MRI changes in dogs with Neosporosis vs Meningoencephalitis of Unknown Origin (MUO)

Well folks, we’re back to talking about Neospora caninum infections this week. BOY have I been seeing a lot of these! Are you holding them special for me or are we seeing a global increase in neosporosis in dogs?

This week, I reviewed an article that was published in the Frontiers Journal (doi.org/10.3389/fvets.2024.1517256) in January 2025. The purpose was to describe the MRI and biochemical findings in dogs diagnosed with Neospora caninum and compare them to those diagnosed with meningoencephalitis of unknown origin (MUO). Quick refresher:

MUO: non-infectious, inflammatory (suspected auto-immune) inflammation in the brain, spinal cord and nerves that can affect dogs or cats. Diagnosis is obtained via a combination of MRI, CSF and clinical history findings in conjunction with negative infectious disease testing.  Treatment is immunosuppression. Not curable.
Neospora caninum: a protozoal parasite that can affect brain, spinal cord, nerves or muscles. Diagnosis is obtained via positive serum titers and/or histopathologic observation of the encysted organism. Treatment is clindamycin or sulfa antibiotics, in most cases. Maybe curable?

Riddle me this: What do you do when you see a dog with multifocal neurological signs, and you’ve identified inflammation on MRI and spinal tap but don’t have the infectious testing back yet? Statistically, about 98% of dogs have MUO… infectious meningoencephalitis is only about 2% of the population. Infectious meningoencephalitis could be caused by fungal, bacterial, protozoal or viral infections. Infectious serology/PCR takes 7-10 days to come back in many cases. So, what do you treat? This article attempted to identify markers of neosporosis on MRI to improve early identification BEFORE serology is available. Here is what they found:

• CSF analysis: no statistical difference between dogs with MUO and those with Neosporosis in WBC or protein.

• CK: Dogs with Neosporosis had significantly higher CK compared to those with MUO. (median 1423 U/L vs 161 U/L).

• MRI: Dogs with neosporosis had inflammation more frequently in the masticatory muscles compared to dogs with MUO. The presence of muscle changes had a sensitivity of 27% and specificity of 96% to predict a diagnosis of neosporosis. The odds ratio was 8.25 but not statistically significant.

Take home message:

• If you have a dog with multifocal neurologic lesion localization, run a CK on your routine biochemistry testing. If it’s pretty darn high, run a Neospora caninum titer on serum (IFA)!

• If I see masticatory muscle inflammation on MRI, I’m going to suggest we treat with clindamycin while awaiting serology results…just..in..case.

• Keep up the good referrals! We’ll keep trying to figure out why Neospora caninum has become so prevalent in Wisconsin.

Thanks for reading! I hope you have a great week!

"Doc, The Dog is Having A Seizure!"

No one likes to hear those words (not even neurologists). Upon hearing those words you rush into the exam room and are faced with a convulsing dog on the floor. Here is your preemptive stop and think moment (yay!):

Why do we want to stop seizures, anyway?

Prolonged seizures can result in hypertension, tachycardia, acidosis and hyperthermia with secondary neuronal cell death and hypoxia. These changes negatively affect the brain and may have systemic effects as well. The goals of acute seizure management are to stop the seizure as quickly as possible thereby limiting secondary brain and extra cranial organ damage.

Give me the "Go-To"!

Look no further than your Benzodiazepine class of drugs. Benzodiazepine drugs (Diazepam, Midazolam, Lorazepam) were introduced in the 1960s for human status epilepticus. A human meta-analysis identified that benzodiazepines are the “best” first line IV drugs and identified the therapeutic concentration to be between 150-300 ug/ml. To date, there have not been any veterinary studies identifying which drug is ‘best’ for acute seizure management. We’ve always used benzodiazepines so, we continue to do so.

• Rectal, at home care: Home care with liquid rectal diazepam is often recommended for patients at risk for cluster seizures. Compounded suppositories are not currently recommended. Rectal midazolam and lorazepam are not recommended! We also know that chronic phenobarbital use reduced plasma concentrations of diazepam. With this knowledge we recommend dosing rectal diazepam at 1-2 mg/kg if the patient is receiving chronic phenobarbital therapy.

• Intranasal diazepam and midazolam: Intranasal diazepam, using an atomizer, resulted in detectable levels in about 2.5 minutes which makes this drug a viable alternative for at home anticonvulsant care. Midazolam was even more rapid and had a better outcome than rectal diazepam in one study of epileptic dogs so it is currently my drug of choice for at home (or non-IV) care. 

All the "cool kids" are using levetiracetam. Should I?

Well, maybe yes, maybe no. Levetiracetam's use has been documented in veterinary medicine since 2004. It is considered a relatively safe drug, with few reported side effects. This drug is typically used as an add-on or alternative to intravenous benzodiazepine therapy for acute seizure management at doses ranging from 30-60 mg/kg IV. Adding diazepam and levetiracetam together resulted in improved seizure control in epileptic cats so this is currently my recommended way to give IV levetiracetam. (Unless diazepam is contra-indicated such as with hepatic failure.)
Rectal levetiracetam may be on the horizon according to one study in 2014. However the first sampling time was 10 minutes therefore it is unclear if this drug will be useful in acute seizure management.  

Is Propofol Still Used?

Yes, but I don't have any new information. We all like shiny, new things, but propofol may still have a place in acute seizure management. There are a small number of published studies addressing this use in veterinary medicine. This drug is only recommended for intravenous use. Care must be exercised when using propofol due to its respiratory suppressor effects. Occasionally, intubation may be required if apnea is encountered during bolus therapy. Propofol withdrawal may result in distal limb twitching which may be difficult to distinguish from seizure activity. Extended exposure in cats to propofol may result in Heinz body anemia therefore a CBC analysis is recommended every 24 hours during constant rate infusion of propofol with cats.

Thanks for reading! I hope you have a great week and look forward to working with you soon!!

Quiz Time! Test your Lesion Localization Skills!

It's Monday morning, and your first case is presenting for "not walking well". Let's review some neuroanatomic lesion localization so you can be awesome on a Monday morning!

Signalment: 4 year old FS Labrador X
History: The dog was outside playing in the backyard last night when suddenly she yelped and fell over. The owners use this dog for sport as well as for a pet, so she is known to be a very stoic dog. Right away they worried about pain because she vocalized. It was apparent that she couldn't walk back into the house, so they put her on a blanket and carried her inside. She was able to stand up but couldn't use her right front or right rear leg normally. They gave her dinner (which she ate) and allowed her to rest until the visit today. (Why didn't they take her to ER? I don't know...I'm just the neurologist!)

Physical examination on presentation was unremarkable. (Yes, you examined her stifles, and they appear stable). 
Neurologic examination:
Mentation: BAR, very excited to see you (she's very excited to see EVERYONE)
Cranial nerves: all normal (high five for doing a full cranial nerve exam!)
Gait: She has an ambulatory right hemiparesis, with frequent falling to the right. She is able to walk 5-6 steps, unassisted, before falling or having her right limbs slide out. Note, the definition of ambulatory is the ability to walk a minimum of 5 unassisted steps IN ALL LIMBS. 
Reflexes: No withdrawal reflex in the right front leg, absent bicep and triceps reflexes right front leg. The reflexes are normal in all other limbs
Postural reactions: Absent paw replacement right front leg a right rear leg. Normal paw replacement in both left front and left pelvic limb. 
Palpation: No signs of pain on palpation or cervical ROM. 
Nociception: She has motor in all four limbs, so you do NOT need to test nociception (deep pain)

Neuroanatomic lesion localization: Right C6-T2 myelopathy (spinal cord)

Why? We know the dog is mentally normal and has normal cranial nerves. She does not have a seizure history therefore there is no evidence of intracranial disease. You can cross that body part off. Therefore, the lesion must be caudal to the foramen magnum. A forelimb AND pelvic limb are affected which means this lesion must be cranial to T3. If the lesion was caudal to T3, only a pelvic limb, or limbs, should be affected. That narrows our window of concern to C1-T2, correct? From there, you need to evaluate the reflexes. If they are normal, the lesion is likely C1-C5 but in rare situations it is C6-T2. Normal reflexes aren't super useful to narrow this window further. However, she has reduced to absent reflexes in the right front leg. Reduced to absent reflexes suggest a lesion in the reflex arc itself, which is located C6-T2 in most dogs. Why did I say this was a spinal cord, not a peripheral nerve injury? If you guessed it was because the pelvic limb on the same side was affected you'd be correct! The long tracts (paw replacement testing, upper motor control) going to or from the pelvic limb must travel through the C6-T2 part of the spinal cord. If the dog has sustained damage to the spinal cord, the tracts to the pelvic limb should be affected. If the nerves to the front leg are damaged peripherally (i.e. with brachial plexus injury) the pelvic limb should be normal. You did it!

Differential diagnoses: This dog has an acute onset, non-painful spinal cord disease. I would include an FCE, AHNPE (acute hydrated nucleus pulposus extrusion) and possibly at Type I disc herniation on the top of my list. As we learned last week, we cannot ever take meningomyelitis off the list so that goes on the list, but lower. Lastly, although trauma wasn't witnessed, this was an acute onset disease, so trauma goes on the bottom of my list until proven absent. 

We performed an MRI and diagnosed her with a suspected FCE. She entered rehab and supportive care and is doing well! With mobility and deep pain present, she is likely to make a good recovery but may not have completely normal mobility in the front right limb because the plexus was involved. 

Did you enjoy this case? Did you find it difficult? Please let me know if have any topics or a lesion localization case that you wish I'd cover on a TidBit Tuesday. Have a great week!

Vaccination and Seasonality in the Development of MUO

A study was published this Month in JVIM entitled “Vaccination and Seasonality as Risk Factors for Development of Meningoencephalitis of Unknown Origin in 172 Dogs”. I don’t know about you, but this is a super-hot topic in my world, so I immediately thought we needed to get this into a TidBit Tuesday!

Overview

MUO (meningoencephalitis of unknown origin) is a clinical diagnosis based on MRI findings, identification of a mononuclear pleocytosis and negative infectious disease testing. The authors proposed to investigate the association between vaccination WINDOW and the development of MUO. What is a vaccination window? A vaccination window is a categorization of the time from most recent vaccination to onset of clinical signs (that were later diagnosed as MUO) that was placed in 45 or 90 day intervals for analysis. For example, there was a window of 0-45 days and 46-90 days. Additionally, the authors evaluated the presentation season.

Results

172 dogs were included in the 2 year prospective study. The median age at onset of clinical signs was 5 years (range 0.18-15.3 years). Interestingly, Labrador and Labrador-X dogs were most common (13/172) followed by French Bulldogs and then Chihuahua/Chihuahua X. This should be a reminder that MUO can affect anyone, regardless of breed, age, sex, and size. It should always be on your differential diagnoses list for dogs with neurologic disease!
More dogs received vaccinations within 450 days of the onset of signs, so >450 days was considered “referential” for analysis. Looking specifically at dogs vaccinated within 450 days of the development of MUO, the highest risk for development of MUO was associated with vaccination in the first 45 days after vaccination (9x higher). This was not a case-control study, so we don’t know what the incidence of development in a breed or time. All that the authors are stating is that of the dogs with MUO that had received vaccination within 450 days of the development of signs, being vaccinated within 45 days resulted a 9x higher risk of developing of MUO.
The type and number of the most recent vaccinations administered was also evaluated. The number of vaccinations administered ranged from 1-7, median 4, in all dogs with MUO.  NO association with the type (Bordetella vs distemper, etc.) or number of vaccinations administered at one time was associated with the development of MUO.
Lastly, there was no associated with the season and the development of MUO.

Take home message:

• Dogs get MUO frequently so keep it on your differential diagnoses list

• Dogs who develop MUO have a 9x higher chance of developing it within 45 days of vaccination. (This doesn’t mean that dogs have a 9x higher chance of developing MUO overall!)

• MUO is not apparently linked to season

• We need to learn a lot more about MUO but likely there is a genetic risk that is triggered by something and that something might be vaccination.

 
If you found this article interesting and would like to read the entire thing it can be found at https://onlinelibrary.wiley.com/doi/10.1111/jvim.70013.  

Thanks for reading! I hope you have a great week and look forward to working with you very soon.

Neurologic signs of Hypertension in Cats (This is an oldie, but a goodie)

Hypertension is common in cats. It can be associated with a predisposing disease such as chronic kidney disease or hyperthyroidism, or idiopathic. Idiopathic hypertension is diagnosed when all predisposing causes have been eliminated (and hypertension is documented on 2 separate occasions)  and accounts for less than 1/2 of the cats diagnosed with hypertension (about 40%). 

Target organs for hypertension are the CNS, kidneys and cardiovascular system. Despite under recognition by clients, several studies have suggested that hypertensive encephalopathy might be present in 30-40% of cats. 

Neurologic manifestations of hypertension in cats

Seizures, mentation changes, vestibular signs (central), behavioral changes (disorientation), tremors, sudden collapse, cervical ventroflexion, paraparesis, cerebellar ataxia with hypermetria, cranial nerve deficits and cortical blindness (not retinal blindness). That's quite a list, isn't it?? It's amazing that these signs are the reason for presentation to a vet in only 10-20% of cats! 

A small study was recently published in the Journal of Feline Medicine and Surgery that aimed to identify the clinical occurrence of hypertensive encephalopathy in cats. In this study, 31 of 56 cats were diagnosed with neurologic signs associated with hypertension. Retinal lesion were identified in 28 of the 30 cats that under went fundoscopy. 

Cats with neurologic signs presented most often with proprioceptive ataxia, some with vestibular ataxia. Additional signs included hiding, disorientation, sleeping in unusual locations, increased and inappropriate vocalization, and increased appetite. Three of the 31 cats had seizures. Neuroanatomic lesion localization was predominantly prosencephalon, second most commonly vestibular signs and lastly spinal cord signs. Many cats had multifocal neurologic signs. 

Treatment and Outcome

Amlodipine was used in 22/31 cats. Telmisartan was used in 4/31 cats. The remaining cats received combination therapy. Follow-up was available for 25 of 31 cats. Fifteen cats had complete recovery after starting antihypertensive medications including one cat with severe seizures. Partial improvement was noted in 8/25 cats with residual ataxia or seizures manifesting most commonly. No initial response to treatment was noted in 2 cats with subsequent euthanasia within 1 week of treatment initiation. 

Key points:

• Feline hypertension is common (they enrolled 56 cats in less than 2 years!)

• Neurologic and behavioral signs occurred in more than 1/2 of the cats in this study but clients weren't aware of the significance!

• Treatment with antihypertensive medication can result in improvement

• Routine monitoring for hypertension is recommended in at risk cats, especially those with neurologic signs!

Reference: https://doi.org/10.1177/1098612X231153357

Thanks for reading! If you noticed that I failed to respond to your texts recently, I have good news! Texting is back up and running now! After some diligence I have convienced the FCC that Barnes Veterinary Specialty Services is NOT a spam threat. :) 

Myoclonus and Lafora’s Disease

Movement disorders are increasingly recognized in veterinary medicine. Perhaps we’ve had a shared patient where I have proclaimed this diagnosis, and you’ve thought… “It’s a what?” Let’s spend this TidBit Tuesday talking about movement disorders, and specifically, movement disorders related to a common storage disorder called Lafora’s Disease.

What is a movement disorder?

A movement disorder is classified by clinical appearance, anatomic origin or etiology in human medicine. In veterinary medicine we classify them as hyperkinetic (those associated with increased muscle movement) and hypokinetic (those with reduced or absent muscle activity). Even more confusingly, some of the hyperkinetic movement disorders can be associated with seizures. Myoclonus,  a type of hyperkinetic movement disorder, is one of the more common movement disorders that we see. An example of a myoclonus is a rapid lip twitch, eyelid twitch or even hiccups! Although probably annoying, they haven’t been shown to result in brain damage, or respond well to anticonvulsants, so generally treatment is benign neglect.

What is Lafora’s Disease?

Lafora’s disease is an autosomal recessive storage disorder that is unique compared to some of the other lysosomal storage disorders. Signs of Lafora’s Disease onset in adult hood, typically between 6-9 years of age. Dachshunds are commonly affected. Most other lysosomal diseases are juvenile onset. What it does is clog up the inner workings of the brain with these Lafora’s bodies resulting in blindness, behavioral changes (aggression) and, yes, myoclonus. Some dogs will also develop seizures, too. The myoclonus is typically visually stimulated. When something briskly approaches the dog’s face the eyes will shutter rapidly, and the dog may move its head and neck rapidly back and forth. Myoclonus can occur for reasons UNRELATED to Lafora’s disease but in combination with loss of vision, and possibly seizures or behavioral changes, I would suspect Lafora’s Disease in a patient with mature adult onset visually stimulated myoclonus. Sadly, we do not have any treatment to date for Lafora’s Disease. The disease is progressive, and unresponsive to anticonvulsants, however some dogs may temporarily improve with muscle relaxants.

Key Points:

·         Movement disorders are not seizures and can be hyperkinetic (increased movement) or hypokinetic (decreased movement).

·         Myoclonus is a type of hyperkinetic movement disorder

·         Lafora’s Disease causes myoclonus, blindness, behavioral changes and sometimes seizures

·         Animals with Lafora’s Disease often have visual myoclonus that can be triggered by a visual stimulus

·         No treatment is available for Lafora’s Disease

Thanks for reading! I’m still working on getting texting reinstated for my business. Please continue to email or call me with case questions. I sincerely apologize for the inconvenience.

Arachnoid Diverticulum - Spider-What-Now?

 
Arachnoid diverticuli (AD) are an increasingly common diagnosis on MRI, specifically for Pugs, but also for many small breed dogs. Arachnoid diverticuli are a focal dilation of the arachnoid space in the meninges. The result of this dilation is an abnormal CSF flow through the region and spinal cord compression. If you don’t remember the layers of the meninges, let’s take a quick moment to remember. The outer most layer is the dura mater, which is a very tough, fibrous protective layer. Above the dura mater is the epidural space (think epidural anesthesia here) and under the dura mater is the subdural space, which doesn’t have much purpose. Deep to the subdural space is the arachnoid layer. The arachnoid layer is connected through spider-y like connections to the underlying pia mater (the 3rd and last layer of the meninges). Between the arachnoid layer and the pia mater is the subarachnoid space. Cerebrospinal fluid courses through the subarachnoid space. Getting back to the pia mater, it is stuck right up against the spinal cord therefore there isn’t a space between it, and the underlying cord. Can you picture this now? I hope so!

So, what happens when the arachnoid layer becomes dilated? Clinical signs often include gait deficits such as proprioceptive ataxia, and paresis, and frequently fecal and/or urinary incontinence. The later signs are notable because these animals often drop or dribble but are still ambulatory animals. For an animal with a disc herniation, this type of incontinence wouldn’t be expected unless they were non-ambulatory approaching a plegic state. Fecal or urinary incontinence in a walking dog is usually a red flag for me to consider an arachnoid diverticulum in a patient! This disease is not typically painful, but occasionally we might detect spinal discomfort on palpation.

How is it diagnosed? MRI. That’s a pretty simple answer but there isn’t much else to add here.

What do we do about AD? There are medical and surgical treatment options. Medical treatment options are geared at decreasing CSF production, reducing inflammation, and managing pain. Prednisone, or other corticosteroids, are the cornerstone for treatment due to the suspected CSF-reducing properties and potent anti-inflammatory properties. Surgical treatment options haven't been very encouraging thus far, however a recent study outlining a retrospective, non-randomized treatment trial was published in Veterinary Surgery (2025: 1-11) comparing two surgical techniques. The first surgical intervention is the more common one and that is a durotomy followed by either durectomy or debridement of the dura. The other treatment option was a durotomy with shunt placement. Twelve dogs were enrolled in the durotomy alone group (which they called the control group, and we will too) and 14 were enrolled in the shunting group. Breeds were similar, as were neurologic grade between both groups. Here were some highlights from the paper:

• Immediate post operative (< 24 hour) outcome: not significantly different between groups

• Short term outcome (4-8 week recheck): no significant difference between groups

• Long-term outcome (> 6 months): the shunting group was statistically more likely to have improved than the control group. They reported 12/14 dogs improving (85.7%), compared to 5/12 (41.7%) in the control group.

• Recurrence rates were similar between the two groups (5/12 in the control group and 2/14 in the shunting group).

• No difference between the groups was noted in long-term presence of urinary or fecal incontinence.

 
Previous studies have reported significant difficulty with the shunt placement including a greater likelihood of a non-ambulatory state postoperative. This study did not report this difference, but their technique was slightly different. Did that cause the improvement? It’s hard to say because the number of dogs is so small in each group. The take away for me is that there may be hope on the horizon for a different, more successful, surgical intervention for AD than we’ve had thus far. It was notable that the dogs that experienced signs of recurrence were placed on prednisone and all improved. The ~40% improvement on the standard treatment (not shunt placement), and the possibility of recurrence has historically deterred me from recommending surgery at the start. If patients improve with medical management, I often do not recommend surgical intervention. Perhaps the new shunting techniques will change that recommendation. As with all new things, keep your ear to the ground and I’ll let you know what new data comes down the pipe about corrective surgery for AD.
 
Thanks for reading! I hope you have a nice week and enjoy some of the weather that March has to offer. Many of you know that March is a busy time for my family, so my hours are a little more restricted than usual. Please be patient with my email responses – I promise I will respond but there may be a slight delay as I play chauffer to two Irish Dancers during St. Patty’s Day season!

Highly Pathogenic Avian Influenza A (H5N1) Neurologic Manifestation in Cats

 
I have been following the news about H5N1 infections in cats with interest (and other emotions!) due to the repeated mentioning of “neurologic” signs. I had to do some digging to find any specifics, but I finally found some details and wanted to pass them along. On February 20, 2025, the CDC’s Morbidity and Mortality Weekly Report (MMWR) included information from two household cats in Michigan that were confirmed positive for HPAI-H5N1 on necropsy in May of 2024. Clinical signs for both cats were described. Although these reports are from 1 year ago, I think the information is still relevant today. A link to the CDC report can be found here (https://www.cdc.gov/mmwr/volumes/74/wr/pdfs/mm7405a2-H.pdf) or I’m happy to provide a copy of what I have if you send me an email. The second report was from 2023 out of Nebraska (Journal of Comparative Pathology 205 (2023) 17e23). There were 3 cats in the Nebraska report diagnosed with H5N1
 

Neurologic Signs
The signs reported come from the two cats in Michigan and 3 cats in Nebraska, so given the small sample size additional neurologic signs may be present and not reported in these cases. Initial signs appear to involve loss of appetite, grooming and change in behavior. In the Nebraska cats, case 1 is described as having anisocoria, injected sclera, nystagmus, loss of proprioception, tremors, hyperesthesia and pyrexia. Signs progressed to seizures which resulted in euthanasia. A second cat from the same house developed compulsive circling and inappropriate mentation 24 hours after the first cat’s signs. This cat was stable with supportive care but acutely progressed on day 10 to lateral recumbence and tremors which resulted in subsequent euthanasia. A third Nebraska cat (unrelated household) developed difficulty ambulating, lethargy and anorexia and was presented to a veterinarian. The Michigan cats were reported to have nasal discharge, decreased mentation, ataxia, swollen right jaw and anorexia. One other household cat in Michigan developed signs of URI but did not test positive for H5N1 and did not die. Most cats have been reported to die within 7 days (reports are 1-7 days) of experimental infection so survival to 10 days is unusual for the one naturally occurring infection. The household cat that developed an URI did not test positive and therefore must be assumed to have an unrelated illness due to their lack of fatality, however this is an assumption.

Clinical Pathology
No significant abnormalities were noted on CBC or serum biochemistry.

Necropsy
Not surprisingly, lesions were present in lungs and brain but also some other visceral organs were affected as well. The brain had wedged shaped laminar necrosis and vasculitis. Mild to moderate spongiosis and other signs of inflammation were present in all cases. The third Nebraska cat had more profound inflammation than the other two, but it was similar in characteristic. Areas of malacia were present in the cats.
 
Recommended Diagnostic Testing
Based on the data collected, if you have a cat with signs of respiratory and neurologic disease collecting nasal swabs for PCR testing might be useful antemortem test. If the cat is euthanized the authors of the Nebraska paper suggest random brain samples for viral testing. I would add that PPE should be strongly considered given the rapidly adapting capabilities of this virus.  According to their website The WVDL can test for Influenza A virus (https://www.wvdl.wisc.edu/testsandfees/) but I’m not a virologist so I’m not sure if this is inclusive of the H5N1 variant. If you have a patient who needs testing, I recommend calling the WVDL to ask (608-262-5432).
 
Treatment
To date, supportive care has been unsuccessful for managing H5N1 variant infection in cats and no specific treatment is available.
 
I hope this very quick summary has been useful for your practice. As I said above, I am not a virologist so please reach out to WVDL where the very smart people can give you better information about the virus itself. These reported cases help me see that this is an intracranial disease for cats, and a terribly inflammatory one with lots of thrombi and vasculitis so I am better able to identify cats with possible infection. On that sad note, I hope you are enjoying the pleasant shift of the weather, and I look forward to working with you soon!

Use of CBD Oil for Refractory Epileptic Dogs

Did you know that WI vets could not SPEAK about or recommend CBD oil containing products to clients until recently? We are permitted to speak about CBD oil containing products but cannot recommend or prescribe products. However, clients need our direction! Several years ago the folks from Colorado State University present data from a double blinded, placebo controlled prospective study evaluating CBD oil in resistant epileptic dogs. To date, this has been the most thorough study I've encountered about CBD oil use in epileptic dogs. If you're aware of better data that I haven't mentioned please let me know! 

How the Study Worked

51 client owned dogs, taking at least 1 ACD (anticonvulsant drug) and continuing to have 2 or more seizures every month, were included. Resistant epileptics are already the hardest subset to manage so this was a really tough crowd for the researchers to target. The dogs were given either placebo or CBD oil for 3 months and then switched and given the other compound for 3 months. Initially, they dosed at 2.5 mg/kg PO q12h but no effect was noted so after 12 dogs the dose was increased to 4.5 mg/kg PO q12h. 

Key Points

• ALP and ALT were elevated in this study. This is the first study to document elevated ALT during CBD administration in dogs. The researchers aren't sure why this happened but hepatocellular damage of some sort was suspected. Bile acids were normal in all dogs except 2.

• No significant difference in response (response = a > 50% reduction in seizures) was noted between the placebo and CBD administrations group even with dose escallation.

• Total number of seizures/month and seizure days/month was reduced in the CBD group compared to the placebo group BUT over all seizures went UP with both groups

Should we use CBD to manage seizures for resistant epilepsy?

Sorry, not based on this study. It's not compelling enough to suggest that we should be using this drug PLUS it showed evidence of liver enzyme changes that could be concerning AND phenobarbital serum concentration went by 11% when the dogs were on CBD. That said, they targeted resistant epileptic dogs so could this be effective in "easier" to control dogs? Maybe. Could this increased phenobarbital concentration mean that we could lower the dose of phenobarbital in these pets? Maybe. Do we need to check out different doses? Maybe - but at least with this question I am cautious because of the new elevation of ALT at this higher dose. Can we safely increase the CBD dose? Unknown. 

This is a good step forward but alas, we still don't have enough compelling evidence to say CBD should be a part of seizure therapy and at what dose.

Keep up the good work managing epileptic dogs! I'm available if you have questions about a case or need a second opinion. Have a great week!

Levetiracetam and Dogs with Chronic Renal Disease

Levetiracetam and Chronic Renal Disease in Dogs

I dislike starting sentences with “Little is known…” but alas, that is how I wish to start this TidBit Tuesday. Little is known about the effect of levetiracetam on the kidneys of dogs with chronic kidney disease (CKD). Human epileptics with concurrent CKD have a longer levetiracetam half-life than patients without CKD. Therefore, the dose is often adjusted (lowered) to account for poor renal function. Thanks to a colleague, I was reminded of a paper from 2021 on this very subject in vet med. Gim SY et al (2021: Veterinary Sciences doi.org.10.3390/vetsci8110263) published data about 20 dogs with CKD and compared them to 17 dogs without CKD. I thought you might find a quick review of the data valuable:

CKD group

• Mean age 12.5 +/- 3.78 yrs

• Mean weight 5 +/- 2.78 kg

• Many breeds

• CKD IRIS stage 1: 60%

• CKD IRIS stage 2: 40%

• Initial dose 21.9 +/- 8.36 mg/kg q8-12h

Non-CKD group

• Mean age 10.26 +/- 3.73 years

• Mean weight 5.44 +/- 5.56 kg

• Initial dose 20.58 +/- 8.72 mg/kg q8-12h

Results

The authors note that the typical starting dose for levetiracetam is 20 mg/kg PO q8h (30 mg/kg PO q12h if using extended release) in dogs. Therefore, the dogs with CKD had a mean starting dose HIGHER than the standard dose, which is odd. One would expect a reduced dose for animals with CKD. Sadly, the authors did not obtain serum levetiracetam concentrations to document a difference in drug accumulation in the two populations. Not surprisingly, dogs with CKD were reported to have more adverse effects (85% vs 53%) than dogs without CKD. Adverse effects most commonly reported were ataxia, sedation and anorexia. Although a known adverse effect, anorexia may have been worsened by the underlying CKD. Throughout the study period, a clinically relevant, statistically significant increase in serum BUN, serum creatinine or both was noted in the CKD group. The authors postulate that sedation may have contributed to reduced water consumption, worsening the renal disease, however this was not objectively measured or observed.

Take away message

Based on our knowledge of renal elimination of levetiracetam, the authors suggest starting with a dose lower than 20 mg/kg PO q8h in dogs with CKD. Based on clinical experience I recommend starting at a 20% reduction (16 mg/kg PO q8h)  and monitoring BUN/creatinine every 2-3 weeks for several rounds. If seizures are poorly controlled and BUN and creatinine do not increase, an increase in levetiracetam could be considered.
I hope you have found this helpful! It isn’t a very robust study, but it brings to light the discussion of monitoring dogs with CKD who are taking levetiracetam, a worthy topic.

On a different note, I’m having issues with my phone carrier and therefore texting isn’t available for at least the next 3-4 weeks. I can see texts that you send me, but I cannot respond. For the time being, please email me with all nonurgent questions and use the old fashioned telephone to call with any urgent questions. I’ll do my best to respond to the phone calls as timely as possible! Thanks for your patience as I work through this stupid new regulation.

How to Localize a Cranial Nerve

Time for another terrible joke. Why did the neuron get in trouble at school?? (Answer at the bottom)

Let's review the cranial nerves and how we use them this week. First, there are 12 paired cranial nerves. Cranial nerve1 localizes to the olfactory bulb and cranial nerve 2 localizes to the thalamus, but the remaining 10 localize to the brainstem.  You might even argue that CN 2 localizes to the thalamus, which is an embryological part of the brainstem but...well, then we should have a coffee and get to know each other better!  Let's stick to the idea that CN 3-12  have cell bodies in specific brainstem segments, thus making it possible (dare I say easy??)  for us to localize a lesion to either a specific brainstem segment OR the peripheral nerve. 

What are the names of the brainstem segments, again? (Mesencephalon/midbrain, metencephalon/pons, myelencephalon/medulla oblongata). Okay, whew! Now that that is over, how do you decide if a deficit is coming from the nerve nucleus in the brainstem OR the peripheral nerve?

Take the following steps:

1. Identify the cranial nerve affected (i.e. facial nerve = CN 7).

2. Identify the segment of brainstem associated with the nucleus of this cranial nerve. Don't remember what cranial nerves are associated with which brainstem segment? Let's review...Midbrain = CN 3,4; Pons = CN 5, Medulla = CN 6-12

3. Are any ipsilateral long tract deficits (postural reaction deficits, hemiparesis) or mentation changes (obtunded, stupor, coma) present?

   1. If yes, the lesion is in the brainstem segment associated with the cranial nerve (i.e. medulla).

   2. If no, the lesion is affecting the peripheral portion of the affected nerve

Let's give this a try. The following findings are from a 6 year old FS Lab X
Mentation: normal
Cranial nerves: inability to perform blink reflex on LEFT, menace response or lip twitch with hemostat pinch on LEFT. Right side and all other remaining CN are normal. 
Gait: normal
Postural reactions: normal paw replacement in all limbs
Reflexes: normal in all limbs

What is the neuroanatomic lesion localization? Let's go through the steps.
1. Identify the cranial nerve. The dog cannot MOVE it's lips and eyelid on the LEFT. Movement is caused by CN 7, so this is a CN 7 deficit.
2. What brainstem segment does this CN associate with? CN 7 comes from the medulla oblongata.
3. Any long-tract signs? No paw replacement deficits, no mention of hemiparesis and no mentation changes. 

The neuroanatomic lesion localization for this pet should be peripheral CN 7 on the left. 

Guess what? You can apply these steps to any deficit affecting CN III-XII. Yay!
 
Do you need help performing the neurologic exam? I'd love to help! Looking for the answer to the joke? The answer is: it just couldn't control it's impulses! Thanks for reading and Happy February 2025!

Medication Compliance and…the Cat

Administration of medications, topically or orally, is often a required part of cat ownership. As veterinarians, we ask clients to perform this job at home, and are often concerned that it isn’t performed as prescribed. As a neurologist, I become especially twitchy about the maintenance of anticonvulsant dosing because the consequence of skipped medications can have dire results. A variation in the serum drug concentration can be MORE harmful than the absolute value of the serum drug concentration. Missed doses, or variable dosing times, can mean that breakthrough seizures are more frequent. Sadly, poorly controlled seizures is one of the leading causes of euthanasia for seizure patients. Topically applied transdermal medications are often the “go-to” solution for medicating cats however a recent study identified reduced compliance with topical as well as oral administration in a limited number of cats. This study came from New Zealand, and included 66 cat owners that responded by survey. In this survey, 39% of cat owners reported noncompliance. Compliance was defined as the extent to which a client follows the prescribes recommendations. This can be dose or timing related. In this group, 1 owner was noncompliant with topical medication and the remainder were non-compliant with oral administration.  Clients were asked about several factors, including veterinary visit experiences. Over 90% of owners strongly or somewhat agreed that the veterinarian spent enough time explaining how to administer the medication, and the reason for prescribing the medication. Furthermore, more than 45% of cat owners were shown by the veterinarian (why aren’t folks delegating this to techs??!), 14% were shown by a veterinary student and 40% were not shown. Interestingly, in univariate analysis, only medication class was associated with noncompliance. When further evaluated, antimicrobials were the most common medications associated with noncompliance.  In multivariate analysis, owners of single cats, and medication class were statistically associated with noncompliance.

The authors suggest that demonstrating how to administer the medication, using a liquid or tablet or trying both, and considering client characteristics such as prior pet experience should be a part of the discussion or consideration when prescribing medications for cats. Remember, topical and oral medication can be problematic, so this advice applies to both situations. When relating this to seizure medications, a trial of tablet, liquid, and transdermal applications could be considered when recommending an anticonvulsant for cats.
 
Thanks for reading! I hope you have a wonderful rest of your week and look forward to working with you soon!

FDA Review of Librela 2025

The Food and Drug Administration (FDA) recently published a review of reported adverse events for Librela and I thought it was worth bringing it up in a TidBit Tuesday. Many of you prescribed Librela, and have seen wonderful results, for patients with orthopedic disease. To be clear, there are no indications to use this medication to treat neurologic disease. The preliminary studies did not identify significant neurologic risk in the population studied however this has been questioned as more data comes out. Many of you have asked me about adverse neurologic reactions to Librela and it has been a discussion of amongst neurologists as well. Well, the FDA has weighed in. This report was performed on data received prior to March 31, 2024. The review was published September 10, 2024 and I’ve attached the link here if you’d like to review it for yourself. (evaluation of adverse events)We will focus on the neurologic adverse events reported in this review but other adverse events were included in the summary.

As of 4.18.24 , 3674 cases reported Librela related adverse reactions. Ataxia was noted in 160 cases, and 27 (17%) of these were considered probably associated with Librela. Three cases had a positive rechallenge after a subsequent dose. Ataxia was reported to occur within the first week for 110 cases (70%).
Seizures were reported in 42 dogs, with 7 (17%) having a probable association with Librela. Almost 70% of the seizures occurred within the first week, and after the first dose.

Paresis was reported in 64 cases, 17 (27%) of whom were probably associated with Librela. Three had a positive rechallenge on subsequent dosing. Paresis is challenging to decide if it is orthopedic or neurologic given the indications for Librela administration. Paralysis was reported in 24 cases, 3 (12.5%) of whom were considered probably associated with Librela administration. Signs occurred in the first week for 68% of cases and after the first dose in 16 cases, but it is unclear if the 3 cases most likely to be associated with Librela were in that group.

Proprioceptive deficits were noted in 60 dogs, and 10 (17%) were considered probably associated. Approximately 65% of the cases had signs starting within the first week and after the first dose in 42% of cases.

Lastly, muscle tremors were noted in 28 cases, and 9 (32%) of these cases. Urinary incontinence has been frequently discussed amongst neurologists and this was not followed in the report.

What does this mean? It means that neurologic side effects are being reported and are considered likely to be associated with Librela. Does it mean that you shouldn’t give the medication in a dog with pre-existing neurologic signs? Not necessarily, however I personally think it is worth mentioning the risks to all owners considering starting the medication. What if a patient develops adverse effects? Report! You can report them directly to Zoetis (the manufacturer) 1-888‑963-8471 or to the FDA www.fda.gov/reportanimalae. A pre-treatment neurologic examination is strongly recommended and if adverse effects develop, a (repeated) neurologic examination is even more strongly urged. Pre-treatment examinations for orthopedic procedcures, limb amputations and now for Librela is a frequent part of my job. Please reach out if you would like to schedule a neurologic consult related to Librela administration.

Thanks for reading! I hope you have a really great week, wherever life takes you!

Degenerative Myelopathy

Degenerative myelopathy is a slowly progressive, fatal spinal cord degenerative disease that has been linked to the SOD1 gene in German Shepherds, Corgis, Boxers, Rhodesian Ridgeback and Chesapeake Bay retrievers. The disease is currently diagnosed via histopathology which can only be performed post mortem. Degenerative myelopathy (DM) presents initially with proprioceptive ataxia of the pelvic limbs, progresses to paraparesis and then a loss of the patellar reflexes may occur followed by tetraparesis and eventually loss of respiratory and cranial nerve function. Most owners euthanize prior to the development of tetraparesis but not all. What else can present with the initial signs of a slowly progressive proprioceptive ataxia and paraparesis? Right! Intervertebral disc disease, myelitis, or spinal neoplasia. Each of these diseases has their own subtle differences but the typical history is similar among all of them. As a result, neurologist struggle to confirm a diagnosis of degenerative myelopathy.

Diagnosing Degenerative Myelopathy

The SOD1 gene mutation can be identified on a genetic test, readily available from several sources. If found to be a homozygous carrier, is that enough to diagnose DM? Approximately 78% of neurologists and 50% rehabilitation specialists thought so according to a recent study published in the Journal of Veterinary Internal Medicine (Bouche T, Coates JR, Moore SA, et al JVIM 2023). What if the dog was unlucky enough to have developed an intervertebral disc extrusion AND was a SOD1 homozygous carrier. Can they have both diseases? Can they have a disc herniation and not (yet) be clinical for DM? According to the article, 43% of neurologist always or sometimes required an MRI plus the SOD1 genetic testing to make the a presumptive diagnosis of DM. I require both to make a diagnosis. Dogs can be at risk for something but have something else and we are not doing them a good service if we assume a diagnosis without eliminating the most common other options.

Treatment
This will be a short paragraph. None. We cannot successfully treat DM as of 2025. However, a very small study (Kathmann I, Cizinauskas S, et al. JVIM 2006) found that the time to non-ambulatory status was delayed with intensive PT 3-5x daily along with weekly hydrotherapy, massage and passive ROM compared to a cohort with moderate or no treatment. For this reason, most neurologists and physical therapists recommend consistent physical therapy. This recommendation was also frequent in the 2023 study as well. The mean survival is 10-36 months, so any little bit helps! If you have a patient with a minimal progression after 36 months, reevaluate your diagnosis.

Take away message

• Diagnosing DM requires histopathology

• A presumptive diagnosis is obtained through a combination of SOD1 gene testing and MRI

• Treatment is physical therapy centered but will not eliminate/cure the disease

Happy New Year everyone! I hope you had a safe, enjoyable holiday season. January’s schedule is a little different due to my children’s schedules so, as always, please reach out if you cannot find a suitable time for a consult. The regular schedule resumes in February. One of the perks of being the owner is that I can control the schedule!

Omeprazole and CSF Production

Cerebrospinal fluid (CSF) is a protein-poor fluid that is an ultrafiltrate of blood produced in the choroid plexus in the brain. This all-important fluid provides a way to remove waste, cushioning, and a nutrient source in some situations. As with most things, you can have too much of a good thing. In diseases like hydrocephalus, syringomyelia or hydromyelia there is excess CSF in parts of the nervous system which can result in clinical abnormalities. These abnormalities may include seizures, behavior changes, pain, phantom scratching, difficulty with ambulation and blindness. Studies have determined that omeprazole, a proton pump inhibitor, can decrease CSF production when administered IV or intrathecal (in the ventricle). As a result, many neurologists, me included, prescribe omeprazole for dogs with hydrocephalus or Syringohydromyelia. Our goal is to improve clinical signs through a reduction in CSF production.

In 2016, a group from Belgium (The Veterinary Journal 209 (2016) 119–124)) evaluated oral administration of omeprazole in a group of clinically normal research beagles to determine if CSF production was reduced. A few notable points here – 1) these were clinically normal beagles and therefore were expected to have normal CNS anatomy and 2) this was an indirect measure of CSF production via the albumin quotient calculation. The albumin quotient, which is a common way to indirectly measure CSF production, is calculated by dividing CSF albumin by the serum albumin. As CSF production goes down, the quotient should go up. No statistical difference in the albumin quotient was noted after 14 days of omeprazole administration, however a slight overall increase in the quotient was noted. Why did this happen when it was previously shown to reduce CSF production via IV or intrathecal administration? We have a few options here…

• Oral absorption does not have as great of an effect compared to IV or intrathecal. A 0.2 mg/kg IV dose given to rabbits showed a whopping 25% reduction in CSF production. We typically recommend 1mg/kg PO. Perhaps we should be giving more? The PO study did not measure omeprazole concentrations in the CSF, so it is unknown how much transferred after oral dosing.

• Chronic administration may result in a lesser response over time (the other studies were single dose studies) OR we needed more exposure to affect a response. Subjectively, clients do not report an immediate improvement on omeprazole therefore perhaps exposure longer than 14 days was needed.

• Normal beagles are, well, normal. Animals with hydrocephalus or Syringohydromyelia may have different CSF production mechanisms (upregulated? Down regulated?) which could result in a more profound shift when exposed to omeprazole.

 
What is the take-away message? Based on this study, omeprazole has fallen out of favor with many neurologists. However, I continue to recommend this medication because the IV/intrathecal study was fairly convincing, and I think I have seen remarkable clinical response in some patients. Notice the modifiers to that sentence! “I think” and “some patients.” Here’s the thing though…adverse effects are rare with omeprazole, so I also don’t think there is a big downside to trying it. I continue to have clients report a favorable response to phantom scratching events (times/day and/or severity) as well as cognitive function. Seizures and gait deficits tend to respond less, in my experience. I do, however, tell clients about the results of the PO study so that they are (hopefully) realistic in their expectations. Nonetheless, it continues to be part of my armament when treating excess-fluid-diseases in the CNS. Why subject an animal to steroids if omeprazole will work?
I hope you are enjoying your start to January and look forward to working with you soon!

What is the BEST tool in neurology?

Okay, perhaps you'd want to stop and have a cry if you were stranded on an island with 100 neurologic examinations to do. Hear me out...
Imagine this scenario instead: 2-year-old MC Labrador, with a history of 2 seizures in the last month. The owner is coming to see you and wants to know what is going on!? What do you do first?
Hopefully your answer is a...

THOROUGH NEUROLOGIC EXAMINATION!

What if you don't have the time, staff or patient patience to do a complete exam? If you focus on a few specific parts of the neurologic examination, you can get a good picture of what that pesky forebrain is up to. (The part of the brain that causes seizures.)

Okay, grab your pen (or what ever writing implement you use these days), here are the 4 things to focus on when you perform a neurologic examination on a patient with a history of seizures:

• Assess mentation: Signs of obtundation or stupor can indicate a lesion in the forebrain (but also the brainstem, so don't be narrow minded if the pet is mentally inappropriate. Do a full exam!)

• Menace response, paired with pupillary light reflex (PLR): A unilateral absent menace, with a normal PLR and blink reflex, indicates a CONTRA lateral forebrain lesion. 

• Gait assessment: Specifically, do you see circling? Unusual compulsion? If so, animals generally circle TOWARDS their lesion. E.g., circling left, I’d worry about a left forebrain lesion.

• Postural reactions:  Deficits will be CONTRA lateral to a lesion causing seizures. E.g. an animal with a left pelvic limb paw replacement deficit may have a deficit on the right forebrain. Note: the new name for CP is paw replacement deficit. Also, remember that those tracts for paw replacement can be abnormal with anticonvulsants, or from other neurologic diseases. When in doubt... do a full exam!

Beware! The neurologic examination may be abnormal after IV administration of anti-convulsant drugs, during the post ictal phase, or if the pet has received long-term anti-convulsant drugs.

Did you know that 90-95% of dogs with idiopathic epilepsy will have a normal inter-ictal neurologic examination??

Furthermore, dogs with an abnormal exam are 16x more likely to have structural brain disease than their normal counterparts! Seriously. The neurologic examination is one of the biggest tools used to predict a diagnosis in an epileptic dog (and I might add, cat). 

Statistics never predict an individual’s condition but by focusing the neurologic examination on these areas you can gain important insight into the health of your patient’s forebrain. Please note: if you find an abnormality, the entire neurologic exam should be performed to make sure that you're not missing multifocal disease. Ultimately guiding owners, helping dogs, and improving everyone’s quality of life is what we’re after, right?

Not feeling confident on the neurologic examination? I'd love to help. The vast majority of my business is identifying IF neurologic disease is present in a given pet so that we can build a reasonable differential diagnoses list.  

Some of you very astutely noted that my schedule went a bit wonky this week. For some reason, the calendar program decided that I didn't need to work until the end of January. (Perhaps AI is more advanced than we know??) As much as I'd love to hibernate, please note that the schedule is now fixed and appointments are now available on the schedule for the end of December and January. Thank you to the vets that reached out!! The only way I knew that something was amiss was because of you so please, please don't hesitate to reach out if you cannot find a suitable time for a consult. It might be because I'm super busy, but, lit might be for other, fixable, reasons, too! 

Have a great week and please fill up the schedule! :)

Epilepsy in Labradoodles

How many of us are old enough that a Labradoodle wasn’t labeled as such when we first started practice? The labradoodle was officially “started” in 1989 as a breed intended to have low shedding potential. They have gained in popularity over the years and are now extremely popular as a breed worldwide. They are not a recognized breed by the AKC as of 2024, but that hasn’t stopped many breeders from providing pedigrees. Although typically considered a mix of just a labrador and a poodle, they can also be mixed with Irish Water Spaniels, Curly Coated Retrievers and even Cocker Spaniels. One of the proclaimed benefits of a mixed breed dog is the perceived lower risk of health problems. Several studies have refuted this and certainly we see a similar incidence of seizures in Labradoodle dogs compared to Labrador dogs. Idiopathic epilepsy has a known genetic inheritance in the Labrador, and it is suspected in the Poodle. A recent study evaluated Labradoodle dogs with idiopathic epilepsy, presumptive epilepsy and those with epilepsy of unknown origin. They included 40 dogs in the study. Males were over represented in this study (supported in other studies) and most of the dogs were neutered before their first seizure.

Generalized seizures were noted in 25 of 40 dogs, 12 of 40 had focal and generalized seizures and three displayed only focal seizures. The average age of onset was 2.3 years +/- 1.3 years which is similar to the Labrador. Note that the study limited age as an inclusion factor so this could be slightly skewed. The average number of seizures per year in this cohort was 5.4 seizures +/- 6.5 seizures, also similar to the Labrador. Poodles tend to have fewer, less frequent seizures and rare status or clusters. There were similar numbers of seizures in the treated, and non-treated groups, but remember that we treat frequent seizures, and don’t tend to treat infrequent seizures!  Seizures were scored for severity on a 1-10 scale (1: not severe, 10 – very severe) and, although a subjective measure, was considered 6.9 on average +/- 2.0. About 33% of the dogs had cluster seizures (more than 1 seizure/24 hours) and the other remaining dogs had occasional clusters or no clusters.

This study utilized a questionnaire to determine the personality of the dog, and home setting. Eleven dogs were described as nervous/anxious dogs and the remainder were described as vivid, cheerful and stable. Although more seizures/year were noted in the anxious group, this was not statistically significant. No correlation was noted between tick/flea/food and vaccinations in this group of dogs. However, all owners thought that they identified precipitating factors that were all considered ‘stressors.’  Some examples provided included visits to the groomer, vet visits, home visitors and sounds. Both the ictal and post ictal phase were considered stressful for some of the owners, however more owners referred to the ictal phase as the most stressful part of the event. Owners scored their own and their pet’s QoL as fair to good for most of the study. However financial cost was considered a moderate problem (an average of 5.1 on a 10 point scale) for owners.

What should we take away from this article? An awareness of the prevalence of idiopathic epilepsy in Labradoodles should be an important take away from this article. Secondly, it is helpful to note that generalized seizures are common, however focal seizures are also reported in Labradoodles. If you have a desire to read the remainder of the article it can be found here: https://doi.org/10.3389/fvets.2024.1459260

Thanks for reading! I hope you have a good week and stay warm!

Vestibular Disease in Cats

As we reflected on our familys, and leaned back in our chairs last week around the Thanksgiving table (sorry, Canadians, I know yours was last month) I thought - wait - vestibular disease in cats! (That, and why did I eat so much pie?) First, I have been asked "Do cats get vestibular disease?" The answer is: yes. They have the same anatomic structures and roughly the same neural pathways that influence the vestibular pathways as dogs do. Let's look at a case:

Signalment: 4 year old FS DSH
Neurologic Examination:
Mentation: normal
Cranial nerves: right head tilt, horizontal nystagmus FF left, positional strabismus OD, remainder of the cranial nerves are normal. 
Reflexes: normal
Postural reactions: normal tactile placing all four limbs
Gait: ambulatory with mild vestibular ataxia and staggering right when turning.
Palpation: Non-painful spinal palpation and cervical ROM

Peripheral Vestibular Disease

The basic players in the peripheral system are 1) The receptors, 2) cranial nerve VIII or vestibulocochlear nerve. Cats with peripheral nerve disease may have a head tilt, nystagmus, positional strabismus, vestibular ataxia and falling/rolling. The head tilt is towards the side of the lesion. The nystagmus are a bit trickier. In the old days we used to track the direction of the nystagmus as a localizer. Remember when we said horizontal nystagmus indicated peripheral disease, vertical nystagmus indicated central disease and rotary was either? Welllll..... that isn't strictly true anymore. While it is true that horizontal nystagmus are typically associated with peripheral disease, they can be seen with central disease, too. The same is true for vertical nystagmus. Nystagmus that develops only when the head is placed in a specific position (positional nystagmus) are more common with central disease, but unfortunately are no longer strictly associated with that neuroanatomic lesion localization. So how do we localize peripheral disease?? We localize based on the lack of specific findings on the neurologic examination. What they won't have is ipsilateral paw replacement deficits, ipsilateral hemiparesis and/or reduced mentation (obtunded, stupor, coma). These last three findings are identified with brainstem vestibular disease ONLY. 

Brainstem Vestibular Disease

The players in brainstem localization are the paired vestibular nuclei in the rostral medulla oblongata. The tracts for proprioceptive function, descending upper motor neuron and level of alertness (mentation) are also nearby. Therefore, if a disease in the brainstem is affecting vestibular function, it is also very likely to tick off one of those nearby pathways, therefore creating deficits. They don't need to have all 3 deficits, just one will do. So, a cat with a head tilt, nystagmus AND an ipsilateral tactile placing deficit is more likely to have a brainstem localization than peripheral disease. 

Cerebellar localization
The last group of neurons influencing or being influenced by the vestibular system are the cerebellar nerves. In the cerebellum there are "marionette" nerves that exert their influence on the brainstem vestibular system. By "pulling strings" the cerebellar influences the output from the vestibular nuclei.  Without this influence signs such as hypermetria, intention tremors and truncal swaying are noted. To localize to the cerebellum, signs of vestibular disease (head tilt, nystagmus, positional strabismus) are present PLUS hypermetria, truncal sway and intention tremors. When localizing to a specific side, follow the hypermetria. If an animal has hypermetria on the right front limb, the localization is right cerebellum. Occasionally delayed paw replacement is present, but this will be due to difficulty repositioning the limb rather than a solid paw replacement loss. 

Have you figured out the neuroanatomic lesion localization for the case? That's right - peripheral vestibular disease! Differentials for cats are very similar to dogs with the exception that we see more polyps in cats, and more PSOM in dogs. Therefore, I would consider otitis media/interna, polyps, neuritis (infectious or inflammatory), hypothyroidism (yes, in a cat!), diabetes, and peripheral neoplasia. These differential diagnoses are then tailored to the specific case based on the history. 

That wasn't too painful, was it? Let me know if you have a topic you think should be covered in a TidBit Tuesday!