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!

How to Name Pain, and How to Treat Pain

I was taking a deep dive into different types of pain this week (for an article I'm working on) and I thought this list of terms was especially susinct and might be useful to you. It is from an article by the wonderful Dr. Clare Rusbridge (https://doi.org/10.1177/1098612X241246518) from the Journal of Feline Medicine and Surgery (2024). I strongly recommend reading the entire article entitled Neuropathic pain in cats: mechanisms and multimodal management for more detailed information. I have abridged the list from the article so if you would like the entire list please check out the article!

1. Nociceptive pain - pain that arises from activation of nociceptors during actual or threatened damage to non-neural tissue and transmitted by normal functioning nerves to the central nervous system. The pain is localized to the area of damage and removal of the insult results in resolution of pain. This term is used with a normally functioning nervous system.

2. Nociplastic pain – pain that arises from altered nociception, despite no clear evidence of  (i) actual or threatened tissue damage causing the activation of the peripheral nociceptors or (ii) disease or a lesion affecting the somatosensory system. It is possible to have both nociceptive and nociplastic pain.

3. Neuropathic pain – pain due to abnormal somatosensory processing in the PNS or CNS. This term must accompany another diagnosis (e.g. sciatic nerve damage with neuropathic pain) and is not used to describe the feeling of pain.

4. Hyperalgesia – increased pain reaction/behavior from a stimulus that normally provokes pain.

5. Allodynia – pain from a stimulus that does not normally provoke pain. (e.g. light touch perceived as burning.)

6. Analgesia – inability to feel pain

7. Hypoaesthesia – decreased sensitivity to stimuli, excluding special senses (sight, hearing, smell, taste)

Are you looking for some pain control medications now? Read further to see a few of the treatment options discussed in the article. 

1. Anti-NGF monoclonal antibody – chronic painful stimuli increase NGF, a neurotrophins that binds to TKA. When the NGF-TKA complex is translocated to the DRG it results in overexpression of substance P and calcitonin gene-related peptide leading to peripheral sensitization and neurogenic inflammation. Think of frunevetmab (Solensia).

2. Glucocorticoids – block transcription of inflammatory genes, upregulate anti-inflammatory genes and have excitatory and inhibitory effects of lots of neuronal systems. They can be applied locally (epidural methylprednisolone) or orally (prednisolone).

3. NSAIDs – prostaglandins contribute to the development of neuropathic pain.

4. Local anesthetics – injectable lidocaine can be considered for cats undergoing dental procedures to reduce the likelihood that the procedure will stimulate central sensitization (causing FOPS??). Topical lidocaine has been useful for humans but is less so for veterinary species.

5. Topiramate – an antiepileptic drug useful for neuropathic pain and self-mutilation. It is often called a voltage-dependent sodium channel blocker which results in a reduction of ectopic firing in PNS and DRG however there are central mechanisms as well. The central mechanisms may include potentiation of GABA neurotransmission, inhibition of the excitatory neurotransmitter glutamate and inhibition of voltage-activated calcium channels.

6. Carbamazepine/oxcarbazepine – a voltage-sensitive sodium channel antagonism which reduced high frequency repetitive neuronal firing and glutamate release. This could be useful for FOPS but is the most common treatment for human trigeminal neuralgia.

7. Gabapentin/ pregabalin – prevent the release of glutamate, among other things. Pregabalin is 5x more potent than gabapentin and the ½ life is longer therefore q12h dosing is appropriate. Transdermal route is unpredictable so stick with oral dosing for now (2025).

8. Amantadine – NMDA receptor antagonist and possibly potentiate dopaminergic neurotransmission and has anticholinergic activity. There is not much data published in cats!

9. Phenobarbital – reverses hyperalgesia via GABA actions and reduction of glutamate release, among other channels. This medication is not just for your seizure patients anymore!

 
If you are looking for drug doses, please see the referenced article. The article is also the place to look for references related to these drug treatments if you want to see the originally published data (always a good idea in my opinion). Spoiler alert - multimodal pain control does a better job for cats than single mode therapy. Prednisolone + phenobarbital or topiramate, NSAIDS + pregablin, or acupuncture + local anesthetics... you get the picture. 

Thanks for reading! Please reach out with any questions or check the article for dosing recommendations. Have a great week and thanks for reading!

Feline Orofacial Pain Syndrome (FOPS)

What is it?

This is not a seizure, we don't think and shouldn't be confused with orofacial seizures in cats. FOPS is a behavioral manifestation of oral discomfort and occasionally tongue, lip or gum mutilation in cats. There is some suspicion that this is a neuropathy arising from the trigeminal nerve or the ganglion processing from CN V. 

How does FOPS present?

This disease is more common in Burmese cats but can be seen in any breed at any age. Signs are often linked to dental work, tooth eruption or oral surgery. According to data from one study (link below), the median age was 7 years at first onset of signs, with the majority of cats having repeated or ongoing signs after the onset. 

Can it be diagnosed?

Anything called a “syndrome” should be your tip off that we don’t have a definitive cause or diagnostic routine. Rule out underlying dental disease, or oral pain, or diet-related causes for automatisms of the mouth following eating or other activities (e.g. wet food for a cat without teeth). If you’ve performed oral radiographs, a dental cleaning, looked for oral masses or wounds and tried diet changes without improvement, it might be time to think about FOPS.

How is it treated?

Not well.... oh wait, that is not what you mean, is it? Sadly, it is the truth. What treatments have been tried?

• Dental procedures: 35/53 cats improved following a dental procedure, but it was not sustained in 9 cats. 

• NSAIDS: 18 cats received NSAIDS of some variety. This was effective in 6 cats

• Corticosteroids: 7/17 cats had relief with steroid use. 

• Antibiotics: 2/12 cats attained improvement with antibiotics (unknown type, dose)

• Combination treatment (anti-inflammatory and antibiotic): 9/21 cats found this effective

• Opioids: 4/14 these were effective

• Phenobarbital: 14/14 cats, effective (this was combined with a dental 2 cats)

• Diazepam oral: 13/14 cats this was effective (combined with a dental in 1 cat)

• Gabapentin: only used in 1 cat and was effective *I would try pregabalin now*

• Chlorpheniramine: effective in 2/4 cats
  Take Home Message

It is very important to read the numbers regarding treatment carefully. This data is reporting a subjective response to treatment, with variable doses and types of drugs within one class, in a small group of cats. This data suggests efficacy with phenobarbital or diazepam use but other treatment choices may be effective. These medications are proposed to be effective because of their anti-allodynic effect, not anticonvulsant effects. Human patients with a burning sensation for their neuropathic pain find phenobarbital particularly effective and it may be the reason for improvement in FOPS. Also, remember that oral diazepam can cause idiosyncratic hepatic necrosis and therefore should be used with caution in cats. 

Have a great week, and thanks for reading!

Link to an article for additional information: https://doi.org/10.1016%2Fj.jfms.2010.03.005

A New Study Evaluates a Seizure Questionnaire

                 A large multicenter European group recently published data regarding a new survey designed to help more closely evaluate seizure semiology (appearance) to help us better classify seizures vs dyskinesias (abnormal movements that aren’t seizures). Over 600 dogs were included in the initial survey. You can view the survey here: https://dogepilepsyresearch.org/us/. The owners were instructed to proceed through 7 steps during episode description.

Step 1: report the seizure appearance in their own words

Step 2: Read a description of one of 4 episodes and see which one best fits their pet. These included 1) generalized seizures 2) non-generalized motor events 3) sudden falls without movement and 4) episodic impaired awareness (stare into space with behavioral arrest). The survey provides verbal descriptions of the categories as well as videos.

Step 3: Owners answer specific questions about the seizures include pre/post ictal signs, signs at first onset, description of the position, muscle tone, responsiveness during the event, age at onset, triggers and a few other questions.

Step 4: Historical questions about familial history, a history of head trauma or puppyhood diseases are asked.

Step 5: Veterinary exam results

Step 6: Medications and medication history

Step 7: Interictal changes in behavior

Results

The most common breeds were Labrador retrievers, Siberian Huskies and Border collies. Median age at onset was 2 years (IQR 1-5 yrs) with 80% experiencing their first episode between 6 months and 6 years old. Only about 50% of the dogs has neurologic examinations (what??!). Interestingly, owners described generalized seizures in about 58% of dogs, non-generalized motor activity in 58% of dogs, sudden falls in 6% and episodic impaired awareness in 15% of dogs. Over 25% had multiple types reported. Overall, reviewers agreed with owner classification about 90% of the time. Similarly, for dogs with multiple different types of seizures, reviewers agreed with classification about 86% of the time. The questionnaire was considered usable and/or easy to complete by about 70% of owners.

Interestingly, Labrador retrievers were more likely to have one classification, and it was the non-generalized motor event. This was compared to Huskies and Border Collies who were more likely to have generalized type seizures. Within the Labrador group, the majority of cases were consistent with dyskinesias NOT seizures (70%) and focal motor seizures in 24%. The remainder were undefined in classification.

Key Points
This questionnaire is a great tool for those researching seizures (um…me) but might be worthwhile for all of us to look at to make sure we are asking the right questions. While they did not set out to differentiate between dyskinesias and seizures, they state that this questionnaire might be the right tool to do so. My goal in showing you this article was to make you aware of the existence of this seizure questionnaire. Your clients can contribute to the ongoing data collection (by completing the form), and you can become familiar with the types of questions that might be helpful when faced with a dog with a possible seizure disorder.

If you’d like to watch the videos linked to the survey please see the article: https://doi.org/10.1111/jvim.70077

Thanks for reading! I hope you are finding time to enjoy this wonderful fall weather!

Phosphate concentrations and Seizures vs. Syncope?

Seizures Vs. Syncope

We've all been there, right? An elderly small breed patient with a grade II or III heart murmur presents to you with a history of "passing out". Clients aren't more descriptive than that, and they didn't catch a video. Is this syncope or was this a seizure?

You have several things to ask and look for (see prior TidBit Tuesday on syncope) but recent research has given us one more tool in our belt to help differentiate between these two diseases. 

Human patients with generalized tonic-clonic seizures demonstrate a reduced phosphate level within several hours of the event and patients with syncope do not. A study from Israel published data in January 2023 that strongly suggested a link between hypophosphatemia and seizures in dogs, as well. According to this study, 87 dogs with seizures and 26 dogs with syncope were included. Phosphate was evaluated within 3 hours of the "event" in question and noted to be decreased in 28 (32%) of dogs with seizures. None of the dogs with syncope had a low phosphate level. Dogs were excluded from the study if their creatinine was above the normal range to eliminate those cases with hypophosphatemia from renal causes. Median phosphate levels were significantly different between the two groups!

Key point: With an optimum cutoff value of 0.97 mmol/L (about equal to 3.0 mg/dl), evidence of hypophosphatemia has a 100% specificity and 44% sensitivity to diagnose seizures. 

Importantly, this tool should not be used as a stand alone finding to differentiate between seizures and syncope! However, identification of hypophosphatemia, within 3 hours of the witnessed event, could suggest a generalized seizure was more likely than a syncopal event if all other historical, physical examination and biochemical findings are concurrently evaluated. Important note: This has not been verified in dogs with focal seizures or complex partial seizures OR cats! 

This week's TidBit Tuesday is short and sweet. Have a wonderful week!

Reference: https://doi.org/10.1016/j.tvjl.2022.105914

Are Vertebral Malformations in French Bulldogs Painful?

Many of us have evaluated a spinal radiograph on a French Bulldog and thought “is this dog painful”? A recent study out of UW-Madison tried to evaluate this question in a prospective study.

Methods

Twenty-five client owned French Bulldogs, and 12 non-French Bulldog breed dogs were included as case and control animals, respectively. All dogs were perceived to be neurologically normal and non-painful by the owners. It is unclear if the researchers performed a neurologic examination to confirm this suspicion, but I assume that they did. All dogs had full spinal radiographs performed and mechanical sensory threshold (MST) testing was performed at 3 separate vertebral sites. The maximal force was 11 lbs. – which seems adequately weighted to assess for pain.

Results

What do you think they found? This study found no significant difference in MST testing between dogs with vertebral malformations and those without. This means dogs with only radiographic vertebral malformations do not need pain management. If you palpate a patient and elicit spinal pain, do not assume the pain is due to the underlying vertebral malformation. Keep digging! This pet may have a disc herniation, or articular cyst, or even meningitis causing its pain.

This week’s Tidbit Tuesday is short and sweet…just like summer! Enjoy the last few weeks of summer with those you love, and I look forward to working with you soon!

Reference: Pinal K, Zidan N, et al. Mechanical Sensory Threshold in Neurologically Normal French Bulldogs with Vertebral Malformations. ACVIM abstract 2025.

Epidural Steroids for Disc Herniation in Dogs?

Epidural Steroids for Disc Herniation in Dogs?

Epidural steroid administration has been a common therapeutic option for humans with low back pain secondary to intervertebral disc herniation (IVDH) but is rarely employed for veterinary patients. This option was recently evaluated in a double blind evaluation in 41 dogs.

Methods
The dogs were randomly assigned to either the control group (given epidural saline) or treatment group (1 mg/kg epidural methylprednisolone sodium succinate: MPSS). All dogs underwent surgical intervention (decompression) and the saline or MPSS was applied in the epidural space at surgical closure. Post operative care was similar between both groups.

Results

The dogs that received MPSS walked at a median of 3 days (range 1-8 days) and control dogs walked in a median of 7 days (range 1-17 days). This was a significant (P=0.01) difference between groups. Bodyweight did not affect recovery, however age did influence recovery. Younger dogs walked faster than older dogs, but both groups contained similar age ranges nullifying this finding as a cause for the significant difference.

One dog in the treatment group became non-ambulatory after regaining the ability to walk. This dog developed discospondylitis secondary to Staphylococcus aureus and dygalactidae which was ssumed to be seconcary to MPSS application, however an N=1 makes this association challenging to make. The dog was treated with antibiotics and subsequently regained ambulation.

Key Points

Although this isn’t the first report of intrathecal MPSS use in dogs, it contained the biggest case count. The significant difference in ambulation leads me to wonder about using this as another treatment option for dogs unable to undergo surgical intervention. Given the sufficient safety data from this and prior studies, it appears safe to administer with a less than 10% chance of serious adverse effects (discospondylitis). If you have a patient that is non-ambulatory but cannot go forward with surgery, and we have a high index of suspicion for IVDH, let’s talk about intrathecal MPSS. If you are a general surgeon performing spinal surgeries, or a neurosurgeon, I’d love to know if you give epidural MPSS or if you’re inclined to do so after reading this report. In case you’d like to read the full study you can find it here: DOI: 10.1002/vetr.4962

Thanks for reading!  Have a wonderful week!

Sleep and Neuropathic Pain in Cavalier King Charles Spaniels

A study was presented at ACVIM this year (2025) by Drs. Parker et al that evaluated sleep scores, neuropathic pain scores and perceived QOL by owners in a cohort of Cavalier King Charles Spaniels. The premise for this study was that poor sleep might exacerbate chronic pain in humans. They enrolled 68 CKCS, 37 of whom were diagnosed with caudal occipital malformation syndrome (COMs). Of these 37 dogs, 19 of them were considered to be clinical for the diagnosis and 18 were not clinically affected. Interestingly, dogs with clinical COMS also had greater difficulty falling asleep, ability to stay asleep for long periods of time, and overall poorer sleep quality. It was noted that more dogs slept with their heads propped up than not in the clinically affected group.

Why are they sleeping more poorly?

The authors propose that dogs with COMs may have chronic pain, which results in greater sleep disturbances. Additionally, part of the COMs complex is kinking of the brainstem which is where respiratory centers and the reticular activating system (RAS) are housed. The authors proposed that disrupted sleep could be due to alterations of these systems as well. Lastly, these dogs are brachycephalic which can result in snoring while sleeping, which is also linked to poorer sleep scores.

What do we do about it?

Owners can purchase a “fit bark” or other activity monitor that tracks their dog’s sleeping patterns. If frequent sleep disturbances are noted, initiation of pain management, investigation into brachycephalic airway surgery, or allowing for a “propped” head position might be indicated to improve sleep. The pain management medication I suggest in these cases is gabapentin or pregabalin, however excessive sedation should be monitored.

Although not exactly in line with our summer of cranial nerves, I thought this study was interesting and worth sharing. Stay tuned for more Tidbits gleaned from the national meeting this year!

Thanks for reading. I hope you have a wonderful week and enjoy these dog days of summer with those you love.

Time For a Tongue Twister!

For my "old-timers" this is a repeat TidBit Tuesday from 2021 (wow! time flies!). This is a really cool case about a cranial nerve deficit that we don't see very often. Enjoy this week's installment of our Cranial Nerve Summer Bonanza!

Signalment: 12 year old MC Mixed breed dog, 45 kg
History: 1 month history of change in bark, with a 1-2 week history of difficulty eating and drinking. The owners also identified difficulty walking in the last few days and a decrease in the dog's interaction with them. 
Physical Examination: Grade II/VI left heart murmur, previously noted and not progressed. The remainder of the exam was unremarkable.

Neurologic Examination

Mentation: Mildly obtunded. The pet interacted when asked, but otherwise seemed content to stare at the floor. 
Cranial nerves: Decreased to absent gag reflex, tongue atrophy (see the photo above), all remaining cranial nerves were normal. 
Gait: Ambulatory mild proprioceptive ataxia in all four legs
Reflexes: Normal spinal reflexes including c. trunci and perineal. 
Palpation: Non painful spinal palpation however pain elicited with cervical ventroflexion
Postural reactions: absent right thoracic and right pelvic limb paw replacement test, normal left paw replacement thoracic and pelvic.

Neuroanatomic Lesion Localization??

To do this, we need to break it down and identify all of the possible anatomic localizations each neurologic deficit could be noted. I prefer table form, but flow charts are also great.

DeficitWhere are ALL the places this abnormality could localize?Likely localization for THIS patient and whyObtundedCerebrum, diencephalon, midbrain, pons, medullaMedulla due to cranial nerve deficits noted.Gag reflexAbsent CN 9 and/or 10. This localizes to the medulla OR the peripheral nerves of 9 or 10Unable to determine if it has affected 9 or 10 however a central (not peripheral) lesion localization is suspected due to the concurrent paw replacement deficits and obtunded mentation.Tongue atrophy (right)Right CN 12 or right medullaSuspect medulla due to concurrent right sided paw replacement deficits and obtundationProprioceptive ataxia in all 4 legsC1-C5, medulla, pons, midbrain, prosencephalonSuspect medulla due to other findings but this does not localize all by itselfPain on cervical ventroflexionIncreased intracranial pressure (also called referred spinal pain), C1-C5, C6-T2 myelopathyLikely intracranial referred spinal pain due to concurrent cranial nerve deficitsAbsent right thoracic and pelvic paw replacementTo cause ataxia in both front and back legs, we need to assume the lesion is cranial to C6. Therefore, possible locations include C1-C5, medulla, pons, midbrain, prosencephalon.Likely medulla based on concurrent CN 9, 10 and 12 deficits noted above.

Do you see what I did here? I listed all  of the possible locations that the affected deficit might involve and then narrowed down the lesion localization two ways:

1. Find the common denominator. In this case, the medulla. OR

2. Find the cranial nerve(s) affected and determine if the pet also has: a) abnormal mentation, b) hemiparesis ipsilateral to the affected cranial nerve or c) paw replacement deficits ipsilateral to the affected cranial nerve. If they do, it is central. If not, it is a likely a peripheral neuropathy. 

Neuroanatomic Lesion Localization

Medulla, right side.

Differential Diagnoses

Neoplasia, meningoencephalitis (infectious or inflammatory)

Case Conclusion

This dog had normal CBC, serum biochemistry, UA, chest radiographs and abdominal ultrasound. Brain MRI identified a discrete contrast enhancing extra-axial mass in the right caudal fossa affecting the right side of the medulla. This finding was most consistent with a meningioma. A spinal tap was not performed due to the proximity of the mass to the cerebellomedullary cistern. Based on the working diagnosis surgical decompression, radiation therapy or supportive care were discussed with the owners and they elected supportive care.

Thanks for reading! I hope you have a great week. If you have a new colleague in your clinic please ask them if they'd like to sign up - the more the merrier!

Recurrence of Cervical Disc Herniation following Prophylactic Fenestration

Today we're going to take a small break from our cranial nerve evaluation to look at the recurrence rate of confirmed and suspected cervical intervertebral disc herniations in dogs with or without prophylactic fenestration. A study published in Veterinary Surgery by Berthome et al detailed the recurrence rate in a group of dogs that received prophylactic fenestration to those that did not.
What is fenestration? Fenestra means “window” in Latin, which is exactly what we’re cutting in the disc. This procedure is performed in dogs with a concurrent Type I disc herniation after removal of the herniated disc. This surgery is performed on the discs that did NOT herniate; thus, it is called prophylactic. During surgery, many neurologists, me included, cut a small window in the outer annulus fibrosis and “scoop” or attempt to remove the nucleus pulposus from the intervertebral disc. Fenestration is supposed to reduce the risk of herniation via three ways: 1) remove of the offending nucleus decrease the amount of material available to herniation. 2) provide a different path of least resistance for the disc to herniation (in the neck this will be ventrally away from the spinal cord) and 3) the scar tissue that forms after mechanical fenestration holds the remaining nucleus pulposus in place.
Results
The study by Berthome et al included 55 dogs, with weights less than 20 kg. Of these 55 dogs, 18 received prophylactic fenestration, and the remaining 37 did not. Neurologic grades were similar between groups, as were surgical sites for the herniated disc. Recurrence was defined as confirmed if advanced imaging was performed and a new disc herniation was noted. It was defined as suspected if clinical signs of new neck pain or worsening gait changes were documented by a veterinarian, but no advanced imaging was performed. A recurrence rate of 25% was noted (14/55) and all 14 dogs were in the non-fenestrated group. Only 1 dog had a confirmed new disc herniation, the remaining 13 were suspected. Surgical times were significantly shorter (p = 0.017) for dogs not undergoing fenestration compared to those that underwent prophylactic fenestration. Complication rates were similar (p=0.838), and no major perioperative complications were found in this study in either group.
Take Home:

• Prophylactic cervical disc fenestration may reduce the risk of disc herniation

• Srugical times may be longer if prophylactic fenestration is performed, leading to higher anesthetic costs (significance unknown)

• Recurrence was not confirmed in most of the cases so take this will a little grain of salt

Reference:DOI: 10.1111/vsu.14303. Vet Surgery J 2025

 
As I mentioned above, I do fenestration and have been an advocate for this for years. If you perform ventral slot surgeries and are unclear on the fenestration technique let me know; I’d be happy to teach you. Based on this data, hopefully we can reduce the risk of recurrent neck pain on our small dog population that is already over represented with cervical pain!Thanks for reading. I hope you’re staying cool in this summer heat.

Visual Fixation Test

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

What is Visual Fixation testing?

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

Visual fixation testing in dogs?

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

Results

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

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

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

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

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

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

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

Take away message

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

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

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

The Facial Nerve

The Facial Nerve 

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

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

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

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

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

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

Sedating Dogs with Intracranial Disease

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

Study Design

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

Results

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

Clinical application

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

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

Acute, Progressive Tetraparesis in a Large Breed Dog

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

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

1. Does this animal have evidence of neurologic disease?

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

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

4. Does the dog have reflex deficits?

5. Does the dog present or absent reflexes?

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

1. Yes

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

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

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

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

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

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

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