Hi, my name is Emily. I'm a veterinary neurologist and I work in a private referral hospital in the UK. This presentation is about vestibular disease.
We will first discuss the anatomy of the vestibular symptom. System, then the symptoms of central and peripheral vestibular disease. And with the help of cases, we will discuss differential diagnosis, diagnostics and treatment.
I hope you will find this presentation useful. So we will start with the anatomy of the vestibular system. The vestibular system is the part of the nervous system that is responsible for maintaining balance.
It consists of a peripheral component and a central component. The peripheral vestibular system consists of the inner ear. And the vestibular cochlear nerve.
The vestibular cochlear nerve connects the inner ear with the brain. The vestibular organ works in close proximity with the hearing organ. The inner ear is medial to the middle ear and in direct contact with the middle ear.
The facial nerve and the sympathetic nerve passes close to the middle ear. This explains why severe middle ear disease can result in vestibular disease, hearing deficits, facial nerve paralyzation, and Horner syndrome. The central vestibular organ is partially localised in the caudal brain stem and partially in the cerebellum.
The caudal part of the brain stem where the vestibular nuclei are situated is called the medulla oblongata. In the brain stem we have 4 vestibular nuclei on each side. In the cerebellum, the flocular nodular lobe, and the cord of cerebellar peduncle are responsible for vestibular function.
The main functions of the vestibular system are balance, coordination of the posture and the gait, and coordination of the position and movement of the eyeballs. It also plays a role in motion sickness. Malfunction of the vestibular vestibular organ can result in a number of symptoms such as falling over, head tilt, vestibular ataxia, strabismus, dystagmus, and nausea.
An animal with vestibular disease can present with only one or multiple signs of vestibular disease. In the next part of the presentation, we will discuss the symptoms of vestibular disease in more detail. As discussed in the previous chapter, the most common symptoms of vestibular disease are heeled vestibular ataxia, falling over, nystagmus, positional strabismus, and nausea vomiting.
A head tilt is a patagnomic sign of vestibular disease. In peripheral and central vestibular disease, the head is tilted towards the site of the lesion. The only exception is paradoxical vestibular disease.
In paradoxical vestibular disease, the head is tilted towards the contralateral side of the lesion. This is typical for cerebellar lesions. We have 3 types of ataxia, vestibular, cerebellar, and proprioceptive ataxia.
Vestibular ataxia is not a sign of vestibular disease, and I will try to demonstrate the 3 types of ataxia with the video. In this video, you can see that the dog has vestibular disease because he has a right side of the head tilt and has vestibular ataxia. The vestibular ataxia is characterised by crossing over of the legs and falling over or leaning to the side of the head tilt.
This is a dog with cerebellar disease. Cerebellar ataxia is characterised by hypermetric gait. Last but not least, an example of proprioceptive ataxia in a dog with cervical myelopathy.
So another symptom of a similar disease is nymus pathological nystagmus. It is a pathognomaic sign of vestibular disease. There are two types of pathological nystagmus resting and positional nystagmus.
In resting nystagmus, the abnormal eye movements are present all the time. In positional nystagmus, the abnormal eye movements are only present when the head is held in a certain position. A normal animal has a physiological mistus, also called a vestibular ocular reflex.
A physiological nystagmus can be seen when you move the head from left to right or right to left. The role of the physiological nystagmus is to keep a clear vision while the head is turned. The vestibular organ registrates the movement of the head and gives instructions to the cranial nerves who are responsible for the innervation of the extraocular muscles for the physiological nyamus.
This video demonstrates how to test for physiological darkness, also called the vestibulo-ocular reflex. In this video, you can see a dog with a resting pathological nystagmus. In this video, I will demonstrate how you can test for positional stagmus in a cat.
This cat has a pathological missagus when you keep it in a ventral recumbency. So the direction of the nystagmus can be horizontal, vertical, and rotary. Vertical nystomus cannot be seen in peripheral vestibular disease.
A horizontal and rotary nystagmus can be seen in peripheral and central vestibular disease. In horizontal nystagmus, the direction of the fast face is typical away from the lesion. A good way to remember this is the stagmus runs away from the lesion.
A pendular stagmus is a stagmus characterised by small oscillations of the eye which are present all the time. You can differentiate a pendulum nystagmus from arresting pathological nystagmus based on the fact that there is not a slow and a fast phase. It is most common seen in specific cat breeds, such as the Siamese cats, Burmese, and Himalayan cats.
Pendyonist stagmus is a result of a congenital abnormality in the visual pathway. There is a larger percentage of optic nerves that goes over atopticism in cats with pendulum status. So this is a video of a cat with a pendulum stagmus.
You will see very fine oscillations of the eye. Normally, this causes no problem for the cat. And we leave it untreated.
Positional strabismus is an abnormal position of the eye when the head is held in a certain position. The positional starism is typical on the side of the lesion. The photo on the right is from a boxer with a right-sided positional strabismus.
So circling is a symptom that can be seen with vestibular disease, but also with for brain disease. Typically, the dog or the cat circle towards the site of the lesion. Dogs with forebrain disease normally make wider circles, and dogs or cats with vestibular disease make more tight circles.
So there are certain signs that can help you to differentiate between central and peripheral vestibular disease. It is very important to remember these specific signs. An abnormal mentation.
And or poster reaction deficits are an indication of a central problem. The postural reaction deficits are typical on the same side of the lesion. As discussed before, a vertical nystagmus is a sign of a central vestibular disease.
Facial nerve paralyzation or Horner syndrome in combination with vestibular signs indicate a peripheral vestibular problem. But multiple cranial nerve deficits indicate a central problem. This table summarises the signs of central and vestibular disease.
It is important to know that all of these signs can be present but do not have to be present. If based on your examination, the dog or cat has a problem in the peripheral vestibular disease, it is important to keep in mind that you cannot re cannot exclude a central component for 100%. So now it's time for our first case.
Our first case is about Izzy. She is a 9, she's a 10 year old boxer who presented with a 10-day history of a right-sided head tilt. Easy has remained stable in the last 10 days, and the owner hasn't noticed any other clinical signs.
Izzy has no history of ear disease. This video demonstrates the neurological examination of Izzy. Please watch carefully and write down the abnormalities.
What So E's neurological examination revealed a mild right-sided headed, an absent venous response, and an absent palpable reflex on the right, and a positional strabismus on the right. Based on the neurological examination, where would you localise the problem? A, in the right side of central vestibular right side central vestibular disease, B, right side of peripheral vestibular disease.
C, right-sided central vestibular disease plus cranial nerve 7, or D, right-sided peripheral vestibular disease plus cranial nerve 7. The right answer is. I would localise the problem in the right side of peripheral vestibular disease and the facial nerve, but it is important to to mention that when you localise a problem in the at the peripheral vestibular disease that you can never exclude a central involvement for 100%.
So the reason why we localised in the peripheral vestibular system is because there is a head field and a positional strabismus, which are typical signs of vestibular disease. I did not have any mentation changes and her postural reactions were normal. This makes a central localization unlikely.
And the absent menace response and palpable reflex indicates dysfunction of the facial nerve. Based on the history and the neuro neurological examination, what would be your most likely differentials for a dog with peripheral vestibular disease and facial nerve paralyzation. So the most likely differentials are antiti media internal, idiopathic facial and vestibular neuropathy.
Hypothyroidism and neoplasia. For a dog with a sudden onset of vestibular syndrome, I would recommend a blood test, including thyroid hormone testing and an orthoscopic examination to start with. If you think that middle or inner disease is unlikely, you can give the dog a little bit more time to see if there is some spontaneous improvement.
If you think middle or inner ear disease is likely, an MRI or CT of the head is the next step. Examination of the spinal fluid is mainly important to rule out inflammation of the brain. For easy, the blood test and otoscopic examination was normal.
As there was no improvement after the days, we performed an MRI scan of the head which revealed mild enhancement of the facial nerve on the right side. Examination of the spinal fluid was normal. So this is a transfer T2 weighted image of the head at the level of the inner ear.
The ducts here are the inner ear. On the on the MRI you can see that both middle and inner ear appear normal. This is the middle ear.
It also called the bula tympanica, and it's actually filled with air. Because air is black on a tweed sequence. And the inner ear, as we already said, has a normal dark appearance.
On this dorsal T1 weight post-controlled image at the level of the facial nerves, we can see that there is some contrast uptake of the right facial nerve. So this small branches here are the facial nerve, and we can see that on the right side. The facial nerve is enhancing slightly, so it's a little bit more bright compared to the left side.
So based on the history and the neurological examination, blood tests, MRI, and CSF results, I was diagnosed with idiopathic facial and vestibular neuropathy. This is also called benign peripheral vestibular and facial nerve dysfunction syndrome. Idiopathic vestibular and facial neuropathy means actually that you have a sudden onset of loss of facial and vestibular nerve function without a clear underlying cause.
Approximately 30 to 70% of the dogs with idiopathic vestibular neuropathy also have a facial neuropathy. The vestibularcorleal nerve originates in direct proximity of the facial nerve, and both goes together in a common neuronal sheet. Because they are in such a close proximity, we think that if one nerve gets affected by a mild inflammation, that the other one often gets affected as well.
At this stage, we don't understand why these nerves suddenly stop working. In a recent study, It was shown that the endollymph in the inner ear of dogs with idiopathic vestibular disease has a different composition compared to normal dogs. This is a first step in reaching a better understanding about the path of physiology.
Further research needs to be done to understand exactly why and how the composition has changed. So how do you diagnose idiopathic vestibular and facial neuropathy? You have a dog with vestibular signs.
You localise in the peripheral vestibular system. You, you get, you do blood tests which all come back normal, a normal orthoscopic examination. The MRI scan of the head, reveals no major abnormalities.
Sometimes it's possible to see an enhancement of the facial or locochlear nerve on the T1 way to post contrast images. And a marked increase in senior intensity of the inner ear on flare images. Examination of the spinal fluid can be normal or can reveal a luminal cytological dissociation.
Which means that the proteins in spinal fluid are increased, but the cell count is normal. The treatment of facial and vestibular neuropathy mainly consists of supportive treatments. If the dog is nauseous or vomiting, you can give anti-sickness medication and fluids.
For dogs with facial nerve paralysis, it is important to lubricate the eyes frequently. Because of the lack of blinking and reduced tear production, the dog is predisposed to the developing eye ulcer. In clinics, we normally recommend saline eye ointment as a lubricant.
There is no scientific evidence that steroids are beneficial. If the dog is non-ambulatory because of the severe ataxia and falling over, a good mattress should be provided. Help and my partners can be very helpful for dogs that are unable to walk.
The overall prognosis is good. 30% of the dogs recover completely. 70% recover partially.
Sometimes a headed remains of a permanent facial paralyzation remains. Only a small percentage relapse. Overall, the quality of life is good, even if the if the recovery is only partial.
Just to finish, I've had another video of a dog with idiopathic vestibular disease. Sukira, she's she's an elderly Labrador with also very acute onset of a right-sided heels and vestibular ataxia. In older dogs, this disease is sometimes called geriatric vestibular disease.
The signs can sometimes be quite dramatic, but most often these dogs get better spontaneously after a few days. So now our second case, and the the second case is about Ellie. She's a 14 years old, domestic short hair.
She was referred for a 3 day history of circling to the left, falling over anistanus. So on the right, we can see a video of Ellie. You can see she's circling to the left and has a vestibular ataxia.
She also has a marked left side of her tilt. It's not very clear on the video, but she also has a horizontal his anus. So based on this information, where would you localise?
A in the left sided central vestibular at the left sided central vestibular disease, right sided paradoxical disease, left-sided peripheral vestibular disease, and you know you cannot rule out central involvement and the multifocal disease. I would, localise the problem in the left side as the left side that you feel similar disease. So the reason why I localise it in the left, on the left side in the vascular system is because she had a left sided head tilt, a horizontal nyarmus, and you know that horizontal nyarmus can be present in peripheral and central vestibular disease.
She's circling to the left. And the direction is certainly is towards the site of the lesion. She has vestibular ataxia, and I don't think there's a central problem because Ellie does not have postal reaction deficits and she also has a normal mentation.
So what would be your differential diagnosis? Give you 2 seconds to think about it. So my differential diagnosis first otitis media internal poly in a cat and important differential otitis, idiopathic vestibular disease, neoplasia, toxic problems and brain disease.
So, which toxins can cause autotoxicity, you know that amino glycosids, loop theuretics, air cleaning, products as cisplatin, vingosin, and vincosine can cause autotoxicity. So further examination. A general blood test, of any, that's always a good idea if you have an animal with neurological signs, an orthoscopic examination, very good, but, but keep in mind that you cannot see the middle ear or the inner ear because that is hidden behind the tympanic membrane.
If you see a ruptured tympanic membrane or a very bulging tympanic membrane, it can be an indication that there is a problem in the middle ear. You can also do if you're worried about middle or inner ear disease imaging of the head. You can choose between a CT or an MRI scan.
Advantage of CT scan is that it's cheaper than an MRI scan. It is faster, and it's good to look at the gula tympanica. An MRI scan is unfortunately more expensive.
You need a longer general anaesthetic, but you get more details of the inner ear and the brain. If, if your cat, if in the middle, middle ear disease is confirmed, it's always good to do meningotomy, where you actually with make a small hole into the tympanic membrane and you take a sample of the material from the middle ear, which you can send for cytology and culture. And if you have any concerns that maybe, for example, the middle or inner ear infection has Has actually broken into the brain, it's good to do a spinal tap to rule out inflammation or infection of the brain.
So this is a transverse T2 weighted image of the brain at the level of the inner ear. So we can see that in the middle here on the left side. There is an abnormal intensity.
This means that instead of air which is black on MRI. We can see a bright signal which indicates that is that there is fluid-like substance in the middle ear. On this MRI you can also see that the middle ear is divided into compartments, a ventromedial compartment and a dorsolateral compartment.
And you can see here that there's little membranes separating these two compartments. So what would be your diagnosis based on the scan? For otitis media was the most likely diagnosis.
So the path of physiology of otitis media in cats and dogs is slightly different. In cats. Typically develop an a middle ear infection secondary to an upper respiratory tract infection.
In dogs, a middle ear infection is most often caused by notitis external. So Titis media and cats can be treated conservative and surgical. As any was an elderly cat, we decided to try conservative first.
We gave 6 weeks a course of antibiotics, and often a short course of steroids at an anti-inflammatory dose can be useful as well. So surgery can be considered if there's no response to medical management or and also if, if the otitis media is very severe and it's causing inflammation or infection of the brain. So now, a little question for you.
Can you name three nerves that can be affected in cats with otitis media or internal? The three nerves are the sympathetic nerve, the facial nerve, and the vestilocochal nerve. And what syndrome do you get where the sympatic nerve stops working?
With sympathetic nerve dysfunction, you get Horner syndrome. This is a photo of a cat with Horner syndrome. And with Horner syndrome, you get osis, meiosis, protrusion of the third eyelet, and endothalamus.
Sympathetic nerve. A sympathetic nerve innervation involves a three neuron pathway. It includes a first order neuron which travels from the hippothalamus.
To the spinal cord. A second order neuron will travel from the T1, T2, T3 spinal cord segments till the cranial cervical junction. Me, which is medial to the tympanicbula, and a third or neuron will travel from the cranial cervical jureon to the eye.
A phenyl test can be helpful to localise the source of the problem in dogs or cats with horn syndrome. When you do a phenyl ephrine test, you can put one drop of 1% phenyrine in the in the affected eye. And it will create pupillary dilatation and resolve the anothalus to eyelid protrusion and hosis.
The duration until you reach a resolution of the Horner syndrome will help to differentiate between the 1st, 2nd, or 3rd or the Horner syndrome. When it is the Or the Horner syndrome, a localization in the central nervous system can be excluded. So what type of Horn's syndrome do you expect in a cat with middle ear disease, first or the second or third-order Horn's syndrome?
You would get a 3rd out of Horner syndrome. Now it's time for the case 3. So our first case is about Sky.
Sky is a five year old female neutered chihuahua, which presented as an emergency with the sudden onset of left-sided vestibular signs. It started with a mark left-sided head tilt, and it progressed to uncontrollable rolling to the left within 24 hours. Sky doesn't have a history of ear disease or trauma.
So please now look carefully to the video of Sky's neurological examination and write down the abnormalities. The main findings on the neurological examination of Sky were a left-sided he falling over to the left when trying to walk and almost rolling over to the left. She also had a positional vertical nystagmus, and she also had a strabismus.
She had a reduced postural reaction of the left thoracic and left pelvic leg. So based on the examination, where would you localise the problem. A left side peripheral vestibular disease.
The right-sided paradoxical vestibular disease. The multifocal brain problem? The left-sided central vestibular disease.
So, left-sided central vestibular disease is the right answer. So and the reason why we think it is left side of the central vestibular disease, so the heel, the ataxia, positional nystagmus, and arbs already confirmed us that we are dealing with the vestibular syndrome. The abnormal postural reactions on the same side of the head.
And the direction of the stagmus, which was vertical, is an indication that there is a central problem. I think in Sky it was very difficult to to say if the mentation is normal or abnormal as she was actually struggling so much in general with the vestibular disease with the rolling over and apraxia, to, to to be able to properly assess the mentation. So what would be your differentials for a 5 year old chihuahua with an acute onset of central vestibular syndrome?
So the main differentials for me would be a vascular incident such as an ischemic infarct or a haemorrhage. And an inflammatory condition. Neoplasia is possible as well, but you would expect maybe a more gradual onset.
So for a dog with an acute onset of central vestibulosisys, we recommend to do a blood test. MRI of the head and spinal tap. If you have an owner with cost concerns and the onset of vestibular signs is very acute, you can always give the dog some time to see if there is any sign of improvement over a period of 2 to 3 days.
If the dog has a vascular incident, he or she should start showing signs of improvement after 2 or 3 days. With inflammatory disease. Of neoplasia, you actually expect that a dog or cat will get worse with time.
So, with Sky, we decided to do an MRI scan of the head and it revealed actually a poorly defined lesion on the left side of the brain stem. This makes a vascular event unlikely, as a vascular event typically is very well defined. The lesion was mildly contrast enhancing, which is an indication of inflammation or neoplasia.
But there was no mass effect, and mass effect is a typical sign of neoplasia. Based on the MRI we could also see that there was no signs of haemorrhage, as we would get a signal void on the gradient echo sequences. So most likely based on the MRI scan, we were dealing with inflammatory brain disease, but you need to do a CSF test to confirm this if it's of course safe to do so.
So the spinal fluid analysis of Sky confirmed the suspicion or suspicion, and there was an increase in white blood cell count. So Sky had 30 cells per microliter, and normally you should have less than 5. The proteins in the spinal fluid were increased as well.
It was 68 mic litre and normally it should be less than 30. On the cystology, we could see that there was a lymphocytic pleocytosis. So, At this stage, we know that the sky has an inflammation of the brain, also called an encephalitis.
So encephalitis in dogs can be immune mediated or can have an infectious cause. And then the immune mediated encephalitis is most common in dogs. It is called also called meningoencephalitis of unknown origin.
Based on histopathology of the brain, you can further differentiate it in granulomaters, meaning encephalitis or necrotizing encephalitis. Infectious encephalitis is rare and can be caused by viruses, bacteria, parasites, fungi and protozoa. In dogs, probably the most common infectious cause for encephalitis is Neosporra or bacteria.
Rabies luckily is extremely rare. Canine distem appears as well, thanks to the vaccinations and fungal encephalitis is also very rare. In the we suspect an encephalitis.
We will try to rule out toxoplasma and Neosporra, and you can do this by doing a blood test, sociology, or you can also do PCR and the CSF. For toxoplasma, we measure the IgG and IgM antibodies. So we are suspicious of an active infection infection if IgG is above 1 in 400 and or if your IGM is about 1, is above 1 in 64.
A positive PCR and CSF is also diagnosed with toxoplasma. For diaspora, we can diagnose an active infection if the antibodies are above 1 in 400 and or if you have a positive PCR in the CSF. So steroids are the main part of the treatment for meningoencephalitis of unknown origin.
We typically start with a high doses, immunosuppressive doses of steroids, and we slowly taper the dose over a period of 6 months to a year. The majority of dogs will need to be treated with a low dose of steroids in the long term in order to avoid a relapse. And in some patients, we add another immunosuppressive drug such as cytarabine.
The prognosis of encephalitis of unknown origin is guarded. Normally we tell, we tell the owners that the cases can be divided into three big groups. A minority of the dogs dies within days after being diagnosed.
The majority of the dogs responds well to treatment but needs treatment in the long term in order to avoid relapses. And then there's another small group which recovers completely and does not need any medication on the long term. So this is a video of Skype 3 days after diagnosis.
Can still see that she still has a head tilt, a bit of ataxia, but at least she can stand up by herself and do a few steps. She also appears more alert. And this is only after 3 days of treatment.
And, inflammation of the brain in cats is more rare compared to encephalitis in dogs. An immune-mediated encephalitis is very rare, and the most common causes for infectious encephalitis in cats are bacteria and FIP. I briefly would would like to discuss neurological FIP as this is the most common cause of encephalitis in cats.
FIP in general is most common in young cats and purebred cats. Often they present with a chronic history of lethargy and progressive neurological signs. When we do an MRI scan of the head of a cat with FRP, we can find some very specific findings.
The cats often have ventriculomegaly, syringomyelie, obvious contrast enhancement of the meninges ependema, and cover plexy. The spinal fluid can have an abnormal intensity on flare and the one way images because of the high protein concentration. Examination of the spinal fluid typically reveals a neutro neutrophilic pleocytosis and an increased protein concentration.
On histopathology of the brain, we see severe inflammation of the meninges, ependyma, and cho plexy. In the UK, rendecivi is now officially available for treatment of FIP in cats. MRI scan of the brain.
Cats with neurogenic FIP can be very useful. Typical signs of a ventriculomegaly. You see this cat, lateral ventricles, metayphalic aid, and 4th ventricular are severely increased in size.
Cringomy syringomyelia. Here you can see bright signal within the cranial cervical spinal cord. And enhancement of the appendema so the lining, the apical lining of the fourth ventricle.
Undercover plexy. So these are very typical findings in a cat with FIP. And, and to finish, we have a last case.
And the last case is about Darcy. Darcy is a 5 year old Cavalier King Charles Spaniel, and she has a parakeet onset of a left-sided head tilt and inability to walk. The right side of the body appears to be weaker.
Blood tests revealed no significant changes. So please watch the videos of neurological examination of the carefully and write down the abnormalities. So the main findings on the neurological examination of the art was a left-sided head, non-ambulatory traparesis, and the right side is worse compared to the left.
The pole replacement is absent in the right thoracic and pelvic leg. The menace's response was reduced in the right eye, and also Darcy had a position on his arm. So based on the neurological examination, where would you localise a left-sided central vestibular disease, B right-sided central vestibular disease, paradoxical vestibular disease with the lesion on the right side.
Paradoxical vestibular disease is a lesion on the left. Left-sided peripheral disease or right-sided peripheral disease? The right answer is paradoxical vestibular syndrome.
The lesion is on the right side. So animals with paradoxical vestibular disease have a head tilt on the opposite side of the lesion. The postal reaction deficits are on the same side of the lesion.
So in that we could see that the head tilt was towards the left, but the postal reaction deficits were on the right. So with the normal central vestibular disease, the head and the post reaction deficits are on the same site. A paradoxical vestibular syndrome is seen with lesions in specific parts of the cerebellum, such as the flocullomodular lobe.
And the coal cerebellar peduncle. The coal cerebellar peduncle connects the cerebellum with the brainstem. So what would be your differentials for five year old Kavallic and child with a parakeet onset of paradoxical vestibular syndrome?
The main differentials are a vascular inflammatory, a vascular event, inflammatory disease, and neoplasia. Neoplasia is again less likely because it started very acutely. So further examinations that we would recommend blood test, serology for toxoplasma Neosporra, MRI scan of the head, and a spinal tap.
MRI scan of the brain of Darcy revealed a right-sided. Well-defined lesion. If you compare this lesion with the previous lesion I saw of the chihuahua, this is a well-defined with triangular shape.
And that is typical for a vascular lesion. So Darcy was diagnosed with an in fact of the rostro cerebellar artery. Based on a previous study, we know that cavis are predisposed for in facts of the cerebellum.
So treatment and the treatment is supportive for dogs with a vascular in in the brain. Most dogs will start to improve after a couple of days, but full recovery can take a few weeks to months. It's important to know that 50% of the dogs who suffered from a brain in fact have an underlying condition, and the most common underlying conditions are problems with thyroid function, kidney function, Cushing's disease, and hypertension.
The overall prognosis is good, but it depends on the underlying condition. And then, as a last remark, metronidazole intoxication, secondary, the chronic administration of high doses of metronidazole can cause vestibular signs, but it can also cause seizures, neuropathies, and tremors. So if you have a dog who presents with an acute onset of a neurological signs, and it can be vestibular diseases, seizures, signs of weakness, and the dog is on metronidazole, it is good to check the dose and the duration of the treatment, because that can be the cause of the signs.
The treatment consists of stopping the metronidazole and giving diazepam for a few days, as the diazepam will speed up the recovery. Here I have a video of a dog with metronidazole intoxication. The dog presented because of sudden inability to walk.
Taking a good history is very important in these cases, because if you were not aware of the But the fact that this dog was treated with melonitazole for a long time and at very high dose, you would maybe rush this dog into the MRI scan for an MRI of the brain and, and maybe the neck as well. So the dog was normallay tetayretic. And sometimes we could see a spontaneously time as well.
I was testing the, the vestibular ocular reflex. Meniscus responses. And this is a video of the dog a couple of days later, after the metronidazole was stopped and the treatment with diazepam was started.
So thank you for watching the CBD and please contact me if you have any questions.