. Who's riding and what is their age, so anyone under the age of 18 riding a neurological course should be not doing it unless the the the parent gives permission, so that becomes a whole another youth, their problem. Intended use, insurance, they're all difficult questions and I, and it's a difficult one to answer, and I don't think you can give a a a a rule to any of this, and often that's why referral or second opinions are required, and often if I'm sitting on the fence, I'll get another person here to come and have a look and give me their second opinion.

Summary, I think like with all examinations, it's really good to have an exact plan and to stick to it every time you do these examinations, because then you're not gonna miss everything. You're a bad vet for not looking rather than anything else, and it's so easy just to skim over a and the static examination because we don't see it very often in the UK, but you should do it in every single neurological examination. Once you've done those parts, you can neuro local neuro localise appropriately and then deem the most appropriate diagnostics at the next stage as the best way to spend money.

Once you've got that diagnosis, you can make your treatments and your future plans and make a decision as to whether that horse is neurologically safe to ride, or if it's AEHV start the treatment as appropriate. Well, thank you very much for listening and I hope that's been helpful for neurological examinations.