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!

Recurrent Cervical Pain

Imagine with me that you are presented with a 10 kg small breed dog on Tuesday morning with a history of neck pain. This dog had a history of neck pain 1 year ago that underwent full work up, at your local University or specialty hospital, and was diagnosed with a disc herniation. The clients pursued surgery, and recovery was smooth and complete. The clients were thrilled...until yesterday. Now, they're angry.

How likely is it that this dog has herniated ANOTHER disc in it's neck?

It is a good question, and one that we have some recent data that might help answer this question. A study out of the UK looked at the recurrence rate of cervical pain in dogs that had a prior disc herniation diagnosed via advanced imaging.
119 dogs in the study, 36 dogs had signs of recurrent neck pain or a cervical myelopathy.

• 36/119 had medical management following diagnosis of IVDH

  • 13/36 (36%) had a recurrence of signs

  • Recurrence was more likely at the same intervertebral disc space

• 83/119 had surgical correction following diagnosis of IVDH
  

  • 27/83 (33%) had a recurrence of signs

  • Recurrence was more likely at neighboring intervertebral disc space to the original disc herniation

• Surgical correction did not decrease the odds of recurrence in this study. Important: We don't know if these dogs underwent surgical fenestration at the time of their first surgery, or not.

• Recurrence was within 2 years of the original diagnosis of a disc herniation for 80% of the dogs in this study. (Note: this means that 20% it was longer than 2 years!)

** We don't know that every one of the dogs had a second disc herniation but the few that did have work up did have a disc herniation confirmed.

The data reported in this study suggests that medical and surgical correction of cervical disc herniations does not change the risk of new onset cervical pain. Reported ranges in the literature for recurrence of cervical pain with surgical correction are between <10-30% (and probably more towards the 0-15% range in the cervical spine) so it is at the high end of reported recurrence. Reported recurrence with medical management is slightly more difficult to track but may be in the 30-40% range. Therefore, it is surprising that the authors saw a similar recurrence for medical vs surgical correction. This may come down to the surgical correction performed, which we don't know from this study. We do know that none of the dogs with surgical correction had a recurrence at the site of correction.

What should we tell the client before us? Surgical correction for a ruptured disc corrects the issue at that disc, but may not address degeneration at distant sites. Sadly, their pet may be faced with a recurrence of another disc herniation. If they're up for another workup and possible surgery, it's time to start the process for referral. If they'd like to give medical management a try, get started on some pain management and bed rest (avoid those steroids if you can in these cases!) and keep a close eye on the dog. Weekly neurologic exam would be recommended, if possible.

Link: https://onlinelibrary.wiley.com/doi/epdf/10.1111/jsap.13480

This Tidbit took a slightly different approach than my usual updates. I typically try to pull 1-2 key points from an article that I find useful, and that I think you'll find useful. This time, I decided to represent a study that wasn't highly powered, that also didn't provide clear, convincing data to support a specific question. We all like black and white scientific data that we can read, digest and apply but honestly, that is a minority of what I read on a daily basis. This TidBit had more "waffling" in it because I wasn't fully convinced the data provided would change my practice. How did this report strike you? Did you find it useful, or not? As always, thanks for reading!

Have a great week and keep those consults rolling!

Status Epilepticus

Status epilepticus (SE) is defined as continuous seizure activity for more than 5 minutes or two seizures in which consciousness isn't resumed in between. SE has a potentially fatal outcome in dogs and humans and is devastating to watch, try to fix, and explain to clients. I wish it wasn't so.

A recent study out of the UK (see below) outlined risk factors for short term mortality (death during hospitalization for SE) and long-term recurrence of SE in dogs. Here are some key points but, as always, if you want more depth please read this open access article.

Short-term mortality:

• 124 cases included, 87 survived to discharge (70%)

• Increasing age, shorter duration of hospitalization, onset of SE before hospitalization and SE being caused by a potentially fatal etiology were related to mortality.

• Of the survivors - 42 had idiopathic epilepsy ( this was the first seizure in 6 dogs), 21 had structural epilepsy (first seizure in 12 of the dogs) and 8 had reactive seizures (first seizure in 10 of the dogs).

Recurrence of SE

• 74 of 87 dogs had follow-up information after discharge. Recurrence happened in 20 of 74 dogs.

• Pharmacoresistant epilepsy and having focal seizures were the only significant risk factor identified. .

• 50% of recurrence was within 2 months from discharge

What do we make of this?
Status epilepticus is a serious form of a seizure. We cannot fully prevent it, but we can counsel clients on the possibility if their animal has one of the predisposing factors identified above (advancing age, fatal etiology or focal seizures). Do not delay on treatment of seizures. Waiting and seeing can result in SE and avoidance is definitely the best policy for management of SE.

JVIM (2022): 36: 353-662.

Thanks for reading! Happy Easter and Passover to those of you that celebrate. Safe fast to those of you in the midst of Ramadan. I look forward to continuing to work with you and your staff to help pets with neurologic disease.

Spinal Trauma

We all know not all vertebra look the same, however did you know this means they don't behave the same way during trauma, too?
Let's look more closely at the cervical vertebra, for a moment.

C1-C2 are a common site of subluxation, especially in young small breed dogs. Congenital C1-C2 subluxation is not considered a traumatic subluxation in most situations. Traumatic C1-C2 subluxation does occur in developmentally normal dogs especially in circumstances when a collar may have resulted in a rapid deceleration of motion (hanging). Cervical vertebra are also "roomier" meaning that the ratio of cord to canal is smaller resulting in more fat in the epidural space compared to the thoracolumbar vertebra. This allows for a traumatic event to cause less clinical neurologic disease and may be a reason why dogs with cervical fractures and subluxations often recover well with medical management. Finally, cervical vertebra have more rotation and flexion or extension capacity compared to thoracolumbar vertebra therefore making them more resistant to fracture and subluxation.
Did you know that 5-10% of dogs have a site of a second spinal fracture/subluxation that is masked by a more cranial trauma? Please consider taking radiographs of the entire vertebral column in a post traumatic patient NOT just in the area of neuroanatomic lesion localization.

Three Column System of Stability
There is some debate about the validity of this system but I will mention it because many surgeons and neurologist ascribe to the principles. This system is used to determine the need to treat a fracture and does not base the need to treat solely on neurologic signs. (Although these are still important!) Instability is considered likely if 2 or more of the columns are affected.
Dorsal column: Dorsal process, dorsal laminal and dorsal ligaments
Middle column: Dorsal longitudinal ligament, dorsal anulus, middle, dorsal part of the vertebral body
Ventral column: Ventral longitudinal ligament, ventral anulus, and ventral body with lateral processes or rib heads.

How to use this information: Evaluate the fracture in two views, whenever possible. If two or more segments are affect, surgical correction should be entertained with the owner (and local surgeon/neurologist if you aren't correcting it yourself). If not (ex: fractured dorsal process), you may be able to avoid surgical correction. There are exceptions to every rule, so if you're unsure please reach out! (As a side note: I don't perform fracture reduction surgery but I am happy to help with the neurologic assessment, and to help facilitate referral.)

A few other notes about the difference between cervical and thoracolumbar vertebra:

• Fractures/subluxation in the C6-T2 region may carry a worse prognosis due to disruption of the LMN to the thoracic limbs.

• The paraspinal musculature of the thoracolumbar region is protective! Don't disrupt it if you don't need to.

• The lumbar vertebra have large articular processes, which protect them from subluxation.

Thanks for reading and I hope you have a great rest of the week! As a reminder - I'm off to Texas for the week so please email if you have any questions but calling/texting may be time delayed due to my lecture schedule.

Seizures in the Post Operative Period

Seizures in the immediate post operative period can indicate a poor prognosis for humans undergoing brain surgery. The same is suspected for dogs, but isn't known. A recent article (see below) recently discussed this question and I thought you might be interested in reading some key points from the article.

Key points:

• 88 dogs underwent 125 procedures. Most had either a brain biopsy or a brain surgery, but some had both.

• All included surgeries were rostro tentorial because caudal tentorial surgery and tumors have a very low incidence of seizures.

• Most dogs (72%) had seizures before brain surgery was performed, therefore diagnosed with structural epilepsy.

• All types of seizures were noted (35% generalized only, 29% focal and generalized and 17% focal only)

• Forty-one of 88 dogs (46%) had a normal interictal neurologic examination. This is MUCH higher than some other studies have shown and is worth noting in general practice. The neurologic examination can help guide you towards advanced diagnostic testing, or not. According to this study, almost 1/2 of the dogs had a normal exam and had a brain tumor!

• About 42% of dogs had an abnormal neurologic examination consistent with a focal lesion and 11% had examination findings consistent with multifocal disease.

What I learned from this article

This article was full of data, so if you're a practicing brain surgeon, it is worth a full read. That said, there were a few points that may benefit the non-neurosurgeons amongst us. I've summarized them below and included a link to the open access article at the bottom if you'd like to read more yourself.

• Early post-operative seizures in humans, are diagnosed in the first month after brain surgery. One of the hypotheses was that dogs receiving anticonvulsant drugs (ACD) would have a lower incidence of post-operative seizures. Interestingly, this article did not detect a difference in post operative seizures between dogs with or without ACD pre-operatively!

• Tumor location nor brain herniation were associated with the development of post operative seizures.

• Curative intent surgery carried a higher risk of post operative seizures when compared to biopsy procedures.

• Dogs with glioma had a higher incidence of seizures compared to other tumor types, except meningioma.

• Dogs with early post operative seizures were less likely to survive to discharge.

• Early post operative seizures occurred in the first 24 hours for all dogs, and were associated with longer hospitalization.

Take Away Message

What does this mean? It means that seizures are a small, but mighty way for the brain to express it's displeasure with human touch. Even the most careful surgeon risks causing seizures that could be life threatening for their patients. I still give ACD pre-operatively but am compelled, by this data, to consider stopping that practice. Why administer an ACD if it isn't associated with a lesser chance of seizures? For most of you, brain surgery is not a part of your daily practice, so I would suggest that the most important take away from this article might be that almost half of dogs had a normal neurologic exam and yet were diagnosed with a brain tumor. Also, if a client asks you about post operative seizures, you can refer to this article! Thank you, Science.

Thanks for reading all the way through! I hope you have a great week and look forward to working with you, and your patients, soon.

Article links: https://onlinelibrary.wiley.com/doi/full/10.1111/jvim.16391

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 in 2019, 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).

Thanks for reading! This was an oldie, but a goodie and I hope you enjoyed revisiting it along with me. Please reach out if you have any questions. Have a great week

The Case of the Shrinking Head

Signalment: 4.5 year old MC Shepherd Mix

Clinical history: The dog had a 3 week history of left unilateral temporalis muscle atrophy when I met him. Hyporexia and nasal hemorrhage from the right nostril were noted when the signs first started, but they had improved by our consult. The atrophy, however, continued to progress.

Physical and Neurologic Examination:
The physical exam was normal.

Mentation: BAR
Cranial nerves: moderate left temporalis muscle atrophy, otherwise normal. No sensory abnormalities noted.
Gait: Ambulatory, no evidence of lameness, weakness or ataxia
Reflexes: normal all limbs
Postural reactions: Normal all limbs
Palpation: Non-painful spinal palpation and normal CROM

Neuroanatomic Lesion Localization?
Let's walk this through. First, what nerve innervates the temporalis muscles? (CN 5: trigeminal) So, our problem is a) peripheral trigeminal b) brainstem at the trigeminal motor nucleus or c) muscle. How do you sort between these? Right! Let's rule out the easy one first. Signs of brainstem disease include changes in mentation, paw replacement deficits (ipsilateral to the atrophy) and/or hemiparesis. Any one of these three abnormalities is present and voila! it is a brainstem lesion until otherwise discovered. We ruled out brainstem disease in this dog. Is this, then, peripheral trigeminal nerve (motor portion) or muscle? This differentiation can be hard on the neurologic examination so I actually included both of these possibilities on this dog's final neuroanatomic lesion localization. However, without a sensory deficit (he didn't have one) a trigeminal neuropathy is less likely. That said, if the CK is normal, it's hard to make a story for a myopathy. His was normal. So...I left both on the final list. You could have said "neuromuscular" and you would have been correct because that localization includes peripheral neuropathy, neuromuscular junction and myopathy.

Differential Diagnoses?
Neuropathy: Neoplasia, neuritis (infectious or non-infectious), hypothyroidism and trauma.

Myopathy: Masticatory muscle myositis (3M), infectious myositis (toxoplasma and Neospora caninum are most common causes of infectious myositis.)

Diagnostic Results
CBC, serum biochemistry: unremarkable.
T4: normal
Neospora antibody M titer: > 1:200 (positive!)
Toxoplasma IgG/IgM titer: Negative
3M antibody titer: < 1:100 (negative)

Conclusion
This patient was diagnosed with a Neospora myositis based on positive titers. We placed him on sulfa antibiotics and tracked the titers. Clindamycin is also an acceptable antibiotic choice for fighting protozoa myositis.
2 months later: 1:200
4 months later: 1:100
1.5 months later: negative.

Unfortunately, this patient developed an adverse reaction from the sulfa that included blood dyscrasias and hypothyroidism 5.5 months from the original diagnosis. The sulfa-based antibiotic was discontinued and clindamycin was started. My goal is to have 2 negative Neospora titers before discontinuing antibiotics but we will have to see if we get to meet that goal with this guy!

Key Points:
1. Muscle atrophy (especially unilateral) should prompt a toxoplasma (cat) and toxoplasma and Neospora titer (dog). This is a lesser known infection in Wisconsin dogs!
2. Treat with either a sulfa antibiotic or clindamycin to the point of two consecutive negative titers to ensure clearance of the infection. Titers are typically checked every 4-8 weeks.

This was a very interesting case and a great one to remind us all about protozoal infections in house pets. Remember - when we work together, we all learn!

I look forward to working with you soon.