Good evening everybody and welcome to another webinar proudly brought to you by the Webinarett and TM UK. Tonight's topic is a very interesting one on management of epilepsy and we have an absolutely amazing speaker for you tonight. His, credentials are beyond reproach and he is a really good speaker.
But before we get over to introducing you to Laurent and, getting on to tonight's presentation, we just have a little video that we want to play from our sponsors. I'd like to say thank you to TM for sponsoring tonight. It makes it possible that we can bring Laurent to you because of their generous sponsorship.
So, Paul, if you'd like to start the video for us. Hi everybody, good evening. My name is Will.
I am a vet working for TDM UK as a product manager. Thanks to Laurence for presenting this presentation this evening for us on epilepsy. We just wanted to sponsor a webinar, on epilepsy for you, just so you could take time to learn a little bit more about epilepsy and how to deal with cases effectively.
And also at TBM we have a neurology range which we are looking to promote and just make you whereabouts. So for those two reasons we approach webinar but just to kind of, give this presentation for you guys. So, one of our products in our neurology range which we've just launched is Solid Fen.
So Solophan is a phenobarbital, generic tablet, which I'll explain a little bit more about in a minute. It forms part of a neuro neurology range with Zyoppa. So Zyopal we have is a, a, a diazepam injectable, licence for dogs and cats, and obviously that can be used in the acute management of seizures, so it kind of fits in with this presentation.
And Solifem being phenobarbital, as you're well aware, is for more long-term management of seizure control, and we have a licence for dogs with Solifem. Similarly to our antitox range and our ophthalmology range that we have with TVM, with those, when we launched those, we gave a lot of practise support materials out alongside the products. And we've done the same with neurology as well.
So, if you go onto our website, you can actually see we've got a lot of downloadable content that you can, Take down for yourselves, download as PDFs and just have a new practise, or we can actually post them out to you as well in hard copy. And it encompasses things like, seizure information booklets for owners, and seizure guidelines, so how to manage kind of long term, seizureing patients, with things like phenobarbital, and also we have a status epileptic guideline as well that you can download, which you might want to pop in your crash kit, for instance, that, can just help you in, in an emergency situation. With regards to Solien, we're unique with the phenobaral generics in that we have bioequivalent to the market leading brand.
So TVVM have done a study that just basically demonstrated that, this bioequivalence meant that we could, have an on label swap. If you're thinking about swapping from the market leading veenobarbital brands to Solien, you could now do this on label, because we don't have a caveat on the SPC that prohibits that. If you look closely at any of the other generics, they, they actually have that in the SPC.
If you've got a stable patient, then they wouldn't recommend switching, whereas with Solophan we don't have that. So you just have a little bit more protection and a bit, bit more peace of mind if you did decide you wanted to swap over to Solife. And also, obviously, if you get any new epileptic patients into your practise, then certainly Solifen is appropriate to use in those as well.
The benefits are that Solifen is a tablet that you can divide, so they come in 60 milligramme tablets with little small lines down them so you can snap them into quarters, which means that you can get 50 milligramme dosing increments which allows you to get more accurate dosing when you're titrating up and down. Cause usually we have to kind of go up or down by about 20-30% when we're switching the dose, when we need maybe a dose increase, for instance, in the early stages. And also you can just have one product for the shelf, the majority of dogs as well, rather than having lots of different tablet sizes that you've got to stock.
It's flavoured, so, the flavouring is liver flavoured, which hopefully will help with compliance for our patients, which, you know, can be an issue sometimes, and compliance is of the utmost importance when we're dealing with epilepsy. Also, Tablets are blister packed as well. So, like I say, they come in boxes of 60.
It means you don't have to keep a lot of stock on the shelf, especially if you're a small practise, that might be beneficial. And just being blister packed, it means that it's safer to handle, you're not having to directly handle the tablet. And it's easy to dispense and count when you're doing stock stock counting.
Also, the list. Price is quite attractive, so against the market leading brand, you're saving about 3. So that can actually, give a significant saving to clients per year, depending on what size of dog that you're treating them with.
So that saving can obviously be passed on to the client if you want, which can then fund extra blood tests or extra, other treatments that you might want to. If you would like to get any more information on Solifen, then please just go to our website www.tbmuk.com or email us at our [email protected] email address.
And we can certainly answer any questions or send you out some literature should you want it. Thank you very much for this introduction and thank you for the webinar that for hosting this webinar and for TVM, our sponsor. And what I'm going to do today is to give you an overview of how to manage epileptic dog, and what I've decided to do is to take you from the first moment with, you know, the client and the dog into your consultation room to the management of this patient in terms of what Treatment to give.
So we're going to review all the things we should have in mind. The first one being getting a good history from the owner. Remember that, you know, the dog won't be for the large majority of case sing in front of you.
So we're going to go through what kind of questions to ask to the owner to ensure that you're actually dealing with an epileptic seizures and we're going to review what could be over mimic that could put you in the wrong path and then. We're going to discuss when should you do further tests, and when are you going to suspect idiopathic epilepsy, and when some red flag should be coming up to say, Hold on a sec, I don't think it's idiopathic epilepsy. I think we should do further investigation to look for, for example, metabolic or structural brain disease.
And then. We're going to focus on the treatment of idiopathic epilepsy looking at when should we start and what to use in the first place, what kind of drug. I will give you my personal opinion.
What do I prefer between the different first line licenced drugs. And then how should you monitor this patient? What to expect, and when should you use an add on antiepileptic drug and there still a lot of confusion.
Should you add something? Should you replaced by something? And then we finish with this sometimes very annoying situation, annoying and obviously for the owner and the patient and annoying because they tend to be often out of hours sometimes you're relaxing on a Saturday night.
You get this phone call, you got a dog in status epilepticus, or having cluster seizures during the last few hours, and you have to go to the clinic and stop this dog seizing. So that's the plan for this evening, and we're going to spend about an hour and I hope you enjoy this presentation. In case you don't already know, TVM has put together some fantastic brochure.
I'm a big fan of this kind of algorithm. And that's the way my brain tends to work and this tree, and you can download that from TVBM website where you got this algorithm about what how to manage this scale and it pretty much summarised this presentation starting, you know, is it actually an epileptic seizures and what tests you should do, what kind of drug to start, and so on. So I really Recommend, have a look at their website and download this decision tree.
It's totally free, so please, you know, enjoy yourself and have a look. So first step, we are going to take you back to the consultation you've got on your computer. The next patient is the dog office.
Mrs. Smith is presented for seizures. What should you do next?
Well, The first step is really to sit down with the owner and to ask a few key questions to ensure that the animal is actually having an epileptic seizure and not something else. Remember that 99% of the time the dog is not going to put a show in front of you having an epileptic seizures, and you are. To rely on the description to make sure that it is an epileptic lesion and not something else.
Remember, you know, it could be very difficult for a pet owner to describe an event like that. It's easy, you know, to get confused with all the mimic. They're not medically qualified and if there is the first take on message that if you're not sure, ask the owner to get the video footage.
The mobile phone technology these days very easy to do so. What is an epileptic seizure? An epileptic seizure to me as a neurologist is a symptom of a dysfunction of the front part of the brain, what we call the forebrain, which is, you know, in front of the brain, in front of the cerebellum membrane stem, and whatever the And cause there is an imbalance between excitation and inhibition.
That's the way the neurons communicate and usually there is a very fine harmony between neurons keeping everything under control, and a seizure will occur when there is a riot in part of the brain. With this either too much sexitation, not enough inhibition, and then things get out of control and you've got the equivalent of an electrical storm spreading throughout the cerebral cortex. In terms of phenomology, usually epileptic seizures tend to occur out of the blue.
The owner will usually say first thing middle of the night or early hours of the morning, but in general it is when nobody is expecting it. And also it's exceptional to have a seizures during exercise or excitement, with a few exceptions, for example, the myoclonic seizures that could be triggered by visual auditory stimuli. But the large majority of seizures will occur out of the blue when you're not expecting.
There are usually sometime I should say pretal sign where the animal may be a bit more clingy, you know, with recurrence it may pick a subtle abnormality in the behaviour of the dog, and then you're going to have the actus, which is the sever itself, and the eus last. In general, 1 to 2 minutes, most pet owners will tell you it sounds like an eternity, you know, 2 minutes watching your dog having a fit really sounds like a long, long time. And during these secs, depending on the type of seizures, if it is a generalised seizures, then the animal will collapse.
Lose awareness. The eyes are open, but there is no awareness of the dog of the surroundings. There will be chatting of the jaw, chattering of the jaw, hyper salivation, violent tonic or clonic movement in the limb, and sometimes over autonomic signs like salivation and defecation.
That's the most common type of dog, also known as a generalised tonicoclonic seizures or. Seizures and then the least common seizures would be the partial seizures. And while with the generalised seizures, this electrical storm affects the entire cerebral cortex at once and with the partial seizures, this electrical storm in the cortex is only confined to a region of that cortex and obviously depending on which region is affected, the manifestation will vary.
But most often you may have twitching on one side of the face, salivation on one side maybe twitching on one limb as well. The third category would be the partial seizure with secondary general, generalisation, and then after the accus, which usually lasts 1 or 2 minutes, the dog will enter a postal period which is a bit like the hangover of an epileptic fit where the animal will be confused. It may be attacked, bumping into things, maybe want to drink more, to eat, and sometimes it may be more aggressive.
Which is obviously not very often seen, thankfully. So here is an example. If you've never seen a generalised t called clonic seizures, which is the most common type in dog, the dog suddenly collapsed on the side.
You can see the eye open, and the owner would describe a glaze appearance. There is scattering of the jaw, violent tonicoclonic motor activity and hyper salivation, and sometimes not only this dog urination and defecation. So that is what the owner will often try to describe, but it really, it's really an art to get this information from the owner and you need to be very mindful not to lead the owner to give you the answer you want to hear.
And so it takes a bit of practise, but what I want to know is when does he occur, how long does he last? Is the animal aware? And what I mean by that, when you call, is he responding?
What is he doing with his limb, any autonomic sign, and how long he lasts. Regarding how long it lasts, be very mindful. For a pet owner, if you just ask this question, how long it lasts, it will be from the onset of the excuse to the recovery phase, the end of the recovery phase.
Well, how long he lasts is I'm mostly interested by the excuse itself, so be a little bit more specific when you ask that question. Because that would be a key amount to distinguish from a mimic of epileptic seizure. So what would be condition that could mimic epileptic seizures?
Well, the most common one is what you're going to see on that video. And what you can see on that dog is that initially he's standing up and he has this involuntary flexion of the thoracic limb starting with the left one. When moving to The affect again that limb and it will slowly move to other limb, but the striking thing is that this dog is fully aware of his surroundings.
And then you can see the dog lay down and he's going to start lifting. Now lifting again the left wall. He's also flexing the hip.
And then he's going to do that on the other limb, but you can see how easily it is for an owner to give you the wrong information. If you say, does the animal collapse? Well, for a pet owner, this dog is collapsed.
What is he doing with his limb? And if you even mimic, you know, the tonic clonic movement, the owner may tell you, yes, that's exactly what he does. But you can see that on this video there is a big, big, big difference.
And again the video speaks a million word ends. Any doubt obtain a video footage. So what you see here is probably the most common mimic of epileptic seizures, and this type of condition is named paroxysmal dyskinesia, also known as paroxysmal movement disorder.
It is seen in any kind of breed. However, It's something that we've known for many years and for many years we've been labelled as partial epileptic seizures even from some of my colleagues, veterinary neurologists, and we only started to scratch the surface with regard to Standing this condition and I will tell you in a sec how much do we know or how much little do we know, but you may have heard this condition with different names because in some breeds they've been seen for many, many years and labelled. In cavali King Charles, for example, episodic falling or collapsing cavalier, the first report was nearly 50 years ago, and it was thought initially was a muscle disease.
In Bauerrier, dyskinesia has been labelled in the past CS or spike disease in Scottish terrier they've been labelled Scotty cramp. What to take of that is, you know, there is a kind of rule in human or veterinary neurology when you don't do anything. In terms of pathophysiology, you try to find a very complex name but no one can pronounce CCS canine epileptoid cramping syndrome, or you give it your own name, spike disease, which was a dog in the Netherlands.
But the bottom line is that Don't try to see past of this, you know, weird name. Beyond this, it is the concept of paroxysmal dyskinesia, which is a common mimic for epileptic seizure. So as I say, we know very little, but here is an example of the so-called canine epileptoid cramping syndrome, and all these mimics look very similar.
The dog remains fully aware of his surroundings. He's having this involuntary flexion or extension of the limb. Sometimes they got also mild tremor of the head, the episodic event, but they can last as, you know, short as a seizures, but they can sometimes last up to a couple of hours.
Absolutely love this video that you're watching now because as the dog is recovering, it looks like the owner is having another form of collapse. He's on the floor, not sure really what's going on there. Here is an example of the episodic falling in Cavalic King Charles.
Again, the dog will suddenly collapse and while being fully aware of his surroundings, the dog is having this. Increase involuntary motor activity with cramp affecting all four limbs. And in Kavaing Charles, like in any other breed, it may last a minute.
It can last 1 to 2 hours, which is an important factor to differentiate with an epileptic seizures. The other main differential to recognise is not an epileptic seizure is the fact that while the motor activity affects all four limbs, the dog remains fully aware of its surroundings. So what do we know or how little do we know about this condition?
Well, in Kabale in Charles, which was the first condition I started to look nearly, you know, 18 years ago, we were extremely lucky to find with a small number of affected dogs a genetic mutation causing this episodic falling. So at least. In Kalic insurance there is now a genetic test that will allow you to diagnose that condition and for most of these paroxysmal dyskinesia, they are functional disorders, so you can't really rely on the MRI and CSF or CT scan to diagnose them because all these investigations will come back normal.
What is important is to recognise them on video footage and in Kavala in Charles you can establish a diagnosis with a genetic mutation. In terms of treatment, and here is an example here where I discussed the treatment with you of another affected cavalier. A long time ago, we're talking nearly 18 years ago, I was treating Cavalier with clonazepam, which worked very well and it usually starts at a very young age.
These dogs are usually 3 to 4 months of age when they start. The problem with clonazepam is a benzodiazepinem and in dog very quickly they develop functional tolerance, which means that You know, the effect of the drug will lessen with time, and we then move on to try a drug that is commonly used in humans with dyskia called acetazolamide, and acetazolamide provides a complete relief of the symptoms. However, it is only a symptomatic treatment.
It doesn't get rid of the genetic mutation, and you need to treat these dogs for life, but they respond extremely well to acephallamide. The second breed that we investigated with this dyskinesia because of the large number we're seeing was the so-called canine epileptoid cramping syndrome, and we've done a number of publications on that compared to Cavalier, well, they have the same phenotype. They look exactly the same, you know, when they are having this episode, but they tend to occur at any age pretty much.
They also were showing often mild tremor of the head. But one thing that keeps coming back when we did that phenotypic study is that the owner was mentioning this gut sound what we call bog boring me, and he looked like the dog was having some abdominal cramp, you know, when he's having one of these episodes. The other important factor is that the others were telling us that.
Changing diet or giving treats can sometimes make the episode worse or actually make the condition better. So that wanted us to look at the diet and see what common denominator there was between all these anecdotal reports from Petuna and the common denominator in Bauer was the gluten in the diet. And we did this second study that shows that border TIer with this paroxysmal dyskinesia are very high antibody tighter for gluten.
There's two antibodies like the anti-gliadine and anti-transcontaminates, and if you put affected border teria on the gluten-free diet, well, and we monitor them over 9 months, not only the antibody type return to normal value, but the dog stopped having this cramping syndrome. And if you reinstate a diet that contains gluten, these dogs were relapsing. So in border, and we've only established that link in that breed.
We know that they have a genetic predisposition for gluten sensitivity and in that breed only gluten is a trigger for this dyskinesia mimic of epileptic seizures, . So the treatment in that breed is a gluten-free diet. What would be over mimic of epileptic seizures that the owner may confuse or give you wrong information.
Here is an example here where we see a lot and they are often referred to us for seizures, sometimes labelled as partial seizures. It's the so-called idiopathic head bobbing or head tremor, . Quite a good idea to show you a bulldog because they are the number one breed for that condition.
Usually they are young adult dogs. There's also a predisposition in Doberman, but it can pretty much affect any breed. So compared to an epileptic seizure, this dog is fully aware of the surroundings.
But also if you interact with the dog, for example, give him a treat or call him or give him a toy, then you can stop this tremor which you cannot do if he was an epileptic citizen. This is an idiopathic condition likely a functional disorder. And again, if you do an MRI, you expect to find nothing.
There is only one dog, but we find a thalamic tumour, but it was an older dog, whether or not it's comorbidity, and that was triggering, you know, this as a stress related this tumour, we don't know, but in the, in the very, very large majority of dogs, the diagnosis is made on video footage. And there is no treatment. However, with age, about 2/3 of those will enter spontaneous remission.
Finally, a last mimic of epileptic seizures will be. Fortunately, the video doesn't work, but I'm sure you can imagine what this dog is doing is the so-called fly catching syndrome dog that follow in your room or at home, imaginary fly and try to catch them with their mouth. And this fly catching syndrome was for a long time labelled as a psychomotor seizure, and there is this recent paper that And look at this hypothesis of partial sever versus more likely a behavioural type disorder, and they find that there was, you know, very little evidence that this fly catching syndrome was an epileptic activity, but these dogs tend to respond for the large majority to antidepressants while a minority respond to anti-epileptic drugs, so.
The thought these days is that we're dealing with a behavioural disorder and the treatment of choice would be antidepressants like clomramine or imipramine. So what to take from this first point, making sure that the owner, you get a good history from the owner, but we're dealing with an epileptic seizure and asking them when did that start, the circumstance, the duration, is he aware of his surrounding presence of involuntary motor activity and autoic sign. And if you have any doubt, remember common thing are common, and if the episodes are frequent enough, then try to get a video, and the video may provide some clue.
Otherwise there is nothing wrong putting the dog on the trial anti-epileptic drug for a few weeks and see if the frequency. Decrease, but to do that we need to have a good idea of the frequency prior to the treatment so you can compare before and after. In humans, to distinguish all of that, we will do an EEG, which you know can be done, but in the interectile phase it's not very common.
You will find interectal abnormality confirming the suspicion of an epileptic seizure. Second step, when you're pretty sure you're dealing with an epileptic seizures or you got a video to support that, is to know, am I actually dealing with idiopathic epilepsy? Should I worry about an underlying cause?
As you know, epileptic seizures can of course find inside the brain or outside of the brain. Causes outside of the brain coming into the the remit of the umbrella I should say of reactive epileptic seizures, and reactive epileptic seizures means that the brain is totally normal, but it is reacting to something abnormal in the blood, and this abnormality could be metabolic or toxic. Now toxic disease, you know, do not cause recurrent epileptics with maybe the exception of lead poisoning, but usually it's something that happens over a few hours and with other systemic signs vomiting, diarrhoea, salivation, tremor, and then cluster seizures.
With regards to metabolic seizures, metabolic cause of severe food, there is a very large catalogue that you will find in many texts in my experience. The most common will be portosystemican, congenital one, in especially in pure breed dogs, usually young, very young dogs, and they are often associated with other signs of hepatic encephalopathy. And then all the dogs with hypoglycemia are often related to Ninoma after that to that puppy.
We breed dog with hypoglycemia, and finally hypocalcemia and as well, polycythemia. That's pretty much what I've seen the most over the last 22 years of, of doing clinical neurology. And then the other category would be intrareal cause and they split in.
To symptomatic epilepsy where in that case the epileptic seizures are the symptom of a structural disease in the brain and that could be anything from tumour infection, inflammation, or potentially stroke or previous head trauma. In that case, by doing further tests, MRI, CT, CSF, you will be able to find a structural cause causing the seizures. The last category is the overall most common cause in dogs and in humans is the so-called idiopathic epilepsy, which relates to a functional disorder in the brain.
The best way to expand it to another, an abnormal wiring the dog is born with and will live with for the rest of his life and exceptionally die of. So when to suspect idiopathic epilepsy? Well, the age of onset of the first seizures can sometimes give you some idea, but that is only giving you the balance of probability.
So if you experience your first seizures between the age of 6 months and 6 years. The balance of probability is more likely that you have idiopathic epilepsy than something else, and if you're outside of the range, then the balance of probability is more likely that you will find a cause for the severe metabolic or structural brain disease than idiopathic epilepsy. However, you could still have a structural disease in the brain causing the fit in between 6 months and 6 years, and the reverse you could have an early onset idiopathic epilepsy or a late onset epilepsy, but at least to give you some guide as to when to start thinking, hm, maybe there is something else that idiopathic epilepsy.
The other thing is that as a minimum I will do a targeted neurological exam in any epileptic patient. Now if you've ever listened to me lecturing, you know I'm not a big fan of doing a full neurological exam. I think it doesn't make any sense and it's the best way to get lost in detail.
I tend to do a targeted neuro exam, which means I use my neuro exam to answer a question and the question relates to the problem the dog is presented for. So for an epileptic dog, I'm going to focus on the mental stages. Especially, you know what the owner report as changing behaviour in the dog.
I'm going to look at the gait if the animal are toxic, if it's circling to one side. I'm going to look at the postal reaction because when you do the propositioning or the hopping that involves the contralateral forebrain. I'm going to test the Mona response as well.
Because again that will test with the PLR, the contralateral forebrain. If you've got an abnormal menace on one hand with normal PLR, then that will point toward a lesion in the contralateteral forebrain to the eye tested. And the last one is the response nasal stimulation.
So what I want and I played a video there to show you here the palpable reflex that you do prior to testing the menace. And on that dog, what I'm looking for, I'm testing this forebrain function. Manas is intact on the right.
Then I'm going to do the mannas on the left. And you can see that this dog has nona on the left eye. So what I'm looking here is, is the examination between the feet normal or not?
And if it's abnormal, do I've got symmetry or asymmetry in my neurological deficit? Here we've got very clear asymmetry. Why it is important.
Because if we come back to the three large main category of causes of seizures, if I got a symmetry, then that can only fit with a structural brain disease. With metabolic and even with toxic, you should have, if there is associated neuroscience, they should be perfectly symmetrical. So in that situation you can be guaranteed that there is an underlying disease in the brain.
If the neuro exam in between is abnormal, but I've got symmetrical neurological sign, then the first question to ask yourself, when was the last seizures? Because as you know, shortly after a fit, the animal may be postal. And the protal sign can last up to a week.
So in any doubt, if you're examining the dog on the same day as an epileptic fit and you find neurological abnormality, then repeat the examination maybe a couple of days later and see these abnormalities are still present. But if I've got a symmetrical neuroscience not relating to the proctal, then the first thing I'm going to do is to do a metabolic workup. And if that is normal, then look for structural brain disease.
If my neuro exam is normal, then I very much rely on the edge. If it's a dog before or before 6 months or older than 6 years, then I will do further tests to look for an underlying cause. You could, as you saw in this picture, which actually is a cat, not a dog, but sometimes pathology like brain tumour can cause isolated seizures, especially if the tumour has started growing in an area of the brain that the dog doesn't choose to be a dog.
Here at the front is affecting the olfactory lobe. Well, he can use it all the olfactory lobe to smell his food, so you won't see anything and any manifestation on the dog. So if the owner wants to be 100%, what should you do?
Well, in theory, to know if it's definitely neuropathic epilepsy, some pet owner, even if, you know, they tick all the box with the edge and the neuro exam is normal, then. The worker will be ruling out metabolicals by doing blood to HMD balacid, and then ruling out structural brain disease by doing MRI, ideally was a second option CT and then CSF analysis. And to expand very clearly in that situation to the owner and tend to do that prior to the test, but finding nothing has a meaning.
If you find nothing, it means you're dealing with idiopathic epilepsy. Step 3, when should you start treatment? What should I use?
Well, it's very important before to go into the detail of that to understand where we are at with idiopathic epilepsy. If you have idiopathic epilepsy, you're born with that, but you're going to live with that and die with that and very rarely die of idiopathic epilepsy. Ideally, what we're trying to achieve is very much the balance there is to control the seizures, which may mean having no feet or more realistically to limit the number of feet to something reasonable and it's very subjective what one person will find reasonable number versus another one.
I will say if a dog is having one fit every 6 to 8 weeks. That is, you know, good enough in some dog. Well, you know, for some pet owner, they will only take good enough if the dog has no feet at all, because the downside, you know, giving antiepileptic drugs is that this drug can have side effects, and we're trying to find the right balance between having no feet or limiting the number while having no side effect or the least side effect, but also the best quality of life for the dog and the owner.
Again, among all the practise support information provided by TM, and this is to remind me and it's something you can download on their website, but it's very important to encourage your pet owner to keep a diary of when the dog is having a fit. So when they come back to you, usually when things are not going well, you can objectively look at the frequency of the seizure and decide, you know, further action. So when should you start treating?
Well, there are situations where there is no doubt and there is the rest is very much opinion based. If the dog is having even the first episode of static epileptic cluster seizures and there is no known exposure to toxin. And no metabolic cause identified, then I will start treating straight away.
One example in the UK would be border collie. They tend to be prone to cluster. They can be quite aggressive in terms of frequency of the feet starting at 1 year of age.
If I go to border collie, first episode is having 4 seizures one day, then I will start antiepileptic treatment straight away due to the predilection. The rest is very much will be on there and personally I tend to start when the dog is having 1 or more than 1 fit a month. But before to do that, I will, you know, have an observation phase where I will wait for the dog to have minimum 3 seizures before to say yes, it's happening at least once or more than once a month, .
You know, some people would advise 250/6 months. I think it's a bit overkill personally, but again it's only my own opinion, so. Take it or leave it.
What I tend to do at least 2, you know, 1 or 2 ft a month, I will start treating after an observation period of at least 3 seizures. And then the other indication would be you've got a very jare dog, for example, a Great Dane, having, you know, not very often epileptic seizure, but one is having one is very positive. That could be enough.
You know, for some pet owner to decide, well, if we can stop the feet happening or make them as infrequent as you can, I want to go down that route, same thing very rarely a dog may be aggressive after a fit because they're confused, because they're blind, you have young children in the family or another dog and this dog gets attacked. It may be another reason, even if the feet are not very frequent, for the UN owner to decide to start the dog on antiepileptic drug. So what are the drugs available for dogs?
Some of them are licenced phenobarbital, and you know there are a number of formulations. The latest one is obviously lien released by TBM this year. You've got also hemipetoid and phenobarb and hemipetoin, also known as Pexion, are the only two first line licenced drugs in the UK.
And then we've got bromide, but as a licence as an adjunct to phenobarbital in refractory case. Then you got the off-license drug that we commonly use. The most commonly used, at least in my practise is levetiracettam, and we discussed as well the use of toyramide, Zonegram, zonizamide, and pregabalin.
Overall, the first line antiepileptic drug. We estimate that we get this balance between good and side effect in about 25% of dogs, which means that there are still 25% of dogs not doing well despite antiepileptic medication. And to put your mind at rest, you know, in humans, they're not doing better than we do, you know, there's still a number of patients that would be pharmaco resistant.
What not to use? Well, definitely, you know, using diazepam tablets and some practitioner may do that because they don't want to give phenobarbital and they want to try something else initially they go with oral diazepam, it's a waste of time to give it as an anti-epileptic drug, waste of time because the half life is too short. The half-life with chronic administration will even get shorter.
And you've got functional tolerance and risk of hepatotoxicity. So diazepam is a very good anticonvulsant, meaning it's good intravenously to stop the fit as it occurs, but it's not an antiepileptic drug in orally. So I will not encourage his news.
The two first line treatments are phenobarbiton and hemipitoin. Penobarbiton has been available for many years. We're very familiar with that, and we know again that about 3/5 of dogs will have a good response on phenobarbital.
Phenobarbital can be used twice a day because of its long half life, and I usually recommend starting 3 mix perk BID orally or around 3 mixs per gig. At the end you need a reasonable tablet size, and the advantage of fullyan is that with one tablet you can actually split it in 1530, or 45 and 60 milligrammes. Phenobarbital has been used for a long time and we know that about 90% of dogs will have a response if they are within the therapeutic range of 20 to 35.
Below that, a small number of dogs can still respond and above that you got the top. Toxic range where some dog may need to be at that level to have a response, but what we want ideally initially is for the dog to be in the therapeutic range. When you give phenobarbital, it will not have its effect straight away, and it will take about 2 weeks to reach a steady state level.
And that's why 2 weeks after starting the drug, you need to have, you know, to come back to do a serum level to make sure that you reach a therapeutic level. If you keep giving phenobarbital long term, what will happen is that phenobarbital will induce his own metabolism, and that will cause for the half-life to drop. Consequently, if you carry on, for example, on that graph, giving if you start two tablets and that puts you right in the middle of the range, with time, the serum level will slowly drop.
That could happen in a matter of weeks, months, and some it may never happen. But that's the reason why you need to do regular blood tests to be able to monitor the serum level and as a result of that if the serum level drops, you may have to increase the number of tablets to keep the dog within the same serum level. When should you do blood level of phenobarbital, as I say, when you start two weeks later, check if you are within the therapeutic range.
Ask the owner to keep a diary, and if you observe that the frequency of the feet is increasing, then this should be a trigger for them to bring you the animal. When you start in the Barbiton, I usually recommend to do it every 3 months with, you know, HMB to monitor for side effects and then if everything goes fine, do it every 6 months. If you have to treat the dog for other conditions that imply the use of drugs that may interfere with the metabolism of yobarb, steroids, cyclosporin, then I think it's good practise to test the serum level before you introduce this other drug and then 3 weeks later to make sure it's not affecting the serum phytobarbital level.
If you see side effects that could be fidomar related, for example, sedation, ataxia, then it is a reason to do it. And finally, every time you're going to change the oral dosage, check two weeks later what you achieved. Do not assume that by increasing.
So by doubling the number of milligrammes orally, you're going to double the serum level. There's no direct link between the two. Does it matter when you do the blood level?
Well, in theory, if you reach the steady state serum concentration, there should be minimum fluctuation between thick and trough. So in theory, that should not matter when you do it, . And it would be unmanageable if you have all your epileptic patients turning up when you open the practise and before you close.
What I would recommend is as good practise to do it always at the same time on the same dog. That would be probably the best. There is only in dogs that stopped to respond to fiobar.
They've been on fiobar for a long time, then it could be useful to check the pick and trough. Because in that case, the half-life may have dropped below the interval of administration and there is this handful of dogs that we require TID administration of in a bar, but they are very rare scenario. So when you start feeling the barbiton, what you're going to do, start around 3 weeks per kick.
As you need to come back 2 weeks later. If the serum level is within the therapeutic range, then I usually ask them to come back 4 weeks later again, so at 6 weeks to recheck that we're still within the therapeutic range. Why that?
To preempt this auto enzyme induction and and phenobarbital inducing his own metabolism. If the level is below the therapeutic range, then I'm going to increase the number of tablets, check again two weeks later, and I'm going to do that until at the beginning I'm well within the therapeutic range. If the level come back above the therapeutic crunch and the dog is having no side effects.
Then I'm going to leave him, as you know, to come back 4 weeks later and I will only decrease the oral dose if the level is still above the therapeutic range. Following that, how do I make decisions about dosage? Well, I rely primarily on the clinic, clinic meaning, do I've got improvement in the seizures?
Do I've got side effects? And I only use the serum level as a secondary, element in my decision. For example, I've got a dog that is within the therapeutic branch.
But the seizures are not improving or they're not good enough, then it all depends where is this dog in the therapeutic range, because if it's still in the bottom half, then I'm going to increase the oral dose to bring the dog to the top half of the therapeutic range to see if it improves the situation before I something else. If I've got a dog below the therapeutic range and he's having no feet, then I'm going to keep him like that. I'm not going to change anything.
And if that same dog starts to have more feet, then I'm going to increase the oral dose. In some situations, you can't really afford to wait 2 weeks. And that would be again a dog having, for example, 1 ft on Monday, then he's having 3 ft on Tuesday, and he's having 5 ft on Wednesday.
In that case, I need to load the door on phenobarbiton, and the way I do that is I'm going to use intravenous phenobarbiton. The loading dose is 18m per kick, but instead of giving it in one go, which may cause excessive sedation, I'm going to give policies of 3 mixs per kick given every 30 to 60 minutes depending on how sleepy the dog is after each li. So I give 6 bolus of 3 mixs per kick, and that will help me.
Within 3 to 6 hours to reach therapeutic level. And then on that same day, I will start the oral dosage of 3 mix perk. What are the side effects of phenobarbital?
Some of them are idiosyncratic, which means they are not those of time related. Hyperoxidability very rarely acute hepatotoxicity, probably a bit more common bone marrow dysrexia, neutropenia, anaemia, thrombocytopenia, and superficial necrolytic dermatitis. So if you're facing any of that.
Then you have no other option than stopping phenobarb and replacing by something. We will discuss that in a minute. And then you got dose related or transient effect, PUPD, polyphagia, sedation, and ataxia.
With regard to the liver, if you give him a barbiton, you can expect that the liver may increase in size. But more importantly, from a bio biochemistry point of view, you will see an elevation in LLT or LP which reflects the auto enzyme induction. A whether parameters such as AST, bilirubin, or palacid should not be affected.
Hepatotoxicity relating to phenobarbital is a rare phenomenon probably overrated by the owner. And if I ask, you know, all of you how many times you've seen it, I'm sure you may have seen it at least once, but it's not very common. Usually you have over sign.
A related to liver dysfunction. But if you want to explore, you know, if a dog is having liver toxicity, then what I would recommend is to use parameter that should not be physiologically affected by phenobarb and the best one would be paracide. If your balacid is high and even more if your albumin is low, then I will do an ultrasound.
And then get a biopsy to establish what kind of liver disease we're dealing with. Is it related to phenobarbital or not. Mechanism is unclear with hepatotoxicity, but it's often related to those that have been poorly monitored and where the serum level has been kept too high for too long periods of time.
If you want to test the dog on phenobarbital for thyroid or adrenal function, be aware that phenobarbital could affect thyroid function. It could cause decrease in total T4 and 3 T4. It could cause increase in TSH to mimic from a biochemical point of view, hypothyroidism and the cholesterol could be high.
So in theory you can test hypothyroidism. On a dog on phenobarbital, but at least you can do a T4. If the T4 come back normal, you know the dog is not hypothyroid.
On the other hand, phenobarb has no effect on adrenal function. The other first line treatment for epilepsy in dogs in the UK is hemipitoin, released about nearly 5 years ago now. A number of advantages for that drug, the fact that he has a short half life, so he tends to work very quickly within 48 hours.
He's metabolised by the liver, but there is no liver enzyme induction. There is no need for regular blood tests, no evidence of liver toxicity, and the recommended starting dose is 10 weeks per BID. And depending on the response, if the dog is not responding well, you may have to increase on a weekly basis 20 and then 30 milligramme BID.
Initially the efficacy was reported to be comparable to phenobarbital, and the side effects initially reported were rare polyphagia. Now some dogs that we've seen anecdotal report have developed ataxia and depression. But it's not a common phenomenon.
And in terms of what would be my preference, one thing is sure is if a dog is having cluster seizures, I will definitely use phenobarbital. In terms of efficacy, I still prefer to use phenobarbiton as well, and I will tend to use peion if I've got a pet owner that is really worried about the very rare hepatotoxicity due to phenobarbital. If I got a dog that is difficult to sample because it may be aggressive and in that case I may useexion or I may useexion as well if I've got a pet owner that wants to start a dog on on antiepileptic drugs, but the ss are very infrequent.
In all the other scenarios, my preference is still remains phenobarbital. Step 4, what to do when things are not doing well and not doing well if we come back to the definition of the more what the aim of the treatment, anti-epileptic treatment is to find this fine balance between reducing the seizure with no minimum side effect. So I'm going to consider a few scenarios for you to understand when do we add another drug or when do we replaced by another drug and We are in a scenario of poor seizure control in about 25% of dogs with idiopathic epilepsy.
This is related to a phenomenon known as pharmaco resistant with multiple pathophysiological explanations going from multi-drug transporter to drug targeted sensitivity or modification in the neuronal network, but overall some dogs with time will stop responding to anti-epileptic drug and often. You get this honeymoon effect where you introduce another drug and then they improve and then after a few months they go back to their seizures behaviour. So, I'm going to consider a few scenarios for them depending if the issue is the control of the feet and all the side effect.
The first one, and you know I haven't put a slide for that is if you have started the dog on epitoinexxion and it's not doing well, what should you do well? The first thing is to make sure you're using Pexxion to the maximum recommended dose. So if the dog is on 10 mg per kick, then increase to 20.
And if it's not responding after a week, increase to 30 mg per kick before you decide to add something else. But what I will add in Bad Dog, I will ask phenobarbiton, and they've been two recent publications that I've shown that in combination of the two, dogs tend to do well when you add phenobarbital toexion and vice versa. So I think, you know, the way things have been marketed initially was very much.
They were the enemy and actually together they do a good job as well. So if the dog is infection, not responding well, use the maximum dose and then add phenobarbital. And what to do after that?
Well, if the dog is well controlled, then after 3 months I will start taking the dog offexxion over a 3 month period. If a dog is on phenobarbital but not doing well in terms of seizure control and not having side effects, first thing to do is to check the serum level. If the serum level is in the bottom end of the therapeutic range, then try to increase the oral dosage.
Check the serum level, making sure that now you achieve the top end of the therapeutic range and see if it helps. If it doesn't help. And you are the top end of the therapeutic range, then I will add something else.
And probably what I will choose initially would be hemipetoin, Texan. Other alternative would be to use bromide, and in theory, using the cascade, you need to use either of these two drugs. If a dog is on phenobarbital, the sever are not well controlled, but is also having side effects, then it depends very much what kind of side effects we're dealing with.
If the side effects are PUPD polyphagia, then in that case you need to be very careful what you add, making sure you don't add an anti-epileptic drug that have cross side effects. And in that case, adding bromide will only make things worse because it will add to the side effect. In that case, I will probably add levetiracetam.
And when the dog is better controlled with the seizures, if you achieve that, try to reduce the phenobarbital by at least 20 to 30% to see if you can improve the side effects. If now the dog is not well controlled on yobarb and the side effects are idiosyncratic, especially bone marrow dycretia, which is a life threatening condition, then what I will do in that case, you have to take the dog off phenobarbital, but you can't do that from one day to another one, otherwise you risk to have severe withdrawal seizures. In that case, the options are I will use lebeti acetone.
Start the dog on that and over a week, slowly take the dog off in the barbiton. If you count the 4th levetiracetam, then I will, if the seizures are not too bad, start on hemibitoin. Or you can load the dog on bromide, and I will give you the dosage in a, in a minute.
If the seizures are well controlled with phenobar, but the dog is having side effects, then if the side effects are PUP polyphasia, then I will try to reduce the phenobarbital by let's say 20 to 30% and see that by doing so I'll limit the side effect while not destabilising the seizure control. Well, if the dog is well controlled on fiobar, but I've got idiosyncratic side effect, then. We have no other option than stoppinginobarb over a week, and at the same time we need to start another anti-epileptic drug to keep the control of the feet again, if the feet are not too bad, then I will try probably Texion.
Otherwise, if the feet are quite severe, I will probably go straight away for levetivacetam or roy loading if they cannot afford levetivaceam. Alternatively, if they can't For levityra long term, you could always start on both roma and levitiracetam together. And bromide will take about 3 months to reach steady state, and when you know with blood testing you reach steady state, take the dog off levetivacetan.
If everything goes well, what is my recommendation then to do every 3 months initially serum level and CBC biochem to monitor for side effects and after a year to do it every 6 months. So what are the addons that I've just mentioned bromide 30 mg per kg once a day, and if the dog is quite sleepy or is having vomiting because of obviously bromide being a soul could irritate the gut, then I will sit the dog the dosage twice a day. If you have to load the dog on bromide, the loading dose is 150 milligrammes per kg per day given over 5 consecutive days, and obviously you don't give that in one go, you split it in 4 or 5 dosage every single day for 5 consecutive days.
Levetiracetam. I usually start 20 per kg, TID, but you can give it 40, even 60 per kg. The limitation here is very much the the cost of the drug and also the more you give, the more likely they may have side effects like sedation or ataxia.
Also in some dogs that have a pattern where they tend to have feet for a few days on a regular basis, then you can always use levitiracetam for a short period of time after the first fit until you stop having feet that week and then using them this way could save you, you know, quite a lot of money as well as supposed to give it every single day. In some pet nerve that still want to carry on and try despite the dog being on phenobarb, bromide levitiracetam and not responding, what are the other alternatives. You can use zonnizamide, you can use pregabalin, but to be honest with you, when a dog doesn't respond to 2 or 3 drugs, the chance of responding to more is pretty very small.
I use rectal diazepam in situations when the dog is known to have cluster seizures as opposed to only having single feet. If it's having cluster seizures, then I will instruct the owner to give as soon as practically feasible during or shortly after a fit at least 1 to 2 weeks per kick rectally and to be given up to 3 times. So after the 1st, after the 2nd, after the 3rd.
And if after that the dog is still having feet, then to contact you to bring you the dog to stop this cycle. Briefly, we're going to mention the emergency treatment. Again, fantastic, you know, decision tree available on the TVM website with the management of status, which I would encourage you to download and stick it somewhere in your clinic to be ready for the next dog.
Very important when you manage emergency seizures like severe cluster status, not only to focus on stopping the fit. But also focusing on the systemic stabilisation and not losing sight of what could be the underlying cause in that dog. Systemic stabilisation is very important because When you're having a prolonged, yes, it could damage the brain, but it could also a lot of damage to the body, especially the heart, the kidney, and also the muscle, and you're going to have, you know, predisposition after prolonged seizures.
All the compensatory mechanism to keep the metabolic demand initially will fail. You're going to have hypotension, hypoventilation. You're going, but we're going to predispose to cardiac arrhythmia, decrease kidney perfusion, myonecrosis, myoglobinuria, that will aggravate the kidney, the kidney issue.
So overall it's very important to treat the systemic cause as well as the its manifestation itself. So how to stop the fit? Well, at some point, I'm afraid this dog is going to need to have an ID access, and yes, they don't always turn up on a Saturday night with an ID.
They turn up without, for obvious reasons, and, you may. Want to use in that case rectal diazepam one mix perk to buy you a bit of time to try to put an IV catheter. But at some point you need to isolate the limb and give this drug IV and what I will do.
Is initially to give one bolus of benzodiazepinem. You can use diazepam or midazolam, and TVM has released recently Xiapa, which is the first licenced diazepam for use in cats and dogs. So you can use benzodiazepam once and if the dog doesn't respond, then I repeat that bully straight away, but I had as well a free mix per kick in aarbiton.
If the dog is still not responding, then I repeat this combination of benzodiazepinem followed by phenobarbital one more time. If the dog stops and he's never been on phenobarb, then I will loading on phenobarb using a total loading dose of 18 per kick. If the dog is already on phenobarb, then I will give him in total 3 times 3 mixs per kick, taking into account what you've already given to stop the fit.
If the dogs stop feeding, very important to check the airway to make sure there is no excessive secretion of blood, to make sure they are patent. Put the dog on oxygen mask, give him oxygen. If the dog cannot stop ventilating or is anaesthetized as a result of his bud and the postictal phase, then I will intubate the dog and ventilate until he recovers spontaneous ventilation.
I will put the dog on IV fluid, check his blood pressure, and if it's hypotensive, then give bodies of crystalloid 10 mL per kick until you restore normal blood pressure, and I will keep a close eye on the rectal temperature with profound with prolonged seizures, the animal could go from being hypothermic to hypothermic. If the seizures do not respond to the policies we just described, then in that situation I will use the CRI, and you've got the choice between using benzodiazepine sterile, or propofol infusion. I personally tend to use propofol, and what I do is practically fill up a syringe and give the propofol to effect until I stop the physical manifestation of the feet.
And then put the dog on a CRI or propofol. In that dog that didn't respond to the initial policies that we discussed and need to go on a CRI, then you need to keep it for at least 3 hours on on propofol. And then after 3 hours I will slowly take the dog off propofol.
When you do so, some dogs could be very agitated and it can give you some sometimes the false impression they're having a fit. And if you're not sure if it's propofol recovery versus epileptic fit, then turn the dog on on external recupancy, and if it stops, you know it's propofol. A recovery.
In that case, I will try to manage the dog while I take him off propofol by giving either a bolus of ACP or dexeditomidine, and you can even put the dog on the CRI of dexeditomidine while you slowly take the dog off propofol. As an alternative between the bullies of benzolano IV and the CRI of propofol, then if you can afford it in your practise, then I will recommend to use Keppra injectable using 60 milligrammes per kg IV bolus, and then you can put the dog on the CRI as a way. Before to use propofol infusion.
Yes, it is expensive, but it may save you having a dog on propofol for 6 hours, which obviously takes a lot in terms of manpower and also a cost for the owner. After all that, very important not to walk away, as we say, to look at the ABC, making sure the dog is ventilating well, especially after all these drugs. You may have anaesthetized the dogs, you may need to be intubated.
It may be hypotensive. It may be hypothermic, so important to keep a close eye on the systemic consequence, to have a successful recovery from this emergency severe situation. So, again, if you haven't done so, have a look at the TVM website to download this very useful decision tree and as I say, you know, stick it somewhere in your practise, you will find them very useful one day.
I wanted to finish this presentation to, again, thanks, the webinar vet for hosting this webinar. Thanks as well to TM for sponsoring, this very, hope you find this useful webinar. As I say, I'm joining CVS referral, next week, to, grow the neurology service across the network as well as, offer tele neuroradiology.
And I wanted to finish by making you aware if you haven't had a look yet at the Facebook page that Simon Platt and I created 2.5 years ago called Veterinary Neurology, we put every, every week a lot of interesting video of neurological case, a lot of practical tips. It's totally free, so feel free to join us and to follow us.
We have now 31,000 followers across the world. And the last word will be to make you aware of a fantastic charity called VettLife. You may be aware that mental health in the profession is at an all-time high and only today in the BBC news was an article about the rate of suicide in the veterinary profession, which has 4 times the average rate in the UK.
Very lucky, but people at that time do a fantastic work, and I've decided this this year to support this charity for my CPD and I will throughout the year give my fee to that life, which is what I wanted to do tonight via this presentation. So everything will be given to this fantastic charity, and I hope you will also one day do the same and support them. Thank you very much for your attention.
I hope you enjoy this webinar and I passed again the microphone to the webinar vet. Lorraine, thank you so much for that absolutely amazing presentation. And it was finished off so beautifully with supporting VELife.
It really is an amazing charity and I urge everybody to support them. We did a webinar for them the other night and folks, I, I just support and echo what Laurone has just said. They really are worth looking at and worth supporting.
They are amazing. Lorraine, thank you for your time tonight. It, it really has been fascinating.
We have run over a bit, so folks, if you want to leave, please feel free. Lorraine, we have got quite a few questions. We're not gonna get through all of them, but if you're happy to answer some questions, there are some real good ones here.
I think the first one, comes in from Lucy. You were talking about running metabolic tests and everything else. And Lucy says, would you routinely test for Neosporra and Toxo when you have a fitting patient?
That's a good question. The answer is no. And I think, you know, when you look at how much it costs to run serology, it's about, if I'm correct, maybe 100, 110 quid.
I will only do that if I've got a dog showing neurological sign. And I've got, I've done an MRI and the CSF, and I suspect an inflammatory process on MRI and CSF. Then the next step for me is to if there's a protozo cause behind that and That will help me.
There is no protosol cause to, you know, diagnose an immune mediated encephalitis. If you've got a dog that is not showing any neurological signs and is only having isolated seizures, it's very, very unlikely to be due to toxor neurosporra. So my answer is definitely not in that case.
Excellent. Couple of questions coming through about various supplementations, when, you know, when, when you've obviously got them on phenobarb and the liver. What are your feelings with omega oils, milk thistles, skullcap and Valerian, etc.
Etc. I don't have much experience, so I prefer to leave people that know more about this supplement to talk about it than me. So, you know, I'm, I'm afraid I won't be able to answer that, you know.
However, you know that there is a food range now from Purina that has been, released. And I think that that could be a good adjunct, you know, to the treatment to put the dog on, on that kind of, of diet. You know, I don't think you got anything to lose and Certainly a lot of owner will be quite attentive to that kind of, you know, add on treatment to anti-epileptic medication.
Excellent. You were talking a lot about building multiple drugs into, into your therapy. One of the questions that's come through, is when you have started, on Pexian and not phenobarb, you gave us phenobarb and add on and everything else.
But if you've started on Pexian, what would be the dose of phenobarb that you would introduce as your second line drug? Yeah, so you can use yobarbital at the usual dose of 3 mix per kick. However, you know, this recent publication has looked into that, and even a lower dose of 2 mixs per kick twice a day may give you a good response.
And I didn't mention it. When you do the reverse, you got to do on fiobarb. It's not responding well, addingexion.
You know, can work and together they can have a good effect, and you may be able to get away with giving as little as 10 to 15 weeks per infection. OK. Just to go back to what you were saying about nutrition and everything else, Paul, my controller in the background, has just reminded me that, Holger Falk did a whole webinar on feeding the epileptic brain fairly recently, on the Purina food and everything else.
So it is on our website, if you want to go and have a look at that, folks, the recording is up there. We have another question that has come in. Is there any evidence that either diazepam, incorrectly or midazolam IM or even intranasally is a better route over each other in an emergency?
You know, so there, there's been quite a lot of study done with the pharmacokinetic of intranasal and it's been shown that it's a very, you know, good route. I always find it practically difficult. To stick anything in the nose of a severing dog.
I mean, you've seen, you know, this box there having a general clinics, and I think for a pet owner, I would feel more comfortable advising them to go by the back end than the front door, you know, which is putting something in the nostril when the dog is having violent chattering. Of the jaw, to be honest with you. And with regard to IM, definitely I am diazepam is very poor, so you would not achieve what you want to do in terms of stopping the feet.
The alternative would be IM midazolam would be probably best, but overall my preference would be rectal diazepam or rectal midazolam. Real approach doesn't tend to bite as badly as the front end. That's it.
Kiara wants to know if you have a patient that is waiting for surgery for a report of systemic shunt, what sort of drugs would you choose, to try and stabilise those fits? Well, you may find it strange, but I still use phenobarbital in these dogs. It's been shown that, you know, people were advocating the use of levity acetone because it's not metabolised by the liver and so on, but phenobarbiton still seems to be the way to go.
However, you may have to use lower dose because the dog may not be able to cope with, you know, the usual dose. So yeah, I will go for enobarb. This might be a very, loaded question and it may be, a topic for another webinar, but, any tips on a planned general anaesthesia in stable idiopathic epilepsy patients?
You know what a lot of myths, for example, people used to say do not use IACP in epileptic dog. Every single dog with MRI for investigation of seizures are pre-med with ACP and methadone, and then the anaesthetized with isofuran. So, you know, that would be commonly used in practise.
That would probably what I would recommend to do. That's, that is, quite a statement because, for many, many years, the, ACP was considered to be, you know, completely contraindicated and even bordering on malpractice. And it's a myth, I'm afraid it's been demonstrated that, this, you know, is, is not funded, practise at all.
So don't hesitate to use ACP in that case. And even you've seen, if a dog, a dog recovering from propofol infusion, but is too agitated when you can give bodies of ACP, low dose, to try to smooth the recovery. Oh, excellent, excellent.
Lauren, I have to tell you that I'm, I'm sifting through. We have got so many comments coming through about fabulous webinar, absolutely brilliant. Thank you for an interesting presentation and it, it really, there's just so many comments thanking you for a brilliant, brilliant webinar.
Folks, I'm afraid we have run very far over time. We are not gonna have any more time to be carrying on with these questions and that, . I do apologise, but I think the presentation that Lauren has given us has been absolutely incredible.
I know I've learned a lot and Lauren, thank you so much for your time tonight.
