Bile Acid Testing For Dogs with Seizures

Case scenario: You are presented with a 2 year old Labrador retriever with a history of 3 seizures in the past 1 month. The seizures are consistent with generalized seizures and last less than 1 minute. Further questioning of the client reveals the dog to have normal activity, appetite, and mobility at home between seizures. You perform a neurologic examination (yay!) and no abnormalities are found. 

What is the likelihood of idiopathic epilepsy in this dog?

According to the International Veterinary Epilepsy Task Force, a diagnosis of idiopathic epilepsy can be made, at a Tier I level of confidence, if a dog is between the ages of 6 months and 6 years, has had 2 or more seizures, has a normal interictal neurologic examination AND has normal CBC, serum biochemistry and dynamic bile acid testing (that means pre and post feeding testing). We know Labs are commonly diagnosed with idiopathic epilepsy and that a genetic inheritance is known or suspected for most of the breed. So, do we really need to do a bile acid test? 

First, a little background. Minimum data base (MDB) pseudohepatic function tests include glucose, BUN, albumin, ALP and ALT. A pre-prandial bile acid test alone, called a resting bile acid test, is different than a dynamic bile acid test which includes both pre and postprandial samples. 

Do we Reallllly Need to Perform Dynamic Bile Acid Testing?

An article from England recently addressed this question in a publication in the Veterinary Record

Questions asked:
1. If  a dog has a normal MDB, how likely are we to finding an elevated postprandial bile acid test? Answer: 24 dogs out of 202 dogs

2. How likely is a dog with a normal MDB and a normal pre-prandial bile acid test to have an elevated postprandial bile acid test? Answer: about 9 out of 100 dogs

3. What is the prevalence of a clinically significant hepatopathy in a dog with a normal MDB and normal pre-prandial serum bile acid test (if we don't do a post-prandial bile acid test)? Answer: 1.29%

The authors compared this to the risk of missing a significant brain lesion in a dog less than 6 years of age with a normal neurologic exam in which an MRI is not performed. (About 2.2% of cases would have had a brain lesion missed.) The question always begs, how much of a risk taker are you, or your client?

Based on the information from this study, here is what I propose we do:

• ALWAYS check CBC, serum biochemistry for every dog with a history of 2 or more seizures.

• ALWAYS recommend a pre AND post bile acid test for every dog presenting with a history of 2 or more seizures, even if CBC and serum biochemistry are normal. When making this recommendation I suggest that we make clients aware of the less than 2% chance that their dog could have a significant hepatopathy that will be undiagnosed if we do not perform these tests. This hepatopathy may be the reason for their seizures or, and perhaps more importantly, it could affect how they metabolize many of the anticonvulsants that we use. I'm looking at you phenobarbital, zonisamide and diazepam! Poor hepatic function could result in poor metabolism of these anticonvulsant drugs even if the hepatopathy isn't severe enough to be the seizure etiology. 

• ALWAYS perform a neurologic examination to document any abnormalities before starting any medications for seizures. (Okay, so this wasn't part of the study but I still think this is a must!)

Thanks for reading! This was a very informative article so check it out for more detail!  (DOI: 10.1002/vetr.2585).

Have a seizure patient and need backup? Seizure management is my passion so I'd love to help! Email me or hop on my website to schedule a consult. 

Next week starts one of the craziest months of my calendar and it's not due to work. Two of my kids are Irish dancers which means St. Patty's Day is a very busy time of year for us. Please be patient as I try to answer emails and phone calls over the next few weeks. Thank you! 

Geriatric Vestibular Disease of Dogs and Cats

Geriatric vestibular disease (GVD) is characterized by an acute onset, unilateral failure of the peripheral vestibular system. The cause remains unknown but causes such as inflammation (viral or immune mediated) or atrophy have been hypothesized. A study back in 2021 (DOI: 10.1111/vru.12893) by Sungjun Won and Junghee Yoon out of South Korea identified a significant size difference in the utricle, one of the parts of the bony labyrinth in the ear, in dogs with GVD compared older dogs without GVD. Necropsy evaluation has shown a reduction in the size of the peripheral CN 8 and the affected ganglion, further supporting atrophy as a cause. And yet, it is difficult to explain the recovery that most dogs and cats experience 1-6 weeks after onset of signs if this is atrophy. Perhaps this is occult hypothyroidism? Calcific deposits in the endolymph? They typically recover, which means that necropsy diagnosis are uncommon and therefore we don't know the true etiology of this disease. 

Common Clinical Signs

Animals with GVD are middle age to older dogs and cats that demonstrate peracute onset of signs, often proceeded by vomiting with no clinical worsening after 24 hours. These dogs and cats usually have very severe vestibular signs such as head tilt, nystagmus, ataxia (if ambulatory), positional strabismus and rolling/nonambulatory vestibular ataxia. IF you are able to have the animal stand, mentation, limb tone and paw replacement should be normal. Many of these dogs and cats are so severely affected in the first 24 hours that we delay assessment for 24-48 hours. Do not provide antibiotics or steroids during the first 1-2 days!  This is a self-resolving disease therefore providing those treatments can muddy the diagnosis AND it isn't necessary! 

Differential Diagnoses for Peripheral Vestibular Disease
Remember, this is a peripheral vestibular lesion localization so consider diseases that affect the peripheral system as differential diagnoses. This may include: 

• Hypothyroidism

• Otitis media/interna

• Neoplasia (peripheral CN 8 cancers such as lymphoma or nerve sheath tumor)

• Neuritis (rare)

• Topical antibiotics

Geriatric vestibular disease is diagnosed by exclusion . Although the report referenced above does provide measurements for the utricle on MRI, it is not yet a diagnostic marker for GVD. Exclude all other causes using chest x-rays, blood work including T4, brain MRI and spinal tap. 

Treatment?

This is a self-resolving disease. The head tilt is commonly permanent, but all other signs of vestibular disease should resolve over several weeks. Signs begin to improve 24-48 hours after the onset but may take up to 1 week to start improving. Signs should fully resolve by 6 weeks. If signs wax and wane, or progressively worsen, GVD is not the proper diagnosis. Supportive care such anti-emetics. diazepam or meclizine for anti-vertigo effects, and nutritional support such as hand feeding (only when sternal!) , may be used. IV fluids may be needed for severe or prolonged nausea. 

Prognosis

Don't euthanize these pets in the first 24 hours! They look miserable...but they can recover with time and supportive care. This can be very difficult for clients to witness and, because the pets are elderly, may result in a triggered response to consider euthanasia. If you can, please hang in there for a few days even if that means hospitalization. Remember - recurrence is possible but many repeats warrants a full diagnostic investigation. 

Thanks for reading! I'd love to hear if you have any suggested topics for TidBit Tuesdays. If you have a question, chances are that other readers are interested in the topic too! I tend to pick things that I think are timely or interesting (or both!) but then again, I find everything interesting in neurology so help me narrow this down! :)

Have a great week!

Discospondylitis Meta-Analysis in Dogs

A recently published (January 2026) meta-analysis of discospondylitis (DS) in dogs was a good review of what we do, or should do, when faced with these cases.

This was a meta-analysis, which means that the authors undertook the difficult job of evaluating the available literature about DS and deciding if it was bias, and what the collective “take away” message could be.

• All 48 included studies were retrospective case series or cohort studies, all with moderate–high to high risk of bias. There were no standardized outcomes, further complicating the knowledge gained.

• Surgical and medical management were comparatively effective, remembering that surgical correction is reserved for very selective cases. (69 and 75% respectively).

•  Practical implication: This paper does not justify earlier or more aggressive surgery in otherwise stable cases.

How should you manage a case with suspected discospondylitis based on this meta-analysis?

Imaging

• Radiographs are the first line diagnostic tool, but evidence is often delayed (2–8 weeks after clinical onset).

• CT and MRI are equivalent for detecting DS lesions, with MRI offering better soft-tissue and epidural assessment.

Culture

• Disc sampling (CT- or fluoro-guided) has the highest diagnostic yield.

• Blood and urine cultures are important but less sensitive.

• Empirical antibiotics before sampling were common and contribute to bias—but also reflect real-world constraints.

Take away: If the patient is stable enough, delay antibiotics until cultures are obtained

Antibiotics

• Culture-guided antibiotics are strongly recommended (although about 1/3 of bacterial DS is culture negative at the time of diagnosis)

• Most commonly reported empiric choices: Amoxicillin–clavulanate and Cephalexin because they readily cross into bone and are broad spectrum.

• Mean duration of treatment: ~105 days (~3.5 months). Remember, this is a study evaluating studies so some of these patients stopped treatment and relapsed, some stopped treatment due to euthanasia and some stopped treatment with stringent criteria. I stop treatment after radiographic evidence of disease resolution which typically means 6+ months of antibiotics. I (knock on wood) haven’t had any relapsed cases in 20+ years but perhaps I’m OVER treating?

Antifungals

• Ketoconazole, itraconazole, and fluconazole were effective in reported cases.

• Fungal DS remains uncommon but should be suspected in German Shepherds, systemic illness, or poor antibiotic response.

Monitoring response

Across studies, follow-up quality was inconsistent, but practical trends emerge:

• Neurological exam + pain assessment were the most reliable indicators of response.

• Imaging was variably used; MRI/CT follow-up was uncommon.

• Radiographic “healing” lagged behind clinical improvement.

Surgical Treatment

Surgical intervention is complicated. Anytime we go to surgery on an infected site we risk spreading the infection, so it is often reserved for dogs with vertebral instability, pathological fracture or subluxation or progressive neurological deficits AND we think instability is the cause. This study also listed failure of adequate medical management as a reason to pursue surgery, but I struggle with this reason. What constitutes failure? That doesn’t automatically mean a surgical treatment is needed, does it? This study reiterated that surgical correction is adjunctive to medical management but does not replace antibiotics or antifungal treatment.

What is the big-picture takeaway (clinical bottom line)

This systematic review reinforces what most of us already do in practice:

• Medical management with prolonged, targeted antimicrobials remains first-line for the majority of canine DS cases.

• Surgery is clearly indicated in specific scenarios (instability, neurological deterioration, failure of medical therapy).

• Evidence quality for these studies was uniformly low, so decisions should be driven by clinical status, imaging findings, and response to therapy, not perceived “success rates” alone

• Counseling owners on the long term need for treatment is important up front.

Thanks for reading! I enjoy reading studies that remind me that sometimes the basics are really the best route for our patients. We all love shiny new surgical treatments or fancy sounds medications (me included), but we shouldn’t lose sight of the tried and true treatments either. Thanks for reading! I hope you have a good week and stay healthy out there!

Reference: Vallios VI, Sourla E, Low D, et al. VetRecord 2026. DOI: 10.1002/vetr.70334

Comparing Dog to Human Temporal Lobe Epilepsy

Temporal lobe epilepsy (TLE) is a specific form of epilepsy that has specific pathology. As you might imagine, the pathology is found in the temporal lobe and consists of given cellular degeneration, loss of neurons and sprouting of mossy fibers (what a great term for a fiber). Clinically, TLE often shows facial automatisms (focal seizures) and is commonly drug resistant. As a result, patients with TLE may under go radiation or surgical intervention to manage their epilepsy. A group from the University of Wisconsin Neurology service recently investigated a cohort of 7 dogs with clinical seizures suggestive of TLE to determine if the same pathology was represented in dogs.

Materials and Methods

Seven dogs with focal facial seizures who were euthanized due to progressive disease were included.

Key neuropathologic findings

·         No significant hilar neuron loss was identified in any dog. Cell counts fell within a relatively narrow range, and no hippocampus showed neuron numbers >2 SD below the group mean.

·         No hippocampal asymmetry was detected in neuronal counts between left and right hippocampi.

·         Mossy fiber sprouting was mild in all dogs (median score ~1.1/5), with no cases showing extensive sprouting typical of TLE.

·         No asymmetry in mossy fiber sprouting was found between hippocampi.

·         Overall, none of the dogs met human neuropathologic criteria for TLE, despite having focal seizure semiology.

What does this mean?

These findings indicate that focal seizures in dogs with idiopathic epilepsy are not necessarily associated with TLE-like hippocampal pathology, contrasting with humans. The mild hippocampal changes observed may reflect seizure-related or age-related alterations rather than a distinct epileptogenic lesion. Importantly, previously reported MRI hippocampal asymmetry in some epileptic dogs may be a consequence of focal seizure activity, not evidence of true TLE. This data does not support pursuit of radiation therapy or surgery in dogs with resistant epilepsy, however there may be specific individual differences that warrant considering these treatments on a case-by-case basis.

I thought this article was worth discussing even though the results were negative. Maybe because the results were negative? We always think we could or should be doing more for some pets who are suffering from refractory seizures – and we should keep trying – but this study did not support similarities between human TLE and canine focal seizures. Therefore, without similar pathology, we cannot pursue similar treatments.

Hope you have survived the January vortex and are beginning to get out and enjoy all that winter has to offer in Wisconsin (or wherever you live!). If you enjoy reading the TidBits, please tell associates, new graduates and your veterinary friends. Thanks for reading. I look forward to seeing you soon. 

Reference: https://avmajournals.avma.org/view/journals/ajvr/aop/ajvr.25.07.0260/ajvr.25.07.0260.xml

How to Diagnose Canine Cognitive Dysfunction Syndrome

At the end of December 2025, the Canine Cognitive Dysfunction Syndrome Working Group published guidelines for diagnosis and monitoring canine cognitive dysfunction syndrome (CCDS). Many of the veterinarians on this working group are also on the Dog Aging Project, providing a nice cross over of ideas.
The guidelines were intended to clarify CCDS and provide ways to make a diagnosis of this illusive disease and attempt to develop a standard grading program.
 
Definition: “Canine cognitive decline syndrome is a chronic progressive age-associated neurodegenerative syndrome characterized by changes in cognitive functions that are severe enough to affect daily life.”
People describe the changes using the following acronym DISHAA
D: disorientation
I: impaired social interactions
S: Sleep disturbances
H: House soiling, learning and memory deficits
A: Activity changes (increased or decreased)
A: Anxiety and fear (increased)
The this is a syndrome, not a singular disease. This allows room to inclusion of other forms of neurodegenerative diseases not yet identified but that present with progressive cognitive decline signs. Currently, canine dementia is the only disease that falls under the umbrella term CCDS, but this could change in the future.
A three tiered grading system is recommended by the working group:

• Mild: subtle signs, preserved function

• Moderate: functional impairment requiring management changes

• Severe: debilitating deficits requiring comprehensive support

There is a nice flow chart (Figure 2) in the article which I recommend printing and keeping at your fingertips. The key points are:

• Screening is recommended every 6-12 months starting at age 7 for most dogs (maybe earlier for giant breed dogs).

• If progressive changes in DISHAA dementia are noted on the screening, proceed to the typical senior diagnostic testing (PE, NE, CBC, serum biochemistry, UA, BP).

• If everything is normal, including the neurologic examination, reassess in 2-8 weeks.

• If signs continue to progress, a level 1 antemortem diagnosis of CCDS can be made.

Note that it takes at least 2 evaluations (surveys) to make this diagnosis. I will be instituting a survey, extrapolated from the supplements included in this article, for use in patients with signs of cognitive dysfunction. It will come as a link, just like the seizure questionnaire. If you would like to create something similar for your clinic please look at the supplements section of this article.
Level 2 antemortem diagnosis of CCDS is made when an MRI and CSF tap are added to the diagnostic plan. Currently, these diagnostic procedures are mostly used to exclude other diseases and therefore by elimination, diagnose dementia. We know that brain atrophy occurs with age but distinguishing age related brain atrophy on MRI from neurodegenerative CCDS brain atrophy hasn’t been fully elucidated.
What are the key points?

• Canine cognitive dysfunction syndrome (CCDS) is being diagnosed more frequently, and we need to support our senior patients, and their caregivers, through the process.

• Diagnosing CCDS requires at least 2 separate completed surveys (preferably by the same caregiver) with evidence of progressive signs. The surveys, combined with normal routine screening, support a tier 1 level diagnosis.

• Other diseases can look like CCDS and are therefore important to exclude in older patients. These may include metabolic, orthopedic, neurologic, or behavioral diseases.

 Reference: https://doi.org/10.2460/javma.25.10.0668

Thanks for reading! Progressive dementia is a COMMON reason for consultation so don’t feel like you need to go at this alone. Reach out if you have any questions! Have a great week, stay warm, and I look forward to working with you soon.

How do I use the Menace Response?

Picture this...You are presented with a 4 year old Pug with a history of "bumping into things" recently. You do a complete physical exam, including a fundic exam and neurologic exam (self high five!) and find the following changes:
Mentation: Quiet, alert and responsive
Cranial nerves: Absent menace OS, intact PLR, intact ocular movements, normal remaining cranial nerves
Gait: normal
Postural reactions: absent left pelvic limb, all others normal
Reflex: normal all limbs and cutaneous trunci
Palpation: non painful.

 
First question: Does this patient have neurologic disease? 

Golly, if it didn't this would be a silly TidBit Tuesday, wouldn't it?  It seems odd to ask this question but I feel it is a good habit get into, to ensure you're not trying to make a non-neurologic problem into a neurologic one. Interestingly, a recent report identified 8% of pets referred to a University Neurology service had "pretenders" disease (ex: cruciate rupture that was mistaken for a neurologic condition). 

Second question: What is the neuroanatomic lesion localization?

Start with basic anatomy. In a very simplistic sense, menace uses CN 2 (sensory) and CN 7 (motor) with a pass through the prosencephalon to connect the two CN. This is a complex pathway that we don't fully understand but the true bare basics are CN2, pass through the prosencephalon and CN 7.  Damage to 2, prosencephalon or 7 will result in a menace deficit. Now, expand the anatomy to include the pathways. The left eye uses left CN 2, crosses and uses right prosencephalon and then back to the left CN 7. 
We still don't know if it is CN 2, prosencephalon or CN 7 that is affected, right? Isolate CN 2 from CN 7 by doing PLR. 
PLR = CN 2, midbrain, CN 3. 
Deduction would say that if PLR is normal then CN 2 must be normal too, right?
Now we need to sort out if the menace deficit is due to disease of the prosencephalon or left CN 7. So, isolate CN 7 from CN 2 by looking at the blink reflex.
Blink reflex = CN 5, and 7.
If you tap the medial and lateral canthus and they blink, CN 5 and 7 must be intact! In the case above, we said all cranial nerve tests, other than the menace response, were normal. Therefore, CN 7 must also be normal. 

 
Voila! Neuroanatomic lesion localization is RIGHT prosencephalon!

What about that postural deficit in the left pelvic limb, you ask? 

That pathway goes from the pelvic toes --> up sciatic nerve -->up left spinal cord --> up left brainstem to cross in the midbrain --> ends in right prosencephalon.

This dog has a right prosencephalic lesion (aka right forebrain) giving both a left menace deficit and left pelvic limb deficit. Well done! You now know WHERE the problem is coming from and can build your differential diagnoses list for a focal prosencephalic lesion and/or refer them to a neurologist (instead of an ophthalmologist) for further testing.

Want more? I can do personalized CE at your hospital. We can go through neuroanatomic lesion localization, discuss seizure cases, or any other topic you and your colleagues might find helpful for your practice. Email me for additional details.

Have a great week and stay warm!

Cluster Buster Protocols

What is a cluster seizure?

Cluster seizures are defined as 2 or more discrete seizures within a 24 hour period. Cluster seizures are different than status epilepticus (any one seizure lasting for an extended period of time, or 2 seizures in which poor recovery occurred between seizures). Cluster seizures pose a special concern for seizure patients because of they have been linked with poorer outcomes compared to dogs without a history of cluster seizures. 

The goal with cluster seizure management is to minimize the number and duration of seizures. A secondary goal is to reduce the need for hospital visit or stay thus reducing the financial burden to the client. 

When should I provide a cluster seizure plan to a client?

• If a patient has a history of 2 or more episodes of cluster seizures

• If the patient has a history of status epilepticus 

What drug choices, routes of administration and doses can I offer?

Levetiracetam

1. Rectal administration – 40 mg/kg per rectum (PR) at the time of seizure, repeated once if needed within 24 hours. Results suggest an improvement in seizure management in the medium term using rectal levetiracetam AND standard anticonvulsant therapy according to one study

2. Oral administration – start 20-30 mg/kg PO q8hr (NOT Extended release) levetiracetam after a pet experiences the first seizure and has recovered well enough to eat. Continue q8hr dosing for 2 days beyond the pet’s last seizure. The levetiracetam is then stopped, and the pet's long-term anticonvulsant therapy is continued. Clinical experience suggests this approach will reduce clinic visits, number of seizures during the cluster event. However, clinical side effects such as sedation or ataxia may be present during the dosing period. Note: This approach should NOT be used if levetiracetam is part of a patient’s standard oral therapy for long-term seizure control. Suddenly discontinuing an anticonvulsant medication can lead to breakthrough seizures or status epilepticus.

Benzodiazepine
Diazepam has been the main acute anticonvulsant treatment for veterinary patients.

1. Rectal -  Be sure to target the rectum, not colon, to avoid hepatic metabolism. Start 1-2 mg/kg PR. Compounded suppository formulations of diazepam have not demonstrated reliable serum diazepam concentrations in dogs and therefore are not currently recommended.

2. Intranasal – preferred by some due to the ease of administration, and avoidance of the first pass effect of metabolism. Start with 0.5 mg/kg intranasal. 

Midazolam

1. Intranasal – this is my preferred route and drug for at home benzodiazepine administration. Additionally, it was reported to be favorable compared to intravenous midazolam in 44 dogs.Start with 0.2 mg/kg intranasal. 

2. Intramuscular – this route is favored by some but is not my recommended route of administration for clients at home in emergency situations. In a clinical situation, intramuscular administration can be effective when intravenous access is limited. Starting dose of 0.2 mg/kg is recommended.

3. Rectal – do not use midazolam rectally due to erratic and unpredictable plasma concentrations at standard doses.

 
Phenobarbital
Patients receiving daily phenobarbital administration can benefit from an increase, or pulse, of phenobarbital therapy during a cluster event.

1. Oral increase – in clinical practice we regularly recommend increasing a dog from q12h dosing to q8h dosing and continue this plan for 2 days beyond the last seizure. An example of this would be if a dog had a seizure Saturday morning. Upon recovery from the seizure an additional oral dose of phenobarbital (at the same oral dose administered) is recommended followed by q8hr dosing Sunday and Monday. Tuesday the dog would return to the standard twice daily dosing interval. This approach provides a slight increase of serum phenobarbital concentrations which may protect against further cluster seizures. Clinical adverse effects such as increased sedation, ataxia, polyuria, polydipsia, and polyphagia may become evident during the increased dosing period.

Summary
Providing options at home for cluster seizure care can reduce the need for hospitalization, and clinic visits. Additionally, any of the above treatments can be provided in hospital during seizure observation should that be needed. All the treatment choices discussed above are targeted for dogs and are rarely used in cats.

I hope your Tuesday isn't a cluster of craziness! As you well know, I enjoy helping you, help your patients with seizures live their best lives so please reach out if you're working through a case and need a little extra help. Have a great week!

Rabies in Dogs

Rabies Virus Infection in Dogs

I'm hopeful that most of you heard of the dog diagnosed with a Rabies virus infection in Chicago, Illinois in December 2025. If not, here is the story: (https://www.cookcountyil.gov/news/cook-county-department-animal-and-rabies-control-confirms-rabies-positive-dog). This is a sobering reminder that Rabies virus is still out there and that being vaccinated does NOT eliminate the possibility of a rabies virus infection. This feels like a good time to review our knowledge and resources for Rabies virus infections, don't you think? 

Etiology
Rabies is a neurotropic rhabdovirus that causes fatal infection in dogs, cats and (usually) humans. Infection is caused by inoculation from saliva by means of a bite.  The virus then spreads into the CNS via peripheral nerves.  Once the brain is infected, the virus spreads back out through peripheral nerves to the salivary glands – at this point, the animal can transmit rabies.

Signalment
Any dog, cat, horse, cow, HUMAN
Clinical Signs
Two syndromes are described:

• Furious syndrome (forebrain signs) - seizures, mentation changes, aggression/sedation, visual changes. 

• Paralytic syndrome (lower motor neuron signs ascending from the site of the bite). Paralysis in one or more legs can be an indication of ascending infection. This means a paraplegic dog could be considered for rabies observation if they are NOT vaccinated. Be aware! 

Once neurologic signs are present, progression is rapid, and most animals will be dead within several days but it has been reported to last up to 3 weeks in a few pets. Remember, the ONSET to clinical signs after exposure can be much longer. 

Rabies should be considered as a differential diagnosis in any animal with acute onset, rapidly progressive neurologic disease especially if there is a poor vaccination history or exposure to wild animals.
 
Diagnostic Tests
  Key point: A definitive diagnosis can only be achieved postmortem, and requires fluorescent antibody staining of brain tissue to demonstrate rabies antigen. A serum RFFIT (Rapid fluorescent foci inhibition test) can be performed to evaluate for evidence of previous vaccination however it should NOT be used to make a diagnosis of active rabies infection. One of the cases I evaluated had a negative RFFIT test and was confirmed to have the rabies virus on necropsy. Due to the neurotropic nature of rabies it can remain undetected by the immune system and therefore cause a negative (false negative) RFFIT result.

What do you do if you've been exposed? Contact your local heath department immediately. 
What do you do if you have a patient that you suspect has a rabies virus infection? Contact your field vet (Wisconsin: https://datcp.wi.gov/Documents/AHVetsMap.pdf)

Further reading
If you're interested in reading about a case of Rabies virus infection please check out this article. https://doi.org/10.5326/0390547. I saw this case a number of years ago, but the disease hasn't changed much in 20 years!

Thanks for reading! A rabies virus infection is something worry about for those of you out there on the front lines. Be aware, be cautious, and when in doubt - put on PPE!! Please reach out if you have any questions.

Other good resources:
The Wisconsin Rabies Algorithm: (for exposure or sick animals) https://www.dhs.wisconsin.gov/rabies/algorithm/algorithmcategories.htm
Illinois Rabies information: https://www.ilga.gov/commission/jcar/admincode/008/00800030sections.html

Audiogenic Reflex Seizures, Anyone?

Crinkling wrapping paper, crackling fires, and music - can any of these things cause seizures? 

What are they?

Feline audiogenic reflex seizures (FARS) start in cats late in life (> 10 years of age) and are triggered by a sound or sounds. The seizure phenotype (appearance) has a myoclonic component (a rapid twitch) but may also have absence or generalized seizures, as well. Absence seizures don't have any muscle movement associated with them and generalized seizures are charicterized by tonic clonic movements.

What causes FARS?

Any noise, but usually a high frequency sound such as clinking a spoon in a tea cup triggers the seizures. Some cats will have spontaneous seizures in addition to FARS and others will purely have FARS. If you are seeing an older cat with new onset seizures, consider having the client keep a "sound diary" for a few weeks to see if there is a correlation. 

Why bother identifying this...you're going to tell me to give phenobarbital!

Au contraire mon frere! A sentinel study was published in 2017 by Lowrie, et al (https://doi.org/10.1177%2F1098612X15622806) that showed a marked improvement in cats on levetiracetam in a randomized, controlled, open-label study with phenobarbital. 100% of the cats in the levetiracetam group obtained seizure control compared to 3% in the phenobarbital group. So you're correct that I typically prefer phenobarbital for feline seizures...except for FARS!

What causes FARS?

Interestingly, the majority of cats diagnosed with FARS in the published studies have had idiopathic epilepsy with a small portion showing progressive signs suggestive of active forebrain disease (neoplasia, meningoencephalitis).  

Merry Christmas to those who celebrate! Wishing everyone a happy, healthy holiday season filled with family, friends and good food. Thanks for reading and I look forward to working with you soon! As a quick reminder, I am out of town December 25-January 2nd. See you in 2026!

Tidbit Tuesday: Fungal Discospondylitis

Discospondylitis is a common cause of spinal pain in young to middle aged dogs. German Shepherds have been over represented, likely due to their immune deficiency. We’ve all probably seen a case or two of bacterial discospondylitis, but did you know fungal discospondylitis is also a worry? A study by Okonji S et al, published in JVIM in 2025, looked specifically at the presentation, diagnostic tests, treatment and outcome of 11 dogs diagnosed with fungal discospondylitis.
This was a retrospective case series of 11 dogs with confirmed mycotic discospondylitis. The organisms found cytologically in urine (5 dogs: Aspergillus spp and Candida albicans.), surgical curettage (3 dogs: Aspergillus spp. And Penicillium spp.), CT guided disc aspiration (2: Aspergillus spp. And Saccaromyces spp.). One patient had fungal hyphae noted on CSF, but they didn’t classify what they were.

Clinical Presentation
German Shepherd Dogs were markedly overrepresented (7/11), reinforcing prior evidence of breed predisposition. Dogs were typically middle-aged (median age 5.1 years), medium-to-large breeds, aligning with systemic aspergillosis demographics. Spinal pain was universal (100%), and gait abnormalities occurred in 82% and were often progressive and chronic. Most dogs localized neurologically to T3–L3 (10/11), emphasizing that mycotic discospondylitis should be considered in painful thoracolumbar myelopathies, especially when progression is insidious.
Pyrexia and inflammatory markers were inconsistent: only ~50% showed neutrophilic leukocytosis and elevated CRP. All dogs with leukocytosis had an elevated CRP as well. This highlights that absence of systemic inflammation does not exclude mycotic discospondylitis.

Diagnosis
MRI was the most sensitive modality, detecting lesions missed or underestimated on radiographs. Multifocal discospondylitis predominated (median 2.5 discs; up to 10), which is more frequent than typically reported with bacterial discospondylitis. However, imaging findings were not specific for fungal versus bacterial etiology.

Treatment strategies and response
Itraconazole was the most commonly used antifungal (7 of 11 dogs), often combined with analgesics and empiric antibiotics. Fluconazole and Amphotericin B were the other antifungals tried in this population. While temporary clinical improvement occurred in some dogs, sustained response was rare. Prognosis was poor despite treatment, with 10/11 dogs dead at study end and a median survival time of only 30 days. Only one dog survived long-term (>3 years). Bottom of FormThis is pretty sobering, isn’t it? Although a less common cause of discospondylitis, mycotic discospondylitis should be on our radar when evaluating a dog with spinal pain especially if multifocal discospondylitis is evident on imaging.
Thanks for reading! Happy Hannukah to all who celebrate! As a heads up – I will be closed December 25-January 2nd. You’d think I’d take this time to go somewhere warm and relaxing, right? Nope! I will be trekking to lovely Pittsburg to enjoy my family and to watch my daughters compete in a dance competition. May your holidays be full of friends, family and fun! 😊

Novel Surgical Technique for COMS/Chiari-Like Malformation

This week, I put ChatGPT to work on a TidBit Tuesday. I read the summary provided by “chatty” and made some changes. What do you think? Can you tell it isn’t me writing it?
A little background information…
A new surgical technique for the management of clinical signs associated with Chiari malformation (caudal occipital malformation syndrome: COMS) in small breed dogs was published. In a nutshell, the technique places a small gap between the underlying neural tissue and the titanium mesh used to make the new skull formation after foramen magnum decompression is completed. Not many of my readers are performing this surgery however I felt it was an important advancement in our surgical understanding of this disease. My biggest complaint about doing foramen magnum decompression is that u to 20% of dogs have a recurrence of signs. That, plus a lack of resolution of clinical signs with surgery, makes me very reticent to perform this surgery on patients. This technique was little different with a very different outcome. Read on to see how they did…
 
1. Pathophysiologic Basis of CM/SM
Chiari-like malformation (CM) results from congenital occipital hypoplasia causing caudal displacement of cerebellar tonsils and occasionally the medulla through the foramen magnum. The resulting foramen magnum crowding disrupts normal craniospinal CSF pulsatility, creating pressure differentials that drive syrinx formation. Syringomyelia progression reflects damage to neural spinal tissue which explains neuropathic pain, phantom scratching, and proprioceptive deficits.

2. MRI Grading Does Not Reliably Predict Clinical Severity
Historically, MRI evaluations demonstrated that CM grade did not consistently correlate with ventricular dilation or syrinx dimension. Some dogs with mild CM had substantial ventriculomegaly, while others with advanced CM had mild dilation. This supports that CSF flow disturbance—rather than anatomic grading alone—determines clinical impact, reinforcing MRI’s role for diagnosis but not prognosis.

3. Biomechanical Rationale for the Titanium Mesh (TM) Gap Technique
The modified technique preserved a deliberate 5–6 mm gap between the decompressed surface and the titanium mesh. Maintaining this “decompression space” is critical because contact between implants and dura can transmit external forces and encourage fibroproliferation. By allowing tissue ingress without compression, the technique aims to prevent postoperative adhesions, recurrent stenosis, and dorsal spinal cord indentation.

4. Avoidance of PMMA Improves Safety in Small-Breed Dogs
PMMA wasn’t used in this surgical technique.

5. Preoperative CT Planning Improves Implant Fit and Reduces Complications
3D-CT reconstructions were used to identify the thickest occipital cortical areas for screw placement and to plan appropriate mesh curvature. This prevents iatrogenic damage to thin occipital bone, minimizes risk of screw pullout, and ensures mesh contouring matches the native skull dome, which distributes forces during neck flexion-extension.

6. Surgical Technique Standardization Minimizes Reoperation Risk
All 87 dogs were operated on by the same surgeon, reducing technique variability. Essential components included:

• Modified decompression without dural grafting or Gelfoam (both associated with excessive scarring)

• Placement of 1.5-mm cortical screws as anchor posts

• Pre-shaped mesh to restore occipital curvature

• Verification of safe clearance during cervical flexion intraoperatively
  This uniformity likely contributed to the 0% revision surgery rate, markedly lower than the 8–30% reported in human studies and up to 25% in previous veterinary reports.

7. Postoperative Imaging Validates Long-Term Decompression
At 6 months, CT confirmed that the decompression gap remained intact with no mesh deformation, screw loosening, or dorsal compression. Maintenance of this space is essential because scar tissue maturation occurs over months; persistent patency supports the hypothesis that the mesh provides a long-term, stable barrier to re-occlusion.

8. Clinical Outcomes Demonstrate High Long-Term Efficacy
87% (76/87) of dogs had sustained improvement over a median of 35 months. Improvement included reduction or resolution of phantom scratching, neuropathic pain, and ataxia. Only 13% required persistent pharmacologic management. Importantly, no deterioration requiring reoperation occurred, despite follow-up up to 73 months (range 27-72: median 35), validating the durability of the surgical construct.

9. Older Dogs and Chronic Cases Showed Reduced Response
Non-improved dogs were disproportionately older (≥6 years) and frequently had long-standing clinical signs (≥1–2 years). This supports that chronic syrinx formation causes irreversible spinal cord damage, gliosis, and loss of neural plasticity, limiting postoperative recovery even when biomechanics are corrected. Early surgical intervention may yield superior functional outcomes.

10. Study Limitations and Clinical Implications
Although this retrospective study shows excellent outcomes, limitations include lack of blinded neurological scoring, reliance on owner-reported improvement after 6 months, and incomplete long-term CT follow-up in many patients (after the mandated 6-month scan). Nevertheless, the extremely low complication rate and consistent improvement strongly support the modified TM technique as a preferred decompression strategy in toy breeds, where limited occipital area complicates traditional grafting methods.
 
Given the chance, I’d definitely consider this approach on my next foramen magnum decompression! I’m away speaking at a conference in Texas until Thursday, but I look forward to working with you upon my return. Thanks for reading!
 
Reference: Park SS, Park JY, Han HJ. Outcomes of 87 small-breed dogs surgically treated for Chiari-like malformation and syringomyelia. Vet Surg. Nov 2025

Head Tremors in Cats

Tremors have been well documented in dogs however data is lacking about tremors in cats. A study by Liatis T et al, published in February 2025 classified the phenotype (appearance) and underlying etiology in 105 cats. Although a rare clinical sign, knowing common causes of tremors in cats can help direct further testing and treatment if you happen upon one of these cases.
 
What is a tremor?
Tremors are loosely defined as an involuntary, rhythmic movement of a body part with symmetric velocity in both directions. Picture a pendulum swinging in an arc. The pendulum swings just as wide from the center point in both directions, resulting in symmetric velocity in both directions. Tremors may be caused by central generators (such as the cerebellum) or peripheral generators (such as demyelination of a peripheral nerve).
 
Results
As mentioned, 105 cats met their inclusion criteria. This was a retrospective case-series utilizing medical records review and video assessment provided by owners.

• Median age 1.1 years (range 10.8 months – 17.3 years)

• Focal tremors were most common (62/105: 59%) followed by generalized tremors (43/105: 41%). Focal tremors included just the head in 58 cases or only a limb in 4 cases.

• Intention tremors accounted for almost half of the cases, while nonintentional and both types accounted for the other half.

• Top 7 causes of any tremor (focal or generalized): degenerative encephalopathy (19/105), FIP (17/105), hepatic encephalopathy (17/105), intoxication (permethrin and unknown cause: 16/105), polyneuropathy (8/105), suspected CNS lymphoma (4/105), and thiamine deficiency (3/105).

• What is a degenerative encephalopathy? The authors included cerebellar cortical degeneration, lysosomal storage diseases, congenital spongiform encephalopathy and the dreaded “unspecified”. 

What is the take away?
If you have a cat with a history of a tremor, especially an episodic head tremor, consider thr top 7 causes and fine tune your differential diagnoses list based on the cat’s signalment and history. Full CBC, serum biochemistry and a bile acid test are appropriate initial diagnostic tests for cats with tremors. Supplementation with thiamine, if a diet change or poor diet is present, should be considered. Brain MRI would be helpful to diagnose degenerative causes, FIP and the lymphoma causes. Lastly, interrogation of the owners regarding possible intoxication might indicate permethrin exposure. Other signs such as mydriasis and generalized hyperesthesia could be present in these cases as well.
 
Short and sweet TidBit Tuesday this week! I hope everyone is staying warm and successfully navigating the snow. Stay safe! Thanks for reading; I look forward to working with you soon!

Finding a Pain in the....

 
On your schedule today is a 9 year old German Shepherd Dog with a history of struggling to sit and stand. The owners have been noticing signs for about 3 months and think things have been getting worse. This dog is one of your favorite patients and is wonderfully cooperative when in the clinic!

Physical Examination: A little bit of resistance to full hip extension, remainder normal.

Neurologic Examination:
Mentation: normal
Cranial nerves: No worries here!
Gait: mild pelvic limb weakness (paraparesis), no significant ataxia or lameness
Reflexes: reduced withdrawal in the right pelvic limb, all other reflexes and all other limbs are normal.
Postural reactions: normal paw replacement testing in both TL, reduced to normal paw replacement left pelvic limb, reduced paw replacement testing right pelvic limb
Palpation: marked discomfort with tail jack, and direct digital pressure to the lumbosacral region
 
What do you do next?
I am working on a neurologic examination lab for an IVECCs conference and in this lab the participants will be asked to seek out next steps. So, what do you do? If it was me, I would localize the lesion.

Neuroanatomic lesion localization
If you draw a little stick figure of a dog, you can safely cross off the head and thoracic limbs. We don’t see evidence of cranial nerve deficits, mentation changes or thoracic limb changes. That focuses our gaze on T3-L3, L4-S3 and neuromuscular causes. Working backwards, we can eliminate neuromuscular because we don’t typically see focal spinal pain (only) with painful neuromuscular disease. How do we differentiate between T3-L3 and L4-S3 myelopathies?
 
Reflexes, you’re right! How were those pesky things? The withdrawal reflex was reduced in one limb, wasn’t it? The withdrawal reflex tests the sciatic nerve (L6-S3). If we have a reflex deficit, we have a problem in the nerve or the associated spinal cord segment. Why the paw replacement deficits? The right leg is easy to explain – the sciatic nerve carries the proprioceptive information to the spinal cord. If there is trouble in the peripheral nerve or the spinal cord segment of that nerve (L6-S3 in this case), we can see delayed proprioception. The left limb doesn’t have evidence of decreased withdrawal, so you’ll have to believe me when I tell you that this is still likely due to sciatic nerve involvement. The sciatic nerve is HUGE so damaging one small part could result in a minor delay of paw replacement without a clinically observable reflex deficit. So, in conclusion, our lesion localization is L4-S3, with a focus at L6-S3, more on the right.

What are your top differential diagnoses?
One of my top concerns for this dog is a lumbosacral degeneration. This typically involves intervertebral disc degeneration, ligament hypertrophy and bone changes including articular facet osteoarthritis and coning of the vertebra. The best way to diagnose this is to do an MRI. That allows us to look at the soft tissues (nerves, disc) and the hard tissues (bones).

A recent study by Medina-Serra et al  (2025) showed that over 30% of patients undergoing a spinal MRI had 3 or more painful etiology identified! That means they diagnosed an intervertebral disc herniation, nerve root entrapment and  facet disease in 1 patient – each of these can cause pain on their own. They also found a normal MRI in 20% of patients with detectable pain on evaluation. We need to pair the neurologic examination findings, with the physical examination findings (osteoarthritis of the hips? Stifle disease?) AND the MRI findings when trying to sort out what is the root cause of a patient’s pain and how best to treat it. Without the MRI we could have assumed this was osteoarthritis of of the hips. Without a complete physical or neurologic examination, we might have assumed this was only lumbosacral disease based on the MRI. 
I don’t have all the answers but hopefully a TidBit of knowledge will help you be proactive for your elderly, large breed dogs with  pain BEFORE they progress too far.
 
If you’d like to read more about this study you can find it here: https://doi.org/10.3390/ani15050761
Thanks for reading! I hope you have a pain free day!

Horner's Syndrome and Cervical Myelopathy

How many of you feel comfortable localizing Horner’s syndrome in a dog? If you do…skip the first section and read the data from a recent study about cervical myelopathy and Horner’s syndrome.  If not, please carry on and join us for an interesting look at Horner’s syndrome with cervical myelopathies.

 
First, Anatomy

The sympathetic pathway to the eye is a 3-neuron system. Neuron 1 starts in the thalamus, travels through the brainstem and cervical spinal cord to T1-T3 thoracic spinal cord segments where it synapses. Neuron 2 starts here and travels cranially, through the ansa subclavia along the vagosympathetic trunk (right next to that jugular vein you’re about to do venipuncture on!) to the caudal aspect of the bulla. From there, the 3rd order neuron takes a path through the tympanic bulla, along the ventral aspect of the skull (in the cavernous sinus) and hops a ride with CN 5 (trigeminal) to make a beeline to the eye. This neuron innervates the muscles of the iris, eyelids and orbit. It is the most indirect path anyone could design but I might argue that you can break it down into several key parts when localizing Horner’s Syndrome.

• Intracranial

• Cervical

• Brachial plexus

• Jugular groove

• Tympanic bulla

• CN 5

Cervical Myelopathies and Horner’s Syndrome

After reviewing the anatomy, it might be easy to see how a cervical lesion may cause Horner’s syndrome, right? The 1st order neuro travels from the intracranial structures via the cervical spinal cord to the upper thoracic spinal cord segments. Interestingly, a 2022 study looked at Horner’s Syndrome and cervical myelopathies* and found an incidence of only about 10% of Horner’s syndrome with concurrent cervical myelopathy. Therefore, although the anatomy makes sense, it is a fairly protected neuronal pathway and therefore a cervical lesion rarely causes Horner’s signs.

What Causes Horner’s Syndrome and a Cervical Myelopathy?

I’m glad you asked! According to this study, more dogs with Horner’s syndrome had noncompressive lesions compared to the control group (dogs with cervical myelopathy without Horner’s syndrome). Noncompressive lesions are often caused by fibrocartilaginous embolism (FCE) but hydrated nucleus pulposus extrusion (HNPE) and intramedullary neoplasia, noncompressive spinal trauma, Syringohydromyelia and inflammatory myelitis were found to cause Horner’s syndrome.  Also of note, Horner’s syndrome can be unilateral OR bilateral with cervical myelopathies.

Did having Horner’s Syndrome Affect Prognosis?

Nope. The underlying disease predicted prognosis and having Horner's Syndrome did not significantly negatively or positively influence outcome. However, seeing Horner’s syndrome on the neurologic examination would suggest that a surgical lesion is less likely to be identified.

 
Do you have a patient with Horner’s Syndrome? Do you suspect a cervical myelopathy? I’d love to help! Please reach out via email or schedule a consult online. Stay safe on these slippery roads and have a great week!

Reference from the TidBit Tuesday: https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.16588

Central Vestibular Signs in Cats secondary to Extension of Otitis Media

Have you evaluated a cat for a head tilt, nystagmus, and some vestibular ataxia recently? If so, you may have seen a cat with intracranial complications from otitis media/interna (OMI). “That’s not possible!” you say, “This cat did not have a history of prior otitis and their tympanic membrane looked fine!” First, great job doing an otic exam on a cat. Secondly, according to a study of 19 cats with intracranial complications from OMI, 63% of the cases did not have a prior history of OMI and over half of the cats lacked evidence of middle ear disease on otoscopic examination. Let’s dig into that study.
 
This was a multicenter retrospective study published in 2019 (DOI: 10.1177/1098612X18764582) that evaluated 19 cats who were diagnosed with intracranial complications from OMI. In this report, 15 cats received a lesion localization of central vestibular disease, and 3 cats were diagnosed with peripheral vestibular signs. Only 6 cats (33%) had evidence of Horner’s syndrome and NONE of the cats had evidence of facial nerve paralysis. Remembering neuroanatomy, the facial nerve and the ophthalmic branch of the sympathetic nerve course through the ventral bulla, which is the middle ear. It is interesting that so few cats had evidence of disease in the bulla, but it also tracks with what we typically see on clinical evaluation.

There were some interesting CT and MRI findings that you can read about in the paper. All of these cats except 1 were noted to have intracranial extension of the ear disease. The 1 cat without cross sectional imaging evidence had evidence of a neutrophilic pleocytosis on CSF analysis. Speaking of CSF analysis, 10 cats had a CSF analysis performed, and all 10 cases had a neutrophilic cell dominance, but not all of them had a pleocytosis.
Cultures were submitted on 21 samples from 18 cats. The most common source was fluid from the myringotomy or ventral bulla osteotomy (VBO) and the most common bacteria isolated was Pasteurella (n=4). Pasteurella is often found in the nasal cavity of cats. This suggests that the bacterial infection can occur through eustachian tube access rather than through the external ear.
 
Treatment
The treatment was surgical (VBO) in 12 cats and medical in 6 cats. Medical management included myringotomy in 3 cats. All cats except 1 were prescribed antibiotics, and 14 cats were prescribed a short course of a steroid.  Overall outcome was successful (improved or resolved signs) in 14 cats (74%), and unsuccessful (static, declined or euthanized) in 5  cats (26%).  A successful outcome was recorded for 83% of cats that underwent VBO and 66% for those managed medically.
 
Key points:
1. Do not discount the option of intracranial spread of OMI in cats based on examination alone. Consider advanced imaging (MRI) for any cat with signs of central or peripheral vestibular disease.
2. Consider Pasteurella when choosing antibiotics. Amoxiclav should be successful against this organism.
3. Cats, unlike dogs, do not always show signs of facial nerve paralysis or Horner’s syndrome with OMI.
 
This article came across my radar because of a recent case of extension of OMI in a cat. The article is a little bit older,  but I think it was worth revisiting. Hope you enjoyed this week’s TidBit Tuesday! I look forward to working with you soon!

References: Journal of Feline Medicine and Surgery; 2019, Vol. 21(2) 148–155

Using AI to prediction function outcome in dogs with disc herniation

Yes, you read that title correctly. A new study, the first of its type, is using “machine learning” to predict outcomes based on CT data, and neurologic grade. I will admit that I do not understand all of the system input data and how it was analyzed. I feel like I need another degree to grasp some of what is presented in this paper. If you’re analytically minded and want to learn more, please check out the paper for the full story because I may not represent it fully.
Historically, we have predicted neurologic recovery based on the most reliable factor which is the presence, or absence of deep pain (nociception). If an animal is paraplegic (no motor in the pelvic limbs) but has deep pain intact, we predict a 90% or greater chance of recovery for that pet. Timing and other variables play a minor role in recovery potential, too. If the same animal loses deep pain, their odds of recovery drop to around 50%. We have tried to predict myelomalacia, or motor recovery with MRI or CT characteristics over the years and have not been fully successful. Clients have higher expectations now, in the digital age. They want to know: will MY DOG walk again? Not what are the population odds? Although this paper doesn’t exactly say that we can do that, I think we’re edging closer to that possibility.
Based on this paper, the authors propose that this new learning tool can look at the neurologic grade on examination AND the CT properties and predict ambulation. (If I could insert the mind blowing emoji here I would!) Okay, maybe that’s a bit of an oversimplification but…it’s close.  While they don’t say it’s predictive for an individual, it gets us closer than before.
Results

• 214 dogs were included, of which 74 were Dachshunds and 65 were Frenchies

• 128/214 dogs were deep pain positive (DPP)

• 86/214 dogs were deep pain negative (DPN)

• The recovery rate for all dogs with 77%; 123/128 DPP (96%), 42/86 DPN (49%). These stats line up with what we already would have predicted

• None of the radiomics features were associated with recovery on UNIVARIABLE analysis. I.e. one feature didn’t stand alone

• The AI model outperformed simply knowing the DP status for predicting recovery to ambulation (p=0.02).

• Neurologic grade was the MOST IMPORTANT feature in the AI model’s decision making process but, as I read it, the AI model did a better job of predicting WHICH dog would recover and which wouldn’t.

 
Is the future here? Are we going to see imaging centers offering AI prediction models? Are we edging people and examinations out of the equation? Not so fast. Do any of you use a calculator in your daily work? I do. Sixty years ago, the calculator was a wild idea. People who knew how to do math could do math faster using a calculator. The data put into the calculator was accurate, and the people inputting in knew it was accurate. People who couldn’t do math, relied on calculators and hoped the answers were correct because they couldn’t know if the output was the number expected because they didn’t understand the input numbers. I think the same is true of AI. If we know how to perform a good neurologic exam, and then pair it with a CT, the results put out by the AI algorithm could be more powerful than just doing recovery predictions based on the exam alone. However, if we do an incomplete or incompetent neurologic examination, we won’t know if the AI prediction model is giving us good data. Or, worse yet, we won’t know that we didn’t do a good exam, and we will believe the AI prediction data without knowing that the data input was bad. Also, don’t forget, the most useful part of the AI prediction model was the neurologic grade. Neurologic grade is obtained by doing a good neurologic examination. If you lose the exam, you will lose data. In 2 years, I will likely look back at this TidBit Tuesday with a different reaction than today. But today – I’m still feeling pretty confident that we need to touch our patients!!.

What do you think of AI? Many of us are using it for note taking and some for radiology. Do you have an AI receptionist? I hope you enjoyed this week’s TidBit Tuesday. I look forward to working with you soon!

Reference: Machine Learning and Quantitative CT radiomics prediction of postoperative functional recovery in paraplegic dogs (Low D, et al) ACVS 2025

Ondansetron for Nausea in Vestibular Disease

Vestibular disease, whether it is central or peripheral in origin, can result in nausea and vomiting. The exact mechanism is unclear, but it is suspected to be via neuronal projections to higher centers (forebrain) and associated with activation of 5-HT3 receptors. Ondansetron is a selective 5-HT3 receptor antagonist (blocker). It has been shown to be effective on subjective observation, in controlling nausea in vestibular patients, but a recent double-blind placebo controlled study took it one step further. In addition to observation of signs of nausea, such as lip licking, facial expression, behavioral clues and hypersalivation, they evaluated blood levels of arginine vasopression (AVP) which has been positively correlated with nausea scores. 

Materials and Methods

Eighteen dogs were enrolled, 14 were included in data analysis. Six dogs received placebo first, followed 2 hours later by ondansetron (0.5 mg/kg IV, diluted 1:1 with 0.9% saline). Eight dogs received ondansetron first, followed 2 hours later by placebo. Dogs were observed at hourly time points for signs of nausea (pre and post treatment) and had serum samples for AVP measurements taken at pre-treatment, 2 and 4 hours post initial treatment. 

Key Results

• Dogs given ondansetron, showed a rapid, significant reduction in nausea compared to dogs given placebo. 

• Only 4 dogs vomited, in addition to signs of nausea. ** Vomiting should not be the only sign you watch for to say a pet needs an anti-nausea medication!

• Serum AVP concentrations decreased significantly after administration of ondansetron, compared to placebo. 

 
Based on the data presented, it is reasonable to assume any dog with recent onset vestibular signs should be administered ondansetron if signs of nausea and/or vomiting are noted. It would be helpful to educate clients on the signs of nausea (not just refusing food or vomiting!) when performing at-home observation of their pets with vestibular disease.

Interested in learning more about the nausea scores? Please consider this reference:
1. Kenward H. Development of an objective means of assessing nausea in dogs. London:EThOS British Library; 2015. 

Thanks for reading! I look forward to working with you soon. 

Feline Cognitive Dysfunction Syndrome

What is Cognitive Dysfunction in Cats?

Over 20 years ago when I left my residency and started out as a newly minted neurologist, feline cognitive dysfunction syndrome (CDS) was not on my radar. That has changed. As we learned more about aging in cats, CDS has become a more recognized disease by yours truly, as well as many others. If you're like me and need a Tidbit-Tuesday style refresher...read on!

What is cognitive dysfunction syndrome?
Cognitive dysfunction syndrome (CDS) is a term used to describe deterioration of mental capabilities associated with age.  Clinical signs of cognitive dysfunction can also be associated with other age-related illnesses (e.g. osteoarthritis, structural intracranial disease such as neoplasia, or cardiovascular disease) which makes it difficult to diagnose. See table 1 for an outline of behavior changes seen in cats with CDS.
The underlying etiology of CDS is yet unknown. Causes such as oxidative stress/damage, neurodegeneration  and vascular changes are among the leading hypothesis for human and canine CDS, and therefore suspected to be similar in feline CDS.  Deposits of extracellular B-amyloid and intracellular accumulation of microtubule-associated protein tau have been seen in human patients with cognitive dysfunction. Similarly,  B-amyloid deposits and increased tau have been detected in aged cats with cognitive decline, however the significance remains unclear. 

What are the clinical signs of cognitive dysfunction in cats?
There is a handy article, published in the Veterinary Clinics of North America in 2020 by Dr. Miele and associates that echoes what others have been reporting in a very concise little table. (See reference at bottom) I have replicated this table, with a few modifications, here. Note: There are other signs such as decreased appetite or thirst, that don't usually drive an owner or veterinarian to seek consultation from a neurologist so I haven't included them here. 

Table 1: You’ll need to subscribe to the TidBit Tuesday email to see this table. Visit www.barnesveterinaryservices.com and click on “TidBit Tuesday Blog”.

How is CDS in cats diagnosed?
Oh, this is as tangled of a web as the tau proteins we chase. (A little CDS humor here...the tau proteins can cause the "tangles" seen in human CDS!). Currently, the diagnosis is made by ruling out structural brain disease and systemic causes for diseases that mimic CDS. This may include complete blood count, full biochemistry panel including thyroid screening, urinalysis, chest radiographs, blood pressure assessment, brain MRI and possibly a spinal tap. Imaging changes associated with canine CDS include increased depth of the sulci, dilation of ventricles secondary to neuronal loss (called ex vacuo hydrocephalus) and a measurably small interthalamic adhesion. Exclude everything else, and it's probably CDS.

How can we help these cats age easier?
Currently, there are no proven treatments for feline CDS.  The addition of antioxidants (B vitamins, vitamin C, other) as well as fish oil were evaluated for use in cats in one study and showed promise. The use of S-adenosyl-L-methionine (SAMe) has been recommended for cats based on a study that identified improved performance on cognitive testing. This study only found significant improvement in cognitive function testing in the least affected cats. In addition to medical management, environmental management with ready access to food, water, litter box and areas of comfort (beds, hiding spots) is recommended. Environmental stimulation with low impact toys, or bird feeders in which the cat can choose to ignore any activity if they do not feel inclined to engage, are recommended. Finally, focused veterinary visits can be important for cat owners to feel supported through the aging process. Focus your exam to specifically evaluate body weight, urine production (to assess for signs of dehydration), behavior changes and mobility. This may help detect signs earlier in the course of disease and to identify concurrent morbidity that may contribute to, or be confused with, cognitive dysfunction.

Did I forget anything? Most of you treat and see this more than I do. What have you used (successfully, or not) for treatment? 

Reference:
Miele A, Sordo L, Gunn-Moore DA. Feline Aging: Promoting Physiologic and Emotional Well-Being. Vet Clin North Am - Small Anim Pract. 2020;50(4):719-748. 

Using Corticosteroids in Neoplasia

Corticosteroids have long been the mainstay treatment for dogs and cats with MRI diagnosed neoplasia. Approximately 85% of brain tumors demonstrate peritumoral edema (PTE) so it stands to reason that corticosteroids would reduce this edema. A recent study set out to determine the clinical response as well as the MRI response to corticosteroid use in dogs with suspected glial cell tumors or meningiomas. The dose of corticosteroids was not consistent or controlled in the study, nor was the use of anticonvulsants.

Materials and Methods
Seventy-two dogs were included in the retrospective study. Dogs were diagnosed with a glioma or meningioma on MRI, which was later confirmed with histopathology. They were then administered prednisone or prednisolone and a second MRI within 3 weeks of the initial MRI. At the second MRI, a quality of life questionnaire was provided to the owners.

• 50/72 glioma – a mix of oligodendroglioma, astrocytoma and unclassified glioma along with a mix of grades.

  • 45/90 were in a cerebral hemisphere (90%)

• 22/72 meningioma – most were grade I tumors, but a few were grade II.

  • 10/22 (45%) were in cerebral hemispheres

Results
A total of 38/72 (53%) were classified as clinical responders, and 34/72 (47%) were classified as clinical non responders. The most common clinical signs to improve were proprioceptive deficits, central visual deficits and other gait abnormalities.
A total of 23/50 (46%) of dogs with glioma and 14/22 (64%) of dogs with meningioma had detectable decreases in peritumoral brain edema volume. A significant difference in total tumor volume and contrast enhancing tumor volume was noted between responders and non-responders with glioma. This was not observed with meningiomas.
 
Discussion
This study outlines what we had long suspected: corticosteroids can improve quality of life and neurologic signs in dogs with glioma and meningioma brain tumors. What we didn’t know, and what this study showed, was a detectable decrease in measurable tumor volume with the use of corticosteroids. Did it work for everyone? No. Can it help? Yes, about 50% of dogs improved and no major adverse effects were noted from administration of the medications. Another little tidbit that I found interesting from this study was that among non-responders, 42% of dogs with glioma and 72% of dogs with meningiomas had seizures as their only clinical signs. This is in contrast to responders in which only about 10% of dogs had seizures as their only clinical sign. Another interesting finding was that 2 dogs, classified as clinical non responders, showed a 50% decrease in peritumoral brain edema. This means that the tumor was a bigger deal than the edema in these dogs. Location, location, location, I suppose.
 
Clinical Key Points:

• Corticosteroids, such as prednisone or prednisolone should be considered part of the palliative care package for dogs with glioma or meningioma.

• Dogs with meningiomas and seizures as their only clinical sign may have a poorer response to corticosteroids compared to dogs with other neurologic deficits,

 
I hope you enjoyed this week’s TidBit Tuesday. Let me know if you have any questions or saw a recent article that you think we should review. Have a great week!
 

Reference: doi.org/10.1111/jvim.70126
 

Not Walking Well...Is this Case Neurologic in Origin?

 On your schedule today is a 4 year old FS Beagle-X with a 3 day history of difficulty walking in the back legs. The owners described swaying, falling and occasional vocalization as if in pain. She has a history of a stifle injury about 1 year ago, but no other important medical history. Today is a lesion localization practice case, so grab a pencil and let's get cracking!

Physical examination: Mild thickening of the right stifle but no evidence of drawer, or instability in the stifle or any other joint. The remainder of her physical examination is unremarkable, other than the neurologic examination. 

Neurologic examination:
Mentation: BAR, anxious
Cranial nerves: normal
Gait: Ambulatory, paraparesis with moderate proprioceptive ataxia in pelvic limbs only. 
Reflexes: normal withdrawal in all four limbs, normal patellar reflexes bilaterally and normal anal reflex. The cutaneous trunci reflex stops at L2 bilaterally. 
Postural reactions: Absent paw replacement testing in both pelvic limbs, normal in both thoracic limbs. Normal hopping in both thoracic limbs, absent hopping in both pelvic limbs. 
Palpation: Spinal pain at TL junction, the remainder is non-painful. Normal cervical ROM and tail ROM. 

The first questions we ask ourselves is "does this dog have evidence of neurologic disease?"
The answer, of course, is abnormal, so let's break it down. At this point in the exam you could draw a "stick figure" dog to help you navigate the lesion localization. I find this trick quite useful for visual learners so don't be shy! Label the stick figure with the spinal cord segments below. Carrying on...

This dog has normal mentation, no cranial nerve deficits and no history of behavior changes or seizures so I think we can safely assume the lesion is NOT intracranial. Cross off the head on your stick figure. This leaves spinal cord, peripheral nerve, neuromuscular junction, or muscle to choose from. Let's start by assuming it's spinal cord in origin but if the lesion doesn't localize to ONE spot on the spinal cord you should then move on to considering the neuromuscular system. When looking at the spinal cord, you have four localization segments to choose from:

C1-C5
C6-T2
T3-L3
L4-S3

The C6-T2 and L4-S3 segments are where the lower motor neuron cell bodies are housed and when a reflex is performed on the examination, these lower motor neuron cell bodies are used. That means that a DECREASED reflex must have a lesion in either C6-T2 (if a front leg reflex is affected) or L4-S3 (if a back leg reflex is affected).Look at the reflexes listed on the neurologic examination. No spinal reflex deficits are noted, except for c. trunci, correct? We'll get to the c. trunci reflex in a minute.  This means you can consider C6-T2 and L4-S3 "free" of disease, or normal. Cross off C6-T2 and L4-S3 on your stick figure. This leaves us C1-C5 and T3-L3 for possible lesion localization. To do this, we must look at the gait description. 

What is paraparesis? Paraparesis is a weakness in the pelvic limbs. Monoparesis = one limb weakness, tetraparesis = all four limb weakness. Make sense? 

What is proprioceptive ataxia? There are 3 forms of ataxia, and proprioceptive ataxia is the most common one. This gait deficit occurs when the sensory nerves running from the toes --> peripheral nerve --> spinal cord --> brainstem --> forebrain become disrupted. When the nerves are disrupted, anything "downstream" or caudal to that disruption may show ataxia. In this case, it is just the pelvic limbs, therefore the lesion is caudal to the thoracic limbs. Caudal to the thoracic limbs is T3. We've already decided that we don't have reflex deficits therefore the lesion must be in front (cranial to) L4. Voila! The neuroanatomic lesion localization for this case is T3-L3 by process of elimination (and by doing a thorough neurologic examination). 

What about the cutaneous trunci reflex? This reflex has sensory nerves that run from about T1 or T2 to L6. When stimulated (pinch the skin), the impulse travels UP the spinal cord to synapse on the lateral thoracic nerve that originates C8-T2. This motor nerve then activates the panniculus muscle to "twitch". If you pinch the skin at L6 and don't get a reaction (a "twitch") move cranially vertebra by vertebra until you DO get a response. In this dog, that response was at L2. Because of the pathway of the sensory nerves, we typically count 1-2 spots cranially from where we see the twitch and assume the lesion is there. Therefore, this dog has a lesion T12-T13 or T13-L1. Most importantly, when this reflex is reduced, the lesion is in the T3-L3 segment. If it is normal, it doesn't mean that the lesion CAN'T be in this segment. To make it more confusing, this reflex is completely unreliable in cats! 

DDx: The most common differential diagnoses for this dog with spinal pain and acute, progressive T3-L3 myelopathic signs would be an intervertebral disc herniation, meningomyelitis,or trauma. I wouldn't exclude neoplasia or discospondylitis however they are less likely based on her history. 

Plan: Spinal radiographs can be used to diagnose discospondylitis but cannot be used to diagnose disc herniations or meningomyelitis. If vertebral neoplasia is present, spinal radiographs may be helpful. If spinal cord neoplasia is present, spinal radiographs will not be diagnostic.  3D imaging is needed to look at the spinal cord which would be a myelogram with CT, a CT alone or an MRI (my personal favorite). If the client is willing to pursue imaging and possibly surgery, if indicated, consider a referral. If the client is not willing to pursue these findings, a referral may still be useful (second opinion, confirm lesion localization or for assistance with medical management). Spinal injection of steroids may be an option for clients unwilling to pursue surgical management so reach out if this describes one of your cases!

How did you do? Was this easy-peasy or more challenging? I'd love to know! Please feel free to email me your comfort with the localization on this case so I can introduce either more or less challenging localization practice in the future. 

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