Good evening, everybody, and welcome to a Thursday night members webinar. My name is Bruce Stevenson, and I have the honour and privilege of chairing tonight. Tonight's session is, gonna be a really good one as we are getting used to on the webinar vet now.
I don't think we've got any new members, so not a lot of housekeeping to do. We will keep all the questions over to the end as we normally do. So let's get on to introduce our wonderful speaker for tonight.
After qualifying from the University of Palma in Italy in 1996, Louisa completed an internship at the Veterinary Teaching Hospital of Palmer University and subsequently at a referral practise in Paris. From 1998 to 2000, she worked as a visiting resident at a neurology service at the Veterinary Teaching Hospital of North Carolina State University. Louisa obtained a PhD at the University of Palma, where she was appointed as a lecturer and subsequently a senior lecturer in neurology and neurosurgery.
In 2004, she successfully passed the examination of the diploma of European College of Veterinary Neurologists. In 2005, she joined the neurology and neurosurgery Services of the Animal Health Trust as a senior clinical neurologist. And since 2007, became the head of the unit.
In 2017, she was appointed as the head of clinical research at the Animal Health Trust and has been awarded the Royal College of Veterinary Surgeons Fellowship for meritorious contributions to clinical practise on the 12th of July 2018. Louisa has lectured at several continuing education and scientific meetings, published several studies in peer-reviewed journals, and a book on canine and feline epilepsy. So who better to talk to us about epilepsy tonight?
Louisa, welcome to the webinar vet, and it's over to you. Thank you for the introduction and thank you to the participants for being connected and to those that will view this presentation as a recorded presentation. The aim of this evening is to review a number of concepts that can help us, deal with patients presenting with a history of epileptic seizures or other seizure-like episodes that can be challenging to differentiate from epileptic seizures.
I would start with reviewing terminology. I promise this is the only slide on terminology, but it's important to, review it and understand that, an epileptic seizure. Is the result of abnormal and excessive cerebral neuronal activity, which can result in a variety of clinical manifestations from just focal twitching of a few muscles or just one muscle to generalised on.
Chronic violent movements with or without impairment of consciousness and autonomic signs, and epileptic seizures can result from both intra or extracranial causes. So there is also quite a large variety of underlying etiologies to consider. The faces associated with the seizure include a prodrome or pre-etal phase.
This can last sometimes up to hours. It is not always recognised by the owners and it does not always occur. But when it does occur, it does represent a very important therapeutic window because if it lasts for hours or 30 or more minutes, we can use antiepileptic drugs such as levetiracetam, which is a rapid onset due to its short half life, and we can even prevent the actual occurrence of the ICTA phase, which is the more damaging phase to the brain.
During the prodrome, owners that are very observant and have dogs with recurrent epileptic seizures will observe some personality changes. So dogs that are very clingy then becomes withdrawn and vice versa, or there is anxiousness, restlessness, sometimes vocalisation. The is the actual seizure phase associated again resulting from the excessive.
Neuronocortical activity and then As the brain recovers from sort of this electrical storm, the posttic phase occurs. This can be last seconds or days. It quite commonly occurs and it's quite obvious to the owners.
So questioning the owners on the occurrence of those faces is quite important in identifying epileptic seizure activity and differentiating it from other paroxysms. During the postictal phase, a variety of clinical signs associated with impaired mentation, movement, coordination, or even vision and behaviour can occur. The first case I'm going to show you.
Is a boxer. With an adult boxer with acute onset of this activity that lasted 30 to 60 seconds and I suppose we will all agree here that this is generalised tonic clonic epileptic seizure. There were tonic clonic movement affecting all.
Muscles in the body, the rhythmic contractions of the jaw muscles and the muscles and the fact that the contractions are rhythmic is relevant and it's helpful in differentiating epileptic seizures from other non-epileptic paroxysm. There is hypersalivation, and there was also urination. So All those variables make the identification of epileptic seizure activity fairly straightforward.
But there are numerous conditions that may mimic epileptic seizures that present in a less obvious way than the case I've just shown. Paroximal dyskinesias or movement disorders are increasingly recognised in dogs and they've been characterised in certain canine breeds and our knowledge of those conditions is increasing. There are a number of publications in peer-reviewed literature in the past couple of years, and we will review some cases tonight.
And those conditions ah often are primary, so there is no underlying structural cerebral abnormality and so like in idiopathic epilepsy, all diagnostic investigations ranging from blood tests, urine tests, MRI, CSF, they're all normal. So the key to differentiate the an idiopathic epileptic dog with epileptic seizures from a dog with a movement disorder is actually clinical acumen, clinical knowledge. The time we spend talking to the owner, obtaining details of the clinical features of these episodes, this is on what we base our diagnosis.
And there are some paroxximal dyskinesia for which the underlying genetic mutation has been identified. So if we have a strong clinical suspicion, then with a simple genetic test, we can achieve a diagnosis. Other conditions that could be misinterpreted as epileptic seizures, including narcolepsy, cataplexy, so when the animal following a pleasant stimulus like food or the owner coming back home from work, they basically collapse, they lose postural tone in all four imbs, and they fall asleep.
And then they wake up and they are completely normal. And if they get excited again, the circle continues. Vestibular attacks can be transient sometimes, and as the animal is laying on his side, struggling to get up and paddling, this could resemble an epileptic seizure tonic clonic movement, and sometimes making this differentiation can be challenging unless we witness the episode or there is good video footage.
Syncope, we all know, can result in impaired or absent consciousness, awareness, and loss of postural tone. Some neuromuscular disorders can have episodic presentation and impair posture and locomotion and sometimes again this can be confused with an epileptic seizure. Some compulsive behaviour disorders have quite a strong overlap with epileptic seizures.
It is now well known that dogs with idiopathic epilepsy can suffer a number of behavioural disorders and conditions such as fly catching can both result from compulsive disorders as well as visual seizures, so hallucinatory seizures. Sleep disorders? There's limited knowledge of those in veterinary medicine, but they can easily be confused for epileptic seizures and also episodic pain, behaviours.
Have to be considered in the different diagnosis of epileptic seizures. A lot of conditions to be familiar with and to consider when we are presented with a patient with a history of seizure or seizure-like episodes. I spend a few more words on the movement disorders because they are again increasingly recognised in our canine patients and probably are the most challenging conditions to differentiate from epileptic seizures.
Those conditions are characterised by episodes of sudden abnormal and involuntary muscle contractions, which result in abnormal posture and movements of variable duration. Consciousness is preserved and there are no autonomic signs. These conditions can be inherited or acquired and when inherited, Sometimes the genetic test has been developed when the underlying mutation has been identified and here at the Animal Health Trust, we had identified the mutation underlying cavidoincho spinal periodic hypertonicity.
So that's a, a genetic test that is commercially available and the condition, actually the, the prevalence of this condition has dramatically decreased following the introduction of the Genetic test because that allows to identify also the carriers and so responsible breeding can be done to eradicate the disease. Most commonly they are primary, so again, even harder to differentiate from epileptic seizures or secondary to underlying disorders including structural brain disease. If the underlying structural brain disease can be treated, the movement disorder can resolve.
And Most commonly, movement disorders do not respond to antiepileptic drugs. So if our clinical diagnosis is incorrect at the start, our therapeutic intervention will not give a favourable outcome. So again, dedicating time to collect all the pieces of the puzzle and establish a strong and robust clinical diagnosis on whether the condition is a movement disorder or epileptic seizure is probably a great investment of your time and the client time and there is no diagnostic test unless again, there is a genetic test available that can replace the clinical skills in differentiating between those conditions.
There are numerous factors to consider. All those listed in blue in the list that will soon appear are supportive epileptic seizures and others can occur with paroximal dyskinesis or other conditions. There are some paroximal dyskinesis in which the abnormal muscle.
Tone resulting in abnormal posture and gait or inability to to walk are secondary to a trigger such as excitement, anxiety, stress. But, seizures themselves can sometimes result from stressful events, although there is not. And necessarily an immediate cause effect relationship.
The pre-event changes like the prodrome we saw earlier are suggestive of epileptic seizure. A detailed event description from the owner along with a good video footage of the episode is extremely helpful. The level of consciousness is impaired with numerous types of epileptic seizures, but not all.
But we know that it's always normal in dogs with paroxyal dyskinesia. So that's a very important discriminating factor. Autonomic signs, as said earlier, can occur with epileptic seizures, sometimes even with focal seizures.
So seizures affecting a region of the body or just one side of the body. There can be prof salivation. And with other conditions, this would not occur.
So it's important, an important discriminating factor. The muscle tone, we are used to seizures with tonic clonic movements or spastic activity, but there are a tonic seizures that sometimes can occur and then in those cases, the muscle tone is flaccid. With paroxximal dyskinesis, typically, the muscle tone is increased and again there is sustained muscle contraction.
The movements, they are often rhythmic muscle contractions in dogs with epileptic seizures. Lateralizing signs are probably more common with epileptic seizures than paroximal dyskinesia, and a feature that is quite typical for certain paroxximal dyskinesia is that the animal, because the mentation is normal, they want to continue doing what they wanted to do. They want to continue playing, they want to continue walking.
Sometimes they even want to continue eating or toiletting while they are having the abnormal posture and movement. So this is a, a useful trick to recognise paroxximal dyskinesia. The duration of the episode can also be helpful.
Seizures generally last seconds to 1 to 2 minutes. If it's more than 5 minutes, the status epilepticus, which can obviously occur, but it would be unlikely to occur at, you know, if there was no underlying aetiology. As the first episode.
Approximal dyshesia can last several minutes, sometimes up to an hour. So that's also a useful discriminating factor and then the occurrence of the postictal signs as we saw earlier can be quite helpful in recognising epileptic seizures. So being aware of all those factors, trying to collect the pieces of the puzzle, put them all together, should help your clinical diagnosis of those.
Episodic paroxysms. It's very, very important to have a systematic diagnostic approach. Again, take time to take the medical history.
Ask specific questions to understand all the features of the episode, anything that happens just before, during, and after the episode. The age at onset of the episode is relevant for, especially for particular conditions that are well characterised in certain canine breeds that they have a sort of a typical age of onset. We know that idiopathic epilepsy is associated with the first seizure occurs between 6 months and 6 years of age.
The episode phenomenology, the duration, the frequency, as many details as you can obtain from the client. If you are under time constraints, providing the client with an epilepsy questionnaire and asking them to complete it before the consultation or soon after the consultation can help you obtain those relevant details in a time effective manner. Of course, we need to perform a thorough general physical and neurological examination and then depending on the findings, we decide the next steps.
Most commonly, haematology, comprehensive serum biochemistry, including electrolytes, pre and postal bile acids and urinalysis would be required, and then depending on the results. We will establish if there are any conditions specific laboratory investigation to perform. Whether MRI of the brain is indicated, and this is often the case with dogs with epileptic seizures or paroxximal dyskinesia, and CSF analysis and eventually electroencephalography.
Obviously, this is all applies in dogs in which we have ruled out intoxication and any metabolic condition that can result in epileptic seizures. So I think we have had enough of theory. I hope you're all still with me, with your attention level because now we're gonna look at 7 clinical cases together.
And they will be affected by a variety of conditions. Some would have approximal dyskinesia, some will have epileptic seizures due either to a structural brain disease or other causes, and others may have other conditions that are non-epileptic in nature and are not movement disorders and may not even be neurological in nature. So we look at the video, we will review some clinical details and then I encourage you, I invite you to try to make up your mind on which disease group you would assign the case in question, not necessarily an iologic diagnosis, but at least Try to lean more towards movement disorder versus epileptic seizure versus other.
And again, some of those cases are challenging. They may have conditions you haven't seen before, but the purpose of this talk is also to generate sort of a critical approach to those cases and increase your knowledge on conditions that have been relatively recently described in veterinary literature and therefore would not really be in all books or will not be at all in books because they were published in very recent times. So the first case is an 11 month old female boxer.
She was completely normal until Very recently before being presented and she had been those clinical signs constantly. Until the time of presentation. She had no previous illnesses.
She was regularly vaccinated, no exposure to toxins. She was unable to stand up and walk during the episode. And the episodes was constant twitching of the facial muscles.
You can see rhythmic twitching, repeated leaking, the wetness on the shoulders due to her saliva, so she was hyper salivating, sometimes you can see the white. On the lips And also her mentation doesn't look right. It seems that she's looking at things that don't really exist.
We try to call her to distract her. You probably don't have the audio, but there is somebody calling her and trying to attract her attention, but, she kind of seems in her own word. So, what do you think?
What could this be? So in this case, it is an epileptic seizure and unfortunately, this dog presented with constant seizure activity due to a structural brain disease which was basically encephalitis and encephalitis. She had what we call orofacial involvement, so the facial muscles were affected by this rhythmic involuntary contractions.
And there was the hydro salivation. And the mentation was clearly altered. Again, assessmentation in a video can be quite challenging and sometimes misleading, but obviously we had the opportunity to witness the case in person.
So this is a case where again the, the, the abnormal muscle contractions are rhythmic, facial muscles, there is the hyper salivation, there is the othermentation, so all those elements are supportive of epileptic seizure activity. The second case is a 2 year 2 month old female spade board terrier. She presented with a history of 3 episodes that they looked all alike to the one shown in the video.
And those occurred in the past 5 months. And she was completely normal in between episodes. And again, although it's not very easy to assess, try to make up your mind on the dog'sation, and cognitive function during the episode and also her ability to walk, her posture.
Let me see if I can get the video started. Here we go. So the dog is going to the owner, although struggling to walk, the owner obviously wants to show, to record the video, so it's trying to Move the dog away.
But the, the dog knows who the owner is. He's trying to follow her everywhere, it's wagging the tail, so apologies for the twisted. Video, but the dog is clearly aware of who the owner is, but has increased.
Muscle tone in all four limbs and probably in the back muscles resulting in this very stiff abnormal gait and the difficulties in moving. And these episodes can go on for several minutes. And then she rapidly returns to normal.
So what do you think, is it an epileptic seizure, a moor disorder, or other paroxysm? OK, the dog is completely normal between episodes, and the episodes are characterised by abnormal muscle tone, sustained muscle contraction, resulting in abnormal posture and gait without any impairment of Awareness, consciousness. And otherwise, the dog is fully healthy.
So probably because also of the breed, those of you who have encountered the so-called spike disease or canine epileptic cramping syndrome as it used to be called a couple of years ago, and most recently this condition has been termed paroxximal gluten sensitive dyskinesia. It is a proximal movement disorder. The mean age of onset is 3 years in different studies done in different countries by different investigators.
Episodes can last from 1 minute to 1 hour, generally it's a couple of minutes. And the frequency is highly variable from once a month to once a year. Sometimes dogs tend to have a couple of episodes clustered over a week and then no episodes for several weeks to a couple of months.
Some triggers have been identified such as sudden movement of stress, but this is not consistently the case for all cases. As it typically happens for primary paroximal dyskinesia, clinical examination is normal as well as all laboratory and other diagnostic investigations such as MRI and CSF. An interesting publication in the Journal of Veteran Internal Medicine published in 2018.
Has reported the clinical features and also serological markers for this condition in border terrier. All dogs, including the study, they were 45, had sustained muscular or peritonicity similarly to the dog shown in the video, resulting in a difficulty or inability to stand up and walk. Consciousness and awareness were normal.
Again, this is typical for paroxximal dyskinesia. There was no facial twitching. Again, the facial twitching, especially as rhythmic as in the boxer we have seen, is often very suggestive epileptic seizures as well as the autonomic signs.
Those do not occur in paroxximal dyskinesia. And these dogs also had frequently concurrent signs such as atroy and or gastrointestinal disease. They measured basically anti-gluten antibodies in these dogs, and the majority of them had raised levels.
Now, the anti-gluten antibodies can be raised. Because of a gluten sensitive proximal dyskinesia and be part of the pathophysiology of this condition as the author suggests, but can also be the result of the dermatologic and gastrointestinal disease. So by themselves, they are not.
Specifically diagnostic for proximal dysian border terrier, they cannot be interpreted by themselves and they have to be tested in the only lab in the UK where the normal values for border tarriers have been developed and the technique in theSA is being developed. But as for any laboratory tests, we can't interpret it in in isolation. We have to Complement the clinical aspects and if the case is not very straightforward, also consider conducting MRI and CSF.
What is very interesting is that in those cases where all the pieces of the puzzles added up to support a diagnosis of epilepto cramping syndrome or proximal dyskinesia of the border carrier. Feeding exclusively a gluten-free diet resulted in resolution of the clinical signs, so no more episodes of paroxximal dyskinesia and also in return the, the serum levels of the gluten. Antibodies.
Return within the normal reference range for for the carriers. So this is all very interesting and obviously if we We are able to eradicate the episodes simply with the diet, that's an excellent result, but we shouldn't be giving gluten-free diets to every dog where we think there may be a proximal dyskinesia. To date, gluten sensitivity is the underlying cause of Paroximal dyskinesia has been identified only in border carriers and not all the border carriers with parroximal dyskinesia have gluten sensitivity.
So they not all of them will respond to the gluten-free diet, but several of them will. And generally, once we start feeding exclusively the gluten-free diet, as early as one month after the diet change. We can see an improvement, so a decrease in the frequency duration and occurrence of the proximal dyskinesia episodes.
So we can move to dog number 3. It's a 7 year old male neutral miniature white-haired dachshund. So here the clinician is clapping the hands, making a noise and a sudden movement, more or less in front of the head of the dog and the dog is having this kind of sudden brief muscular contraction.
Of the head and trunkal muscles resulting in sort of this backward movement. This will happen at home as well with any sudden movement in front of the face of the dog or any loud noises or even the light of the TV in the dark room. What do you think this could be?
The dog in between episodes was considered normal by the owner and in general physical examination there were no abnormalities, no exposure to toxins, regularly vaccinated, warmed, flea prevention and so on. So what do you think it could be? The clinical manifestation shown in the video is known as reflex myoclonus.
And this is one of the cardinal signs of progressive myoclonic epilepsy or Lafora disease. This condition is an autosomal recessive myoclonic epilepsy caused by mutations in the AEPM2A gene which encodes for Glycogen phosphatase lafera or EPM2B gene, which encodes for the ubiquitine E3. The underlying pathophysiology of Lafora disease is transformation of spherical and soluble soluble glycogen to a more linear and insoluble glucan called polyglucosan.
So there is gradual precipitation and aggregation accumulation of the polyglucosan within the neurons and within the muscles. And this results in so-called Lahora bodies which are neurotoxic to the neurons and result in neurodegenerative epilepsy. This is essentially a structural metabolic epilepsy, secondary to a genetic defect.
As I said earlier, it is autosomal recessive and has a late onset, and the condition is unfortunately progressive. A high prevalence of the genetic mutation for Lafora diseases being identified in the wider hair dachshund population in the UK and this very interesting paper published last year reported the results of a nationwide in the UK genetic testing towards elimination of Lahora disease from miniature white haired dachshunds. The study included 548 miniature white haired dachshund between 2012 and 2017.
7.1% were on mozygous for mutation, which means they had either already developed Lafora disease or they were going to develop it later in life. And 35.2% were carriers.
So if bred with another carrier, they would have produced. Offsprings with the condition. Either on the zygos, probably about 25% of the litre, and then half of the litre would have been carriers.
So the prevalence of the carriers is quite concerning. And the genetic testing, which is quite a sophisticated type of genetic testing, has been commercially available since 2013 and has resulted in introduction of the condition. And over the years, hopefully, the, the prevalence will reduce even further.
Fortunately, it has become a requirement for the UK Kennel Club assured breeder scheme since 2014. Looking a bit more into the clinical aspects of this condition. This study Reported the clinical details of 27 miniature white-haired dachshunds.
The average age of onset of the clinical signs, which were basically the same as in the video I've shown you, is nearly 70 years old, and the dog of the video I showed you was just over 7 years of age. The range goes from 3.5 to up to 12 years.
So even much later in life, they can develop this condition. And the most common initial presenting sign was the myoclonus. That reflects myoclonus or even spontaneous myoclonus in the vast majority of dogs.
So the, the, the type of episode I showed you in the video is kind of the cardinal sign at the onset of the disease. Unfortunately, there's more and more polyglucose and bodies accumulating neurons, the severity, the frequency of the Reflex or spontaneous myoclonus episodes increases. Some dogs anecdotally initially report a response to levetiracetam treatments.
But over time they tend to become a refractory. And they develop other neurological signs. One of which is the so called hypnic myoclonus, which is basically jerking as falling asleep and it's quite common.
And these dogs can also develop generalised chronic clonic seizures or focal seizures in the later stages of the disease. There will be cognitive decline with anxiety, impaired vision, and also signs of cerebellar ataxia. So it is quite a nasty disease.
Also in humans, there is a similar condition and it's considered one of the worst type of genetic structural metabolic epilepsies. So it is very, it's great that we have a genetic test to not just to diagnose it, but to prevent its occurrence and decrease the prevalence. And the breeders community has made a huge effort in trying to develop this genetic tests and then obviously use it for selective breeding.
But again, if you remember the video I showed then. There are very, that's quite an important clinical variable in having the suspicion of this condition and then submitting the genetic test. So starting from a good clinical assessment, you can make the diagnosis with a very reasonable cost of just a genetic test.
So moving on to dog number 4. This is a 3 1/2 year old male neutered Norwich terrier. Who had 3 episodes lasting 5 to 10 minutes in the past 4 months.
He rapidly recovers and is completely normal between episodes. So here already, the duration of the episodes should lead to some consideration on the possible underlying aetiology and now we or the disease category, and now we're gonna look at the video. So the dog was quite excited.
It was time to go outside for his walk. And in this video, you have the affected Norwich terrier, which is here, you can see the tail is down, and you will soon see that the Movements are not really normal and there is another no terrier, a control who has normal gait and posture including of the tail. So he really wants to go out, but he can't really stand up and walk.
I've been told by no terrier breeders that when no terrier are stressed, they tend to do this repeated leaking. I suppose it's hard to tell if there is any nausea involved. So he wants to go out, the normal one, off he goes and he has to think about it and then look at the posture of the tail.
It's rigidly. Extended. The pelvic limb muscle tone is increased and that's why he has this very rigid spastic gait.
He wants to go up the stairs, but he has to have a good think about it because again, he's not in full control of his movements. Then off he goes. The thoracic limbs are kind of doing most of the job, and he wanted to go out to pee and he's still trying to perform the intended activity despite the abnormal muscle tone in the pelvic limbs.
And he goes to the toilet. And gradually we see that he can flex his pelvic limb joints a bit more, but it's still quite, the gait is still quite spastic. The tail is returning into a more normal posture for no exterior, and now he can walk faster, although still a bit stiff in the pelvic climbs, the tail has returned to his normal posture.
But still has to think carefully before jumping up. 10 to 15 minutes later, he is fully recovered. He's, this is the, the dog affected by the condition in the previous video, that's his friend.
And this is just 10 minutes later. You can see that the gait has changed. It's much more normal, it's comparable to the other dog.
It's much less. There is no stiffness, there is no swaying of the trunk, and that's him, that's the affected dog. And you will see in a moment that he can run as fast as his friend and he's completely normal.
So happy, healthy, active dog with episodic. Hypertonicity sustained contraction of particularly the pelvic limb muscles, but also the tail and to a lesser degree, the lumbar muscles. No lamentation, no autonomic signs, although this repeated leaking, you know, again the breathers feel is because of distress rather than nausea, but no vomiting, no hyper salivation.
And no impairment of consciousness. So even if we have never seen noraria before, just based on the clinical signs, what do we think it could be? It is a parroximal dyskinesia and we have done some work thanks to the help and support of the breed club of the Noarriers in the UK.
And we contacted owners of Norwich terriers throughout the UK and we identified 26 affected dogs. The age at the first of several episodes was 3 years, both the median and the mean. So this is quite similar to what we've just seen in the border carrier, but not every, proximal dyskinesia that is breed specific would have a median onset at 3 years of age.
Males and females were nearly equally represented, and all dogs were neurologically normal between episodes and all diagnostic investigations were unremarkable, including MRI, CSF, blood tests, and so on. So we suspect that this is a primary disorder, a primary condition, most likely with the genetic basis. What's interesting is that nearly half of the no terriers were aware of the imminent occurrence of an episode of muscle hypertonicity and they were seeking the owner's reassurance.
And as shown in the video, the episodes were characterised by sustained muscle contraction of the pelvic muscle. This was the case in all dogs, including our in our study. Lumbar muscles, the tail muscles were affected in the majority of the dogs.
And sometimes also the in the thoracicines. These repeated leaky movements were recognised in a number of dogs and again, we wondered whether there was an element of nausea but again, no vomiting, no, and they were eating normally as soon as the episode was concluded. And in half of the dogs, the episodes were so severe that they were unable to stand up during the episode.
In the majority of dogs' duration was 2 to 5 minutes. But in some dogs could the episode could last up to half an hour, and the frequency was very variable as we've seen for the border terrier. 42% of dogs had episode clustering, so 2 or more episodes over a few days and then no episodes for 3 to 4 months.
Episode triggers such as excitement, stress, anxiety, exercise were recognised in a number of dogs. And so it's very important when you suspect paroxximal disc easy to question the owner about those factors. And in terms of treatment, other than avoiding the precipitating factors when they are consistently recognised, I'm afraid there is not very much we can do at this stage.
We have done a lot of work on this condition at the Animal Health Trust, and to date, we have not identified an association with gluten sensitivity. However, this is work in progress and we've been working very hard in identifying the causal genetic mutation. And if you see any dogs in which you're suspicious, that could be paroxximal dyskinesia, feel free to email Chris Jenkins.
He's a PhD student who is working on identifying the genetic mutation underlying this condition as well as Idiopathic epilepsy in various canine breeds of dogs and ultimately, it would be wonderful to have a genetic test not only to easily diagnose those conditions, but most importantly to inform the breeders to breed away from this condition. So dog number 5. It's a young male pug and He would have this posture.
Just looking at the ceiling. And even if The owner tries to call him, distract him. He doesn't really engage.
So I'll give you a bit of medical history. He had several episodes of what we called star gazing, although obviously there were no stars, it was just extending the head and the neck and possibly looking at the ceiling. And there were several episodes during the 8 hours prior to the emergency referral.
The episodes lasted seconds to a few minutes, and it could not be distracted. There was no specific trigger. He, between episodes, he was alert, but he appeared a bit quieter than usual, less lively, normal to his owner.
And in terms of general health, you know reported that he tends to have a sensitive stomach and eats stones. So as as most pugs, they obviously had bos, and neuro exam was completely normal. We did blood tests.
It was mildly anaemic. He had a stone on his stomach, his stomach, and also slight hiatal hernia. What do you think could be going on here?
This is quite a tricky case. We are seeing an increasing number of those cases in brachycephalic dogs. Pugs, French bulldogs, the stargazing behaviour manifested as upward extension of the head and neck as shown in the video.
Can be associated with refluxes of ngitis and gastritis and this has been documented quite well in a publication in the Canadian Veterinary Journal. Can be a manifestation of a compulsive disorder or in some cases a focal seizure. In this case, also because of the, obviously the The history of the sensitive stomach and the ingestion of stones.
We did conduct imaging of the gastrointestinal sign and we treated the dog with omeprazole. He defecated the stone fortunately, and he never had an episode again. So Again, starting from a good history, knowledge and understanding of the clinical presentation can lead to sometimes a very cost-effective diagnosis, treatment, and successful results.
Dog number 6, is a 5 year old main neutral Weimar runner. I show the episode first and then I'll tell you a bit more about the medical history. This is at night, the dog was asleep when the episode occurred.
And all the episodes occur when the dog is asleep. So you can see this sort of Uncoordinated, not really rhythmic movements. It's more that he's kicking or running.
The movements are quite violent. It's mainly in the pelvic limbs but also in the thoracic limbs. This is from a different angle.
Clearly, one of the owners was sleeping while the other was recording the episode. So, about the medical history of this dog, the movements that you've seen in the video. Have become progressively worse.
To the point of damaging the furniture, other pets, or even injuring himself. Obviously he was generating a lot of noise that was waking up his owners 5 to 8 times per night. And when awake, he was completely normal, completely normal.
Hyperactive Weimaranner. So what do you think the disease category could be in this dog? So this dog was affected by a condition that has been Termed RAM sleep behaviour disorder.
It is an abnormal excessive manifestation of dream activity during the RIM phase of the sleep, and the face of the dog was not very well, visible in the video, but you can ask the owner to see if during the violent, paddling of the limbs, there are, rapid eye movements so they can see the eye bulb moving underneath the eyelids. The clinical signs are again as shown in the video. Some dogs also have vocalisation, teeth grinding.
And in nearly all the cases, if you wake up, the dog, they can be woken up and they are completely normal after arousal. Unfortunately, those episodes can occur multiple times during sleep, both at night and during daytime. And this condition was first reported in JSAP in 2011, and if you want to know more, here are the details of the paper.
Unfortunately, there is no, I would say scientific evidence that that particular treatment is helpful in this condition. There is some suggestion that potassium bromide treatment may be helpful, but it's not necessarily the case in all patients. So our last case.
He is a 2 year old male neutered Labrador retriever. And this is how his episodes look like. So the episodes occur at home when he's relaxed.
And he just can't stand up. He wants to, he can't. He knows where the owner is, he's trying, this movement is him trying to get up to go closer to his owner.
The owner is reassuring him. He really wants to get up, but he can't. And he has this Abnormal movements.
And abnormal muscle tone. The tail, you see the tail is. He's trying to wag the tail and has the episodes.
Slowly resolves, resolves. The tail is the first part of the dog that is working again, typical for a Labrador. So the medical history was that he had those seizure-like episodes since he was one year of age.
And he had The first episode 1 year of age, the 2nd 4 months later, and then 3 episodes over a week, the 3 weeks prior to referral. The owner thought that those episodes were consistently triggered by excitement. It was sort of above the normal excitement level for him.
All episodes look alike, lasted 3 to 4 minutes. He rapidly recovered and All diagnostic investigations were unremarkable. So we need to make a clinical diagnosis here.
What could this be? It is a paroxximal dyskinesia and this nice paper has reported the natural course of the disease in both laboratory retriever and Jack Russell Terrier. I will focus obviously on the laboratory retriever because this is what I showed you in the video.
In this study, they reported data on 36 Labradors. And the males were overrepresented. The median age at episode onset was 2 years and 3 months.
And they tended to have 1 episode every 3 weeks. With the episode lasting between 2 and 3 minutes and 30 minutes in the majority of dogs. They had a long follow-up in this study and they showed that in the majority of dogs over the years without any treatment, there was sort of a spontaneous improvement or resolution of The conditions.
So the episodes were less frequent or they completely stopped occurring. In a smaller number of dogs, the episodes became more prolonged, severe and frequent. And in the remaining 17% of dogs, there was no change during the long follow-up period.
So in conclusion, there are, as you can see, a number of conditions that could be misinterpreted as seizures or the owner would call fit come to see us and say my dog just had a fit. Give me some medications to fix it, to prevent it. It's very important that we have a systematic approach.
That we dedicate time to characterise the episodes, understand if they truly are epileptic seizures associated with hypersynchronous and excessive neuronal activity in the brain, or there are other type of paroxysmal events. Asking key questions to the owner to understand in detail what's happening before, during, and after the episode is vital to make a correct diagnosis and video footage of the episodes can obviously help. We need to conduct a thorough clinical assessment and the greater knowledge we have of all the potential differential diagnosis, the clinical features and of the breed-related conditions we have seen today, the easier obviously it would be to make a clinical diagnosis.
Some of those conditions, as I've said, can be diagnosed with a genetic test. Others are more challenging to diagnose and require a referral. I hope you find this presentation useful to look after your patients, and I'm very grateful for your attention.
Louisa, that was absolutely fascinating. I, I must say I was completely caught out by the one with the stone. That one I didn't see coming.
But, it's, it's very, very interesting. And, and, some of the comments, like Greg made as well, you know, he was talking about, having a hypoglycemic animal, due to an insulinoma that presented because the owner thought it was having a fit. So they, they can be quite challenging clinical cases.
Absolutely. And obviously, if the hypoglycemia, secondary insulinnoma is significant, the, it will be actually an epileptic seizure because the neurons in the brain will be deprived of glucose, which is their only source of energy. And so this will activate the processes resulting in the abnormal neuronal discharges and the actual epileptic seizures.
But obviously, in those cases, if a blood sample can be collected as close as possible to the seizure event, and then there is obvious, hypoglycemia, then we can assess the fructosamine or other, parameters, look for the insulinoma and achieve a diagnosis. But that's an excellent example of how collecting all the clinical puzzles of the picture would lead us to the correct diagnostic investigation. So here with basically a blood test and potentially an abdominal ultrasound, we can reach a diagnosis.
If we had done an MRI to this dog, to the dog with the insulinoma, the MRI would have been normal and if we were to give an epileptic drugs, the dog would have continued to have the episodes. So, it's an excellent example of how the clinical acumen. Is irreplaceable and there is no expensive diagnostic tool that can be a substitute for the clinical acumen.
Yeah, and, and as you've so clearly demonstrated tonight, the, the, the correct history and actually distinguishing between the, you know, is the animal rhythmic or isn't it? And has it lost consciousness, those are so vitally important and, and will never be replaced by any lab tests at all. Yeah, or even a very expensive MRI scan.
Yeah. Louisa, it's, it was an absolutely fascinating presentation and I'm sure everybody was as spellbound as I was. So thank you so much for your time and the information that you've given us tonight.
Thank you very much. It's been a privilege to be lecturing for the development of vets tonight. Yeah.
And to Dawn, my controller in the background, as always, thank you for making everything happen seamlessly. To all the people who attended tonight, thank you so much for attending. And we really look forward to seeing you on another webinar.
From myself, Bruce Stevenson, it's good night.