Use of CBD Oil for Refractory Epileptic Dogs

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

How the Study Worked

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

Key Points

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

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

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

Should we use CBD to manage seizures for resistant epilepsy?

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

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

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

Levetiracetam and Dogs with Chronic Renal Disease

Levetiracetam and Chronic Renal Disease in Dogs

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

CKD group

• Mean age 12.5 +/- 3.78 yrs

• Mean weight 5 +/- 2.78 kg

• Many breeds

• CKD IRIS stage 1: 60%

• CKD IRIS stage 2: 40%

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

Non-CKD group

• Mean age 10.26 +/- 3.73 years

• Mean weight 5.44 +/- 5.56 kg

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

Results

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

Take away message

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

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

How to Localize a Cranial Nerve

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

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

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

Take the following steps:

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

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

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

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

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

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

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

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

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

Medication Compliance and…the Cat

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

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

FDA Review of Librela 2025

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

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

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

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

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

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

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

Degenerative Myelopathy

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

Diagnosing Degenerative Myelopathy

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

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

Take away message

• Diagnosing DM requires histopathology

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

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

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

Omeprazole and CSF Production

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

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

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

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

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

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

What is the BEST tool in neurology?

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

THOROUGH NEUROLOGIC EXAMINATION!

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

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

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

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

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

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

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

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

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

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

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

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

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

Epilepsy in Labradoodles

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

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

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

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

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

Vestibular Disease in Cats

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

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

Peripheral Vestibular Disease

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

Brainstem Vestibular Disease

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

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

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

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

Thank you!

In this week of Thanksgiving, I am remembering you and your staff.

• Thank you for trusting your patient's care to me. I am humbled by the kindness, consideration and feeling of welcome that I receive when I enter your clinic to help care for your patients.

• Thank you for having a room ready for me. 

• Thank you for having kind, knowledgeable staff to assist me.

• Thank you for giving up valuable floor space (rooms, hallways, office space or even bathrooms!) to allow me to fully examine the patient.

• Thank you for the insight, nuance and personal touch you add when talking about a client or patient. I love being a part of your team. 

• Thank you for being an advocate for your patient and for including me in their health care needs. 

• Thank you for following up with me, giving me feedback, patient updates and answering my emails when I check in. 

• Thank you for sharing new ideas for TidBit Tuesday topics...and then reading the emails!

Most of all, thank you for being you!

Many of you have become my friends over the years. I look forward to seeing you and your staff when I get that "ping" on my phone that signals a consult was scheduled. Keep up the good work. You are valuable and important.  

Happy Thanksgiving!  May you have many of things to be thankful for in life. As always, thanks for reading! :)

This email is a repeat from an earlier year but I just love the sentiment and, although I update it, the core still speaks to me. Appreciation has no expiration date! 

Phenobarbital and The Adverse Effects in Cats

Many of you know that Phenobarbital is one of the most effective anticonvulsant drugs (AED) that we use to help control feline seizure disorders. Data we published several years ago suggested that 93% of cats obtained seizure control with serum drug concentrations between 15-40 ug/ml, regardless of the etiology. Remember, control is either a 50% reduction in seizures or 1 or less seizures every 3 months. Despite its high accolades for control, phenobarbital can cause adverse effects in cats. Phenobarbital does undergo hepatic metabolism but, unlike in the dog, it does not result in an increase in ALP. So, what adverse effects can happen?

Clinical Adverse effects
Clinical adverse effects occur in 46.7%of cats in a 2021 study (Marsh et al). These may be described as Type I or Type A adverse effects because they are secondary to the drug properties and often dose dependent. Keep that in mind!  Sedation and ataxia were the most common side effects, but not the only ones. 
Here are the adverse effects, and percent of cats affected, as reported in Marsh's study:
a. Sedation 89%
b. Ataxia 53%
c. Polyphagia 22%
d. Polydipsia 6%
e. Polyuria 6%
f. Anorexia 6%
Perhaps the last 4 are only notable to the observant owner, or in single cat households. Also of note, side effects in cats are reported less often compared with dogs. Interestingly, 26 of the 36 cats with reported adverse effects had transient signs. The majority of these only occurred in the first 4 weeks of treatment and in cats receiving multiple anticonvulsants. Adverse effects were significantly more likely in this population of cats when more than 1 AED was being used.

Biochemical Adverse Effects
A more severe, and concerning type of adverse effect is Type B. These adverse effects were extremely rare in the recent study, as well as in my experience. Bone marrow suppression did occur in 1 cat (as can be seen with dogs) and it resolved with removal of the phenobarbital. Biochemical adverse effects are much rarer in cats than in dogs. If a cat has an elevated ALP, as a general rule, find a reason other than phenobarbital administration. In both the study we published several years ago, and the study by Marsh et al, no cats showed an elevated ALP on laboratory results.
 
Take home message:

• Talk with owners about the common adverse clinical effects in the first 2-4 weeks of treatment. These should resolve but if not, consider reducing the dose.

• Recheck the CBC and biochemistry within 4 weeks of starting phenobarbital to monitor for those rare Type B adverse effects.

• Phenobarbital is useful, but imperfect, so always look at the cat in front of you when making decisions about seizure management. When in doubt -reach out!

Thanks for reading! I hope you have a good week and are appreciating the slow shift to cold pre-winter weather that we’ve been having. I look forward to working with you soon.

Brain-Gut-Epilepsy Link

This is exciting, folks! It has been well established that comorbidities such as anxiety, ADHD and fear-behavior are present for human and veterinary epileptics. Owners of dogs with epilepsy are frequently troubled by behavioral changes AND the seizures, especially when poorly controlled. Recently, the gut biome has been an area of focus as an area of possible therapeutics for these comorbidities in humans and animals. A group of colleagues from Europe and Asia recently published data looking into this question and... it’s pretty cool! Read on to learn what they learned. 

Material and Methods
Nine dogs with drug resistant epilepsy AND behavioral changes were included in the study. A fecal donor was a dog with epilepsy that did not have behavioral comorbidities and had responded well to phenobarbital. Fecal microbiota transplantation (FMT) was performed three times, two weeks apart. Questionnaires and behavioral tests were performed at 3 and 6 months after the FMT. This, along with urine testing of neurotransmitter concentrations and routine biochemistry and hematology. 

Results
There was a significant improvement in ADHD-like impulsivity, non-social fear and chasing behavior (questionnaire based), AND seizure severity and frequency. Not surprisingly, the care-giver anxiety concurrently decreased significantly. Even more interesting (to me), the excitatory neurotransmitters glutamate and aspartate decreased and GABA, an inhibitory neurotransmitter, increased. Only 1 dog had a partial seizure response (50% reduction in seizures), and several other dogs had a reduction in cluster days during the follow-up period. No dog was seizure-free after the FMT. 

Take Home Message
This was a pilot study, so it isn't clinically applicable yet. YET. But can you imagine having access to FMT to help manage comorbidities like these? I'm sure you can think of at least 1-2 patients right now that would benefit from a decrease in ADHD-like behavior, fear or anxiety behaviors! Although we cannot use this yet to change our patient's lives, keep your ears open for the future. However, as with all new treatments out there, there will be good and bad options as this comes out. Remember that there are a lot of factors that can affect FMT. Specifically, current or historic administration of medications (antibiotics, gastroprotection’s, NSAIDs, and possibly anticonvulsants). A donor with any of these medications in their past may have an altered gut biome that makes them an unfit donor for your specific patient. So, please don't just take any gut biome and assume it will work for another patient!

Thanks for reading. I hope you can feel my excitement oozing out as you read this week, and I hope you enjoyed reading this TidBit Tuesday as much as I enjoyed reading the article. If you wish to read more, please follow the link below. Have a great week!
Link: doi.org/10.3389/fvets.2024.1385469

Neospora in Adult Dogs

Neospora has become increasingly common in veterinary neurology, especially in the last few years. Neospora is an obligate intracellular parasite that causes notable complications in cattle but is not commonly diagnosed in dogs. Dogs are a definitive host, which means upon infection, they will not pass this infection along to other hosts (unless that new host consumes their meat). In other words, do not eat a dog infected with Neospora (!!).

How do dogs  get infected?

The most common transmission is transplacental or juvenile onset neosporosis. Dogs that develop clinical signs at greater than 12 months of age probably have adult onset or the newly acquired form. This form has fecal/oral transmission.

What are the clinical signs of Neosporosis in adult dogs?

There are two forms of disease, which may occur separately or concurrently. First, we can see neuromuscular disease. Signs may include a strict myopathy (difficulty opening the jaw, tetraparesis with normal reflexes), neuromyopathy (myopathy signs plus patchy reduced reflexes) to a full neuropathy (reduced reflexes in multiple limbs along with clinical weakness). The other option is CNS signs, for which cerebellar signs and seizures predominate.

How is it diagnosed?

Adult onset, or acquired neosporosis, is diagnosed via IFA titer. Different papers have listed different “positive” IFA titers. A recent article from Sydney Australia by Kennedy et al(DOI: 10.1111/jvim.17219), listed the positive IFA titer as 1:800. Previous studies have listed anything from 1:200 to 1:800 as the positive titer rate. I typically recommend retesting if you get anything over 1:200. If it goes UP or remains above 1:400 it is likely clinically active and warrants treatment (if clinical signs are present). PCR inconsistently diagnosed Neospora in the recently published study.

How is it treated and do relapses occur?

The first line treatment for most studies is clindamycin (median dose 15 mg/kg PO q12h) x 12-17 weeks. Sulfa antibiotics are the second line of treatment, and several dogs received both drugs in the recently published study. Prednisone is important during active CNS disease to minimize the secondary inflammatory reaction during protozoal die-off. The dose and duration of prednisone is variable, but immunosuppression should be avoided. Relapses were common in the most recent study (9 relapses occurred in 4 dogs) highlighting the need for either longer treatment, or prompt treatment if signs recur. All signs were similar to the initial presenting signs except for one dog.

Take home message?

Remember to test for Neospora caninum when presented with a dog with CNS signs, myopathy, or neuromuscular signs. A simple titer using IFA is the best step, followed by consultation with your local neurologist.

Thanks for reading! I hope you have a wonderful start to November and look forward to working with you soon.

What do you do when you cannot elicit the cutaneous trunci reflex in a cat?

Okay, first let's talk about this reflex. The cutaneous trunci reflex (CTR) is used in dogs to evaluate the viability of the thoracolumbar spinal cord. It is a really LOOOONG reflex pathway. As with all reflexes there is a sensory and a motor component to CTR. The sensory input is each segmental spinal nerve from T1 to L6 and the motor output is via the lateral thoracic nerve found at C8-T1. Sensory and motor innervation is bilateral however stimulation of one side can result in a contraction bilaterally. 

How do you perform the CTR?

Simulate the hairs or the skin paraspinal between T1 and L6. I use my fingers, hemostats or in rare cases a needle to gently poke the skin. The sensory information goes through the spinal nerve, ascends the spinal cord to synapse on the nucleus of the lateral thoracic nerve found C8-T1. After synapses the motor efferent lateral thoracic nerve contacts the panniculus or cutaneous trunci muscle and you see a visual twitch. The effect may be bilateral, even if you stimulate unilaterally. 

What is the significance of the CTR in dogs?

When present and complete to L6, it carries no significance. Dogs can have severe spinal cord injury and still have a present CTR bilaterally. HOWEVER, if it is reduced cranial to L6, especially unilaterally, this can help focus your lesion localization in the T3-L3 segment. For example - CTR is absent between L1 and L6 on the left, the lesion will be 1-2 segments cranial to L1, or the T12-T13 region. What is better than precision?? Tracking lesions! If we take a dog to surgery and remove a herniated disc at T13-L1 and the CTR was cranially advanced to L1 preoperative, I can monitor the CTR for caudal decent to suggest spinal cord healing, or cranial decent to suggest myelomalacia. Perhaps you have seen some of your patients return from spinal surgery with sharpie marks on their back? This is likely because we were tracking the CTR.

Terrific, but what about cats?

Cats are well, different, aren't they? To start, the CTR is unreliable. In some cats it is present, in other cats it is not. A recent study published in the Journal of Feline Medicine and Surgery confirmed what most of us suspected clinically: the CTR has no significance in a neurologically abnormal cat. It cannot be used reliably to localize a lesion and it may, or may not, be present regardless of neuroanatomic lesion localization. One more way cats make us smile...

**Paushter AM, Hague DW, Foss KD, Sander WE. Assessment of the cutaneous trunci muscle reflex in neurologically abnormal cats. J Feline Med Surg. 2020.

This TidBit was a repeat from the archives but, I suggest, still makes for good discussion. I hope you enjoy your week and look forward to working with you soon!

CPs, postural reactions, paw replacement, oh my!

What we previously called CPs (conscious proprioception) we now call the paw replacement test. Yes, if you haven't heard,CP is now the "old fashioned" term and has been replaced with the much less sexy term "paw replacement test". Why?? (You might ask.) The reason is simple: we were lying when we said we were evaluating just the conscious proprioception pathway! When the paw goes on the dorsum, conscious, unconscious and even a bit of motor pathways are involved in righting it to the correct position.  Sometimes the truth isn't sexy, but alas, here we are. 

What parts of the nervous system must work for the paw replacement test to work?

An abnormal paw replacement test almost always indicates a neurological problem however the lesion may be located anywhere along the pathway involved. The pathway is: peripheral nerve --> ipsilateral spinal cord -->ipsilateral medulla and pons --> cross in midbrain --> end in prosencephalon. Some branches also go: peripheral nerve --> ipsilateral spinal cord --> ipsilateral medulla --> ipsilateral cerebellum. You can see that a LOT is involved with this pathway so you really need to put together the remainder of the neurologic exam to appropriately utilize this test. The paw replacement test is one of several ways to test the proprioceptive pathways and they are often collectively referred to as "postural reactions".

What are postural reactions?

• Paw replacement test: While providing support, and on stable footing, turn a paw upside down and place it on the dorsum. The animal should right the paw to the normal position with minimal to no delay, or scuffing. Want to brush up on your technique? See my YouTube channel with this link:  https://youtu.be/vEFEVvO4TCQ  

• Placing (visual or tactile): A useful test for cats. The animal is blinded and advanced towards a horizontal surface such that the paw gently touches the surface. A correct response occurs when the animal places the limb on the surface.  Want to see a video? Check out: https://youtu.be/VDyaL2kHNV8

• Hopping: One leg is on the ground; the other 3 legs are removed from support. Gently, the animal is pushed in the lateral  direction from the direction of the leg on the ground and the animal should hop.

Learning to perform postural reactions can take years...lots of practice...and seeing lots of different animals with different diseases. Paw replacement deficits are critical for localizing many parts of the CNS so, in my opinion, it is worth it to get this test right! If you want to get comfortable with these tests consider performing one or more of them on every patient you evaluate.

Thanks for reading! I hope you have a wonderful week. I will have limited service next week so please plan ahead if you have a case needing to be seen. Thanks!

The Nuts and Bolts of Anticonvulsant Drug Monitoring

The following information is contained in these two tables:
1. What drugs can I run therapeutic drug monitoring levels?
2. Where do I submit samples?
3. When do I draw blood for sampling?
4. What is the standard reference interval?
5. What is MY (i.e. Dr. Heidi Barnes Heller's) recommended reference range
6. How should I collect this sample? Note - all samples for therapeutic drug monitoring should be spun and separated into a plain red top tube. Do not use serum separator tubes! Plasma can be used for some samples also. Please separate the plasma into a plain red top tube as well.
7. What time of the day should I collect the sample?
*** The format became a little messy with the mailer so email me directly if you want a printable PDF of these tables and the mailer doesn't suffice. 

What is not contained in these tables? 
How do I use this information obtained from a drug serum concentration?? Stay tuned for that in a separate TidBit Tuesday! :)

DrugWhere to submitWhen to submitStandard reference range (may vary a little by lab)PhenobarbitalAny commercial lab. Unless you regularly run QC, in-house phenobarbital analyzers aren’t recommendedAfter 14 days on the same dose15-40ug/ml (dog)
Extrapolated for cats: 15-40ug/mlLevetiracetamAuburn University
https://www.vetmed.auburn.edu/ veterinarians/clinical-labs/After 3 days on the same doseNONE verified for dogs or cats. Human range is 5-40, but target may be closer to 20 for “resistant” humans.ZonisamideCornell Animal Health Diagnostic Center https://www.vet.cornell.edu/animal-health-diagnostic-center/testing/protocols/zonisamide
After 14 days on the same dose10-40 ug/ml (human) extrapolated to dogs and catsBromideAny commercial lab.After 12 weeks on the same dose, and/or after completion of a loading dose1-3 mg/dl

DrugMy recommended reference range (pet dependent of course) Other notesCollection timePhenobarbital25-30 ug/ml dog and cat (cat is extrapolated from dog)Plain red top, serum only.Any, if on longer than 14 days of medicationLevetiracetamNone. Use this sample as an internal reference. Not sure what I mean?? Please email me for additional details.Separate serum (or plasma) into a plain red top2-4 hr. post pillZonisamideNone. I don’t think we actually know the range for dogs and cats yet!Separate the serum or plasma and store in refrigeratorJust before the next dose (i.e., trough level)BromideSolo: 2-2.5 ug/dl
Combination with phenobarbital: variable but usually around 2.0 ug/dl.NoneAny time, if at steady-state

Thanks for reading! I hope you're getting in the fall spirit and enjoying all things pumpkin, cinnamon and apple-y! Please reach out over the next few weeks if you need a consult and cannot find a suitable time on the scheduler. I have a lot of days blocked off for family events but may be able to squeeze in a consult or two as needed. 

Episodic Head Tremor in Doberman Pinscher Dogs

We have talked recently (and historically) about idiopathic head tremors (IHT) common in bulldog breeds. There is another head and neck tremor that has been less well described in the Doberman Pinscher dog termed “episodic head tremor syndrome”. This isn’t new, but a recent case made me realize that we hadn’t discussed this form of head tremors in a TidBit Tuesday before. It is high time.

I’m going to refer back to one of my favorite articles (reference: movement disorders, vol 26, No 13, 2011) as we talk about episodic head tremors of Doberman Pinscher dogs. (EHT-DPD) because I think it’s an oldie but a goodie.

What are episodic head tremors in Doberman dogs?

This is an inherited, idiopathic, paroxysmal movement disorder of Doberman dogs. The signs were traced back to 1 sire in the previously referenced study, strongly suggesting inheritance. Episodic head tremors could be a seizure disorder, just like dogs with presumed IHT may actually have a seizure disorder, but for the moment we still classify it as a movement disorder. Movement disorders do not typically associate with autonomic signs (drooling, vomiting, urinating, defecating) or reduced mentation (loss of consciousness) and should not occur during sleep or when the head is fully supported (like lateral recumbence). Those phenotypic descriptions can guide you in the direction of a movement disorder vs a seizure disorder however, as I tell clients, the best way to “know” is to have an EEG performed. That said, EEGs can be misleading, difficult to interpret or so full of background noise that they are uninterpretable. So, we do the best we can, but sometimes it comes down to our best guess for this diagnosis over a seizure. Although idiopathic, EHT-DPD in the referenced study, appeared frequently with concurrent stress. That could include pregnancy, heat, medications and surgery or illness. That doesn’t mean that stress causes this but may unmask it.

What do the tremors look like?

They are rapid, often intermittent, horizontal or vertical head shaking episodes. The oscillations are RAPID, not slow head swinging movements. There is a congenital form, occurring in dogs less than 1 year of age, and a later onset version.

What causes it?
It is idiopathic based on normal EEG, MRI, infectious disease screening, metabolic screening, and CSF analysis in the study mentioned above.

Should it be treated?

No, not usually. It doesn’t appear to be progressive in a negative manner. Breeding is not recommended for dogs exhibiting signs of EHT due to the suspected inherited manner.

Have you seen a case of EHT in your practice? How did it progress? Thanks for reading! I hope you have a good week. Stay tuned for more fun reading next week.

Tetanus in Cats

Tetanus is caused by the action of the Clostridium tetani neurotoxin causing generalized muscle stiffness. This clever neurotoxin gains access to the CNS via retrograde transport up a peripheral nerve to the spinal cord, or brainstem (if it goes up a cranial nerve). Once in the spinal cord, it will irreversibly inhibit the inhibitory interneurons in the spinal cord thus resulting in generalized or partial muscle stiffness and spasm. Cats are more resistant to tetanus neurotoxin compared to humans or dogs, but they can still get the signs. Let’s talk about how to recognize this rare disease, in cats!

A recent retrospective study out of Europe (11 referral centers) was published in 2024 outlining signalment, clinical and neurologic findings, treatment and outcome. In this report, they cite that cats are thought to be 12 to 2400x more resistant to the toxin than humans or dogs. WOW!
This study described tetanus in 27 cats. Not surprisingly, this was mostly reported in the warmer months of spring, summer and fall with few cases in winter. It is interesting to note that this is not the case with dogs. More tetanus is reported in dogs in winter in Europe. The source of the infection was thought to be a wound in most cases; however, 5 cats had a recent history of sterilization.

The initial clinical signs were lameness or stiffness in a limb in 17/26 cats. This was noted as a difficulty manually flexing the joints in one or more limb on evaluation. Progression was noted in most of the cases, peaking at about 4 days from onset of signs. Two cats demonstrated tonic clonic seizures with loss of consciousness. Marked hyperthermia was noted in 10 cats. Unlike humans or dogs, generalized tetanus was less common in cats. Autonomic signs were rarely reported in cats but are more common in humans or dogs and may result in an increased mortality. Signs might include hypertension, hyperthermia, tachycardia, arrhythmias, profuse sweating and bradycardia. Three cases had wound cultures performed and all 3 were positive for Clostridium tetani.

Treatment

Hospitalization occurred in 21/27 cases with a mean hospitalization time of 7 days. Wound debridement was mentioned in 9/27 cats, along with antibiotics (26/27). Metronidazole was the most common antibiotic recommended, followed by Clavamox. The duration of antibiotic treatment was difficult to determine for many of the cats, but the authors report median treatment duration of 15 days (range 7-28). Muscle relaxation was facilitated with oral diazepam (21/27 cats) monotherapy or combined with methocarbamol, alfuzosin or magnesium sulfate (1 cat). Equine tetanus antitoxin was administered in 6/27 cats and no side effects were reported. The most common adverse effects reported included hyperthermia, urinary retention, dysphagia and osteoarticular disease (fractures due to muscle contractures or osteomyelitis). The more severe cases were noted to have adverse effects more commonly.

Outcome

Outcome was available for 25/27 cats. Of these, 23/25 (92%) regained independent motor within a median period of 25 days (range 11-42). The two cats that did not regain appropriate motor ultimately had limb amputation due to osteomyelitis.
 
What’s Take Away?
Even though more resistant, cats can get tetanus just like dogs. If you are presented with a cat with inappropriate focal stiffness and a wound, consider tetanus. Culturing the wound may aid in making a diagnosis. Metronidazole appears to successfully eliminate the infection, however due to the irreversible binding of the toxin the clinical signs may take longer to abate. When in doubt – refer for a consult!

 Thanks for reading! I hope you have a wonderful week and enjoy this summer-like fall weather that we're having. 
 
Reference: https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2024.1425917/full