Seizures are GOOD thing??

Brain tumors in adult dogs are relatively common. There are two primary brain tumor types in dogs: meningioma and glioma. Glial cell tumors are further divided into 3 subtypes varying from less aggressive to more aggressive in growth with rare metastasis. These tumors typically have a shorter long-term survival compared to meningiomas and are less surgically accessible. According to a recent study, dogs receiving palliative treatment have a median survival of about 1 month, compared to dogs receiving definitive treatment. Median survival for definitive treatment was almost 3 months.

This study looked at long-term survival using the new WHO classification scheme and found several interesting findings. The one that is most clinically applicable, and interesting to our pet population, is this:

Dogs with seizures as their first sign had a longer survival, regardless of histopathologic grade, than those with other neurologic signs at onset.

What does this mean? It means that, like in humans, seizures are like a warning shot, letting the rest of us know that something isn't right in the brain and we'd better take a look! If we proceed to MRI and make that diagnosis, dogs survive longer because of early onset palliative OR definitive therapy. This is yet another reason why we really should encourage clients to pursue a definitive diagnosis (i.e. brain MRI, spinal tap) even if they wouldn't consider definitive therapy such as surgery or radiation therapy. Early, aggressive, palliative medical care may actually prolong their dog's life beyond what we might get if we waited to "see what progressed".

I hope you have a good week and look forward to working with you, and your team, soon!

The full results of this study can be found at: https://onlinelibrary.wiley.com/doi/full/10.1111/jvim.16199?campaign=wolearlyview

Hepatic Encephalopathy - UPDATE

Hepatic encephalopathy is caused by changes in hepatic metabolism that result in neuronal damage or swelling. Clinical signs can include neurological, gastrointestinal or urinary due to the abnormal metabolites or the formation of stones. As a neurologist, I see these patients when they have seizures, changes in mentation or behavior, or other neurological signs.

The preferred treatment is surgical correction with slow closing of the offending vessel. As many of us know, this doesn't always correct all clinical signs and some dogs require life-long treatment despite successful surgical closure.
Life-long medical management must provide a high quality protein source, but yet remain a low protein diet to avoid excessive amino acids.

There was an interesting article published recently (https://onlinelibrary.wiley.com/doi/full/10.1111/jvim.16135?campaign=woletoc) that outlined the changes in the different types of amino acids present in the body. There are two main types of amino acids that researchers watch: branched chain amino acids (BCAA) and aromatic amino acids (AAA). In normal animals, the ratio of BCAA to AAA is 3.0 to 4.0, whereas it is 1.5 in animals with a portosystemic shunt. The study goals were to evaluate what happened with the amino acids after shunt surgery.

Results

Interestingly, specific BCAA and AAA did not change a lot, nor were they all outside of the reference range to start. However, the ratio of BCAA to AAA did increase (improve) but did not return back to the normal range. Clinical improvement was noted in most of the dogs, however!

What does this mean? It means that functional recovery occurs faster than biochemical recovery and functional recovery may be more "complete". This also (probably) means that we still need to dig into the amino acids a bit more to see if there are specific amino acids to be more or less worried about.

Yes, I know, this was a very academic TidBit this week and I promised they would be clinically applicable...I'm sorry! I do try to keep it clinically relevant but every now and again I must deep dive into research with you. :)

Keep those consults coming! This has been a terrific few weeks, with interesting cases. I love working with you and your staff to help patients.

Thanks for reading and have a great week!

Update on Acute Seizure Management

"Doc, The Dog is Having A Seizure!"

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

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

Give me the "Go-To", Barnes!

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

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

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

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

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

Is Propofol Still Used?

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

Have a topic suggestion for TidBit Tuesdays? Please reach out!

Need a consult?
Email: barnes@barnesveterinaryservices.com
Telephone: 608-597-0077
website: www.barnesveterinaryservices.com

Happy Father's Day to all of you lucky Dads! Hope you have a safe, relaxing day.

When Should You Start Anticonvulsant Drugs (and Why)?

Following the recommendations of the International Veterinary Epilepsy Task Force I suggest starting anticonvulsive drugs if a patient meets one or more of the following criteria:

• Two or more seizures within 6 months

• History of status epilepticus (one seizure longer than 5 min)

• History of cluster seizures (cluster seizures meet the definition in the first point above)

• Post ictal signs are severe (ex: aggression) or lasting longer than 24 hours.

• Seizure frequency or duration is progressing in the last 3 interictal periods. (ex: 12 months apart, then 8 months then 6 months)

Medications are selected based on the metabolic status of the patient, seizure pattern and client constraints (administration frequency, cost, bias). Phenobarbital and bromide are considered first line treatments by the IVETF and are recommended for most forms of seizures in dogs. Phenobarbital could be considered a first line drug for cats as well (Bromide is a big NO-NO for cats). The level of evidence available to make these recommendations is, at the time of writing, more complete than for the other anticonvulsant drugs. I use the following table to as a guide for starting or changing anticonvulsant drugs; hopefully you find it useful also. Remember that these are guidelines and many animals need manipulation of their seizure control life-long.

Table 1: Indications and limitations of phenobarbital, bromide, levetiracetam, zonisamide and gabapentin as first line anticonvulsant therapy.

PhenobarbitalBromideLevetiracetamZonisamideGabapentinIndication (Dog)Generalized tonic, clonic seizuresFocal or cluster seizuresReactive seizuresGeneralized seizuresInfrequent statusIndication (cat)Generalized, focalnot recommendedReactive seizures, orofacial seizuresLimited data. Consider for generalized?Very little data. Consider as last choice.limitationsAnimals with hepatic disease should not use this drug.Give with care for dogs with renal failure, or renal tubular acidosis (or with zonisamide)Chronic administration may result in honeymoon effectDo not use in cats or dogs with known sulfa hypersensitivity, or liver diseaseNone known

Whew, it's hot out here! I hope you are staying cool, safe and enjoying this blast into summer.

My summer 2021 hours have started! Please email me if you have a case to discuss, cannot find a time on the scheduler for a consult, or just like to chat about all things neurology. :)

I look forward to working with you, and your clients and staff, soon!

Tetanus and Dogs

What is tetanus?

Tetanus is caused by the Clostridium tetani bacteria which produces a neurotoxin that causes muscle contractions. This bacterium is found commonly in soil and is ubiquitous throughout the world. After the bacterium is injected into an anaerobic environment it produces the toxin. The toxin targets inter neurons in the spinal cord, inhibiting their function.

Diagnosis?

A diagnosis is made by observation of classic clinical signs such as limb rigidity, muscle retraction on the face or periocular. Detection of the C. tetani bacterium in the wounds through culture can provide a definitive diagnosis, if obtained.

Treatment?

Wound debridement followed by appropriate antibiotics (penicillin or metronidazole) will result in recovery for the majority of dogs and cats. For severe cases, respiratory assistance with a ventilator, sedation to avoid painful sustained muscle contractions and 24-hour nursing care may be needed.

Seasonality?

An interesting article came across my view recently that identified a spike in tetanus cases in the winter months (December-February) in England. This was surprising because more cases are reported in warm, humid climate than cold ones. The authors didn't provided substantial reasoning for the odd seasonality but suggested it may be related to the exposure by walking in wet muddy environments. Here is the link to the article if you'd like to read more: https://doi.org/10.1111/vec.13068

I hope you have a wonderful, productive, safe week and I look forward to working with you soon. Thanks for reading!

Isoxasoline Flea Treatment and Seizures

Recently published data (2020) suggests that adverse events (AE) - the new word for side effects - are higher than reported by the manufactures of isoxazoline flea treatments. Specifically, researchers looked at Bravecto (fluralane), Nexgard (afoxolaner) and Simparica (Sarolaner) in both the US and Europe.

What did they find?

This is a TidBit Tuesday-style abbreviated summary. For the full report see the link at the bottom. There is a lot of data in this report!

• The survey (called Project Jake Survey) had 2751 respondents. It was compared to the data requested of the FDA and the EMA (European Medicines Agency).

• Almost 69% gave Bravecto, 26% gave Nexgard and a small 5% gave Simparica.

• Overall, 66.6% of dogs had a reaction to treatment

• Of the 911 dogs getting Bravecto, 791 had an AE (86.8%)

• Of the 342 dogs getting Nexgard, 235 had an AE (68.7%)

• Of the 72 receiving Simparica, 44 had an AE (61.1%)
  

What about seizures??

Death and seizures were a focus for this report, however other side effects are certainly noted and were reported. I will focus on seizures.

FDA report: Overall, 5.34% of dogs experienced seizures

• 20% of dogs receiving Simparica

• 2.8% of dogs receiving Bravecto

• 6.9% of dogs receiving Nexgard

EMA report: Over all 30.3% of dogs experienced seizures (!!)

• 60.2% of dogs receiving Simparica

• 18.7% of dogs receiving Bravecto

• 46.69% of dogs receiving Nexgard

Project Jake Survey:

• 4.5% of dogs receiving Simparica

• 14.8% of dogs receiving Bravecto

• 12% of dogs receiving Nexgard
  
  

Why are the numbers SO MUCH higher in the EMA?

Perhaps it is related to genetics in the dog population, better reporting habits, or reporting by vets vs owners (or vice versa). That question wasn't answered in the report. The take home message for me was that Simparica is blowing things out of the park with seizures but that the other two still have a substantial group of dogs with seizures as an AE.
Critically, this report did NOT state if the dogs had ever had seizures prior to administration of the drugs. They did state that at least some of the dogs had novel seizures after administration of one of these drugs...but alas we don't know the details on this.

When do the majority of Adverse Events occur?

Within the first 24 hours. These are supposed to be insect specific GABA mediated chloride channel blockers that are distributed around the body in the first 24 hours so it isn't surprising that this is the highest spike of possible toxicity to the dog. Also, AE were reported as a small spike between 8-14 days.

So, what is the take away?

• Any of the drugs in this report (Bravecto, Simparica or Nexgard) can have seizures as a side effect. Are they a cause of seizures? I'd say probably yes, for at least some of the dogs. Perhaps they lowered the threshold in prone animals too?

• It looks like Simparica may have a higher incidence of seizures

• If a dog has a FIRST seizure (within 24 hours or at 8-14 days) after using an isoxazoline drug, discontinue use and try a different class or different drug in this class.

Link: https://onlinelibrary.wiley.com/doi/epdf/10.1002/vms3.285. Publication date 2020. This was a very interesting read and eye opening for me.

Keep those consults coming! The more we work together, the more we learn from each other.

This TidBit Tuesday grew from a recent spike in questions about flea/tick medications from some of YOU...so, thank you!

I look forward to working with you and your staff, soon!

NSAIDs vs. Prednisone...What Do I Do??

Case 1: A 4 year old Dachshund with 3 day history of back pain. On neurologic examination you find spinal pain at TL junction with reduced paw replacement in both pelvic limbs, normal reflexes and normal gait analysis. Neuroanatomic lesion localization (NALL): T3-L3 myelopathy
What would you rank for a differential diagnoses list?
I'd consider IVDH, meningomyelitis, discospondylitis and neoplasia.

Case 2: A 1.5 year old FS Cavalier King Charles spaniel. On neurologic examination you find moderate cervical spinal pain with reduced paw replacement in the left pelvic limb and marked phantom scratching at the neck when lightly stimulated.
NALL: C1-C5 myelopathy
What differential diagnoses would you consider for this case? I would suspect syringohydromyelia first, followed by less likely meningomyelitis and IVDH.

Case 3: A 2 year old MC Labrador with lumbar pain, a normal neurologic examination and fever of 102.0F.
NALL: Lumbar pain (You cannot have a NALL without neurologic deficits!)
What is your differential diagnoses list for this patient? I'd consider discospondylitis, type II disc herniation, and some non-neurologic causes such as musculoskeletal injury or joint infection. Rarely we see referred pain from prostatic disease (cysts, neoplasia, prostatitis).

We know we need anti-inflammatory medication for pain management, right? Which one?

Case 1: The risk is low for infectious disease in this patient. For confirmed IVDH, neither prednisone or an NSAID has been shown to be superiors for pain control. Without a confirmed diagnosis, we must treat for the top 1-2 differential diagnoses, right? I typically start with NSAID therapy for these patients and if they are unable to proceed with MRI/spinal tap to obtain a definitive diagnosis and clinical signs of pain persist, I switch to prednisone after an appropriate washout period. Is it wrong to start steroids? No. The side effects of GI upset, ulceration and mild immune suppression make them less desirable when treating IVDH but they are not contraindicated.

Case 2: This case has a high likelihood of Syringohydromyelia (SHM) based on the breed and clinical signs. SHM has a high amount of neuropathic pain, which can be mediated by COX-2. Therefore, NSAIDs that target COX-2 may provide some relief. That said, steroids mediate sympathetic pain, decrease substance P expression and decrease expression of lots of inflammatory mediators and may decrease CSF production to boot. Therefore, with a low infection likelihood in this pet and high likelihood of SHM, prednisone is my drug of choice over NSAIDs. If you haven't confirmed the diagnosis, however, it is worth a discussion about the possibility of worsening clinical signs and the side effects of steroids prior to starting the drug.

Case 3: This dog has a high risk of infectious disease based on breed, age and clinical signs. Therefore, in addition to taking radiographs to try to find this dog's discospondylitis (!!), I would NOT use prednisone in this patient. NSAIDs provide wonderful bone penetration and excellent periosteal block of COX-2 mediated pain and would be my drug class of choice.

Steroids, especially prednisone, are not evil and they have a time and a place in neurology. (Understatement of the year😂 ) However, they have a greater chance of adverse clinical adverse effects than NSAIDs therefore they are not needed for every patient with spinal pain. Develop a differential diagnoses list that fits your patient before deciding between NSAIDs and prednisone. Still not sure? Call/email me to discuss your case, or set up a neuro consult!

Heads up - I will be on vacation May 29-June 5th and will have limited telephone and email access. I will respond to emails as I am able but will not be as prompt as usual. Please plan to schedule consults around this window as well. Thanks for your understanding, and support of my small business. I look forward to working with you soon!

The Neurology Checklist

The Checklist

Odds are high that you have probably heard about surgical or operative checklists and, perhaps, some of you employ them in your clinic. This week I wanted to revisit this idea because a recent article reminded me of the benefit of checklist so I thought I'd share it with you!

How Does it Work?

You and your team devise a list of important things to remember for a given procedure and create a checklist. This list then hangs in your OR, or outside of a lab, or wherever it will be used. Ten years ago I read a book called The Checklist Manifesto (https://www.amazon.com/Checklist-Manifesto-How-Things-Right/dp/0312430000). One of the simplest ways to save a life is to know the name of your anesthetist and lead surgeon. Yep, that's it. Instead of bumbling around and saying "hey you...anesthesia..." you can address them by their name and shorten communication time in a crisis. Perhaps you work very closely with your staff everyday and it seems inconceivable that you wouldn't know someone's name! However for new staff members, or in large clinics, this may not be the case.

What is the evidence?

A study published in the Journal of Veterinary Surgery this month identified that surgical times were significantly shorter (p= .005) , antibiotic administration (when appropriate) was given as intended more often (p=.01), and fewer dogs had an unplanned return to the OR (p=.006) when a perioperative checklist was employed. (Reference below.) It takes less than 1 minute to run through the checklist and it may change the course of you or your patient's day!

What is the Take Home Message?

If you don't already have one, consider making a checklist for any procedure in which patient care could be compromised if something was forgotten. This doesn't need to apply ONLY to surgical situations! I make an effort to know the name of my assistant during each and every neurologic examination for this exact reason. I don't expect a crisis during a neurologic examination but everyone feels more committed to the team when we ARE a team! (And I like to be friendly, too!) I also had a checklist hanging in the neurology room when I was at UW and at VCA Aurora to remind trainees of the parts of the neurologic examination.

Neuro Checklist:
Mentation
Cranial nerves
Gait assessment
Postural reactions
Reflexes
Palpation
Ask about a seizure history.

Having this list in your work space ensures that you don't accidentally forget to perform part of the neurologic examination and yet, it isn't so overwhelming that you hesitate to read it. (A checklist MUST be short or people hate to do them!)

I hope you enjoyed this not-fully-totally-neurology-related TidBit Tuesday. Please let me know if you have any comments, questions, or requests for topics. Have a great week and keep those consults coming!

Reference: Thieman Mankin, KM, Jeffery ND, Kerwin SC. The impact of a surgical checklist on surgical outcomes in an academic institution. https://doi.org/10.1111/vsu.13629

Back Pain + Fever

The 2 year old MC Poodle with Back Pain

It is Friday afternoon, and you are about to evaluate a 2 year old Poodle with a recent onset history of reluctance to walk. Upon examination, you find back pain at TL junction and a fever or 104 F. The dog stands there, hunched, but has a normal neurologic exam (self high-five!) and normal remaining physical exam so.... now what?

When I hear this story, my first thought is of discospondylitis. (My second thought is steroid responsive meningitis-arteritis (SRMA), one of the many forms of inflammatory non-infectious meningitis. Let's talk about this another day.)

EtiologyBacterial or fungal infection of the vertebral end plates. Commonly Staphylococci, with other causes including Streptococcus, E. coli, and less commonly B. canis. B. canis is zoonotic and can cause abortion in humans so exercise caution when managing a dog with discospondylitis.

Hematogenous is the most common source, with less common direct transmission (bite wound, grass awn).

Fungal infection with aspergillus or coccidiomycosis (SW USA) most common fungal isolates. Rarely blastomycosis.

SignalmentYoung to middle aged dogs, rarely cats.
Large breed male dogs are more often affected (male: female ratio 2:1).

Clinical signsAcute pain, often with fever, anorexia and other signs of systemic illness. Signs of a myelopathy may develop if empyema occurs, or vertebral subluxation/fracture due to loss of bone integrity. <-- EEK!

Diagnostic testsSpinal radiographs may lag 3 weeks behind onset of clinical signs; however, they are an easy diagnostic test with high yield for many cases. If unrewarding and the index of suspicion is high, spinal CT and then MRI provides increasing better detection rates in early disease.
Or, you can treat the pet for suspected discospondylitis for 2-3 weeks and re-radiograph to confirm the diagnosis.

Treatment optionsAntibacterial or antifungal treatment based on blood, urine or disc cultures. If cultures are negative (approximately 30% of cases have no growth), broad spectrum bone penetrating antibiotics are recommended until radiographic resolution is obtained (maybe 9+ months). These include cephalexin, enrofloxacin and sulfa antibiotics. Pain management and exercise restriction in the early stage of disease is important.

PrognosisFavorable with appropriate treatment.

You're doing great!! I really enjoy helping you, help your patients, live their best lives with neurologic disease. Not sure what to do with a case? You can email or telephone with case questions or schedule a consult online at a time that works for you. (Vets and vet staff only, please!)

Idiopathic Facial Nerve Paralysis

Idiopathic Facial Nerve Paralysis

I thought we'd continue our theme from last week about peripheral neuropathies and talk about a neuropathy that we all (I think) see fairly regularly: Idiopathic facial nerve paralysis.

What is it?
Idiopathic facial nerve paralysis (IFNP) happens for, ahem, unknown reasons. There is some type of synaptic block that, as of now, has an unknown cause. The facial nerve is a motor nerve that starts in the medulla (brainstem), courses through the skull and bulla on it's way to the face. Other causes of facial nerve paralysis such as hypothyroidism, neoplasia, otitis media, polyps, and rarely neuritis. Remember: you must localize the lesion to the peripheral CN 7 to include IFNP on your list of differential diagnoses!

What does it look like?
The facial nerve innervates the muscles of facial expression in dogs and cats as well as providing 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), lack of ear movement (especially noticeable in cats), and a dry, red eye with possible ocular ulceration.

Clinical Course
Signs are typically acute in nature with rapid progression to full clinical manifestation. Spontaneous resolution occurs in 3-6 weeks. Yay!

Management
Supportive care, such as eye lubricant, and ensuring lip injury is minimized by limiting chewing toys/bones, is the mainstay treatment. Antibiotics, steroids, NSAIDs and other medications do not improve the recovery time!

It's short and sweet this week. Please let me know if you have a specific topic of interest! Have a great week, and keep those consults coming.

Consults are available Monday-Saturday at various times. Check out www.barnesveterinaryservices.com (press the schedule button in the upper right corner) to schedule. Note: Only veterinarians or veterinary staff may schedule a consult.

Hypothyroidism and Neuropathies

Etiology: The peripheral nerve is the most common target in the neurologic system for hypothyroidism. What causes a peripheral neuropathy due to hypothyroidism? I'm glad you asked....

1) accumulation of mucinous deposits resulting in nerve entrapment
2) demyelination secondary to Schwann cell defect
3) vascular nerve damage secondary to hypothyroid induced dysfunction of BBB
4) disruption of axonal transport

Signalment:

• Typically older dogs, however congenital disease does (rarely) happen. NOTE: dogs are not always overweight, heat-seeking or have flaky-hair coats with peripheral neuropathy signs.
  
  

Clinical signs:

• A polyneuropathy is most common. This results in paresis without ataxia and reduced to absent peripheral spinal reflexes. Signs may be initially mild.

• Cranial nerve deficits such as facial nerve paralysis (VII), vestibular dysfunction (VIII), or laryngeal paralysis (X).

• Hypothyroidism may also cause a myopathy and/or megaesophagus.

Diagnostic tests:

• T4 is a good first step. If abnormal, a full panel is recommended.

Treatment options:

• You guessed it...supplementation!

Prognosis:

• The neuropathy is likely to improve a little or a lot, after several months with therapy if the axonal degeneration is not too severe.

• Cranial nerve deficits may persist even with appropriate treatment.

Frequency:

• Common in older dogs! (And recently seen in one cat with vestibular signs. This job always keeps me on my toes, that's for sure!)

This is Neurology Month for the WVMA. If you haven't seen already, there are 4 virtual talks available to WVMA members, and non-members, for CE credit. I do not receive any payment for promoting this but, I am one of the speakers!

Have a great week, and keep those consults coming. Consults are available Monday-Saturday at variable times so please reach out if I can help you with a case.

Large Breed Dogs and Disc Herniation

A little background...

Dogs greater than 10 kg experience type 2 disc herniation more frequently than type 1 disc herniation. (Refresher: Type 1 = acute extrusion of the center of the disc; Type 2 = bulge of outer ring of the disc into the spinal canal.) An estimated 10-30% of the time large breed dogs have type 1, depending on the study.

How is a type 1 disc herniation different for a large breed dog?

The answer is rather obvious, but glossed over frequently. They are bigger! That means nursing care is harder, surgery takes longer and is more extensive, and as a result there can be a greater expense for some of our larger dogs.

Does the prognosis change for a medium to large breed dog?

Yes. Dr. Woelfel from NCSU recently published data from a cohort of dogs > 10 kg that had both acute disc herniation and extensive spinal cord hemorrhage.

(Spinal cord hemorrhage occurs infrequently for large and small breed dogs and was shown in a few studies to have a minimal effect on prognosis as a stand alone feature. Meaning, the prognosis was still mostly based on the presence or absence of deep pain and didn't depend on spinal cord hemorrhage identified on advanced imaging.)

Okay, back to big dogs with disc herniation and spinal cord hemorrhage. The NCSU study reported a worse prognosis, and a higher complication rate, compared to overall data for small breed and chondrodystrophic dogs.

The details in summary:

• No deep pain before surgery, recovery about 38% (general population: 50%)

• Deep pain present before surgery, recovery rate about 77% (general population:90-95%)

• Complication rate was about 24% (general population: 10-15%)

Post Operative Complications Noted in the Referenced Study

• Decubital ulcers

• Pneumonia

• Self-mutilation

• Fever of unknown origin

• MDR UTI

• Sudden death

• Progressive myelomalacia

What is the take home message?

When talking with an owner of a medium to large breed dog with acute onset paraplegia, I suggest emphasizing the need for intense at-home nursing care, possible complications (along with the higher incidence) and a realistic prognosis if the dog is diagnosed with a disc herniation on advanced imaging. Remember that other differential diagnoses can cause acute onset paraplegia! Please do not interpret this paragraph as a call for euthanasia for large breed dogs with acute paraplegia. A 38% recovery rate is not zero! But a honest, open, vet-to-client discussion is the best way to achieve an informed decision for the client.

Not sure if you are interpreting the neurologic examination appropriately? Not sure if you are doing the neurologic examination properly? Please reach out! I am happy to work with you to help guide your clients in a compassionate and informed way.

Happy Easter to those that celebrated last weekend. We welcomed spring with big smiles around my house this weekend!

Reference: Woelfel, CW, Robertson, JB, Mariani, CL, Muñana, KR, Early, PJ, Olby, NJ. Outcomes and prognostic indicators in 59 paraplegic medium to large breed dogs with extensive epidural hemorrhage secondary to thoracolumbar disc extrusion. Veterinary Surgery. 2021; 50: 527– 536. https://doi.org/10.1111/vsu.13592

Important Questions to Ask When Evaluating a Seizure Patient

Do you know the most important questions to ask a client when evaluating a seizure patient?

Careful questioning of the owner is required to determine if the episodes described ARE seizures. Syncope, vestibular signs, neck pain, and movement disorders (think Scottie cramp) have episodic presentations with similarities to seizures. Nothing is fool proof, even an EEG, but here are some tips to get you going in the right direction.

Describe the event, please!

• Clinical appearance, including a description of any autonomic signs is critical. Videos can be priceless!
  

• Level of mentation can be confusing and difficult to determine (especially for those pesky night time seizures) so don't spend too much time grilling an owner on this one.

• How long do the events are lasting. This question is subject to tremendous bias, but if the owner says "all day" I start wondering about other non-seizure events.

How often have the events occurred?

Okay sorry, I need to harp on this one. My pet peeve is hearing "about once a month" as an answer! This is an easy one and something we should encourage ALL clients with seizure pets to do: Keep a calendar! Tell owners to write it down, put it in a spreadsheet, mark it on their phone, keep a list - the choices are as varied as the seizures they record! You will NEED this to be in place to help you direct treatment. The single biggest reason to change treatment is that the seizures do not meet the seizure goals for epileptic pets.

Your second goal here is to uncover information about possible cluster seizures. If the animal has 2 or more seizures in 24 hours that is defined as cluster seizures. Cluster seizures need at home cluster seizure management (another topic in a different TidBit Tuesday, I might add). Furthermore, some drugs work better for dogs with cluster seizures than those with single seizures. I personally believe that bromide is a terrific option for cluster seizures and will readily use it for patients with this type of pattern.

How long is each seizure?

This question is utilized to learn about status epilepticus. Any seizure longer than 3-5 minutes (people argue about what is the correct time) is considered status. Status warrants emergency management with injectable solutions (intranasal, intravenous, other). Untreated status can set an animal up for systemic side effects as well as increase the risk of permanent brain damage.

What does the animal do after the event is finished?

Your goal here is to evaluate the post ictal phase so that you can decide if a change in treatment is needed. Based on the rules outlined by the International Veterinary Epilepsy Task Force, severe post ictal changes (such as aggression) warrant treatment even if the other parameters for treatment haven't been met. I also use this question to determine how the owner is feeling about the event. Answers such as "he was fine" or "he paced and paced and seemed really upset" give me a window into how they feel about as much as how the dog did. Helping owners cope with seizures is also part of our job.

Are you working with a seizure patient and need some backup? Please reach out, I'd love to help. It is my job to help you care for your patients with seizures more confidently. We can do it!

Also, a super big thank you to those of you that have contributed head tremor cases to the database!! If you're not sure what I'm talking about please email me or check out last week's TidBit Tuesday mailer for more details.

Stay safe, stay healthy and keep those consults coming!

Idiopathic Head Tremor VS Seizures

Idiopathic Head Tremors vs. Focal Seizures

Wow, a lot of you have been seeing head tremors lately and sending them my way! I thought we could take this TidBit Tuesday to look more closely at Idiopathic Head Tremors and compare/contrast to seizures. Please read or skip to the end - there is a plea for data collection and I need your help!

What are Idiopathic Tremors?

Good question!

• Tremors are action-related in veterinary medicine.

• Two classes are: Postural (example is orthostatic tremor, idiopathic head tremors, and hypomyelination) and Kinetic (Intention tremors with cerebellar disease, others)

• Postural tremors happen NOT AT REST. Meaning, the body part isn't supported by the ground/bed/etc. If it is, the tremor stops.

• Further, idiopathic head tremors STOP WITH MOTION. Distract the dog, get it walking, eating, etc, the movement stops.

• Kinetic tremors DO NOT STOP WITH MOTION. They get worse. The classic example is a cat with cerebellar hypoplasia. As they move, the tremor becomes more obvious. This is a kinetic tremor.

So, what causes idiopathic head tremors? We...ahem...don't know. They are classified as a movement disorder but that means it could be from CNS or PNS lesion localization. Movement disorders are a huge box of diseases that are lumped together but may be anything associated with specific movements, or not. There is a really nice, recently published article by Dr. Mark Lowrie that outlines the different types of tremors if you'd like to read more.
(https://bvajournals.onlinelibrary.wiley.com/doi/epdf/10.1002/inpr.3)

How do you differentiate tremors from seizures?

Look for classic evidence of seizures such as autonomic signs, changes in mentation or a lack of stopping when moved, distracted or completely recumbent. Even the head must be recumbent for idiopathic head tremors to stop.

How do you diagnose idiopathic head tremors?

I'm sorry to say that we don't have any diagnostic tests available to make the diagnosis. Also, it is idiopathic, so even if we do brain MRI/CSF all testing is normal. There is a suspected genetic sire in Doberman dogs that idiopathic head tremors can be traced back to, but as of yet there isn't a genetic test available. Stay tuned.

Because we cannot reliably differentiate these from focal seizures AND seizure disorders can be progressive and life-limiting if left unchecked AND some movement disorders do respond to anticonvulsant drugs I always, always, recommend doing a trial of an anticonvulsant medication before simply stating that they are a movement disorder and ignoring them.

One of the tenants of idiopathic head tremors is that they don't respond to anticonvulsant medications but please read this line cautiously. Up to 30% of dogs and cats with seizure disorders do not respond to anticonvulsants (1 or multiple) either so a lack of response to anticonvulsant drugs still does not rule out a seizure disorder.

If the animal has autonomic signs (drooling, lacrimation, urination, defecation, vomiting) concurrent with the movement, they cannot be distracted easily from the movement OR it is present at rest consider this a seizure disorder and keep trying to treat. Or call your local, friendly, mobile neurologist.

DATA COLLECTION

I am looking into the seasonality of head tremors. If you have a case that you have seen with a postural tremor, such as a head tremor, (not cerebellar animals) please consider filling out the short form found online to contribute data to this study. It shouldn't take long to fill out. If you've sent me an email about a tremor, please consider filling out the online questionnaire so I have your permission to include your data. Thank you!!
Link:https://barnesveterinaryservices.com/head-tremor-database
Password: VET2021

I am here to help you, help your patients, live their best lives with neurologic disease. You don't need to be "good" at neurology - that's my job - you just need to be willing to advocate for your patient!

Stay safe. I look forward to working with you soon!

Root Signature Sign: Neurologic Lameness

It's Wednesday morning and your first consult is a limping dog. You nod...you've got this. Upon examination you cannot find any evidence of joint pain, muscle or bone pain. Not deterred, you radiograph shoulder to foot. Nothing of interest is visible.

What if the lameness is neurologic in origin, you ask yourself?

The most common causes of neurologic lameness in dogs are cervical disc herniation and nerve sheath tumors. Most dogs have neurologic deficits along with their lameness so it is worth a close look at the neurologic examination. Deficits could include reflex deficits, postural reaction deficits and/or pain.
Side note: Did you know that lameness from a neurologic cause is called a root signature sign?

Cervical Disc Herniation
Cervical disc herniation with resulting nerve root impingement occurs from type I or type II disc herniation. Many dogs have cervical pain along with the root signature sign, but not all. Cervical radiographs are non-diagnostic for cervical disc herniations and therefore not often recommended. MRI or CT/myelogram are the diagnostic tests of choice with MRI providing greater detail. Treatment may be medical or surgical. My recommendations for medical management vary by pet, but typically include a NSAID, gabapentin and a muscle relaxant. Additional management with opioids can also be included. Best rest is often recommended for the first 3 weeks. Surgical management is recommended for medically resistant dogs, or if the MRI or clinical signs are severe.

Nerve Sheath Tumor
Nerve sheath tumors are typically slow growing, locally invasive (eventually into the spinal canal) tumors. These are best diagnosed with MRI. Definitive treatment is surgical removal. If surgical removal is not pursued, supportive care with pain management (NSAID or prednisone +/- opioid), muscle relaxant and gabapentin are recommended. Acupuncture may provide additional pain relief. The slow growing nature of nerve sheath tumors means that clinical signs may be present for months before the pain or debilitation becomes life limiting.

Not sure if the patient you are seeing has neurologic disease? This is one of the main functions of a traveling neurologist (me!). Sorting between orthopedic and neurologic causes of lameness can be challenging, especially if you're not comfortable doing the neurologic examination. Please reach out, you're not alone! You can find me on email, or schedule directly online using my website.

Okay, now that we got that out of the way, enjoy that Wednesday morning lameness evaluation!

Happy St. Patty's Day everyone. I have two kids that do Irish dancing so we're really missing the festivities this year, but we look forward to celebrating next year.

Stay safe, stay kind, and I look forward to working with you soon!

Paroxysmal Dyskinesia

These words are not uttered by many of us on a regular basis (unless you are studying for boards and talking in your sleep). So, why do you need to know what this is? So that we remember that not all things that twitch have seizures.

Paroxysmal dyskinesia's are one, of a group, of movement disorders characterized by abnormal muscle movements UNRELATED to epileptic discharges. If you take one thing away from this email it is this: movement disorders are not seizures. Not that I suggest you stop reading...

How do I identify a Paroxysmal Dyskinesia (PD)?

This group of movement disorders manifest as sudden cramping in muscles and limbs. It has been identified in several breeds, with increased incidence in Terrier breeds. Notably there is no loss of consciousness, no autonomic signs, and upon recovery from the cramping the dogs return to normal function immediately. These cramping episodes can be triggered with specific activities in some patients (activity or exercise is a common trigger) and may last for minutes to hours. When performed, no EEG abnormalities consistent with epileptic discharges are noted.

What diagnostic testing should I run?

Cramping syndromes may be triggered from metabolic causes as well as genetic causes. A CBC, serum biochemistry and urinalysis are a wonderful way to rule out metabolic causes. If normal, assessment of a video can determine if additional testing for seizure disorder should be pursued.

Are there any treatment options?

Yes! Many movement disorders improve with anticonvulsant drugs such as the benzodiazepine class of drugs. One recent report (reference below) detailed successful treatment of a Welsh Terrier with levetiracetam (20 mg/kg PO q8h) to control signs.

Do you suspect you have a patient with a movement disorder? Please reach out for a consultation - I'm happy to help. I truly love working with you and your staff to help patients live their best lives, with neurologic disease. Keep up the good work!

Stay safe - it's almost spring time and we can make it!

Reference:
Green S, Olby N. Levetiracetam-responsive paroxysmal exertional dyskinesia in a Welsh Terrier. JVIM 2021: https://doi.org/10.1111/jvim.16068

Are we any good at a neurologic exam when pets are vestibular?

How reliable is the neurologic exam for patients with vestibular disease?

We (neurologists) like to think that the neurologic examination is the ultimate-be-all-end-all tool. But in dark corners, we talk about how incredibly hard it can be to do on patients with vestibular disease.
First, there are three parts that we need to consider for the lesion localization, correct?
1) Brainstem
2) Cerebellum
3) Peripheral CN 8
My rule of thumb is this: If the pet has ipsilateral hemiparesis/monoparesis, ipsilateral paw replacement deficits or decreased mentation (obtunded, stupor, coma) it is a brainstem lesion. If the pet has hypermetria, or intention tremors along with the vestibular signs, it is cerebellar in origin. Finally, in absence of those findings the lesion is localized peripherally.

An article out of Europe, dispelled our fears of the neurologic examination failing us and (thankfully) helped us sleep better at night when it was published that the neurologic examination correctly predicted if the vestibular signs were central (brainstem or cerebellum) or peripheral (cranial nerve 8) over 90% of the time.

Interestingly, central disease was more common in this study and, it was localized correctly MORE often than peripheral disease was localized correctly. In other words, dogs with central disease were more likely to be localized on the exam as having central disease compared to dogs with peripheral disease which were occasionally incorrectly localized with central disease.

A few more good reminders:

• Nystagmus are not a localizing sign! (E.g. 8 dogs with peripheral and 5 dogs with central disease had horizontal nystagmus.)

• The onset of disease does not predict it's lesion localization. (E.g. Acute and chronic onset of signs were not statistically different between the central and the peripheral groups.)

• They had a lot of French Bulldogs in the study! Huh..I'm not sure I've noticed an over representation of French Bulldogs in my clinical work. It's good to learn something new everyday.

So, what does that mean for us?

It means if you do a thorough neurologic exam, you'll be correct about 90% of the time when you guide a client towards an MRI and spinal tap (for central disease) or treat for idiopathic or otitis (for peripheral disease). If you're unsure, err on the side of it being a central lesion and recommend a full work up. (Or contact me for a consult!) Oh, and 68% of dogs diagnosed with peripheral vestibular were idiopathic! Idiopathic disease means we have a lot more to learn...so let's get back to it!

(Bongartz U, et al. Vestibular Disease in dogs: association between neurological examination, MRI lesion localization and outcome. JSAP 2019).

My current work days are...well, all of them except Sundays. I'll post on FB or my website if I'm closed on a random day so feel free to check those spots if you're not sure. Otherwise, feel free to call, email or hop online to schedule a telephone, live or video consultation with me. Remember, all live consults are still curbside!

Bromide!!

Bromide tablets received conditional FDA approval this month so I thought this was a good time for us to review Bromide and the do's and don'ts of this drug. 

What should clients (and vets) know about bromide?

Bromide is one of my favorite anticonvulsant drugs for dogs. Seizures happen when there is too much excitability or too little inhibition in the brain therefore neurons fire. Making neurons' less able to "fire" reduces seizures. Below are answers to common client questions about bromide.

How does it work?
This drug makes neurons more negative making it harder to fire a nerve. Less firing = fewer seizures. It does not eliminate seizures, nor does it "cure" an epileptic dog.

Has this drug been shown to be safe in dogs (or cats)?
This medication should ONLY be used for dogs. Cats do not tolerate bromide!

How long does it take to be effective?
Bromide has a long half-life, therefore it takes about 3 months to reach the point of maximal expected efficacy (steady-state). You may notice side effects, and clinical improvement sooner than 3 months however, it won't be fully stable (or fully effective) until at least 3 months. Furthermore, this means that when the dose is adjusted, it won't be fully realized until 3 months after the dose adjustment is made. Key point: Don't give up too soon on this drug. It is slooooowww.

Side note for vets: Please try to take a therapeutic serum concentration at 3 months even if the dog is doing well. This is valuable information should they loose that seizure control in the future.

What side effects are common?
Some pets do not demonstrate any clinical side effects. In those that do,sedation, ataxia, weakness, increased drinking, urinating, appetite and occasionally vomiting can be noted. It is important to understand that bromide and phenobarbital have very similar side effects so if the dog is already on phenobarbital and we're adding bromide, side effects may be additive! Don't blame the bromide! Vets: try reducing the phenobarbital a bit and often side effects will improve. We're adding bromide because we think it may help the dog so don't play with the dose too much (if at all) in the first 3 months.

What other life-style changes do I need to make for my dog?
Bromide must be given every day, at about the same time each day. It isn't as picky as some other anticonvulsant drugs so little adjustments in the administration time is usually okay. Vets: I prefer this medication is given 20 mg/kg PO q12h, but it can also be give as 40 mg/kg PO q24h.
Additionally, this drug will be confused with chloride during excretion through the kidney. This means that your dog must be maintained on a "stable" salt diet. Not restricted, just consistent. In other words, feed the same food, and if you must give "treats" give the same treats, every day. A sudden increase in salt consumption can result in a serious decrease in bromide in the body, resulting in seizures. (Think: 4th of July BBQ when the dog steals a hot dog from the table...)

Incidentally, "bromide" also means: a trite and unoriginal idea or remark, typically intended to soothe or placate. Hmmm, I wonder if I can put this in a sentence in everyday life? :)

For some of you, this was a repeat TidBit Tuesday from November 2019. This is one of those topics I think is worth repeating and I hope you agree.

Stay safe, stay warm and be healthy. I'm available Mon-Sat, if you have a question, or a case that needs evaluation.

Seizures vs Syncope

In honor of Valentine's day this past weekend, I thought we might discuss when the heart tries to act like the brain...known as syncope vs. seizures.

Seizures and syncope are both described as a temporary loss of consciousness. Clinical signs of seizures often include collapse, some form of somatic movement, and a display of autonomic activation (e.g. urination, defecation, salivation, pupillary dilation) but these signs can be subtle in some patients. Clinical signs of syncope may also include collapse with occasional loss of bladder or bowel function. However, the pathophysiology, differential diagnoses, diagnostic testing and treatment plans are markedly different therefore differentiation between seizures and syncope is critical! What are my top 5 ways to differentiate between seizures and syncope?

1. Autonomic signs: Loss of bladder control has been reported with syncope and is a common finding with seizures. Other autonomic changes such as loss of bowel function, salivation, lacrimation and dilation of pupils have not been reported with syncope and are regularly reported with seizure disorders.

2. Post ictal phase: blindness, disorientation and at times, aggression can be seen for minutes to hours following a seizure. Animals with syncope may appear momentarily disoriented but typically they are back to normal within seconds of a return to consciousness.

3. Timing of the event – It is more common for seizures to occur when the pet is at rest, and syncope to occur when the pet is in motion or accelerating. We know this doesn't apply 100% of the time but can be a very helpful to ask what the pet was doing immediately before it collapsed.

4. Evidence of metabolic disease: Evidence of metabolic diseases known to cause seizures such as hypoglycemia, hypocalcemia or hepatic failure concurrently identified in a patient with a history of acute collapsing episodes should lead the clinician to consider a seizure disorder. Without a doubt, patients with metabolic diseases can also have concurrent metabolic derangement however I will use this as a tool when trying to sort between seizures and syncope.

5. Neurologic examination abnormalities. This one is obvious. If the pet has neurologic abnormalities that localize to the prosencephalon (forebrain) it is reasonable to consider this lesion localization over syncope. You could turn this upside down and say that if the pet has evidence of a cardiac arrhythmia or cardiac disease, syncope may be considered more likely. I have seen several patients that have been unfortunate enough to have BOTH syncope and seizures but, thankfully, that is rare.

I hope this helps you differentiate between seizures and syncope. Let me know if you have any other ways to differentiate between seizures and syncope in your practice.

Thanks for reading and stay warm, my friends! Remember, if you're working with a dog or cat with neurologic disease, I'm an email or telephone call away! Better yet, schedule a consult and we can work through the case side-by-side.

Steroid Responsive Meningitis-Arteritis

It's a cold Tuesday morning and your first patient today is a painful, 6 month old Boxer dog. You dutifully run through the differential diagnoses in your head as you walk into the room. What you see when you arrive is a depressed, febrile Boxer puppy trying really hard not to move their head or neck and wincing when doing so.
After examination you find the dog has the following neurologic examination findings:
Mentation: QAR, especially for this normally hyperactive puppy
Cranial nerves: normal
Gait: stiff, stilted gait but no evidence of paresis, ataxia or lameness. (Although lameness and paresis CAN happen with steroid responsive meningitis-arteritis, a.k.a. SRMA)
Postural reactions: normal paw replacement in all four limbs
Reflexes: normal in all four limbs, normal c. trunci and perineal (you did a great job!)
Palpation: Oh how the dog winces with cervical palpation! (Don't do cervical ROM on this dog, okay?)

Neuroanatomic lesion localization: Well...technically the neurologic examination is all normal, right? So all you can say is "cervical pain" on the record. No neuroanatomic lesion localization when they are neurologically normal.

Differential diagnoses: Trauma, fracture, subluxation, muscle strain, infection/polyarthritis, and yes, SRMA.

What is SRMA?

It is an immune mediated disease that affects the vasculature of the meningitis, and sometimes the joints and it typically affects dogs < 2 years of age, with large breed dogs and beagle dogs over represented.

How do you diagnose it?

First, rule out other causes (radiographs, spinal MRI). Next, perform a spinal tap and identify a neutrophilic pleocytosis (often with a SUBSTANCIALLY increased cell count!). Third, rule out infectious diseases that cause meningitis in your area of practice. For most of us in Wisconsin, this is Neospora (toxoplasma if cat), fungi, and bacterial causes.

What is the recommended treatment?

Steroids at 1-2 mg/kg PO q12h, depending on the literature. I start with 1 mg/kg PO q12h for 30 days and then reassess the CSF. Some studies suggest doing this dose, or a slightly tapered dose, for up to 3 months and then reassessing the CSF. When normal, a gradual taper over 3-6 months is common. Relapses can occur in up to 80% of the studies published but my experience has been a much lower recurrence rate.
A recent study by Giraud et al* found a lower relapse rate with the addition of azathioprine. They used 2 mg/kg PO q24h x 1 month and then tapered from there to an every other day dosing interval for 2 months for a total of 3 months of treatment. The authors suggested that the addition of azathioprine allowed them to reduce the prednisone dosage sooner and more rapidly, thus reducing long-term side effects. Over 80% of the dogs in this study were in clinical remission within the 2 year follow-up time without signs of relapse.
Azathioprine was also reported to have exceptionally long survival times when used in combination with steroids to treat meningitis of unknown etiology (MUE), another immune mediated CNS disease. So...perhaps we're on to something here! Interestingly, azathioprine was suspected not to cross the blood brain barrier initially. Hummm...

Key Points:

• SRMA is often treatable, but relapses do occur.

• A CSF tap is needed to confirm the diagnosis however MRI is often performed before CSF to rule out physical/structural abnormalities. This helps to decrease the risk of harm from a spinal tap.

• Steroids are the mainstay of treatment but azathioprine may be added to allow a more rapid reduction of steroids (thus reducing long-term side effects from steroids).

Have a great week and stay safe out there! It's been a snowy few weeks here in Wisconsin so drive safely if you're out and about!