A cat with a tilt

Welcome! Today is a going to be a busy day! First on your case list is a sick cat so let's dive in. Here is the story:
The cat was presented for a 2-month history of a left head tilt. She was noted to have effusion from the left ear when signs started and was treated with amoxicillin (dose unknown) for 14 days. Clinical improvement was initially noted, but signs relapsed after medications were discontinued and now the owner's are noting a head tilt to the right, with wide head swinging movements (think Stevie Wonder) bilaterally, especially when she first wakes up. She is an indoor only cat, with a history of indoor-outdoor lifestyle over 5 years ago.

Physical Examination

General: T: 99.4 °F/37.4 C Pulse: 180 bpm Resp: 20 breaths/min
Wt.: 3.4 kg BCS: 4/9 MM
Eyes: Corneas are clear, no ocular discharge, normal conjunctiva.
Ears: Mild waxy debris noted in both external ear canals.
Oral cavity: Patient did not allow evaluation
Teeth: Did not evaluate.
Lymph nodes: Normal, no peripheral lymphadenopathy noted.
Heart: No murmurs or arrhythmias, pulses strong and synchronous.
Respiratory system: No nasal discharge, no tracheal sensitivity. Lungs clear on auscultation.
Abdomen: Normal, soft, non-painful, no masses or organomegaly noted.
Musculoskeletal: Not evaluated
Skin and hydration: dry flaky hair, no ectoparasites noted

NEUROLOGIC EXAMINATION

Palpation: No paraspinal pain elicited on palpation
Postural reactions: normal tactile placing and hopping all limbs.
Reflexes: Normal.
Gait: Ambulatory with mild vestibular ataxia and falling left.
Cranial nerve abnormalities: Wide head swinging with an occasional right AND left head tilt, positional rotary nystagmus, mild miosis OS, remainder normal.
Mentation: BAR, occasionally hissing

What is the neuronatomic lesion localization for THIS cat?
This cat has evidence of vestibular disease based on the presence of a head tilt and nystagmus. Cranial nerves 8 are affected by loss of function of the peripheral nerve, brainstem or cerebellum. To differentiate between these three localizations, it is important to evaluate the remaining neurologic examination for clues. Animals with brainstem disease will exhibit a loss of function of the upper motor neurons and ascending proprioceptive pathways which is demonstrated as evidence of ipsilateral hemiparesis and reduced ipsilateral proprioceptive testing. Furthermore, reduced level of alertness (obtunded, coma, stupor) may be noted. If paresis, proprioceptive deficits or reduced mentation are noted the lesion is most likely in the brainstem. Cerebellovestibular disease will manifest with signs of vestibular disease plus evidence of hypermetria, intention tremors and/or truncal sway, suggestive of cerebellar disease. Absence of these findings suggests a peripheral CN 8 neuroanatomic lesion localization. This cat does not have evidence of brainstem or cerebellar disease therefore the signs were localized to the peripheral component of CN 8.
Reduced sympathetic innervation to the eye may occur through damage to the sympathetic pathway. This pathway starts in the hypothalamus, courses caudally through the brainstem, cervical spinal cord, and exits the T1-T3 spinal cord segment and travels cranially in the jugular groove to the cranial cervical ganglion. From the cranial cervical ganglion this pathway runs through the middle ear and along the trigeminal nerve to end in the periorbital muscles, 3rd eyelid and dilator muscle of the iris. Dysfunction anywhere along this pathway will result in miosis in dim light. The lesion in this case is likely in the region of the middle ear due to a lack of neurologic disease noted in the intracranial structures, spinal cord, or along CN 5.

You may be tempted to call this a central lesion because the head tilts BOTH directions but don't! Without signs of hemiparesis, proprioceptive placing deficits or mentation changes a central lesion is unlikely.

Differential diagnoses: The history suggests that we now have a bilateral otitis media/interna but you couldn't rule out a polyp or neoplastic process with a secondary infection.

What did we do?
CBC and serum biochemistry were normal. Thoracic radiographs were unremarkable. The brain MRI showed bilateral debris in the bulla with ring enhancement.

Final diagnosis: Bilateral otitis media/interna. A myringotomy was performed, with ear flushing, cultures and cytology. Unfortunately no growth was noted (this is uncommon!) so marbofloxacin was started and clinical signs improved. She had a left head tilt on presentation for 30 day recheck, and this is expected to be permanent. All other signs of vestibular disease had resolved!

Happy first week of Fall everyone! I hope you and your family had a wonderful summer and look forward to working with you as we dig into what I hope will be a lovely Wisconsin fall.

Anisocoria in Dogs and Cats

** Credit for the amazing hand-drawn image goes to my good friend, and veterinarian Dr. Pam Boutilier.
Anisocoria

Anisocoria is defined as pupil asymmetry and may be seen with ocular or neurologic dysfunction. Malfunction of the sympathetic, parasympathetic, or visual system may result in anisocoria.

Neuroanatomy

Visual Pathway
When light enters the eye, it activates the light receptors in the retina. That information then travels along CN II, crosses in the optic chiasm, and terminates in the thalamus. Optic radiations relay the visual information from the thalamus to the visual cortex in the brain. This pathway can be tested using the menace response test and/or cotton ball testing.

Parasympathetic function: Pupil constriction
The parasympathetic pathway to the eye is a short, two neuron pathway which originates in the midbrain. The two, paired parasympathetic nuclei of CN III (PSNCNIII) send fibers along with the somatic nerves from CN III to the eye. The parasympathetic pathway is best assessed using PLR. When a bright light enters the eye, CN II activates and synapses on the PSNCNIII. The parasympathetic fibers transmit this information to the eye, using cranial nerve III as a conduit, resulting in pupillary constriction.

Sympathetic function: Pupil dilation
The opposing system is the sympathetic system, which causes pupillary dilation. The sympathetic pathway is a three neuron pathway and takes a longer course to the eye compared to the parasympathetic system. In general it goes from the thalamus, through the brainstem and cervical spinal cord to exit in the upper thoracic segments. Fibers then make a U turn and head back to the eye via the jugular groove (don't poke around too much when doing those jugular blood draws!), bulla (ear infection can = sympathetic dysfunction) and then hitches a ride with CN V to make the final leg to the eye. Malfunction anywhere along this pathway will result in a failure of iris dilation in a dark room and a comparatively miotic pupil, typically accompanied with enopthalmus and ptosis.

Putting it together

Let's put this new knowledge to work. If you see a case with anisocoria, how do you decide if it is a parasympathetic or sympathetic dysfunction?
1) Assess the pet in a dark room. Does the eye dilate? If yes --> The lesion is NOT due to sympathetic dysfunction.
2) Asses PLR. Does the eye constrict? If yes --> the lesion is NOT due to parasympathetic dysfunction.

To localize to the appropriate location beyond sympathetic or parasympathetic function requires a full neurologic examination. If you aren't comfortable performing or interpreting a neurologic examination please consider a neurology consultation! I am not comfortable doing a dental...we all have our limitations! :)

If you're interested in digging into anisocoria more deeply, or you have a case with anisocoria consider checking out the following article for a full discussion and more amazing images. Note: I do not receive any royalties or financial impact from this article.
* Barnes Heller H, Bentley E. The practitioner's guide to neurologic causes of canine anisocoria. Today's Veterinary Practice Jan/Feb 2016 pg. 77- 83.

Keep those consults coming; we all get to learn a little bit more with each consult. Have a great week!

Neutrophil-Lymphocyte Ratio in MUE

Meningoencephalomyelitis of unknown etiology (MUE) is a challenging antemortem diagnosis. MUE is the term used when we diagnosed inflammatory, non-infectious disease in the CNS. In the old days, we would have called this GME, NME or NLE, depending on the breed. However, those three inflammatory conditions cannot be distinguished on clinical picture, diagnostic testing, or treatment response, alone. Histopathology is needed to determine if a patient has GME, NME, and NLE. Without a brain biopsy, or post mortem sample, we cannot call it GME, NME or NLE. Several years ago, the term MUE started getting tossed around as an antemortem term for inflammatory brain disease, without a biopsy.

To diagnose MUE, a patient must have:
1) a neurologic examination with deficits identified (or a history of seizures) and
2) have a MRI with classical changes and
3) and CSF tap with a lymphocytic or monocytic pleocytosis and/or elevated protein level and
4) negative geographically specific infectious disease panel. If the pet meets these criteria, they can be diagnosed with MUE. 

MUE does not show up in routine blood work. Inflammatory leukograms are rare, elevated body temperature is not typically reported and pets are not systemically, clinically ill. However, some immune mediated diseases (such as MS) have garnered attention for a neutrophil to lymphocyte ratio present on routine CBC. 

A recent study out of Korea evaluated the ratio of neutrophils to lymphocytes in a standard CBC to see if we could predict a diagnosis of MUE. As it turns out, you can divide the neutrophil count by the lymphocyte count, and get a significantly higher number in dogs with MUE than healthy dogs. Furthermore, the ratio was significantly higher than dogs with idiopathic epilepsy but NOT different than dogs with brain tumors. The neutrophil-lymphocyte ratio was higher in dogs with MUE than all other forebrain diseases (hydrocephalus, idiopathic epilepsy, and brain tumors) but not always significantly so. 

What does this mean for us?

Unfortunately, nothing...yet. This is an interesting concept and a step towards a much needed tool for diagnosing MUE without invasive diagnostic testing. Performing a CBC, and calculating the ratio, is both simple and readily available in most (all?) veterinary practices today. However, if the ratio is high, it does not mean the pet has MUE. It may support a diagnosis of forebrain disease (which you already know from your neuro exam) and may support structural brain disease (i.e. not idiopathic epilepsy). Very importantly - this study did not find a significant difference between dogs with brain tumors and those with MUE. Sadly, brain tumors and MUE are often our top differentials for pets with forebrain disease so this ratio does not (yet) give us another non-invasive tool to differentiate between these two diseases. 
I enjoyed reading this study and learning about inflammatory markers for humans with MS (the human counterpart to MUE) and how this neutrophil-lymphocyte ratio could be used in the future for pets. If you'd like to read more, please see the link at the bottom of the page. 

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

If you haven't heard yet, please note that I am moving my office. Please try to remit any outstanding invoices by August 30th. If you need my new invoicing address please email me, or watch for a note in the mail. 

Reference: https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.16512

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. 

I hope you're doing well and look forward to working with you soon! 

 Reference for article discussed above: 0.1111/jvim.16504

Walk This Way: Describing Ataxia and Paresis in the Clinical Patient

Perhaps you’ve wondered what the difference is between ataxia and paresis? Perhaps you already know, in which case you can grab that cup of coffee and move on to your next email!

Still with me? Okay, here we go. Ataxia is the failure of coordination. This suggests a sensory abnormality and when noted, it is a hallmark for neurologic disease. As you’ll see in the next section, paresis can be noted with neurologic, orthopedic, neuromuscular or muscular conditions, making it much less specific. Ataxia, however, is a failure of neurologic sensory information which means it can only be noted with dysfunction of the neurologic system. There are three forms of ataxia: 1) proprioceptive, 2) vestibular and 3) cerebellar.

• Proprioceptive ataxia is an indication of a spinal cord, brainstem or forebrain disease. Ataxia is not noted with neuromuscular disease.  Signs of proprioceptive ataxia include a crossing of the limbs when walking down a straight pathway, or placing the limbs narrow and wide of the midline of the body without regularity.

• Vestibular ataxia indicates dysfunction of the vestibular apparatus.  When observing a patient with vestibular ataxia, the observer can appreciate a falling or drifting towards one side when walking. This can be especially magnified when the patient is turned in a circle. 

• Cerebellar ataxia occurs with disease or injury to the cerebellum. Signs of hypermetria, truncal sway, and a wide based stance with, or without intention tremor are indications of cerebellar ataxia.

Paresis, on the other hand, is a weak movement or incomplete paralysis. This involves most commonly UMN or LMN, but remember the neuromuscular junction, muscle and bones or joints can be a source of paresis also. A patient with mild paresis will exhibit a reduced joint range of motion when walking giving the appearance of shuffling. Severe paresis may be more profound so that an animal is unable to support weight even with purposeful limb movements.
Common terminology when describing paresis:

• Mono: one limb (any)

• Para: pelvic limbs (both)

• Tetra: four limbs

How can you write the gait abnormality in the record?

• If the pet has only a proprioceptive ataxia: Pet is exhibiting crossing of pelvic limbs, consistent with proprioceptive ataxia.

• If the pet has proprioceptive ataxia AND paresis: Pet shows crossing of pelvic limbs and reduced joint ROM (or weakness /unable to rise/collapsing frequently) consistent with proprioceptive ataxia and paraparesis.

• If the pet is non-ambulatory in the pelvic limbs (cannot walk without support): non-ambulatory paraparesis*

• If the pet does not have any observable motor, even with support, in the pelvic limbs: paraplegia. *

*Comments about ataxia cannot be made once the pet is non-ambulatory or plegic.
 

Hopefully this helps clarify when to use paresis and ataxia when describing the gait. Enjoy your week and stay safe!

Book Announcement!

Small Animal Neuroanatomic Lesion Localization Practice Book

Over the last 18 months I have been collaborating with many amazing neurologists across the globe to write a first ever Neuroanatomic Lesion Localization Practice Book and.... IT'S ALMOST HERE!

I received confirmation recently that they expect to have this baby in the warehouse by November 2022! Self promotion is hard, so hopefully the book will speak for itself.

If you feel the need to brush up on your lesion localization technique, or are entering an internship or residency soon and want to get a jump on the neuroanatomic lesion localization game, or maybe you know a soon-to-be veterinary student that might benefit from this little ditty - you're in luck! Here is the link if you wish to check it out. (http://www.cabidigitallibrary.org/doi/) The book is titled: Small Animal Neuroanatomic Lesion Localization Practice Book. Let me know if you have any questions!

And now...back to the grind. :)

Thanks for reading! I hope you have a good week and stay cool out there in this heat.

Intervertebral Disc Herniation in Cats

Intervertebral disc herniation (IVDH) does occur in cats but is reported at a much lower prevalence than dogs. Is this because the disease is less prevalent or because owners are less likely to pursue advanced diagnostic imaging to obtain a diagnosis? I don't know the answer, however a recently published article reported on 35 cases of feline TL IVDH over 21 years. That sounds like a lot fewer cases than we see for dogs!

Clinical Presentation

Like dogs, the most common presenting complaint is difficulty walking and/or pain. In this study, They found 2 cats had grade I, 20 cats were grade II, 7 cats were grade III, 3 cats were grade IV and 3 cats were grade V on presentation. (Grading scale listed at the bottom). There was no significant difference between outcome at discharge or follow up and initial presenting grade. Does that mean that we shouldn't rush to get cat's seen, imaged, and cut? Probably not. Of the 3 grade V cats (the ones that we would consider a surgical emergency), one improved, one was static and the other was lost to follow-up. What was the timeline for surgery? Unknown. Dogs have a 50% chance of improvement if they are grade V and undergo surgery within 24 hours. This is debated amongst neurosurgeons but as a general rule I subscribe to the plan of cut ASAP whenever possible if deep pain is absent.

Location of the Offending Disc

In the referenced study, thoracolumbar disc herniation was most common at L6-7. This is slightly different from the previous reports in which L7-S1 was reported to be most common, but not far off. I think it is safe to say that cats are more likely to have low lumbar disc herniation than T11-L2 disc herniation, like dogs. Why? Cats are SO MUCH more flexible than most dogs (especially the chondrodystrophic type) that the vertebral dynamics are different as well. Previous reports suggest obesity is more common in cats with IVDH (and in my experience, too) but this cannot be the entire answer. It remains to be seen, why cats are more likely to have a low lumbar disc herniation than TL. When someone knows...I'll tell you!

Key Points:

• Intervertebral disc herniation does occur in cats

• The most common presenting sign is weakness or lumbar pain

• Surgery can be done and SHOULD be done (when appropriate for the patient)

If you have a cat patient with lumbar or lumbosacral pain, reach out. I'd love to see them! Schedule a consult using my online scheduler (for veterinary use only) and let's get your patients feeling better, soon!

Grading scale:
Grade I: normal gait with hyperpathia
Grade II: ambulatory paraparesis
Grade III: non-ambulatory paraparesis
Grade IV: paraplegia with intact nociception
Grade V: paraplegia with absent nociception

Reference: https://journals.sagepub.com/doi/pdf/10.1177/1098612X211028031

Midazolam vs. Diazepam for At-home Care

History of Cluster Buster Protocols

In 1995 Dr. Michael Podell championed the idea of at-home, rectal diazepam use for canine cluster seizures. In that study, dogs that received rectal diazepam had fewer cluster seizures compared to those that didn't receive the drug. Since then, at home cluster care has become standard practice for many veterinarians.
According to human literature, benzodiazepine drugs (midazolam, diazepam and lorazepam) are the "best" first line anticonvulsant drugs to stop status epilepticus. As is typical, we simply adopted this idea in veterinary medicine without data to support it's use. But...the benzodiazepine drugs do show improved seizure cessation so...they probably help our canine patients in some manner.

Which Benzodiazepine is Better?

Here is where the science gets a bit muddy. We've compared rectal diazepam to intranasal midazolam and intranasal midazolam was superior. We've compared intranasal midazolam to intravenous midazolam and intranasal midazolam stopped seizures faster. However, all of these studies involved few animals and ethically we cannot have a group of untreated animals to determine true efficacy. So, which is better? They all work, but intranasal is perhaps faster and easier than other non-intravenous routes when IV access is restricted.

What are the current recommendations?

At this time, intranasal midazolam at a dose of 0.2 mg/kg up to 3 times in 24 hours is my recommendation for dogs with a cluster or status epilepticus history. Do your best to use a nasal atomizer because this has been shown to be the superior technique compared to nasal-drop application. (I have found them at Midwest Vet:https://www.midwestvetsupply.com/products and also carry them in my car. Ask, when I'm at your clinic, if you need one!).

Nasal drop vs. Atomizer?

The nasal drop technique requires the client to drip the midazolam intranasal slowly during the active seizure while also avoiding getting bitten. The atomizer looks like a conical shaped marshmallow that is attached to the end of the syringe and the client is then able to press the atomizer against the nare and dispense the dose in one "push". Not clear on this technique? Please ask me, I am happy to clarify! I do not have a financial incentive or disclosure for this product, or Midwest Vet Supply. :)

I hope you're enjoying summer and all it has to offer! I am at the Dane County 4-H Fair cheering on my kids so my hours are a bit limited. Please reach out if you need me and cannot find a suitable consult time online. Have a great week!

Zonisamide Induced Blood Dyscrasia in Dogs

Really, zonisamide? You couldn't just let this one slide? Phenobarbital already has dibs on blood dyscrasias and I'm struggling to like you as it is. Why did you go and have to do THIS to dogs, too??

If you've been a TidBit Tuesday reader for awhile you'll know I struggle to love zonisamide. Yes, it has it's place in movement disorder management. Yes, it can be a wonderful anticonvulsant. in some dogs. But in my hands, in my experience, it either hasn't worked well or I've seen undesirable side effects that I've attributed to zonisamide. And it is a Sulfa antibiotic. So, there's that worry, too.

New this week, we can read about 4 dogs with blood dyscrasias likely secondary to zonisamide administration.

Dog 1: 7 year old Shih Tzu. Presented for vomiting, lethargy and fever. He had received Zonisamide (ZNS) for 400 days at a dose of 5 mg/kg q12h. Severe leukopenia with neutropenia, monocytopenia and lymphopenia were noted along with an elevated ALP, ALT, hypocalcemia, hypochloremia, hyponatremia, and hyperbilirubinemia. ZNS was discontinued and antimicrobials were started. 19 days later, the leukopenia was resolved.

Dog 2: 1 year old Siberian Husky. Presented for a history of groaning, and appearing tense. He had received ZNS for 29 days at a dose of 17 mg/kg q12h. On presentation the dog was also febrile, had a leukopenia with neutropenia, and increased ALP and hypoalbuminemia. Zonisamide was discontinued and the leukopenia persisted through 40 days. On day 180 from discontinuation, the WBC was within the reference range.

Dog 3: 9 yr old Miniature Poodle. She presented for lethargy, anorexia, labored breathing and reluctance to walk. She had received zonisamide for 20 days at a dose of 8.5 mg/kg q12h. No fever was noted on presentation however overnight a fever developed. Severe leukopenia with neutropenia was documented after the zonisamide was discontinued (within 24 hours, I think) along with increased ALP activity and hyponatremia. Leukopenia and neutropenia resolved by day 6.

Dog 4: 5 year old Miniature Poodle. He presented for vomiting, lethargy and anorexia as well as fever. ZNS was started 1,196 days prior to presentation at a dose of 8.4 mg/kg q12h. Again, CBC showed a leukocytosis with neutropenia and mild thrombocytopenia. Serum biochemistry showed increased ALP, hyponatremia, hypokalemia, hypochloremia and hypercholesterolemia. Zonisamide was discontinued and leukopenia improved within 2 days, and normal by day 3.

The authors attributed the blood dyscrasia to an idiosyncratic drug reaction. Idiosyncratic, of course, means that it is unpredictable in scope and severity and not reliably related to dose. Other idiosyncratic reactions to ZNS include hepatopathies, skin eruptions and rental tubular acidosis. Perhaps all of these reactions are because this is a sulfonamide derived anticonvulsant? Discontinuing the drug is the best way to try to reverse the blood dyscrasia. I found it interesting that in one of the cases they continued phenobarbital (a drug also known to have a risk of idiosyncratic blood dyscrasia) and the bone marrow was still able to regenerate.

Key point: If you find an abnormal CBC for a pet receiving ZNS, please consider an idiosyncratic blood dyscrasia and discontinue the drug (safely).

Reference: https://doi.org/10.1111/vec.13222

Have a great week and thanks for reading!

Abrupt Benzodiazepine Withdrawal in Dogs

Abrupt withdrawal of benzodiazepine drugs can result in withdrawal seizures. A recent report describes withdrawal seizures in 3 young dogs and I thought we could take this opportunity to review this concept.

What is a benzodiazepine drug?

Benzodiazepine class drugs commonly include diazepam, midazolam and lorazepam. These drugs are GABA agonists in the CNS which results in suppression of activity. GABA activation causes inhibition in the forebrain, cerebellum, and in other parts. So, if you activate an inhibitor, you will suppress activity. Got it?

How long is too long?

Abrupt withdrawal resulting in seizures and other signs of CNS overstimulation can occur after constant rate infusion (CRI) use, or chronic oral use. Use of a benzodiazepine drug as a CRI for more than 12 hours usually warrants tapering. The three dogs in the recent report received one of these drugs for 39, 64, and 48 hours, respectively. After abrupt withdrawal of the drugs they experienced ataxia and seizures within 4- 48 hours. A return of the benzodiazepine CRI at a low dose, followed by a 12-24 hour taper, resulted in a successful wean from the medication and no additional neurologic events. All three of these dogs were also undergoing mechanical ventilation, and received other medications, so there is always the questions about a direct link between the benzodiazepine withdrawal and the seizures, however the authors suggest this link follows an expected pattern with abrupt withdrawal in humans and in animals. I agree.

As a general rule of thumb (based on human literature), if I prescribe a benzodiazepine drug for oral use longer than 7 days I taper the medication. Abrupt withdrawal is sometimes called "Jim jams" which, honestly, is a pretty fantastic term but probably not a fantastic feeling. Withdrawal ataxia, cerebellar signs and seizures can be seen from abrupt discontinuation of a benzodiazepine drug.

How do I taper to avoid withdrawal seizures?

CRI:

• Typical dosing range is 0.1-0.5 mg/kg/hr. I reduce the dose by 50% every 12 hours until the pet would be receiving less than 0.1 mg/kg/hr. For example, if we are at 0.25 mg/kg/hr and wish to taper I would start with a reduction to 0.12 mg/kg/hr x 12 hours, then stop, because the dose would then be less than 0.1 mg/kg/hr.

Oral dosing

• Typical dosing is 0.25-0.5 mg/kg PO q8-12hours. If the dog receives the drug for more than 7 days, I would recommend a 50% taper for 3-5 days, followed by another 50% reduction for another 3-5 days and the stop. Cats are at risk of acute hepatic necrosis with oral diazepam administration so I rarely use this medication. However, if you find yourself treating a cat on chronic benzodiazepine drugs, a similar taper can be employed.

Thanks for reading and enjoy your summer! 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.

https://onlinelibrary.wiley.com/doi/epdf/10.1111/vec.13221

Syncope Vs Seizures

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 cool, 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. 

Early detection of Pug Encephalitis

Pug encephalitis, termed necrotizing meningoencephalitis (NME), is a common cause of CNS inflammation in Pug, Maltese, Chihuahua, Shih Tzu and other small breed dogs. The typical presentation is a dog less than 4 years old with acute, progressive, multifocal CNS signs. (However, meningoencephalitis is the great pretender so it may present in ANY age, breed, sex, and with neurologic examination findings!) Many Pugs are reported to be resistant to immune suppression, however this is not a global truth. On histopathology, areas of necrosis are identified, along with infiltration of inflammatory cells which leads to the term necrotizing meningoencephalitis. Antemortem, a diagnosis cannot be rendered. MRI and CSF changes would lead a practitioner to a diagnosis of meningoencephalitis but without histopathology (biopsy or necropsy) the dog would be diagnosed with meningoencephalitis of unknown etiology (MUE). MUE includes the necrotizing meningoencephalitis and granulomatous meningoencpehalitis thus it is not a histopathologic diagnosis but a clinical one.

What if we could detect NME earlier?

Researchers recently published a study with this question in mind. They evaluated 36 pug dogs that were deemed clinical normally by their owners. Genetic studies were performed; 5 homozygous/high risk, 19 heterozygous/medium risk and 12 low genetic risk (previously published data about genetic link) dogs were included. They then performed 2, sequential neurologic examinations on these dogs at least 4-6 weeks apart. Dogs that were considered repeatably abnormal subsequently underwent MRI (spine, brain, or both) and had a CSF analysis performed.

Results of the study

Dogs considered low risk had 0 repeatable abnormalities on neurologic examination. Eight of the 36 "at risk" pugs had repeatable abnormalities. Abnormalities included back pain, menace deficits, ataxia and paw replacement deficits (1 or more). The only statistically significant finding was multifocal spinal pain. The 8 dogs underwent imaging and mild brain abnormalities were noted in all dogs with variable severity. CSF changes were noted in 3 of the 8 dogs.

What is the actionable result of this study?

The take away here is that the MRI was more sensitive to detecting "pre clinical" NME than CSF analysis. Is this actually "pre clinical" if the dogs had repeatable neurologic examination abnormalities? I argue perhaps not, perhaps they were "undetected" by clients rather than preclinical. That said, we don't subject dogs to annual neurologic exams without reason so perhaps this is a reasonable way to conduct the study. (Maybe we should??) I always ask myself: what I would do with the information gained when I suggest a test or procedure? In this case, would I treat this dog with "pre clinical" MRI changes or would we wait to see if this develops into progressive disease? I don't know the answer to this question and they didn't pursue treatment in this study so I don't have an objective answer for you. For me, these types of studies will help us help dogs considered genetic "at risk" for NME. Perhaps we identify treatment earlier? Perhaps we find out that there is a specific environmental trigger? Perhaps you learned that there is a genetic "risk" for pugs. Have a pug patient or pet that you think should be genetic tested? Here is the link: http://www.vgl.ucdavis.edu/services/dog.php

The big question is - at risk does NOT equate to disease - so what do we do with the information??

Thanks for reading today. I really enjoyed reading this study and hope you enjoyed my summary.

Have a great week and keep those consults rolling. My kids will be in and out of different camps this summer so my schedule will be changing week-by-week. As always, please reach out if you cannot find a suitable time for your patient using the online scheduler and I will do my best to find timely spot!

How to handle a jerk

Have you evaluated an elderly patient with a history of sudden, unprovoked jerk movements lasting several seconds and not been sure what to make of it? It's easy to disregard this information because it doesn't fit into one category but perhaps, we shouldn't.

Myoclonic "jerks" can occur as a part of an epileptic syndrome (myoclonic epilepsy) or as a separate movement disorder. As a movement disorder, they may arise from neuromuscular, spinal, cortical or subcortical origin and therefore may have many different etiology. A report in Cavalier King Charles Spaniels came out recently (https://doi.org/10.1111/jvim.16404) which detailed myoclonic jerks in older CKCS. This study was not conclusive about the origin of the jerk, but suggested a cortical or subcortical origin. Several of the dogs in this group had idiopathic epilepsy, diagnosed with MRI/CSF/blood work prior to the onset of the myoclonic jerk so it is possible this is simply a manifestation of their epileptic syndrome. However, several of the dogs were on treatment with primary anticonvulsant drugs (imepitoin and phenobarbital) and the seizures improved but the myoclonic jerk worsened! This suggests a more likely non-epileptic origin. This study was SMALL so it is much too early to draw conclusions about the cause but it does provoke thought.

Here is what I took away:

1. Older adult or geriatric onset myoclonic jerks may be seizure, or non-seizure in origin
2. Phenobarbital (and imepitoin) didn't help
3. Levetiracetam helped in 3 or 6 cases. This could mean it is epileptic or non-epileptic in origin, remember!
4. If non-epileptic in origin, myoclonic jerks do not warrant treatment as they are unlikely to result in progressive neurologic disease (but knowing if they are non-epileptic is difficult)
5. Myoclonic jerks are seen as rapid movements of the face, head or thoracic limbs that are several seconds in duration and do not have a pre or post ictal period associated with the signs. Not sure what I'm talking about? Follow the link to the article and scroll to the supplementary material. There are two videos attached to help you visualize what is being noted.

So what do I do?
1. If the neurologic examination is ABnormal - suggest diagnostic imaging of the brain or spinal cord to determine if pathology is present to account for the jerk motion.
2. If the neurologic examination is normal, consider non-epileptic jerks and either start levetiracetam or monitor if infrequent.

Thanks for reading and have a great week! Stay cool out there and watch out for jerks!

Flaccid Paralysis: Diagnosis and Treatment

Last week we discussed a case of flaccid paralysis that was localized to the neuromuscular system, specifically either neuromuscular junction or peripheral nerve. This week, we'll talk briefly about pursuit of diagnostic testing and treatment for these cases.

Diagnostic Testing
This group of diseases is a diagnostic challenge. In academic, or specialty clinics, electrodiagnostic testing may be recommended to look for hallmark changes amongst these group of diseases. Aside from not being readily available, electrodiagnostic testing is also imprecise when attempting to differentiate between this group of diseases. So what do we do? We attempt to differentiate based on history and physical exam findings. For example, animals with polyradiculoneuritis (Coonhound paralysis) are often hyperesthetic with normal bladder function and may, or may not have a history of contact with wildlife (Racoon). By contrast, those with botulism often have urinary retention, reduced mentation and mydriasis. Dogs with tick paralysis rarely have cranial nerve deficits and may have the mildest signs of the group. Coral snake bite results in rapid death (and is only found in the southern states). Organophosphate toxicity is frequently discovered when reviewing the history. Signs of SLUD (see below) or a history of exposure to organophosphate containing products can help guide this diagnosis. Blood cholinesterase levels can be measured (I've never done it) but they aren't reliable once the neurologic signs are apparent.

Treatment Options
Clinical suspicion can only get us so far. At some point we start treatment for the most likely cause. I will often recommend application of a tick product (example: frontline), even if a "tick check" is negative for the patient. Tick paralysis typically begins to improve within 24 hours after application of the product, further increasing your suspicion of the cause.

Polyradiculoneuropathy can progress to respiratory failure so referral for ventilator support is critical for dogs exhibiting reduced cutaneous trunci reflexes. Evaluation of CO2 levels can help you detect if the animal is not ventilating appropriately. No specific treatment is available for polyradiculoneuropathy. Supportive care with assistance to eat, drink and nursing care to maintain cleanliness are critical during the recovery period. These animals can void voluntarily, however they cannot move away from soiled bedding therefore bedsores are a high risk for this patient population. Physical rehabilitation is helpful for recovery so please get these dogs to PT as soon as you can! Recovery may take 4 to 6 months in dogs with severe disease, or 1-3 months in dogs with mild cases.

Botulism is diagnosed with detection of the toxin in serum, feces or gastric contents. This is extremely hard to do, and rarely is a confirmed diagnosis made. Supportive care with fluid support, urinary bladder catheterization, and management of secondary infections may help reduce the risk of death however Botulism is commonly fatal. An older report (Bruchim Y, The Vet Record 2006) describes the rare successful treatment of a mixed breed dog with botulism utilizing supportive care measures.

My experience with coral snake envenomation is limited to only a few cases during my residency at the University of Florida. Each case had a fatal outcome so I don't have a lot of treatment recommendations or supportive care ideas. If you live in the southern US - reach out to your local neurologist for additional help if you encounter a case.

Organophosphate toxicity results in paralysis from blockade of the acetylcholinesterase in the body, thus causing prolonged exposure to AcH at the receptor. This results in acute SLUD (salivation, lacrimation, urination, and defecation) followed by muscle weakness. No specific treatment is available. Atropine does not help once the SLUD has passed and the dog has progressed into the neuromuscular weakness signs. Supportive care, again, is the way to go. This may include ventilator support, along with nursing care and nutritional support. Signs may improve within 7 days after onset, but death is common. (Hopper, K, et al. JVECC 2002)

Whew! These cases are tough! Sometimes we "treat for the treatable" causes because that is all we can do. Keep up the good work and thanks for including me in your case management. I love working with you on the "easy" and the "hard" stuff!

Flaccid Paralysis in the Midwest

It's Tuesday afternoon and you have an emergency case coming that is reported to be unable to walk. Your staff tells you that you will be seeing a 5 year old Labrador that was found unable to walk in the back legs today. You square your shoulders and remind yourself of the common neuroanatomic lesion localizations for the spinal cord, and enter the room. After performing a thorough neurologic exam (self high five!) you conclude the following findings:

Mentation: BAR
Cranial nerves: reduced blink reflex bilaterally with normal corneal reflex, menace response, PLR, physiologic nystagmus and gag reflex.
Gait: Non-ambulatory tetraparesis
Reflexes: absent withdrawal reflex in both pelvic limbs, absent patellar reflexes bilaterally, absent panniculus reflex bilaterally, and reduced withdrawal reflexes more right thoracic limb than left, but both affected.
Postural reactions: When supported, paw replacement is absent in all four limbs
Palpation: non-painful, normal cervical range of motion

You make a hasty exit from the room and search for the number to your closest neurologist. Just kidding! You take a deep breath and realize that due to the multiple reduced reflexes in multiple limbs and cranial nerves, this must be neuromuscular, not spinal and not brain. Great job! What does neuromuscular actually mean?

Neuromuscular Neuroanatomic Lesion Localization:
Neuropathy - reflexes are reduced to absent, paresis without ataxia.
Junctionopathy - reflexes are typically absent however Myasthenia gravis is a junctionopathy and reflexes can be normal for this disease. Again, paresis or plegia without ataxia.
Myopathy - reflexes are normal, dogs are just paretic and are not ataxia

This dog could be a neuropathy or a junctionopathy.

What are my top 5 differentials for a dog with acute, progressive, junctionopathy?
1. Tick paralysis
2. Polyradiculoneuritis (Coonhound paralysis)
3. Botulism
4. Coral snake envenomation (not common in the Midwest)
5. Organophosphate/carbamate intoxication

Stay tuned for next week's TidBit Tuesday to discuss how we might diagnose and manage these unique cases!

Thanks for reading - have a great week and stay safe.

Neuroanatomic Lesion Localization for Busy Vets

Here is the case: A 5 year old cat that cannot blink one eye. What cranial nerve is affected?
To answer this question, of course you must do a cranial nerve exam. At its most basic level, it is a process of elimination. If you touch the medial and lateral canthus and the cat does not blink what cranial nerves are you testing? (CN 5 and CN 7)

How can you isolate these two nerves from each other to see which is the affected nerve? If you do corneal reflex you're testing CN 5 (sensory) and 6 (motor). Voila! So, if the cat does not blink when you touch the medial or lateral canthus, but DOES retract the globe when you do corneal reflex which nerve is affected? Think you know... scroll (or read!) to the bottom to see the answer. 

Need a little refresher on the cranial nerves and their jobs? The table below has all nerves, and their main jobs, for quick easy reference. 

Cranial nerveFunctionNeurologic examination CN I: OlfactorySmellWatch the dog sniff, ask about eating habits. * Difficult to objectively evaluateCN II: OpticSightMenace, PLR, Cotton ball test, trackingCN III: OculomotorSomatic: eye movement.
Innervates all extraocular muscles except lateral rectus and dorsal obliqueAutonomic: Parasympathetic function to the pupilPhysiologic nystagmus (medial movement), Strabismus (if present this indicates an abnormalities of CN)
 
PLRCN IV: TrochlearEye positionStrabismusCN V: Trigeminal

• Ophthalmic

• Maxillary

• Mandibular

Sensory to the face, cornea
 
Close the jaw (muscles of mastication)Sensory: Corneal reflex, blink reflex, sensory assessment of the nares and lips
Motor: ability to CLOSE the jawCN VI: AbducentSomatic eye movementPhysiologic nystagmus (lateral movement), StrabismusCN VII: FacialSomatic: muscles of facial expression
Autonomic: parasympathetic innervation to the lacrimal gland, 3rd eyelid gland, palatine and nasal glands, taste rostral tongueMenace, blink reflex, lip and ear twitchCN VIII: vestibulocochlearSensory: balance and hearing
Innervates: vestibulospinal tracts, MLF (eye movement), reticular formation, cerebrum and cerebellumPhysiologic nystagmus, pathologic nystagmus,  positional strabismus, head position (tilt), ataxia, hearing test (BAER)CN IX: GlossopharyngealSensory to pharynx
Motor to pharynx
Autonomic: parasympathetic function – taste from the caudal tongueGag reflexCN X: VagusMotor to pharynx
Parasympathetic: taste to pharynx, larynx, heart rate, GI motility, otherGag reflex
CN XI: Spinal accessoryMotor: trapezius, sternocephalicus, brachiocephalicusPalpation of associated musclesCN XII: HypoglossalMotor: tongueMove tongue left and right, visually assess for symmetry and movement.

Answer: Cranial nerve 7 is affected. (5 is normal in corneal reflex therefore it is not the problem in the blink reflex either.)

Thanks for reading and have a great week!

 Do you have a case that is puzzling you? Please reach out - I'd love to help. Did you know I also do onsite or virtual private CE for hospitals? Reach out for more details, if you're interested.

Client Communication Surrounding Seizure Management

Client Communication Surrounding Seizure Management

Client communication is critical during the initial seizure consultation. Many clients arrive in my exam rooms with one or more of the following expectations:

• Their pet will not have any more seizures (this is a common one)

• Medications should not have side effects (yes, this is often requested)

• Inexpensive medication 

• Easy to administer, once to maybe twice daily medication (this is key for cat owners)

These goals do not align with our expectations, do they? Here are my goals:

Seizures will likely continue, if they've had 2 or more already.
Realistically, everybody gets 1 free seizure in their life. If you've had 2, or more, we probably should see your dog or cat and have a chat. If we place the pet on anticonvulsant drugs (ACD), our goal is to have 1 seizure or less every 3 months. That is a reasonable goal. The other option is to have a 50% reduction in seizure activity. This means that we need to know the interval of the seizures before treatment, and then calculate what a 50% reduction looks like for that individual. I am a goal oriented person and most clients also respond favorable to setting appropriate goals. This allow us to feel a sense of success when we achieve them, and a reason to continue to modify treatment if we don't. 

Side effects WILL happen.
Any ACD has side effects, our goal is to have tolerable side effects for that family and pet. Tolerable may mean that they are okay with PU/PD, or it may mean that a level of sedation is acceptable. Each family is unique so this approach is tailored directly to the family I am working with. I am diligent outlining known side effects of the drugs at the time they are prescribed. Be sure to tell the client that many side effects improve or resolve by the time the pet reaches steady-state. This means we can set goals for resolution of signs, too. If the time to steady-state is 14 days (phenobarbital) then give clients that information so that when they see side effects (they will) they know to hang in there for 14 days and it is likely to get better. If it isn't,  we can adjust after evaluating the serum drug concentration at steady-state (when applicable for the drug prescribed).

Cost
The cost of ACD varies over time. Phenobarbital when through a period where it was difficult to obtain and was, therefore, very expensive compared to previous and subsequent years. The fluctuation in cost is really due to production, availability and (as with all things right now), shipping costs. It can be helpful to outline the cost of the drug up front, but ensure that the client knows this can change over time depending on the aforementioned causes. 

Administration is key!
If an owner cannot administer the medication, it doesn't matter how effective it SHOULD be because the pet isn't taking it. This concept is especially near and dear to cat owner's. In human medicine, when a prescription was recommended 1x daily, the compliance was over 80% (the drug was given as prescribed over 80% of the time). However, when the prescription was recommended at a 3-4x daily dosing, the compliance dropped as low as 10-15% in some studies. This becomes especially true in the pediatric world, in which an individual is having something given TO them. I think it is reasonable to translate this to our veterinary world and realize that three times a day levetiracetam, even if the perfect drug for other reasons, may not be a good option for some clients simply because compliance will be low. It has been well established in neurology that the variation between peak and trough can be just as important as one serum concentration at one time point. If there is a wide swing between peak and trough, there may be a greater chance of breakthrough seizures or poor control. Missed doses can result in wide swings of the peak and trough serum concentrations and therefore should be avoided. 

So there you have it! I hope this pep talk has been helpful for you as you help clients navigate the (at times) choppy water of seizure management. If you need help with a seizure case, or feel the client would benefit from a second opinion, please reach out. Seizure management is one of my favorite aspects of neurology!

Have a great week and keep those consults coming!

Hemophilia A and Spinal Hyperpathia?

An interesting case series was published this month in Frontiers in Veterinary Science (see reference below) detailing three dogs with hemophilia A and neurologic disease. I thought we might keep with our vascular discussion this week and chat about this article. Enjoy!

Signalment and Presenting Signs
Three young, male, dogs (4 months, 11 months and 5.5 months of age) were evaluated for signs ranging from spinal hyperpathia alone, to ambulatory paraparesis and proprioceptive ataxia in the pelvic limbs to non-ambulatory tetraparesis and cervical pain. All three dogs had spinal MRI which showed changes consistent with hemorrhage. One dog underwent decompressive surgery at which point a hematoma was confirmed.
Diagnosis
Hemophilia A is an X-linked coagulation disorder that occurs due to genetic mutation and resulting abnormal function of factor VIII.  All three dogs had prolonged aPTT, and normal PT testing. Reminder: aPTT requires functional I, II, V, VIII, IX, X, XI and XII factors so it isn't highly specific when prolonged. PTT evaluates I, II, V, VII, and X. Additionally, genetic testing is now available that can measure the quantity of VIII (more like a percentage of normal) and all three dogs had reduced levels of VIII, supporting the final diagnosis of Hemophilia A in these cases.
Outcome
Two dogs underwent CSF analysis during the diagnostic process, which resulted in hematoma formation and ultimately the demise of one of the dogs. The other dog recovered, was noted to have intermittent cutaneous hemorrhage over the next 5 months at which time it sustained gastrointestinal hemorrhage which was suspected to be secondary to a foreign body and the dog was euthanized. The third dog under went surgical decompression, improved markedly after surgery, and was discharged with a normal neurologic examination two weeks after surgery. No additional follow-up was provided. In dogs requiring invasive procedures with a risk of hemorrhage, fresh frozen plasma or cryoprecipitate is recommended however there is no known cure. Gene therapy is available for humans with hemophilia A however this is not available yet for veterinary patients. A low impact life style is recommended!

Thanks for reading! I am in Michigan this week, and Chicago Vet at the end of the week speaking about super cool neurology-related topics (of course). However, I am reachable by email or telephone if you need me. I look forward to working with you next week!

Reference: Fowler KM, Bolton TA, et al. Clinical, Diagnostic, and Imaging Findings in Three Juvenile Dogs with Paraspinal Hyperestesia or Myelopathy as Consequence of Hemophilia A: A case report. Frontiers in Vet Science (2022): 9,1-9.

Strokes in Dogs

Strokes are an increasingly common cause of seizures and other intracranial signs in dogs (and cats). Why is the diagnosis becoming more common? My theory is that we are simply performing more MRIs, and therefore making the diagnosis more readily, but it is possible that increasing comorbidities or breed related changes may contribute to the increase in diagnosis.

What is a Stroke?
Stroke, or cerebrovascular disease (CVD) occurs when normal brain fuction is disrupted due to hemorrhage or infarction. CVD is typically due to occlusion of an/multiple intracranial vessels however hemorrhagic strokes can occur in rare cases. Around 50% of dogs will have an underlying predisposing facture such as hyperadrenocorticism, hypothyroidism, protein loosing nephropathy, heartworm disease, heart disease (less common as a cause!) or other "hypercoagulable" diseases. The other 50% do not have any identified predisposing factors and are therefore considered to have had an idiopathic vascular event.

Clinical presentation
Acute onset, with progression not typically noted after 24 hours (but it can in rare cases)
Common in older dogs, less common/rare in younger dogs
Gait changes (hypermetria, ataxia) and seizures were the two most common presenting complaints leading to a diagnosis of CVD

Diagnosis
The best diagnostic tool for CVD is MRI. Indication of vascular occlusion can be seen immediately but tell-tale signs may resolve if imaging is performed too long after the onset of the clinical signs.

Treatment
Supportive treatment is often the only treatment needed. Supportive treatment may include anticonvulsant drugs, intensive nursing care if non ambulatory, or rehabilitation if gait abnormalities are identified. A neurology consult may help guide treatment for you and the client.

Outcome
The majority of dogs will improve following CVD but time to improvement and degree of improvement is variable, and based on severity of neurologic impairment, and MRI findings. Recurrence can occur, but is less common. We previously though it was rare, but in one study in Japan (see below) 11 of 50 cases available for follow-up had clinical signs of recurrence of disease after a diagnosis of CVD. Recurrence does not mean seizures - remember they can develop a seizure disorder secondary to a CVD but that does not suggest progression!

Other Cool Facts
The Japanese study referenced below noted August and December as months with significantly higher stroke diagnoses, compared to all other months, and October as the lowest month. Interesting!

Thanks for reading! Have a great week and keep those consults rolling! I will be speaking at the Michigan Vet Med meeting in Lansing and at the Chicago Vet conference the week of May 9th so no live consults will be available that week. However, I will be reachable by email or telephone if you need me. I look forward to working with you when I return!

Reference: Ozawa T, Miura N, Hasegawa H, et al. Characteristics of and outcome of suspected cerebrovascular disease in dogs: 66 cases. JSAP (2022)' 63, 45-51.

Zoonotic Discospondylitis!

This week I thought we could brush up on Brucella canis; an uncommon (in the northern US and Canada) cause of discospondylitis in dogs and a zoonotic disease of importance for humans. Why should we talk about this? Because I was contacted by a Wisconsin vet to help manage this case and I thought we could all benefit from this endeavor. 

What is Brucella canis?
Brucella is an intracellular bacteria that is known to be a cause of abortions and still birth in dogs. Dogs are the known reservoir for this bacterium however other Brucella spp. can be transmitted to dogs on rare occasion.

What signs does it cause?
Brucella canis is known to cause abortion and stillbirth in dogs but it's lesser known signs include discospondylitis, uveitis and fatigue/fever. Have I mentioned this is zoonotic? Wear gloves when handling the dogs, and any excrement. Avoid contact if pregnant.

When should I test a dog for Brucella canis?
Any dog with a history of chronic back pain that is diagnosed with discospondylitis should be tested for Brucella canis. The original case I was involved with had a several year history of "not wanting to be petted on the lumbar spine" that progressed to overt signs of pain over a few months. Another case was imported from Canada (not exactly a hotbed of B. canis activity!) with signs of back pain over several months duration and the most recent case I am working with the dog has a several month history of back pain, as well.

How do you treat Brucella canis in dogs?
Management is NOT recommended by experts and State Veterinarians due to the risk to human health and the poor likelihood of actual cure. No universally accepted treatment protocol is available however several choices in published literature include tetracycline-based antibiotic, aminoglycosides, enrofloxacin or rifampin. Some protocols recommend 2 or more drugs in combination, others have solo management. Repeated screening every 2-6 months, regardless of signs, is recommended. If treatment is going to be stopped, two sequential negative tests are recommended before stopping antibiotics. This is likely to be 8+ months after initiation of treatment...if ever. However, screening should continue life long to catch subclinical relapses. Again, euthanasia is recommended by the veterinary community.

What do you do if you have a suspected or confirmed B. canis infection in a dog?
If you live in in the USA, call your State Vet. This is a reportable disease and must be reported! Furthermore, the state vet can provide additional guidance on treatment, testing and culling.

Wisconsin State Vet contact information:

• Phone: (608) 224-4872, Monday-Friday, 7:45 a.m.-4:30 p.m.

• Email: DATCPAnimalImports@wisconsin.gov

• Evenings & weekends: (800) 943-0003, after-hours. Tell the duty officer you are reporting a potential animal disease.

If you live outside of the USA - contact your local veterinarian for further guidance.

If you wish to read more about B. canis the most recent article from North America that I found is: Cosford KL. Brucella canis: An update on research and clinical management. Can Vet J 2018: 59:74-81.

Thanks for reading! Have a great week and keep those consults rolling!