The purpose of this presentation is to review together a Couple of neurology cases and go through the steps that are very important when we approach a neurological patient. We will review the neurologic examination and how we can achieve a neuronatomic localization, and these are the building blocks to the approach. Of the neurology patient.

The medical history is very important. Investing the time in collecting all the relevant details, all the pieces of the puzzles that we can put together along with the clinical findings of the physical examination and the neurological examination. Are essential to develop a correct and accurate differential diagnosis list, which represents the foundation for the selection and also the interpretation of the diagnostic investigations.

When we are presented with a neuroic patient, we obviously immediately think of expensive and fancy diagnostic procedure. Just like MRI and CT, but actually, the first fundamental and essential step is a good medical history and good clinical skills and clinical knowledge. And I hope that the cases we will look at together today will help you review method, methodical approach to the patients, to the neurology patient, and sometimes a good diagnosis can be achieved in the primary care setting.

Just by using the clinical skills, the clinical knowledge, and giving the Client and the patient the time required to achieve a solid clinical diagnosis. In neurology, when we performed the neuroatomic localization, we often use the so-called neurological syndromes approach and this involves being cognizant of a number of clinical manifestations that can occur when a patient has a lesion in a particular area of the nervous system. Here, we'll review clinical manifestations of Lesions within In the intracranial cavity.

So by forebrain disease, we refer to conditions affecting the cerebral cortex or the diencephalum, and animals with lesions in these areas, sorry, can present with one or more of the clinical signs listed in this box. Some may only have some very subtle behavioural changes that are they are noticeable by the owner at home or in the familiar environment for the animal, and in the consultation room, we will see nothing. So it's very important that we dedicate the time to listen to the owner and we ask key questions to find out.

If there are any signs that could be consistent with a for a brain disease. Other animals may present with seizures or movement disorders as the only clinical abnormality, and others may have persistent neurological signs such as Turning the head or the entire body to one side or pressing the head against objects, bumping into things, circling in large circles, wandering aimlessly and pacing. And on neurological examination, some may present with absent menace and absent nasal or facial sensation.

And if the lesion is unilateral, those deficits are on the opposite side of the for a brain lesion. And postal reactions or some gait abnormalities can also be detected. In patients with lesions affect Active the cerebellum, there can be the following clinical signs.

The cerebellum is in control of the tone of the muscles, as well as the execution of the movements, and then there is a part of the cerebellum which is involved in the vestibular function. So if the vestibular part of the cerebellum is involved, we will see vestibular signs like head tilt, whiteba stands, falling to one side, nystagmus, and If also or only. The part of the cerebellum, involving more the muscle tone, we may see muscle spasticity, hypermetria, and the so-called intention had tremors.

The brain stem is quite a vital area for both us and the dogs and involved in mesencephalon, the ponds and the medulla oblongata, and even a small lesion in this rather essential area of our brain. Could lead to quite severe and pronounced neurological signs, including obtundation, stupor, even coma. The activating reticular system runs within, is located within the brain stem and even a small lesion at this level can result in severe impairment, augmentation and the ability to stand up and walk.

And then within the brain stem, there are the cerebellar nuclei, so we may have cerebellar signs or deficits of the majority of cranial nerves that originate from the brain stem. So a variety of clinical signs, but being aware of these neurological syndromes can be very helpful in Developing our neuroatomic localization and developing the differential diagnosis list. So after this introduction, we we're gonna focus on the clinical signs and I hope you can benefit from this webinar by watching the cases at your own pace.

There will be videos of the clinical manifestations. I will be commenting on the videos, but you may want to watch them first without the audio. So make up your mind on which abnormalities you observe, and then you can replay the video with the audio and listen to my commentary.

The first case is a 10 year old female spayed domestic short hair, and the owners were unsure of when the clinical abnormalities, start. They could say that the cat had been progressively getting worse over weeks, possibly longer, and at the time, the cat was presented to the primary vet and then promptly referred to us, it was quite obvious that there was a neurologic abnormality. So look at the posture of the cat because, when the cat was not, manipulated, not handled, this is the posture the cat would have.

So the thoracic limbs were rigidly extended. The pelvic limbs were flexed. The body was a bit arched here and the neck is also to some extent, to some extent extended.

And I show you the the neurological examination of this cat and I take this opportunity to thank. The colleagues I've worked with, including Professor Simon Platt, who have obviously been involved in obtaining those videos. So this book ha is unable to walk, he's unable to stand up.

The thoracic limbs, as we said earlier, were rigidly extended. The pelvic limbs could be flexed and actually were flex at rest. There were no orthopaedic abnormalities in any of the limbs, and as you can see, the cat has very, very minor voluntary movements in the pelvic climbs, not so much in the thoracic climbs that are rigidly extended.

Because of the hyperextension in the thoracine, I think mentation is fairly challenging to assess in this cat, but it seems to be aware the menace response, as you can see, is present bilaterally and it is very important to cover the opposite eye when testing the menace response. Facial sensation is also normal, the bipedal reflex is normal. And we're gonna look in a moment at the vestibular ocular reflex.

It's bit difficult to appreciate in a video. And here is the gag reflex. The cat is not very keen to open the mouth, but he can, and the gag response is normal.

So, a number of abnormalities and it's very helpful to note all those abnormalities in a neurology examination form and I would highly recommend it. And then try to make sense of all the abnormalities, look at the neurological syndromes, even in the webinar notes, I provided you the the neurological syndromes for all areas of the nervous system. And try to make reach a conclusion on which area of the nervous system is affected by the disease responsible for the presenting clinical signs.

So in summary, the neurological examination in this cat showed non-ambulatory roparassis. The cat couldn't stand up, couldn't walk. There was minor voluntary motor activity, especially in the pelvic limbs.

Mation was challenging to assess even by examining the cat rather than just watching a video as in your case. When cats are unable to move or to, to even sit up, they may look less aware than they actually are. We felt that this cat had a slap some mutation impairment was mild.

What was noticeable is the posture I showed you at the beginning, the rigid extension of the thoracic limb, the flexion of the pelvic limbs, and the opistotinus was mild in this cat. And this is the so-called the cerebellate posture and suggests a lesion in a particular area of the brain we have mentioned earlier. And the postal reactions were absent in all four limbs, and when the cat was put in dorsal recumbens, there was a nystagmus.

Vertical dystagmus in both eyes. This was not that visible in the video, and there were no other abnormalities. So trying to put this all together, allow yourself the time to think where within the intracranial cavity, neuronal structures we discussed earlier, you would.

Localise the lesion. And again, this is a particularly challenging case, and it's more to stimulate the thinking. Then sort of provide a straightforward textbook-like answer.

But again here, feel free to post the recording of the webinar, make up your mind, go back to your notes, watch the video again, if you feel could be beneficial, and try to make sense of the clinical signs and try to establish where the problem could be. And once you've reached your conclusion, then look at this slide. Where I share with you the fact that we felt that the problem was mainly affecting the cerebellum due to the muscle tone abnormalities, the posture of the cat, but to account for the severe abnormalities in the postural reactions and the decrease mentation, the problem had to be affecting also other intracranial areas such as the forebrain and potentially part of the brain stem.

So what next? Differential diagnosis. Considering the age of the cat and the chronic progressive onset, neoplasia, either primary or secondary, was the top differential diagnosis, followed by infectious inflammatory etiologies.

Such as meningoencephalitis, although the cat didn't have any neck pain, encephalitis could occur without any pain. In a brain abscess a granuloma, there were no external signs of a bite, wound or any history of pre-existing bacterial infection, but sometimes in cats, especially outdoor cats, brain abscesses can occur without any external signs. A metabolic encephalopathy was also possible but considered less likely.

So, my question to you is, what would you do next? Take a moment to think. You're in your practise with a cat looking like this.

Would you run any laboratory investigations, haematologists are on biochemistry? Would you measure the blood pressure? Would you take any radiographs, or for example, to look for, a metastatic, neoplastic disease or a primary tumour that could have metastasized to the brain, or would you refer it as an emergency to a neurologist?

The referring vet of this cat decided to Refer it straight to us. Obviously, the neurological signs are quite severe. What needs to be considered also is when a blood sampling is obtained from an animal that has an intracranial pathology, especially if we are suspecting an intracranial mass, space occupying mass, there could be concerns of raised intracranial pressure.

So if we apply pressure on the jugular vein, we may be increasing the intracranial pressure and potentially even lead to brain herniation and death. So even just blood sampling in animals looking like this cat. It could be a life, threatening procedure.

And obviously obtaining blood from a cephalic or sinus vein in, in, in a, in a cat or a small dog also brings these challenges but will not affect the intracranial pressure. Haematologists and biochemistry in this cat were normal, and we performed an MRI. These images are a sagittal T2 weighted image.

The, CSF is hyper intense, so it's white. And a dorsal T1 weighted pulse contrast. MRI image of the brain of this cat.

So we can immediately see that the lateral ventricles are very large. This area I'm outlining here that is full of CSF which is black in T1, are very enlarged and also here on the T2 weighted image, the CSF is white, it's very intense, and this is the third ventricle and it's very, very dilated. And then we can see this area that I'm outlining.

Here and here. And it is a very, very large moss. Adhering to the Occipital bone Ground and severely compressing, very severely compressing the Cerebellum The mesencephalic aqueduct is stenosed as a consequence, and that's why we have the secondary hydrocephalus.

So that's the mask which is updating, taking some contrast, but there are other areas that are not contrast enhancing. So the MRI diagnosis was is a meningioma that is causing severe compression of the cerebellum and secondary obstructed hydrocephalus. So what can we do in a cat like this one, the cat probably had the meningioma for months, several months, and probably initially had just some minor gait abnormalities, which may have gone undetected and until the point that the, Cerebral, the cerebellar parranyma was so compressed that severe dysfunction.

Then became obvious and veterinary attention was sought. In those cases, the treatment of choice is surgical because we need to decompress, the affected brain region. So the cat underwent surgery, we need a suboccipital craniectomy, and, .

The, the meningiomas are fairly easy to resect, particularly in cats, and this is the cat just a few days later, completely, able to walk. There is just a very minor. Ataxia, and, cats generally don't like to walk, in the, consultation room, so we use the carrier.

He clearly wants to go home and it's nearly time to go home, and he can negotiate movements even in narrow spaces, as you can see here, just with a very minor ataxia. So, it's remarkable how particularly in cats. The, cerebral tissue can, recover following removal of space occupying, masses or can, accommodate, and this was a matter of a few days after the surgery.

Phyli intracranial meningomas are the most common brain tumour type in cats, and they are often round or oval, fairly firm. In this case, the T1 post-contrast MRI showed actually quite a good contrast uptake, unlike in the cat I showed you earlier, and you can see that this tumour is about 1.5 centimetres in diameter.

And They are again relatively easy to remove surgically. Prognosis is good to excellent and In a recent study which included 121 cats, the median postoperative survival time was 58 months. So cats that are 10 years or older, may be presenting with intracranial signs associated with a meningioma, and at any time the meningioma is surgically resectable and is large enough for surgery to be the treatment of choice, prognosis is generally good.

So even cats that present with clinical signs that are as dramatic as the cat I've showed you, . Now, they can recover if they receive prompt. And specialised care.

The next case is 6 year, 2 month old female spade cocker spaniel. And she was referred with acute onset of progressive neurologic signs that included gait abnormality for the previous week and also visual deficits were detected over the previous two days. This dog had been previously diagnosed by her primary vet with what was suspected to be idiopathic epilepsy.

And she had been treated with phenobarbital for the previous two years, and most recently, the phenobarbital dosage for the previous 3 months was 5.7 milligrammes per kilogramme twice daily. When we asked the owners when the last seizure was witnessed, they reported it was witnessed one month prior to presentation.

So here I show you the video of Bluebell shortly after admission. And you can appreciate that the gait is clearly abnormal. And you will see throughout the video that also he, she's struggling to stand up and walk at times, balance and strength both do not seem great.

She tyres quite easily and the head is often held low. You will also notice, in a moment that unfortunately she bumps into The fence and she also has some spontaneous knuckling in all all her forelimbs. She tends to fall.

The head is held low. Sometimes dogs that cannot see properly keep the head low because they are guided by smell. Other times the head can be low for other reasons.

Pole replacement responds. Was absent. In the examined limbs as you can see in the video now.

And again, To just in, in the left thoracic limb, there is a delayed response in the other three limbs. The response was absent, but it's quite fatigable and Not particularly lively, facial sensation. Appears normal, but the menace responds.

Is not Normal. Essentially severely decreased to absent. So there are a number of abnormalities that this video has illustrated and I will summarise what we have seen in the video and also provide a few more information that was not available from the video.

So clearly the eye augmentation is not normal, is obtunded. She was obtunded, she bumped into the fence. You may remember from the history, the order felt over the previous two days vision was impaired.

She was a toxic, you know, for limbs and also weak, you know, for limbs. The postal reactions were, decreased to absent and the menace response was absent bilaterally. When we have animals in which there is a concern about vision and we need to establish whether the deficit is due to an ocular pathology, so, or a cranial nerve pathology versus a dysfunction of the perception of the visual stimulus at the cerebral cortex level, there are a number of tests we can do.

First of all, in this dog, the pupil size was normal and the PLR was also normal. That, that would make retinal and cranial nerve number 2, optic nerve disease quite unlikely. And the menace response can be upset for a number of reasons that are related to intracranial lesions.

The cotton ball test can be quite helpful in these animals, because it assessed the, the visual follow, and that was normal. So both PLR, pupil sizes, and cotton ball test were normal, which made a lesion affecting the retina or the optic nerve very unlikely. And the rest of the neurological examination was also normal.

So, here, try to take a moment, review your webinar notes, review the initial slide I showed you with the various. Neurological syndromes and try to, localise the lesion to a particular area of the nervous system. To complete, the puzzle, I have two more relevant, pieces.

Those are more relevant to the development of the differential diagnosis than the actual neuroatomic localization. So you may want to reach your conclusion on the neuroatomic localization first. On physical examination, the mucosal membrane were found to be mildlyteric and on abdominal palpation, we detected epitomegaly.

So in terms of the neuronatomic localization, do you feel the problem is more likely to be in the forebrain? Could it be multifocal, intracranial? Could it be the cerebellum, could it be the brain stem?

So as far as the cerebellum, we've seen that There, there weren't spasticity, there were some issues with, with, with balance at time but the mentation was affected, the ability to perceive visual stimuli was affected, perception was affected. So, overall, we felt that the forebrain was predominantly affected, and differential diagnosis. Could the clinical manifestation be somehow related to the phenobarbital, the dog had been receiving for over 2 years.

The dog is on a, has been on a relatively high dose for the previous 3 months. Unfortunately, serum phenobarbital levels are not being monitored in recent months, so we don't know what, we didn't know at the time what they were. Could the phenobarbiton have resulted into adverse effects, including pototoxicity, or could this dog have suffered a recent epileptic seizure which was not witnessed by the owner and at the time of presentation, was in a postico state.

The postictal state can sometime last several days. However, what would be inconsistent with a postico state unless the dog had repeated seizures or and witnessed seizure over a week was the fact that the clinical signs seemed to be progressive over the past week. Could the dog have a concurrent forebrain disease causing the clinical signs that the dog was referred for, or could the dog have a condition that is extracranial and is somehow affecting?

The brain function. So, a number of hypotheses that I'd like you to consider and maybe select what you feel is most probable or what you would investigate first of these options. I open a brief parenthesis to talk to you about guidelines that have been internationally agreed between specialists in neurology and pharmacology.

To optimise the use of phenobarbital in dogs, phenobarbital is the, oldest and most used antiepileptic drugs in dogs and also people, particularly in, countries that are, still, not as privileged as others financially. The recommendation in dogs with normalpain function is to initiate the phenobarbitin at a dosage that is between 2.5 and 3 milligrammes per kilogramme every 12 hours.

And then it's very important to maintain an accurate seizure diary. And test the serum phenobarbital levels 23 weeks after initiation, when a steady state is expected to be achieved, and then 6 weeks later, And subsequently based on The seizure diary, so if and when epileptic seizures occur, whether the phenobarbital is well tolerated and based on the serum phenobarbital level, we need to adjust the dosage over time. And I recommend to collect the serum phenobarbital level.

Sample, blood sample, always at the same time in relation to the oral administration of the medication and collecting a trough sample, so just before the next oral phenobarbital dosage is due is an easy way to remember to do it always at the same time and it also allows you to find out the lowest serum levels in the 24 hour time interval. And monitoring the seruminobarbutin levels regularly according to the International Veterinary Epilepsy Task Force recommendation is very helpful, it is very important in making the best use of this medication. And it's also highly recommended.

To assess them anytime, seizure frequency is increased, so we can establish if we need to increase the dosage of phenobarbiton or if we need to add a second epileptic drug, we obviously should test the serum phenobarbital levels also anytime we suspect a toxicity or an overdose because we may need to decrease the dosage. And in dogs that have well-controlled epilepsy, it is recommended to test the serum phenobarbin levels as well as haematology, biochemistry, and bias stimulation tests every 6 to 12 months as a periodic health check. And following those guidelines can significantly improve the quality of life of dogs with epilepsy and as a consequence, their owners.

Unfortunately, often those milestones in the phenobarbital treatment are forgotten and And, and, and some very sad outcomes occur. It is also highly, highly recommended by the International Veterinary Epilepsy Task Force to ensure that the serum arbitone levels are maintained below 35 milligrammes per litre because levels higher than this limit have been associated with an increased risk of hepatocysti. And this is very important to us as clinicians are aware of this limit, because unfortunately, several laboratories refer an old therapeutic range up to 40 milligrammes per litre.

So don't rely just on the report of the lab, rely also on your knowledge and the most recent recommendations of the International Veterinary Epilepsy Task Force. Going back to the Coker Bluebell. Here are the 7 biochemistry results, and as you can see, there are a number of concerning abnormalities.

The total bilirubin is incredibly elevated. The liver enzymes, are also elevated, no surprise in a dog on philobarbin. But the total bilirubin is really high, the cholesterol is low, glucose is low, the albumin is at the lower end of the range.

The bylaws its further supported the suspicion of hepatic. Dysfunction and again, this dog was, mildly eric, on presentation. The, liver was considered a large on palpation, and we tested immediately the syno barbitin level, and they were incredibly high, possibly the highest I've seen in the past 10 years, and this made us neurologists and also the internal medicine specialists very, very unhappy.

Those levels were way too high. They could be too high because the, the, the oral dosage was too high for this dog, or they can be too high because the liver is no longer able to metabolise the phenobarbicin and therefore, the levels are nearly twice the top level we would consider acceptable, or over twice. 35 milligrammes per litre.

So this is essentially an emergency. The abdominal ultrasound, confirmed the concern of a severe hepatic condition. There were, diffusiico, the liver was diffusely hypericoic and enlarged.

There were multiple hypoechoic nodules. And a true liver biopsy, the histology, confirmed the clinical suspicion of a severe hepatic disease. So what next?

Diagnosis, advanced liver disease, newly liver failure, the neurological signs were secondary to the hepatic encephalopathy and the excessively elevated serum phenobarbital level. The phenobarbital levels, as I said earlier, were excessively elevated, potentially both because of the high dosage and the decrease hepatic metabolism. Now, there are dogs where a dosage of 5.7 or 6 milligrammes per kilogramme of phenobarbital are well tolerated, are needed, but do not lead to such elevated serum phenobarbital levels.

So the key is to monitor the serum phenobarbital level and monitor the patient regularly. What did we do? First of all, we had to discontinue immediately the phenobarbital.

Now, normally this is not recommended because the animals could have seizures but in this case was obviously necessary, so we stopped it completely and we introduced two antepileptic medications that are not metabolised by the liver. So the potassium bromide and the levetiracetam, both as loading followed by maintenance, and I've indicated only the maintenance dosage in the slide. Fortunately, the dog didn't suffer any epileptic seizures during hospitalisation and also upon, discharge you, and obviously for the liver, a number of treatments had to be initiated that you can see, detailed here, and they were recommended by our internal medicine specialist.

Obviously, some of those like the hepatoprotactant and the diet were performed long term. Other treatment were just for days or weeks. And just 3 days.

Or after, discontinuing the phenobarbital and initiating the treatments illustrated in the previous slide, you can see that the dog is already Walking much better. It's no longer that weak, it can even trot, . He's no longer bumping into things.

There is still a degree of ataxia. Let's not forget that this dog has just completed, loading with both potassium bromide and levetiracetam. And obviously, the hepatic condition has not magically, Disappeared, but you can see what a difference in the perception of this dog.

And I can tell you also in the general demeanour, there was a significant improvement. The menace response is back to normal. And And again, a much livelier, happier dog.

And I show you the follow up over several months of the blood test results in this dog. So a presentation, you can see that also haematology presented some significant abnormalities. And the serum biochemistry has the severe abnormality I showed you earlier, and it took months for ALP and ALT to return to normal.

Whereas other parameters, fortunately, with the treatment recovery was fairly prompt and successful. So, you can obviously stop the video and have a look at those blood test results and monitoring over time and I hope this is of interest to you. Obviously, this, ideally this should have not happened.

Corkers can develop hepatic disease, regardless of being on phenobarbiitin treatment. So, in this case, there could have been more than one condition, and situations contributing to the liver pathology, but it's very, very important to, monitor the serum phenobarbital levels, regularly, according to the international, recommendations and make the best use of phenobarbiton, which is a, can be a very safe and it's definitely a very efficacious antiepileptic drug. And, when we, see dogs with neurologic signs and these dogs are on an epileptic medications, we always have to inquire about the Dosage and the serum level of the medications to ensure that the presenting neurologic signs are whether they are associated to the medications or to a new condition.

Now we have another clinical case, an 11 year old, male neutrid beagle. Who presented with a very acute onset. So very suddenly, in a matter of minutes to a few hours, he went from completely normal to unable to stand up and walk.

He suffered several episodes of vomiting. And that's how he looked on presentation. He needed support to stand up and walk.

So as you can see, the chest harness is being used to support body and help him walk. He has a tendency to lean towards my colleague and without the support he would probably fall on his left side. And also look at the posture of his head.

And again, he was really leaning. And drifting to the left. I, I leave you to watch it here.

You can see that his movements are not very well coordinated. He has a wide base stance at times. And again, he, he's drifting and leaning to the left, and my colleagues has to pull, pull the harness to help him walk straight.

When we assess pro perception, it's very important to support the animal body from underneath and have a non slippery surface, and the fact that when he shake his head, he lost balance and he would have fallen to the left if he wasn't supported by my colleagues. That's also quite a relevant finding in terms of the neurological examination. You've seen the poor replacement response.

That was absent in the left pelvic limb and now it's normal in the other three limbs. And look at the position of the head. I'll stop the video for a moment.

Look at it now and throughout this section of the video, there is. Focused on the head, but piro reflex is normal bilaterally. The menace's response is present.

Look at the head now. Do you feel that the ears are level, or, or is there one ear that is lower than the other? And this is spontaneous position of the head of the dog.

It's not the clinician, . Rotating the head. The menace responds normal.

And again, facial sensation. And but people reflex. Sensation inside the pin now we all normal, you can obviously lick and gag quite well and He was actually repeatedly gagging earlier, maybe he still has a bit of nausea.

And to test facial sensation, stimulating also the nasal septum with the eyes covered is a good way to do so and the gag response was normal. This is the vestibu ocular reflex again challenging to assess in a video, but you may want to look at the ocular globe position and compare the two eyes, do we feel the left? Is normal or there is something different compared to the right?

And again, feel free to, to watch the video as many times as it is beneficial to you. Note the neurological abnormalities you observe and Interpret them and reach a conclusion. On the neuroatomic localization.

So to summarise the analogic examination findings, this dog was obviously a toxic. He had a type of ataxia that I'm not going to mention now, otherwise I will spoil the localization for you, but definitely he was leaning to the left, and if he was not supported with a chest harness by my colleague, he would have fallen to the left and he may have not even been able to walk and stand up. There were balance issues, the, and as a consequence, often he had a wide base stance, especially with the pelvic climbs, and the poor replacement response was delayed in the left pelvic climb.

At times, as when I pointed out during the video, he had a left-sided head tilt and he also had a degree of ventrilateral strain in the left eye. So, The word strabismus can help in narrowing down the neuratomic localization, location and of the Options I've listed in this slide. I'd, take a moment to think what you feel would be the correct one, and then you can move to the next slide.

So, in this dog, the neuroatomic diagnosis is a condition localised to the left central vestibular system. And In the development of the regent diagnosis list, we need to bear in mind the onset was nearly like a switch from normal to severely abnormal, very rapidly. So the top differential diagnosis was a cerebrovascular accident.

Vascular conditions typically have a very acute onset, takes minutes to hours, and they can be either ischemic or hemorrhagic. A neoplasia, either because the neural tissue decompensated or because there was a haemorrhage associated with the neoplasia. Could also be a possibility and it could be the primary or metastatic.

Unfortunately, this is an old dog, so, neoplasia and cerebrovascular accidents are both possible. Infectious inflammatory disease tend to have a more acute to subacute onset, but they were also possible. And a metabolic encephalopathy was also considered, although metabolic diseases tend to have again a more super acute onset.

So the design time graph summarises what can be considered general rules. There are exceptions, but general rules of how rapidly onset and how clinical progression is over time, . In terms of the severity of the clinical signs.

So vascular diseases have a very, very rapid onset, and then the animal either remains stable or, or, or generally improves. With trauma, there is a similar onset, but again, we knew this dog didn't suffer a trauma. So again, this may be a useful guideline for you when considering your neurologic differential diagnosis.

So what did we do? We did haematologist on biochemistry, which were unremarkable, and we did an MRI which I will show you in a moment, and CSF analysis was performed after a CSF was collected after the MRI and this revealed moderate retinosis. And the MRI here we see a sagittal, a transverse, and a dorsal T2 weighted images.

And this is the forebrain, and here we see the cerebellum. And we said earlier that part of the cerebellum is involved in the central vestibular system. So when comparing left.

With right We can see that this area is bright white, so it's called hyper intense, and the symmetric area is The normal intensity that you would expect in the nervous tissue as you can compare to the surrounding. On the nervous tissue. And this area is hyperintense here corresponds to this area in the sagittal image and this area in the dorsal image.

And this is the territory supplied by the left rostrocebellar artery, which is illustrated in this beautiful illustration from the Evans de la Anta. So in this dog, the MRI diagnosis was an infarct, an ischemic infarct of the left rostrocerebellar artery. Resulting in edoema and possibly ischemic.

Process of the left side of the vermis and the cerebellar hemisphere. Other diagnostic investigations were required to identify if there was any underlying aetiology resulting in the ischemic infarct. So we assessed the blood pressure and you can see the results here.

We tested the dimer and coagulation profile, and abnormalities were detected there. And when testing the blood pressure, obviously it's very important to do repeated testing. Have the animal as comfortable as possible and sometimes soon after the cerebrovascular accident, blood pressure may be altered.

So it's important to test it also when the animal is after discharged, being discharged from the hospital, in the following days or weeks. We tested thyroid function, urinalysis, even urine culture, and Thoracic radiography, no significant abnormalities were detected, and then on an abdominal ultrasound, splenic mass and small liver nodules were detected. Those were considered risky for FNA or through biopsy.

So no FNA was performed and it was agreed with the primary care vet that the primary care vet would have, eventually, removed the spleen, for histology of the the mouth. And it is possible that the mass was neoplastic and and neoplastic cell embolus resulted in the ischemic infarction. Generally speaking about cerebrovascular accidents, in, dogs and cats, they tend to occur a bit more in dogs than in cats.

They can be either ischemic due a compromised blood flow to a particular area of the brain, and when the area is relatively large, like in this case, we are talking of a territorial, cerebrovascular accident or territorial ischemic. In fact, and when the area is very small, they are called lacuna. Large dogs tend to have lacuna infarc of the thalamus and or, or other areas of the brain stem, and smaller dogs tend to have territorial infarcts and cavalier uincho spaniel greyhound seems to have a higher prevalence of cerebrovascular accidents than other dogs.

And the Ischemic in fact can be either thrombotic, embolic, or hemodynamic. Hemorrhagic infects can also occur, and they are the results of the rupture of the intracranial vessel, for different types of pathologies, including neoplastic disease and depending on their location within the brain, and intracranial cavity, they are classified as subdural, epidural, subarachnoid, intraventricular, and intraparinal. Onset is paraute, so that's a very useful clinical information.

The animals generally do not deteriorate neurologically after the initial 24 or 48 hours unless sadly obviously they die. And once they reach the highest degree of neurological dysfunction, which is again, Within 22, 48, maximum 72 hours, they either remain unchanged or they gradually improve. And fortunately, in most cases, they do gradually improve even when, when neurotic signs appear quite dramatic at the start, as in this case.

And the neuroatomic localization is often focal and unilateral because it corresponds to the territory supplied by the artery in question. And MRI tends to be more useful than CT with ischemic infarct. And it's very important to investigate for underlying causes, like cardiovascular diseases, hypothyroidism, and renal disease and other conditions that could predispose to ischemic infarction.

Unfortunately, in approximately 50% of the dogs, the underlying cause, has been reported in a large study to remain elusive. The treatment obviously is related to the underlying disease if we, if and when we are able to identify it, but supportive care is very important and prognosis, It can be surprisingly good. This dog made a very good recovery in terms of the neurological dysfunction.

We didn't have feedback on the follow-up regarding whether the splenic mass was malignant or not. So sometimes the prognosis is actually related to the underlying disease. And even dogs presented with quite dramatic neurological signs and quite dramatic MRI findings, can recover with adequate support.

And again, the underlying cause, if identified, if it's not treatable, then obviously the prognosis isn't great. But for dogs where the clinical signs are related exclusively or predominantly to the neurological dysfunction, they can recover within weeks of the onset of the neurological signs only with supportive care. I take this opportunity to thank all my colleagues, particularly those I spent many happy years working with at the Animal Health Trust for, contributing to, the care of these cases and obtaining the neurological examination and the videos.

And I hope you find this webinar, useful and it can help you take care of your patients, in the future. Thank you for your attention.