Good afternoon, everybody. So we'll crack on. Thanks very much for that introduction, Rich.
So, the lame neurologic horse, I, I find these very challenging cases, to be perfectly honest. Many horses may have both, lesions, they may be lame and have a neurological component, and I, and I think the sort of concerning thing really is that the, your diagnosis that you reach has very significant implications for the future of that horse. .
In the many owners, as we know, will be quite happy to retire a horse, which has lameness issues and certainly persist with treatment of lameness issues. But actually, if you do come to a diagnosis of, of a neurological lesion, many owners are very unforgiving of that, and often the often would rather end up euthanizing the animal rather than proceed with treatment. So in terms of what we'd like to try and cover this afternoon, recognise the many reasons for gait abnormality actually, in horses, as a more specific term.
And then talk a little bit about the objective grading of lame versus neurological horses and the grading systems that are out there. Look at how we might try and investigate these animals, and, and how a lameness and a neurological examination differs slightly. Look at some of the different diagnostic techniques that are available to us, and then also touch on some specific neurological conditions, which may result in gait abnormality that is perhaps, slightly confusing with regards to, lameness as a differential diagnosis.
So I think the thing to recognise and and just to remind ourselves of is that the gait abnormality is a very non-specific term. It has multiple possible causes. So we'd all obviously be very comfortable with orthopaedic lameness, pain, we can have gait abnormality through mechanical.
Restrictions. So, fibrotic myopathy is perhaps the commonest one, but also with the scar tissue, some horses may have undergone arthrodesis procedures of, of high motion joints as a salvage, for example, and that will create a a physical restriction of gait but not necessarily lead to discomfort. Uncommonly, but, but sometimes we have horses with myopathy, either as a subclinical poor performance issue or sometimes overt tying up, which can affect the gait quite markedly.
Then we have horses with genuine neurologic issues, some of these can then have a behavioural component to them as well. And then I'm sure everyone's aware of breed-related gait abnormalities, paces, which can be very difficult to assess, hackney carriage horses and and those sorts. And then finally, there is an age-related component as well, and, and, and so, in particular, if you look at young warm bloods, you know, they will often retain a degree of propriceptive abnormality, particularly in the high limbs, you know, for, a number of years and actually may well be, propriceptively abnormal, sometimes you're up to 56 years of age and yet be relatively normal in inverted commas for the breed.
So be a little bit careful when assessing some of these in breeds and needs, of course. Actually think about what these definitions mean, it sometimes helps us to to think about how we might therefore go about investigating them. If you look at lameness per se, the dictionary is really very unhelpful.
So it's a person or animal unable to walk normally due to an injury affecting the leg or foot, which is, as I said, very vague and of no help at all, but it does at least suggest an injury to the musculoskeletal system and therefore, if it's painful, it should respond to analgesia. And you would hope that it should lead to a consistent gait abnormality in most cases. So when we think about how we might localise these lesions, obviously we've got clinical examination, which may identify a swelling area of effusion, area of pain or palpation.
We can also use diagnostic analgesia and diagnostic imaging, but how the animal moves is not particularly useful for us. I mean, I think we would all know of. You know, specific gait abnormalities that can be attributable to a specific way of of going, but there's very few cases that you can watch a horse trotting up and say with absolute certainty that that lateness is coming from a certain area of the lip.
So gait analysis tends to take a little bit of a backseat in terms of trying to provide a specific diagnosis. If we look at ataxia, that is technically a lack of coordination of motor movement, and there's three types. There's cerebellar ataxia, vestibular ataxia, and sensory ataxia, and it's the latter sensory ataxia that really predominates in the horse and certainly is, is, is what we're going.
Most today, sure we all know of cases of vestibu ataxia, for example, temporal hide osteoarthropathy would be a good one, but by and large sensory ataxia predominates that may occur with or without spasticity and paresis, usually paresis of the two, but it doesn't obviously have to. So. Unless we've got a fracture or or some sort of traumatic injury causing ataxia, it's not painful, and it, by definition leads to an inconsistent gait.
And in terms of localising our lesions in these cases, we obviously have our clinical exam, our neurological exam, but we actually place far higher emphasis on gait analysis in these cases, which will come on to a little bit later. We obviously have diagnostic imaging, but we can't use or we don't tend to use diagnostic analgesia. So it's a slight shift in terms of how we go about presenting or or investigating these cases compared with, with lame horses.
We look at paresis or weakness, that's a deficiency of normal movement arising from a reduction in normal muscular power, and there's two types, lower motor neuron and upper motor neuron. With lower motor neuron disease, we tend to see flaccidity, loss of tone, you get profound atrophy, so typical neurogenic atrophy that can happen very, very quickly, and a diminished reflex response, occasionally with fasciculations. Whereas with uppermost neuron weakness, which tends to predominate in the wobblers, for example, we get spasticity, this sort of jerky gait with an increased tone and an exaggerated reflex response.
We don't get atrophy, and we don't tend to see funic regions. We look at how we grade lamenesses, everyone has a different way of doing this, but the AAP scale is probably the most widely published. I have to say it's not my, I, I don't grade out of 5.
I, I use the UK 10 point grading scale most commonly. But if we look at the AAP scale, obviously grade 0 is a, is a sound horse, grade 5 is a, it's a non-weight bearing horse with, with 3 grade grades in between. But actually if you look at the definitions of these, once you start to get to.
Grade one lameness, lameness is difficult to observe and not consistently apparent regardless of circumstances. And so the fact that this git abnormality is not consistently there at all times, suddenly starts to give you some crossover between a very low grade neurological horse, for example, and that's where the difficulty arise. Obviously for grade 2 and a grade 3, those are a little bit easier to spot.
So I said, in the UK we tend to use a 10 point grading scale. There's also an 8 point scale described, which, as I said, I don't use, . And we know that there's considerable intra-observer variability, if it has been some nice research done at inter-observer variability looking at lays it's as low as 0.11 for hind lameness, which is really very, very poor, particularly amongst inexperienced observers.
I suppose the only comforting thing is that, you know, when you're talking of intra-observer agreement, are your ability to grade the lameness the same on, you know, two consecutive examinations, that is far higher, it increases to about 0.57, about 0.6, particularly with experienced observers.
So, The whole point of grading lameness, I guess, is to be able to then see if you've made a difference to it through diagnostic analgesia or through treating the lameness in some way. And I suppose, you know, the fact that the intra observer variability is higher is at least comforting to suggest that we are able to monitor lameness appropriately. But even so, with subjective grading, there can be considerable disparity between observers, particularly for hind limb lameness.
On the outline neurological grading has a similar 5 point scale that most people use. We may have different grades for 4 and hind limbs. And again, there is considerable in observer variability by the very nature of these horses.
They are unpredictable, and they, they do abnormal things and they're not consistent. So, you know, two observers very much may grade them different. If we look at the neurological grading scale that most people are familiar with, that's adapted from, from Joe Mayhew's book.
Grade 0 is a complete normal horse, grade 5 is a recumbent horse and then again, with 4 grades in between, . And As the definition suggests, there is some disparity between the two, and we'll work through these now and have a, have a look at them. So grade 5 horse is fairly obvious, these horses are recumbent, and to be perfectly honest, you know, a, a, a recumbent horse, doesn't have, particularly long to live really, unless there's some fairly obvious, therapeutic option you've got for it.
So, you know, those are relatively easy to grade. If we look at a grade 4 horse, the camera does improve, it's typical student camera work, but a grade 4 horse is stumbling, tripping and falling spontaneously at a normal gait. So if a horse is falling over.
Then it technically has to be a grade 4. This is actually a horse with temporal hide osteoarthropathy, it did actually recover photo course of Jamie. So grade 4 cases again relatively easy to grade.
If they actually slip and go down, or they come very, very close to to falling down, then, then they're a grade 4, which is, is relatively easy. Now the grade 3s, they're still pretty obvious. So I always like to think of a grade 3 is if an owner can look at the horse and easily tell across the yard that there's something wrong with it, then it's probably a grade 3.
Remembering again that there can be a difference in grading between the forelimbs and the hind limbs. But for a grade 3 horse, the neurological deficits are prominent at the walk, so you can really see there's something wrong with that horse, and they have a tendency to buckle or fall when you back turn loin pressure. And importantly, there's postural deficits noticed at rest.
So if you see this horse doing something odd, just standing in the field like this one is, then they, they have to be a grade 3. You could even argue that if this horse has started to sort of slip and fall behind, it might even move into a, a slight grade 4. Again, the grading of of grade 3 is relatively easy to reach if an owner can easily spot it, then it probably is a grade 3.
As we get a slightly more subtle, that's when it has to be a bit more difficult. So if we look at this horse here. This one is probably a grade 1 in the four limbs, so it's very relatively mild neurological deficits in the four limbs, and there's obvious, but, but not as severe deficits in hind limbs.
So a grade 1 horse has neurological deficits just detected at a normal gait, but worsened when you perform tricks. So backing, turning, loin pressure, neck extension. Whereas at grade 2, the deficits are easily detected at the walk and exaggerated by backing turning the pressure, so you could argue there's not a huge amount of difference between those two, but.
I would think that, you know, a grade 2 horse is relatively easy to spot by an untrained veterinary eye. You know, most students, for example, or, mixed general practitioner horses, people with relatively little equine experience would still probably be able to detect the horse has neuro abnormalities. If you look at this horse here, it shows lateral circumduction of that right hind, a bit of interference with itself as well.
It doesn't cross over particularly well. Its placement is poor, but in contrast, it's for limb activity is OK. You'll notice as well, there's a slight, a slight spasticity as well during that action, particularly in the right hind limb.
Again, no muscle atrophy, so uppermost neuron signs as well. In contrast, a grade one, it is far more subtle than that. And as I said, I think.
You know, I would grade this horse probably as a grade 2 behind, but I know there'd be plenty of people that grade this as a grade 3, so some disparity exists there again. Then once you get down to horses like this, then it becomes very challenging. Is this a horse got a great one, hind limb neurological deficits?
Is it mildly hind limb lame, or does it have a combination of both? And, you know, probably we would agree this horse is slightly right hind limb lame at the trot in a straight line. But we would also agree that he doesn't perform brilliantly during a tight neurological test as well.
A bit of interference, not crossing over brilliantly well. But again, these are relatively subtle neurological deficits, so it's hard to know whether this is just discomfort that's causing this horse to move this way, or, or does he have genuine propoceptive or, or a tactic deficit. And clearly, you know, the owner's view to treatment is gonna differ markedly depending on the diagnosis you reach.
In terms of examination, I think history's important. Obviously there's some real markers, travel abroad, but, but also use of the horse, previous use of the horse, level of workload, duration of clinical signs. A lot of these owner, questions owners may sometimes not be able to answer, I guess that's something to, to be aware of.
Signment's important, we know that there's a predisposition, amongst certain breeds and sexs of horses for, for various conditions. Before laying hands on the horse, I'd always encourage you just to step back and have a look at the animal as well. So visual assessment can be really helpful.
Confirmation, as, I think Rachel touched on with the suspensory breakdown. There are certain confirmational traits that will predispose a horse to various injuries, straight confirmation, and predisposing horses to suspensory ligament pathology, for example. So, so have a look at the way the horse is put together and also step back and have a look for any atrophy in asymmetry, and I think this horse on the top right is a reasonably nice example of that.
I'd hope it's fairly obvious, that this horse has, you know, significant underdevelopment of its some cervical, musculature, and this horse did have a. Mid cervical neurological lesion. So, you know, it's not always as obvious as this, but if there is a neurogenic atrophy, or if there is chronic disuse for a specific set of muscle groups, you will get a atrophy and and a symmetry that can sometimes point you in the right direction.
And obviously, I think we'd be fairly comfortable, all of us with our clinical examination, but pay real attention to obviously swelling, heat, pain, reduced range of motion, and depending on the set of clinical signs that you're looking at, obviously, that will, you know, the, the, the various parts of the body that you're examining, will, will vary. If we look at the lameness examination, in terms of gait assessment, I, I very much try and keep, lameness and neurological exams slightly separate, and, and try and keep good notes. There's a lot of, clinical information going in, and you want to make sure you write it all down at the same time.
So, my preference is to do a lays exam and then almost sort of mentally switch gears and then do a neurological exam rather than doing both concurrently. And I think the basic principle of the lamest examination is that we're looking to identify consistent gait abnormality and not trick the horse into revealing a neurological deficit. So, I think everyone would hopefully recognise that this horse is left falling and lame, that we see trotting around.
But really, we're performing the same movement on a flat surface again and again and again, trying to build up, you know, a degree of consistency, so that we, when we do perform an intervention such as, diagnostic analgesia, you know, we hopefully can then document a change in gait. Whereas in contrast, you know, with the neurological exam, what we're trying to do is actually trick the animal into revealing sometimes subtle neurological deficits. So we use obstacles, we use specific ways of the horse, you know, moving tight turns, backing up tails and the like to try and document that.
So, you know, they are inherently very different, processes. In terms of the lameness examination, I do look at these horses at the walk. I think it'd be quite tempting just to trot them on, but actually quite a lot of stuff happens at walk that you really can't appreciate once the horse is moving quickly.
So, look at foot placement, footfall, Fay, hock hyper hyperextension, the fetlocks, for example, you're gonna be quite a lot of clues, and particularly some of the mechanical gait deficits, they're far more easily recognised at walk rather than trot. But then, you know, most of the grading systems certainly work at trot, and we would commonly trot horses in a straight line and then lunge them at trot on a hard and soft surface if it's available. I think one thing I would emphasise is the importance of seeing these horses at Canter, particularly for hind limb lameness.
I, I think, you know, years ago, I would rarely canter horses and, and just trot them, but actually, you know, as time goes by and I see more and more horses with sort of subtle, often bilateral performance limiting lameness, I, I would very much emphasise, how useful the canter can be for these horses. And, you know, we're looking for a nice sort of balanced count canter, but typically with these animals, we'll see. You know, very sort of narrow striding gate that lacks power, lacks the normal sort of cadence and rhythm of the cancer.
Sometimes these horses will disunite behind, and that is actually something that you can, you know, you can improve with diagnostic anaesthesia as well. You know, if the horse disunites every time on the left rein, and then you block it stifle, and it suddenly doesn't disunite anymore, that, that's a positive block. So, Just because you don't see overt lameness at trot doesn't mean there isn't necessarily a, a low grade or bilateral lameness issue there.
Flexion tests, everyone will have a personal opinion on those. I, I certainly don't flex every horse, particularly older horses. I think they can almost be misleading, but certainly for younger horses where flexion tests should be negative, they can be useful.
And then in some cases, a written examination, although it is time consuming, it can also very much help you, particularly for ridden performance issues, well. The little mention of objective gate analysis, which I'm just gonna touch on, I'm sure people have various, experiences of that. Some people are using it widely, some people, not at all.
One thing I would say is it does require a consistent gate at trot to analyse. So you need at least 15 strides at trot, more so on the lunge. So, you know, if you've got a fairly short trot up area or somewhere not really suitable for lunging a horse, then the software doesn't like that.
And what it does do is it prints out this, nice display. And we will, it will obviously in a straight line, give you an analysis of, of lameness and there is. I just switched back, you know, there is moderate evidence of mild right hand impact lameness, but actually, once you get more proficient with using the software as well, you can actually go into it in a little bit more depth.
And I think it's quite important to, to use this lameness analysis tools more appropriately than, probably a degree of proficiency of doing that is, is important. But I think the one thing it does not enjoy is ataxic courses. And in my experience as well, it also struggles somewhat with these very big moving.
Often young sports horses too. So, you know, unfortunately, if you are looking for that answer as to, you know, is this horse a tactic or not, objective data analysis, in my experience tends to you, a, a particularly reliable answer. So neurology neurological examination in terms of the clinical component, is very similar to lameness, but clearly has more of a focus on the neck, the back and, and the pelvis as required.
One thing I would say is that obviously when you're under time pressure, in an ambulatory setting, there's very much pressure to pronounce a judgement on a horse on on day one, but sometimes you do actually need to go back and, you know, have a look at a horse a few times, maybe, you know, one day it's windy and the horse is a bit lit up and. Of adrenaline, you know, sometimes I very much like to get some colleague involved and sometimes get a second opinion from one of the other surgeons or one of the medics, and, and, and that's an invaluable thing to have. So, you know, if, if you're not sure, it's definitely worth getting other people involved.
Multiple exams can be very, very useful. I think there's a safety component as well. Some of these horses are not safe, and you should obviously be aware of that before you start to put them through, to sort of detailed a gate examination.
In terms of our static examination, we obviously would look at the cranial nerves. We're not going to go into that in too much detail because we're going to be talking about horses that have normal cranial nerve function they have or have deficits from, you know, the cervical region quaally. Also look at the cervical facial, tanous trunchi reflexes, anal tone, tail tone, so forth, areas of patchy sweating, focal muscle atrophy as we've discussed.
And then after the static component, we move on to the dynamic examination, that's usually done at walk. Occasionally I'll see a horse trot and then sort of stop abruptly just to see how their, their placement is. But most of the neurotic examination is conducted at walk.
And we would obviously put the horse through, a number of different, movements, serpentine, reversing, turning obstacles and inclines in an attempt to try and reveal a subtle gait deficit. And as we've mentioned previously, the whole point of doing that is that our gate evaluation or gate analysis is key to localising the lesion and this schematic, shows that really quite nicely. So.
We're going to touch, say, obviously say the cranial nerve signs aren't present in the types of horses that we're going to be talking about. If they've got no gait deficits, then obviously they're a normal horse. But if we do have a taxxia hypermetrius spasticity, the distribution between the forelimbs and high limbs very much helps us.
So in most cases. Sorry, let's go back. In most cases, we'll be comfortable seeing the hind limb functions worse than for lib, and that places the lesion solidly within the cervical lesion.
Cervical region, and certainly, you know, in the UK, the majority of cases on neurological cases that we would see would come from cervical pathology. Very occasionally, if you've got a cord or cervical or cranial thoracic lesion, you will see 4 limb signs that are worse than the rear. These are really quite unusual.
I don't see a lot of those. But you can see, there is obviously some crossover between obviously C6-7 in terms of, you know, whether the hind limbs or the for limbs are going to be worse. If our forelimbs are completely normal, and the hind limbs are abnormal, then, then clearly that moves the site of pathology further caudal into the thora of lumbar region.
The only slight caveat I would add there is that you can get some wobblers, you know, some horses with general survive genuine cervical pathology that have really very, very subtle for limb signs and obviously quite marked hind limb signs, depending on the the nature of their cord compression. So you have to be a little bit careful with that, but Essentially, if you've got normal falling function and abnormal hind limb function, then it has to be within the thoracic lumbar region. And then finally, if your limb function is fine, but we have the tail and bladder paralysis, perineal hypogeia, perhaps urinary retention, then clearly we have to have a pelvic or specifically a sacral lesion localization.
In terms of dynamic tests, we don't have time to go through all of these, but, typically we put these horses on a serpentine. I quite like to them to er start and stop, quite. Regularly, so if we start and stop the horse, you know, particularly as we're turning them, you'll sometimes get an idea of where, where their limb placement is.
It's quite nice if you've got a natural barrier for them to try and walk over, you can see, actually assess whether or not they're able to, to sort of avoid it or sort of govern their, their limb placement. But also back these horses up, in an effort to exacerbate, and we may also do these tests at different head positions as well. So sometimes with the head extended, we suspect a vestibular component and the use of a blindfold can obviously be useful, but, you know, currently we're not obviously talking about horses with cranial component to this.
The one thing I would say to be careful of, is I would usually use these abrupt sort of, changes of gait as a way of assessing limb placement or even moving the horse one step to the side. I think you have to be a little bit careful with, limb placement tests like you see down here. Now, this horse does actually have neurological deficits, but you will find that some of these cold blooded breeds will just stand there and let you put their legs in whatever position you want to really not bother about it at all.
So I think if they're a young thoroughbred that were doing this, then clearly that would be abnormal. But I think in some of these perhaps more docile breeds, you have to be a little bit careful, . With their, with their placements.
And as we mentioned, beware young warm bloods as well, you know, they can often have abnormal high limb propriception until they're 6 or 7 years of age, and they will essentially grow out of it. So I want to be very careful not to pass judgement on them too early in their life. Tests for weakness, or obviously similar, the either a tail pull or or pelvic push.
See here, Andy's pushing the pelvis, and you can sometimes get an idea of proprioceptive function as well when you release the test as to how quickly and easily the horse recovers. So some horses, you know, may be weak and they'll struggle to pull against you, but then when you loosen the tail pull, they'll actually overcompensate and overcorrect as well. Again, these are all fairly subjective things, and one observer's assessment is going to be different to to another's.
Test, this is a test of hind limb weakness in the for limb, we tend to try and perform the hop test, as you're asking the horse to to sort of hop across on one leg and assessing how easy to find that. Again, an athletic horse is going to find that awful lot easier than a non-athlete, so there is a degree of subjectivity, and we have to be careful with that. As we mentioned previously as well.
You know, painful lameness can, you know, lameness is often painful neurological conditions are often not painful, so an analgesic trial can often be quite useful as well, particularly, if you're trying to assess a degree of behavioural component as well. Things I would mention about an analgesic trial, it does need an objective owner, and not all pain responds to analgesia as well as anyone with back pain, or, or, or some forms of neuropathic pain will, will tell you, particularly in some horses as well. By the time they, they get to you, you may actually find there's quite a high degree of behavioural component into on top of the, the painful stimulus as well.
But I do use analgesic trials. I think they can be quite useful in terms of trying to determine whether this is a painful condition or not. I think Tend to have a lot more false negatives than you do false positives.
But phenolbusone would obviously be the non-steroidal anti-inflammatory drug of choice. Make sure you dose these horses correctly, you know, reasonably high loading dose for 48 hours, and then down to sort of maintenance dose for 10 to 14 days. And again, I try and get owners to, you know, get the horse into a pattern, almost keep a diary of how they behave and then make the intervention of of the analgesia and try to record as objectively as possible how they respond to that.
Gabapentin, which some of you may or may not have used, can sometimes be useful. Gabapentin is a gabapentinoid drug. It's an analogue of GABA, but actually it doesn't bind to, to GABA receptors.
It actually inhibits voltage dependent calcium channels. And it's used in human medicine for a wide range of things, neuropathic pain being, being one of them. There's a reasonably wide dose range in horses of 5 to 20 mg per kg, and that could be bid or kid, at higher doses, you can get, neurological, signs.
So I tend to use a 10 mg per kg dose, perros twice daily for 10 to 14 days. And, well, I have had a, a, a, a few horses, not, not many, but a few horses that were negative to phenolbutisone, but then did show a positive response to gabapentin, which would very much push you down the line of suspecting a neuropathic, lesion a little bit more. In terms of diagnostic tests, nuclear centigraphy, I think we'd all probably be comfortable in terms of its use in a lameness investigation, particularly for athletes.
I think it's far less rewarding for non-athletic, particularly cold-blooded and often subtly lame horses, but for the equine athlete, it's a very good place to start sometimes. And it is obviously sensitive for some conditions that would cause neurologic abnormalities, vertebral fractures, for example, marked inflammation of the vertebrae. But it does genuinely have, generally have a fairly limited application for neurological cases apart from that, unless you suspect a, a, a overtly traumatic.
And actually the logistics of, of bone scanning of wobbly horse tend to be fairly tricky as well. Serum chemistry, often of limited use as well. Obviously muscle enzymes to rule out myopathy, and sometimes we may get some non-specific markers, giving us evidence of, of information, serum iron, fibrinogen as a longer term thing, SAA, for example.
But by and large, serum chemistry tends to be of little use. Radiography as a diagnostic test is very much limited to the cervical region in adult neurological cases, which is frustrating in some cases, I suppose the only, sort of, good news is, is that the majority of neurological cases tend to come from the cervical region, at least. And, and what radiography is trying to do is obviously identify, identify likely sites of cord compression in an and obviously fracture would be the, the most obvious one, so, fairly obvious in its juvenile horse on the left here.
Which has got a fairly marked fracture, or fairly obvious fracture. Interestingly, this horse did really quite well, so it just goes to show what some necks can recover from. But also cervical vertebral malformation.
We, there are a combination of inter and intra vertebral ratios that can be used to calculate likely sites of cord compression. There's some, quite a lot of literature done on this, so I, I don't know if people are familiar with intra and intra intra vertebral ratios, but we look at the radiograph on the right, and essentially we take, for the intervertebral ratio. We effectively draw a line from the caudal termination of the dorsal arch.
So that's line C to the cranial aspect of the vertebra behind, and we measure a ratio of that versus the widest point of the vertebral body. And then also for the intravertebral ratio, that's A to B. So that's the narrowest point of of the verte of the spinal canal in that vertebra again against the vertebral body, the widest point of the vertebral body.
And it's been shown that there is a reasonable agreement between plain film radiography and sites of core compression, at Necroy, a studied by Levine Etal some years ago that documented about a sort of 65 to 70% agreement, but. In all honesty, with those figures, you really wouldn't perhaps want to be operating on, you know, wobble horses with just plain film radiography alone. A couple of notable papers, Rushmore and colleagues documented an 89% sensitivity, if you have a ratio of less than 50%, so less than 0.5 for the mid cervical region and less than 0.52 at C7.
And in 2008, Caroline Hahn came up with a slightly different figure of 0.48 at the C 3456 sites and 0.56 at C67.
So the exact values are are slightly up for debate, but the point still stands that ultimately, you know, if you've got markedly reduced inter or intra vertebral ratios at any particular site, providing they're down in the 40s, there is a reasonably good chance of more compression at that site. However, that's mainly talking about the type one wobblers will come on to in a moment, you know, in terms of assessing articular process or facet joint pathology, they can be very difficult to interpret. I think everyone's probably familiar with the the interwar variability of the facet joints.
There's a paper by Shelley Down in 2009, I think it was that effectively looked at the cordal cervical facet joints. In a number of clinically normal horses and essentially documented that these horses can have a massive variation in terms of morphology or the radiographic morphology of this fort joints, which can be difficult. It when a lot of cause compression from the side rather than dorsoventral compression, which is what a radiograph is really looking to analyse.
So playing film radiography has its place, try and get as good a films as possible, but again, the sensitivities often. Over Myelography on the other hand, is very much the gold standard for identifying compression, . In the live force, and certainly for plain film radiographic myelography, it's been shown to have a sort of 70 to 80% agreement with necropsy studies, so significantly better than, plain film radiography.
You know, traditionally, it's always been performed radiographically, but that obviously will only allow you to acquire later lateral views, and will therefore only give you an idea of dorsoventral compression. It doesn't give you a sort of 360 degree view. And there's a number of radiographic measurements that have been documented, reduction of the contrast columns to less than 2 millimetres, attenuation of both the dorsal and the ventral columns by greater than 30%, or another one was probably most widely used will be the complete loss of the ventral and greater than 50% loss of the dorsaldi coron column is currently optimal.
I think a recent. Times, CT scanning, use of big ball CT scanners, offers a far superior 3D imaging, and it will happen with time, but I just, you know, large numbers of cases haven't been fully validated yet, but this is, to give everyone an idea of a, a CT myelogram, in a thoroughbred cult. And this is a reconstructed view.
We can see here if we look at two sites, this right hand view here is looking at the C4 5 sites, although we've got complete loss of the ventral die column here, we've still got a reasonable dorsal die column and if we just eyeball that, you can see that the spinal cord has got a reasonable amount of space. Within the canal. But in contrast, if you move one space forward to the C34 site, we've got not only loss of the ventral die column, but we've got complete loss of the dorsal die column as well.
So you can see there's circumferential constriction at that site, and this horse had type 1 CVM at C34. One sort of note, is that C71 seems to be very different, to, there's been some recent sort of PM studies, by Eel and colleagues in 2018, and they documented that C7T1 site seems to have slightly different. Rules and that she's a different degree, a different set of parameters apply.
So, you know, for those reading CT scans, it's just where that sometimes a great degree of die column reduction tends to be path along. But undoubtedly, you know, advanced imaging is, is going to be the future in terms of documenting these sites of pathology more accurately prior to surgical correction order. CSF aspirations, all notes of this are in the the the the pros, notes provided in conjunction with the lecture, but there's, there's three sites we commonly use the Atlantic occipital, C1, C2, and then the lump sacral.
Atlanta occipital, usually done under GA. It has been described standing. I've never done it standing and it wouldn't be my preference too.
Certainly when the horse is under generals, you get far less blood contamination, obviously it's most representative sample of very cranial within the the CSF. The head and neck are held in a flexed position. A 9 centimetre 18 gauge needle is usually perfectly fine.
In the door in the dorsal midline at the level of the cranial aspect of the wings of the atlas, you can see my left hand is just marking that on the upper picture for Jamie to, for, for Jamie to, direct the needle, and then inject the needle down towards the mandibular synthesis, . And normally to a depth of 2 to 3 inches it feel a subtle pop. You normally get free flowing fluid or you can gently aspirate it.
As I said, C1, C2 is an ultrasound guided procedure has been documented in standing horse. We've experimented with that and touch wood it's been OK in a hospital situation, but it is a pretty specialised procedure and not to be undertaken lightly, but as I said, can be done standing. And finally, the one that everyone would be most with with the lumbar sacral tap, as you can see Jamie concentrating very .
Very fixedly on in the bottom picture, but that's a much deeper small space, so ironically, although it's done standing, it's a far more difficult space to hit, and you do occasionally get a violent reaction when you actually perforate the the CSF. Let's touch on some specific conditions now. Musculoskeletal nameus.
One thing I would say is beware of the laminitic horse. I, I think we've all probably, well certainly I've been referred in a few cases, and I think everyone has seen horses with quadrilateral laminitis that can very much mimic a neurological condition. This is a video of a horse that was sent in, who.
Presented from the field of a very abnormal gates, he's got sort of lateral circumduction and placement and it was really as described by the owner and and the initial referring veterinarian as having, you know, quite an abnormal gait suggestive of the neurological deficit, but actually, you know, when we sequentially blocked out all 4 ft, we were able to significantly improve this horse's gait, and it did turn out that he had a significant foot component to his, his gait. Some horses with back pelvic injury can obviously be very uncomfortable and very tight, and present it can be very difficult to fully analyse whether those horses are generally neurological. And then occasionally you just get horses with bilateral orthopaedic pain that can lead to very non-specific gait abnormalities.
So this horse on the right was referred in for weakness and an inability to pick up its hind limbs. But there was really nothing wrong with it neurologically, nothing really to see lameness wise, so. As an older horse, we blocked its TMT, I blocked its right TMT here and you can see that it'll actually suddenly hold that leg up absolutely fine and doesn't mind it.
If we go round to the left hinds, this is the unblocked leg now. You can see that when you go to pick its leg up, it suddenly gets really very, very Uncomfortable with that, and clearly there's obviously a behavioural components coming into this. So, you know, some horses in anticipation of pain can become really quite distressed or or often uncomfortable will show fairly abnormal gait abnormalities, purely as a result of pain, there's no neurological component there at all.
You look at mechanical lameness, so mechanical lameness, by definition should be a consistent gait pattern, but it very much depends on the location, the restrictions. So if we look at fibrotic myopathy, but also things like carpal arthrodesis, betlock arthrodesis, but these are not painful, they won't respond to an analgesic trial and they won't also respond to diagnostic anaesthesia. So, you know, if we look at this horse here, when you trot him in a straight line, I think we all agree he's right behind him lame.
It's really quite hard to see why that horse is right hila, again, it just reiterates that stuff happens very fast, the trot, so it's worth just, spending some time watching these horses walk. If we look at this horse at the walk, he has that sort of typical sort of cordal slap. During the final swing phase of the stride and slaps that down.
So this is caused by tightening and restriction of the semi-membranosis and semitendinosis. And again, this is a purely mechanical thing. This horse actually did have release surgery for that, but, but you can put that horse on as much analgesia as you like and you're not going to change his gait.
So I think fiberrotic mafi would be the best example of of a mechanical restriction of lameness rather than a painful one. Peripheral neuropathy, so peripheral neuropathy is kind of sitting halfway between painful lameness and and neurological lameness, I guess. But again, often very poorly responsive to, to analgesia or certainly conventional analgesia.
It's usually a single limb, and the gait deficits very much depend on the nerve affected. So again, we pay far more attention to how this horse is moving and how it's walking, as opposed to a classic lameness examination. And in acute stage, we tend to get lameness, and in the chronic phase, we tend to get profound muscle atrophy.
So this was here, if you watch the shoulder region or walk, this is a classic case of a super scapular nerve paralysis, normally caused when the horse sort of walks into an upright or jam or something like that. And you get paralysis of the supra scapular nerve as it courses over the scapular spine and therefore we get loss of innovation of the supra and infraspinatus. Now this is obviously a relatively early case, this is quite an acute case because we can see we've not got atrophy of the shoulder musculature, but that will happen with her in a very short period of time.
And as a result of that, we've lost the supporting musculature and you get that lateral luxation of the shoulder. Another one you might see will be bra or plexus injuries. This little horse was jumped on by a bigger field companion, diagnostic analgesia up to the shoulder, blocked this out and this force actually was slightly responsive to to gabapentin, but very much had a tentative working diagnosis of brachial plexus injury.
So the brachial plexus, which, you know, innovates those often protracted muscles within the forimb, and again, a few weeks after presentation developed significant quite profound muscle atrophy. And finally, this is a horse which was hung in a ditch by its left hind limb for some hours before being freed and released, and this developed femoral nerve paralysis. And you can often see these deficits as well with horses that have undergone stifle surgery and had the lay the legs suspended out the back for a long period of time.
We can see here during the weight bearing phase this horse is sort of unable to extend or maintain sort of limb function. And again, thankfully that one gradually got better with time. The other one that I don't have a video of would be something like a radial nerve paralysis.
So for horses that are in lateral recumbency for a prolonged period of time, they may often have, for example, a radial nerve paralysis, which gives very much that sort of dropped elbow, that inability to hyperextend and and fix the leg. Stringholt, exaggerated hot fliction during swing phase. Three types of string hold, again, it's slightly athonomic, gate, really, that hopefully everyone is able to, to recognise.
The idiopathic string hold, as the name suggests, we don't really know why it happens. These cases rarely improve. There is a fairly crude option of performing a tinotomy of the, the long and the lateral digital extents tendons, and there has been some experimental work looking at the use of Botox into the muscular portion of the muscular tendon units, which temporarily changed the gate, if not completely improved it, but certainly classic string hold cases do tend to do fairly, fairly poorly and can can be very upsetting for the owner and negatively affect the career of the horse.
But there are also two other types, pasture associated, which as the name suggests, tends to happen on a herd level with sort of outbreaks. Through ingestion of hyperchois, radica, interestingly, I don't know if anyone else has experienced them in the UK, but we, as a hospital sort of came into contact with a few off the back of our very hot summer that we've just had. So I think that you can occasionally see them in the UK.
And actually, in contrast, the classic spring horses, they, they can show their improvement just by removal from the pasture and a period of rest. And then finally occasionally we'll see horses traumatically induced stringhos they, they have a direct trauma to the extent of tendons, which causes it sort of hyper hyperflexion of . Hyperflexion of the hock during the swing phase of the stride.
Other reasons for gay man worth touching on very uncommon, but myopathy is is sometimes seen, can occasionally present with consistent lameness, but more often not, it's just a non-specific, uncomfortable or poorly performing horse. This is a case that Rachel had in actually, . That had eventually was sent in as a poorly performance, sort of uncomfortable horse rather than a specific lameness, but it was actually right behind them lame as well, and Rachel performed extensive diagnostic analgesia.
In the end, this went for nuclear centigraphy and actually had this really nice patch of uptake in specific muscle groups on centigraphy. CKAS. Are elevated immediately post exercise and a muscle biopsy as well, I sent that to the neuromuscular neuromuscular lab at the RVC and that was actually positive for PSSM as well.
So we don't see them an awful lot. I think as a percentage of our sort of poorly performing abnormal gait cases, they are, they are very, very low, but you do occasionally see myopathy as a cause of that. We look at some specific neurological conditions, that, that lead to gait abnormality, CBM, I think one would be everyone was, is, is sort of aware of.
So, wobblers, two types are recognised. There are, I think, probably some overlap between the two, but essentially type 1 wobblers, tend to occur in young, fast growing male horses, so highly produced thoroughbreds, warm bloods, for example. It's very much more of a male condition, a ratio of 2 to 1 males to females, and tends to cause compression in the mid cervical region, and it, and it's what we call dynamic compression.
So it is generally dependent on head position, usually exacerbated by a flexion of, of the, of the neck. And the pathological changes that we would commonly recognise, we can see here, . Associated with the CT myelogram, but also this pathological specimen as well.
We get malformation of the canal, often there'll be an angle on the canal. We see flaring of the vertebral faeces as well, particularly in the younger animals where they haven't yet closed. And then we see a caudal extension of the dorsal arch or the dorsal lamina.
You can see how now if we refer back to our earlier cervical radiography, you know, this C measurement here is obviously going to be very, very low in relation to our vertebral measurement. And then we would also see osteochondral disease, the articulate process joints. I think the more that we're CT, some of these young wobblers, the more we recognise that their facet joints are also grossly abnormal as well.
Just something to touch upon, CBM type ones is surgery an option. There is some literature out there in the UK certainly owners are fairly, often very reluctant to go forward with that, but you do get occasional owners that enquire about surgery, . Which typically involves into vertebral stabilisation with the use of a curve cut cylinders you can see from, from this radiograph here.
There are some papers out there that can give an idea of prognosis. John Wormsley's paper documented about a 70% improvement or a 70% for one grade improvement. So, you know, if you've got a horse with a single site of compression in the mid cervical region, And it's a grade 2 behind, you can be pretty hopeful that you're going to improve that, certainly a grade 1 behind, maybe a little more, but, but certainly for those horses with with grade 3 signs and above, then it's unlikely to make them completely normal.
I think one thing. That the literature does bear out is that there's a significantly higher complication rate in the cord cervical region, so the C6-7 site, and in particular, you get a lot more problems associated with the the implant and the portal cord of vertebral sites. If you look at the type 2s, so type 2 wobblers, these tend to be older horses, so these very much affect our sort of sports horse population.
It's a cordor location, C5, 67, T1, and this is more static compression, so it's not dependent on, on head position. And that very much involves degenerative disease of the articulate process joints. This is not the clearest radiograph in the world, but I just put it in there just to emphasise that C7 T1 articulation is very important as well.
So although it can be difficult, try, try and make sure, particularly some of these bigger breed horses, try and, image C7 T1 as well, as well as C67. And with type 2 CVM cases, they can have actually a variable range of clinical signs due to multiple effects of the face up property. They've got arthritis, they may have a painful neck, but they may actually have a fall in lameness due to nerve root impingement, that can often be like bilateral.
We'll see a picture of that a little bit later on, and they can sometimes have a taxi due to cord compression as well, so they can be very, very challenging. Definitely worth mentioning, particularly as cases do crop up is HV myoencephalopathy, EH EHV1 viremia affects adult horses usually over the two years of age. So if it's they're very young, and that time tends to rule that out.
There's obviously notifiable and, and I think the important thing, particularly when you're monitoring the outbreak is that the initial pyrexia are very much pre precedes the rapid onset of neurological signs as well. So. Often you get a symmetric para tetraparesis.
These horses often go off their hind legs in particular, that can progress to recumbency, and we may get some additional signs as well. So urine retention, anal tail paralysis, perineal analgia and seizures. And the literature would suggest that there's a reasonably high mortality rate in outbreaks.
So I, I think in particular, if you've got a pyrexic neurological horse, you really need to be aware of perhaps implementing some suitable precautions to try and head off an EHV outbreak if it turns out to be. Obviously, EPM we don't suffer from that here, but it's worth just mentioning, purely because it can be very, very challenging. This is a photo courtesy of Jamie again, two forms of enzootic form, S neurona and a sporadic form from NUI.
And you can get limb ataxia and weakness, often very much mimic a wobbler actually, but, with a variable onset and progression of signs, and certainly if left untreated, then they do progress to, to atrophy. As I said, obviously these horses need to have come from, North or South America, but we certainly do see those horses that have travelled over and it's just worth bearing in mind if, if you do get neurologicalities. Again, finally, it's just worth being aware that you sometimes get multiple lesions as well.
So not all our horses will just have one. They may have genuine orthopaedic pain, and they may have general neurological pathology. We've seen this horse before, so obviously we recognise quite obvious, I would hope, sort of grade 2 slash 3 hind limb deficits in this horse when turning.
And, as you see here, it's obvious sites of mid cervical core compression. This horse actually, although he doesn't trot brilliantly well, was actually, you know, reasonably obviously right hind limb lame as well. And actually, he had marked femo patellar joint effusion and some quite significant ostochondral lesions.
So, although this is obviously a, a fairly extreme example, you know, just bear in mind that if everything doesn't add up, then it may well be that you've got two sites of pathology or that you've got 22 separate lesions, and those can truly be very, very challenging cases. In summary, before we look at a little case example, there are multiple causes of gait abnormality in horses, and they are challenging cases. I find them very, very difficult.
I think everyone does, take good notes and consider that you may have multiple lesions if the clinical signs don't fit with one. Just so we've got a few minutes before question time. I just.
Want to run through a case example that I think hopefully emphasises that this is a seven year old event horse that had a fallout hacking mid February, so preseason stuff was fine afterwards, and you can see from his record, he computed fairly successfully through late March into into April. But then, you know, presented at the hospital for investigation of a right fall in lameness, he's pretty conventionally two tense right fall in lameness straight line. And eventually through diagnostic analgesia, we documented about 50% improvement to the radiocarpal joint.
Diagnostic imaging didn't show up particularly much. And so as I think most people would do, we medicated the radiocarpal joints with triamcinolone, sent the horse home for a period of, of like walking exercise. 3 weeks later, when he was re-examined, sorry, 3 weeks later when he was re-examined by the referring veterinary surgeon, the lameist had improved so he's a much sounder horse, and he returned to work, but the rider still reported that he wasn't right.
So we saw him back at the hospital for a repeaterg evaluation, but very much saw a different pattern of lameness this time. And actually on clinical exam, we saw a reduced range neck of the neck range of neck motion. So this is a seven year old horse.
He should be coming right round to stifle with that. You can see he kind of wants to get to the treats, but almost then sort of tries to snatch at them and then releases and comes back. So, you know, sometimes relatively subtle clinical signs can be important, and again, remembering they may be asymmetric as well.
And actually, you know, when we performed a neurologist exam on this horse, we found that he had very mild hi in ataxia with no evidence of, of weakness. This time when we trotted him up, he showed a very different. Be a number of opinions on where this horse is lame, but for me, this horse shows a relatively typical if there can be such a thing, sort of abnormal gait for, for cord or cervical related lameness.
So, you know, I think you could argue there'd be right and left for lameness components, but this horse has very much a sort of, you know, abnormal neck position, uncomfortable neck position, a sort of skipping, disjointed gait. And if we look at him on the left brain, the right for lib lame miss is a little bit more apparent. And with his neck related cases, you often see the lame miss on the outside, so the lame miss is worse with the leg on the outside, and again, he's got this sort of skipping, hopping gate with a fixed neck position and just generally uncomfortable.
And so it probably transpires that when I was blocking this horse the first time I saw it, I was partially improving maybe a mild degree of carpal lanes, but actually I'm sure there was probably a degree of cervical involvement as well. What do we do with this horse? An analgesic trial was negative, so diagnostic analgesia is a really good horse to blocks, so we, we blocked him up to his shoulder, that was all negative this time.
And we performed nuclear centigraphy and noted some increased rate of pharmaceutical uptake of the C67 region. Difficulty is is that some normal horses will present with that as well. So, you know, it can be a very difficult thing to objectively analyse.
And when we radiographed his neck, we found that he had some arthropathy at the cordal cervical site. So if you see here at C45 got a nice intervertebral forometer, and then here at C56 and C67, we've got some ventral enlargement, but as we know from the literature. What's the significance of that?
You know, unfortunately, this was back in the day before we had the CT, so. We didn't have that option for him, but the diagnosis I came to that he had traumatically induced for arthropathy, nerve root impingement, and cord compression. So very much a combination of orthopaedic pain, but also neurological signs as well.
We medicated his C67 and C56 fort joints, but unfortunately, we're only able to mildly improve him. So in the end, he ended up being euthanized, but just goes to show how these cases can change and they can also be very, very challenging in terms of their gait analysis and investigation as well. I think we've got time, hopefully, for a few questions.
I hope that was useful in terms of how we might have a look at some of these abnormally moving horses. Well, fantastic. Thank you very much, Russell, and hats off to both yourself, Rachel, and Jamie for all time in your presentations to perfection.
So that is also another very good thing. So yeah, as, Russell says, we have got a little bit of time for a couple of questions. I know a couple have come in, .
So the first one I've got here is with regards to the analgesia trial, the base baseline washout, question mark, wash out between negative PBZ trial and gabapentin. Probably a week would be, I think, more than enough, to be perfectly honest. I mean, I think if you look at, you know, detection times just from the BHA point of view, of 7 or 8 days for, for Bute, I, I think if you, if you give a week, then you're probably being overcautious, but it should be fine.
Normally for horses coming into the hospital that have been on a butte trial, I give them 2 or 3 days. And, and so realistically, if you're tight for time, I'd have thought, you know, 2 or 3 days would be plenty. Fantastic, thank you very much.
I think we touched on, I wasn't there chairing this morning's equine session, on lameness as well, but, this also does relate to lameness. Hillary's asking, if she missed this morning's session. Has anyone touched on thermal imaging, and is this of any benefit in working up lameness?
She's received some emails recently regarding the technology and wondered if it was something worth looking into for future. That's a very good question and in danger of stirring up a real on it. Come on, it's 4 o'clock on a Sunday afternoon.
When else we can. My per there is, there is a lot out there. My personal opinion at the moment is that, you know, there isn't enough really sort of published evidence for thermal imaging.
We, we've had, we certainly don't have it at the hospital, and that's that's a deliberate choice, and I have had some. Input from thermal imaging at the owner's request and people coming out, and I've by and large found it fairly unhelpful, in all honesty. I think the trouble is, is that, you know, that they're so prone to artefact through, room temperature, draughts, a bit of sunlight shining on the horse that, as I said, for me personally, I haven't found it to be a useful imaging modality at all, but.
I, I'm sure there will be plenty of people just waiting to say that they have, and certainly it is becoming far more widely available. No problem, but as you say, it's probably as once as everything as technology progress and then it can become more of an accurate, mode then, hopefully that's see how it goes and how we interpret different changes in limb temperature. I mean, I think there's, you know.
There's sometimes when you've got a hot fetlock, and clearly there's fetlock pathology, but then again, you can find that by doing a nerve block. I think the time it would be very, very useful would be if you could extrapolate back, neck, pelvic pain, you know, trunk lesions to different areas of, of skin's temperature. And as far as my experience has been, for those very sort of challenging back pain, pelvic pain cases, that's when it's struggled.
So, as I said, I, I don't think it, for me, it currently doesn't have an application for those in my case, though. No problem, thank you very much. It doesn't look like we've got any more questions.
We've just hit 4 o'clock on the nose. So, what that leaves me to do is to, thank you all for attending Virtual Congress 2019. That is it.
We have, do have one more hour on the farm stream so if any of you are interested in farm, then do shoot over to the farm stream for the last one hour presentation on that. What I'd encourage you to do please is provide your honest and open feedback. We love to get as much feedback as we can, both to provide to the speakers, but also for us to help develop our programme and how we can improve going forward.
Thank you to Lewis. Lewis has been in the background, helping people, with any technical difficulties they may have and answering some questions. So thanks to Lewis for, joining me today.
And obviously, thanks for, go to, Russell, Rachel, and Jamie, for putting together three fantastic presentations, which I'm sure you'll all have found really useful. We are aiming to get these recordings, all the recordings from Virtual Congress up on our website from this Friday, which is the 25th of January. It is quite a big process, so, do, please do bear with us, but I'm sure we'll be able to get them up by then, and we will be sending out emails to let you know they are available for you to watch.
So, wishing you the best of the weekend, and, we look forward to welcoming you onto the webinar soon. So thanks a lot. Goodbye.