Visual Fixation Test

In keeping with our cranial nerve summer theme, I thought you might enjoy this interesting study about visual fixation testing in dogs.  

What is Visual Fixation testing?

Visual fixation testing (VFT) is performed in humans with vestibular disease to help differentiate between central and peripheral lesions. For this test, patients are asked to fix their gaze on a target and then a bright penlight is shone into one eye while the other is covered. Patients with peripheral disease can suppress spontaneous nystagmus during testing, while those with central disease cannot. Exceptions were described such as those with focal cerebellar lesions, however the majority of humans with central lesions fail this test.

Visual fixation testing in dogs?

We clearly cannot ask dogs to focus their gaze, so would this work in veterinary patients? A recent study from the UK asked this question. They omitted the request to fixate and simply covered one eye while shining a bright focal light into the other eye. The slow phase of nystagmus was expected to increase in velocity with peripheral vestibular disease, therefore increasing the number of beats counted in 10 seconds compared to prior to VFT. Dogs with central disease were expected to have no change in beat frequency.

Results

·         Almost ½ of the dogs had spontaneous nystagmus in both the peripheral and central group (48% and 44% respectively).

·         During the VFT, an increase in beat frequency occurred in 33% of the peripheral group

·         Only 1 case (6%) had an increase in beat frequency in the central group.

·         The change in frequency was significantly different between central and peripheral vestibular disease, with more dogs showing an increase in beat frequency in the peripheral group.

·         An increase in slow phase velocity was significantly associated with a peripheral diagnosis and this was significant even after the dogs with idiopathic disease were removed.

·         Dogs with peripheral vestibular lesion localization had a 95% of having peripheral diagnosis with a neurologic examination alone. When accounting for the VFT, this probability increased to 99% (1% of central disease).

·         Dogs with central lesion localization based on neurologic examination alone, had a 17% chance of peripheral disease. If they demonstrated an increase in beat frequency this increased their likelihood of peripheral disease to 52%.

Take away message

While only 1/3 of dogs with peripheral vestibular disease had an increase in beat frequency with the VFT in this study, this tool is one more easy option to attempt to localize vestibular disease more specifically. Central vestibular disease is frequently correctly localized based on the neurologic examination. On the contrary, 20% of dogs with central disease are diagnosed with peripheral vestibular disease. If a dog with suspected peripheral lesion localization has an increase in beat frequency during VFT, this can further support our lesion localization.

Reference: https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.70182

Thanks for reading! I hope you enjoyed this “bright” TidBit Tuesday during this sunny summer day! Have a great rest of your week.

The Facial Nerve

The Facial Nerve 

The facial nerve is a large motor nerve, originating from the medulla, that causes the muscles of the face to contract. These are often called the "muscles of facial expression". What happens when this important nerve malfunctions?

What does paralysis look like?
The facial nerve innervates the muscles of facial expression in dogs and cats as well as innervation to the lacrimal eye glands. Clinical signs are typically unilateral and, result in an inability to move the eyelids (inability to blink), inability to move the lips (dogs may accidentally chew on their lips and look "droopy" ), lack of ear movement (especially noticeable in cats), and a dry, red eye with possible ocular ulceration. They look bored because they cannot make a facial expression. 

What causes facial nerve paralysis?
Facial nerve paralysis can be caused by peripheral or central dysfunction. Diseases affecting the peripheral nerve might include hypothyroidism, neoplasia, otitis media, polyps, rarely neuritis and everybody's favorite - idiopathic. Idiopathic facial nerve paralysis is actually the most common cause of peripheral facial nerve paralysis in dogs. Central facial nerve paralysis occurs when something dysrupts the nerve function at the level of the brainstem. In additional to facial nerve paralysis, dogs will show ipsilateral paw replacement deficits, changes in mentation, and occasionally hemiparesis with central dysruption. The causes of brainstem facial nerve paralysis are often neoplasia, meningoencephalitis or vascular. 

The Diagnostic Challenge
After localizing the lesion, the next step is to make the diagnosis. Animals with central disease are best diagnosed with MRI +/- spinal tap. Animals with peripheral disease would benefit from a T4, neospora IFA, toxoplasma IgG/IgM (and other geographically specific infectious disease testing), and an MRI. Idiopathic facial nerve paralysis is diagnosed when all causes have been ruled out. 

Treatment for facial nerve paralysis is clearly based on the diagnosis. All animals with facial nerve paralysis benefit from eye lube at night (they cannot blink or close their eyelids) and eye drops during the day until the blinking returns. 

I hope this TidBit was useful.  This summer I'm going to spend some time looking at the cranial nerves in TidBit fashion so buckle your seatbelts! Have a great week and I look forward to working with you soon!

Sedating Dogs with Intracranial Disease

Frequently I am asked if a specific sedation protocol should be used for a pet with known, or suspected, intracranial disease. The biggest concern with anesthesia is a shift in the intracranial pressure (ICP), which is directly linked with the mean arterial blood pressure. Therefore, it is commonly recommended that medications are chosen which have minimal effect on blood pressure. Butorphanol is a commonly used premedication for dogs and often part of the recommended protocol for “safe” sedation. A study performed in the UK, and published in Veterinary Anesthesia and Analgesia, evaluated the effect of intravenous butorphanol on dogs with and without intracranial disease.

Study Design

Fifty-three dogs, presenting for brain MRI, were enrolled in the study. Each dog was sedated with 0.2 mg/kg IV butorphanol and the time to recumbency as well as the sedation score were recorded for each dog.  The sedation score was adapted from a prior publication (Grint et al 2009) and was scored 0-4 for six separate categories with a maximum score of 19.

Results

Nineteen of the 53 dogs had intracranial disease, the remaining 34 did not. Ten of the 19 dogs also had signs of intracranial hypertension. The overall median sedation score time 0 was 1 (range 0-10) , and 6 (range 0-15) at 15 minutes. Dogs with intracranial disease had a significantly higher sedation score at both 0 and 15 minutes. This was especially notable at 15 minutes when the dogs with intracranial disease had a median sedation score of 12, compared to dogs without intracranial disease who had a median sedation score of 4. A greater number of dogs with intracranial hypertension achieved recumbency than those without intracranial hypertension.

Clinical application

If you sedate a dog with butorphanol for a procedure (dental, radiographs, other) and the dog becomes recumbent at 15 minutes, it would be wise to continue the anesthetic protocol under the assumption that the dog may have intracranial disease. For example, use propofol instead of dexdomitor so that the intracranial blood pressure (and flow) is less likely to be affected. As the authors point out, it is helpful to remember to account for other sedation medications on board and note any recent seizures that could play a role in the level of sedation that an animal achieves. Nothing will replace an MRI diagnosis of the presence of intracranial disease, however keeping the “butorphanol test” in mind might help reduce the risk of undesirable consequences in patients with undiagnosed intracranial disease.

Thought provoking, right? I hope you found this TidBit useful and look forward to working with you soon!

Acute, Progressive Tetraparesis in a Large Breed Dog

It is time again for a lesion localization practice case. This one is brought to you by springtime: the giver of all dormant insects, infectious diseases and allergies. 

Signalment: 4 year old  MC German Shorthaired Pointer 
History: The dog was noted to have weakness in the left back leg yesterday morning when the owners let him out. By noontime he was weak in both pelvic limbs, and this morning he is struggling to stand on all four limbs. He continues to urinate, defecate and wag his little nub tail. The dog is used as a fall hunting dog (it’s springtime now) and is a house pet for the remainder of the year.
Physical examination: He is a well-muscled, well behaved (for a pointer) dog without evidence of abnormalities on his physical examination. TPR is normal.
Neurologic examination:
Mentation: BAR
Cranial nerves: normal
Gait: Nonambulatory tetraparesis. When he tries to stand, he cannot rise on his pelvic limbs at all, and trembles when supporting weight on his front limbs before collapsing.
Postural reactions: with support, he does have paw replacement deficits in both pelvic limbs and the left thoracic limb. The right thoracic limb is slow, but intact.
Reflexes: Absent patellar reflexes bilaterally, absent withdrawal reflexes both pelvic limbs, reduced withdrawal both thoracic limbs (worse on the left thoracic compared to the right thoracic limb). Absent c. trunci reflex both sides. Normal anal tone and reflex.
Palpation: non-painful spinal palpation with normal cervical ROM and no pain on tail jack.
Neuroanatomic lesion localization
Whew. This is a toughie! Let us start from the top.

1. Does this animal have evidence of neurologic disease?

2. Does the dog have a seizure history, show evidence of mentation changes or have any cranial nerve deficits?

3. Does the dog have weaknesses in 1, 2 or more legs?

4. Does the dog have reflex deficits?

5. Does the dog present or absent reflexes?

Draw out a stick figure of a dog and follow along as we go through the answers. Answers:

1. Yes

2. No. This means the lesion shouldn’t be intracranial. Cross off the head on your stick figure.

3. Yes. The dog is weak on all four limbs. The pelvic limbs are weakest, followed by the left thoracic limb and least affected is the right thoracic limb. This means that the lesion is expected to be in the muscles, peripheral nerves, C1-C5 spinal cord or C6-T2 spinal cord. Circle these areas on your stick figure or cross off T3-L3 and L4-S3.

4. Yes! The reflex arcs for the limbs at C6-T2 (thoracic limbs) and L4-S3 (pelvic limbs). Animals with a spinal cord lesion in these areas will have reduced reflexes in the limbs. It is very rare to have two spinal cord lesions, one in each plexus, therefore when an animal has deficits in both thoracic and pelvic limbs it is reasonable to assume the lesion is in the peripheral nervous system rather than the central nervous system (spinal cord) until proven otherwise.

5. This answer is a little bit subjective, but the question is trying to make us think about the peripheral nervous system. If an animal has a myopathy, we expect them to have normal reflexes. Animals with neuromuscular junctionopathy are expected to have absent reflexes and lastly those with peripheral neuropathies are expected to have reduced reflexes. There are exceptions (myasthenia gravis is a junctionopathy but often animals have intact reflexes!). The dog has absent reflexes in both pelvic limbs, but it also has reduced reflexes in the thoracic limbs. This likely reflects progression of the disease rather than two different diseases so I would consider this most likely to be junctionopathy or a severe neuropathy.

Neuroanatomic lesion localization: Peripheral nervous system (PNS), specifically junctionopathy or neuropathy.
Differential diagnoses: common causes of junctionopathy include tick paralysis, botulism, polyradiculoneuropathy (coonhound paralysis), organophosphate toxicity and fulminant myasthenia gravis.

What do you do now?
Myasthenia gravis: acetylcholine receptor antibody titer (https://vetneuromuscular.ucsd.edu/)
Botulism: evacuating the stomach, supportive care such as IV fluids, nutrition, physical therapy, and nursing care
Tick paralysis: apply an anti-tick medication such as Frontline (no, I do not get kickbacks for saying this).  Provide supportive care and monitor.
Organophosphate toxicity: evacuating the stomach and supportive care like with botulism.
Polyradiculoneuropathy (Coonhound paralysis): supportive care. Some universities will use immunoglobulin. Electrodiagnostic testing and CSF can suggest this is the diagnosis, but we do not have a singular diagnostic test available.

Thankfully, this lovely dog had tick paralysis and was back up and running 48 hours after applying the anti-tick treatment topically.
Tick paralysis is NOT caused by an infection (e.g. Lymes disease) carried by the ticks. This is caused by an autoimmune reaction against the tick “saliva” when it bites the animal. Minimizing tick bites is the best prevention. Removing the tick is the treatment. It does not appear that a dog will develop immunity after developing tick paralysis so keep applying the topical preventative all through tick season!
 
I hope you have enjoyed this week’s TidBit Tuesday. Please reach out with any topics you would like to see covered. Have a wonderful week!

Acute Seizure Monitoring Devices

Recording the number and duration of seizures is the best way for owners to help us manage seizures long-term. Should we start anticonvulsant medications? Should we increase medications? Should we stop medications or try something different? These questions are all dependent on the seizure frequency and duration. If the seizure frequency is acceptable but each seizure is 15 minutes long, adjustments are needed. If the pet is not showing adverse clinical effects, and the serum drug concentration is good, but the pet has 1 seizure per week, we need to make a change. If the pet continues to have cluster seizures, despite adequate drug concentrations, we need to make a change.
There are many data recording options available to owners.

1. Keep a paper log with date, duration and number of seizures (this doesn’t need to be a diary!)

2. Keep a spreadsheet record

3. Use a smartphone app. There are many available and some can even connect to the vet clinic. (RVC Pet Epilepsy Tracker; PetPace; Safetail; SeizAlarm)

What if the owner cannot be with their pet 100% of the time? (This is everyone.) How will we know if we missed a seizure? Here are some options that I provide for owners:

1. Consider a video camera and keep the pet in the room with the camera when you are gone. This works well to document seizures but can increase anxiety in an owner if they witness the seizure but aren’t there to intervene or comfort the pet.

2. Consider using a FitBark monitor. FitBark is like the human FitBit. It detects gyroscopic movements and is an activity monitor. It has also been evaluated as  a “scratch-o-meter” by dermatologists. I have played with it as a seizure monitor but do not have official data to support its use as a seizure alert tool. If a pet has partial seizures (head shaking, jaw chomping, other) it likely will not trigger the FitBark. Generalized seizures are likely to be identified as an increase in activity but the monitor cannot distinguish between running around the house after a housemate or having a generalized seizure.

3. Observe for signs of a seizure upon your return. This is our typical recommendation for owners. If a pet voids during a seizure, they may see urine or feces unexpected. If a pet has profound ptyalism, there may be evidence of drooling on the pet or surroundings. This is the least objective measure and probably has a high false negative result.

Recently a report was published out of Japan (https://doi.org/10.3389/fvets.2025.1558274) detailing a patented seizure-detection system (SDS) that they developed for dogs. This is not yet commercially available but, based on the results, it may be available in the near future. The device was previously tested in laboratory dogs.

Study Design and Outcome
One research Beagle and 12 client-owned dogs were enrolled in the study. The dogs were hospitalized with 24-hour staff who were available for intervention for seizure management. A video system was placed and the SDS was  placed into a custom designed jacket worn by the pet during the observation period. The device was connected to an application on a smartphone.  The SDS detected 25 of 34 seizures during the observation period, providing a sensitivity of 74.3%. The median sensitivity for detection was calculated to be 37.5% for each dog (range 0-91.7%). Three false positives were noted in only 1 dog, one of which was excluded because the jacket fell off. The authors calculated the positive predictive value to be 92.6%. Median latency from onset to detection was 11 seconds (range 6-75 seconds). During the observation period 35 focal seizures, which did not develop into generalized seizures, were observed and none of them triggered the SDS.

Discussion
This device performed more poorly than previously reported data for human SDS. Human SDS have a sensitivity between 79-91% and this device had a sensitivity of about 74%. That said, this is a very positive step toward canine SDS. The time from the onset of the seizure to detection by the SDS was a respectable 11 seconds. This latency is well within the acceptable window of observation expected in a hospitalization scenario or it would allow an owner to address the seizure if they are in the area but not directly observing the dog. This tool may soon be one more option for us to accurately record seizures for pets at home. As with all tools, knowing the limitations (partial seizures) and the expected outcome (low false positive results) will help us guide owners to the best monitoring for their pet.

 
Thanks for reading! Have a wonderful week and I look forward to working with you soon!

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!