Wild West Vet Show - Neuro Questions Answered!

Gait Analysis:

  • No questions

Vestibular:

  • Can you clarify what paradoxical vestibular looks like and how to differentiate?

    • Of course! Paradoxical vestibular is when the head tilt and nystagmus (side) don’t match the proprioceptive deficits. It is considered a “paradox” when they disagree because it can’t exist, but of course - it does! This is most often associated with cerebellar disorders, as the cerebellum inhibits the vestibular nuclei. Think of the cerebellum as “mom” telling the kids to turn down the radio (aka the vestibular nuclei). Normally, when we have a vestibular issue, we damage the radio. I like to think of a peripheral lesion as something wrong with the plug/outlet or the cord (CN VIII). Then, a brainstem lesion fits more with actual damage to the radio. If we imagine a room with two radios (one on the left and one on the right), when we damage these structures, the radio on the same side as the problem (lesion) is damaged is not longer making sound. This means that all the effects we see come from the other radio that is making sound, leading to circling (towards the lesion) and nystagmus - fast phase away).

    • With paradoxical - assume the radios are in two different homes (one on the left and one on the right). The moms are not allowing the radios to be too loud. If Mom in the right house goes to the store (well, mom is away, the kids will play), that right-side radio will increase the noise. Both radios are playing in this scenario, but the one on the right is louder. This makes the body think the left radio is broken, but it’s not; the right side is just SO loud, thus the body acts like a lesion is on the left. This is where the paradox comes from because it doesn’t make sense.

    • You can, however, always trust proprioceptive deficits IN VESTIBULAR situations. In vestibular disorders, proprioceptive deficits are always on the same side of the lesion. If the head tilt and nystagmus don’t match the side of the proprioceptive deficits, think paradoxical!

  • What dose of injectable Cerenia do you give since the oral dose is 8mg/kg for motion sickness?

    • I still do recommend the manufacturer dose since I haven’t seen studies to the contrary looking at the injectable version, especially since it has and uses a different vehicle for drug delivery.

  • With idiopathic vestibular disease, would you worry that nystagmus is caused by head trauma if the animal is overly disoriented?

    • This is an amazing question! I would be looking for other signs of dysfunction with head trauma suggestive of brainstem signs. I have had a few that ONLY had a fracture of the petrous temporal bone (so they presented peripheral), and they did have a heck of a nystagmus as well as head sensitivity. That being said, I have seen mild trauma and severe idiopathic vestibular, so I’m not sure that nystagmus rapidity alone can differentiate as many peripheral localizations can have very rapid nystagmus.

  • What dose of steroid would you use for OMI?

    • Anti-inflammatory, no more than 1mg/kg/day, but likely to fall in the 0.5 to 1 range based on patient size.

  • Do you do both cerenia and antihistamines or go for one or the other?

    • I use Cerenia and ondansetron as a combo pretty regularly. I haven’t used antihistamines in some time, but some people swear by them. I can’t think of a reason why it would be wrong per say.

Neuromuscular

  • To the people who submitted puns - You are my FAVORITE people!!! “Weak in the knees for neuromuscular disease” killed me!

  • Can you please explain the neostigmine testing. I missed it.

    • Of course!!! Edrophonium (Tensilon) is no longer commercially available, so we have had to move to using neostigmine.

    • Here is a paper about the protocol: Link

    • We get ours from Amphstar Pharmaceuticals

  • Why do they have elevated CK with myasthenia gravis since it’s a junctionopathy?

    • In the human literature, it is because they often see concurrent myositis with MG. We don’t have great data on this, but it makes sense and is a purposed theory for why we may see it in vet med as well!

  • With a palpebral reflex that tires, what other diseases may cause that beyond MG?

    • GREAT Question! In theory, anything that hits AcH has the potential to depend on the stage of the disease. Early-stage botulism (before we get a complete lack of release), in theory, could cause fatigue, and muscle weakness disorders (though I anticipate other areas of muscle weakness other than these tiny facial muscles. In vet med, we have a pretty heavy association with MG, but never say never in neurology! (A lesson I have learned the hard way).

  • For Cushing's myotonia, does it resolve with just treating the Cushing's or require additional treatment?

    • Once it is present, to my knowledge and experience, it is present. It does benefit from treating and ensuring the underlying Cushing’s is controlled to keep it from getting worse. Treatment for myotonia can also be directed at stabilizing the muscle fiber membrane. Drugs used for this purpose include procainamide, quinidine, and phenytoin. Serum levels of carnitine were reportedly reduced in a human patient with congenital myotonia and supplementation with L-carnitine might help to alleviate muscle weakness in metabolic myopathies in dogs. Again, aimed at treating progression more than anything.

Seizures - Clusters and Status - See ketamine and other papers (and other questions here!)

  • Do you recommend combining the keppra and pheno or start with pheno to go home main.

    • In a status situation, I like to hit them with the IV keppra first cause it works quicker, but I often am reaching for the phone at the same time. Typically, in a true status situation, I’m going to load on pheno and will lean on that as the only go-home med, even if I used Keppra to help stabilize. It isn’t wrong to keep both, but we might as well see if we can lean on the efficacy of phenol and improve owner compliance with fewer pills.

  • What is your threshold for elevated liver values when choosing to use pheno in an at risk breed for cluster seizures? (Border collie, aussie, boxer).

    • Wonderful question; I don’t worry too much about ALP; ideally, I prefer it not to get too crazy, but when by itself, it can do some wild things. ALT on the other hand I start worrying when getting to the 2-3x mark, and especially over that. I have pushed it on occasion when it was the only thing that worked and used bile acids to really monitor. I am working with a researcher to try to develop a new drug that will protect the liver without affecting pheno! Cross your fingers!!!

  • Do you have a preference for mannitol over hypertonic saline?

    • I don’t other than I was exposed to mannitol first. If I need to ensure volume resuscitation at the same time then I do lean towards towards hypertonic in that situation.

  • For dogs that have clusters but they don’t occur often, can you get away with ONLY pulse therapy after the first seizure? I.e. only occurs every 4-6 months.

    • This is a great question for which I don’t have a great answer. I don’t have a study to support this approach, but I have talked with others (and in one dog myself) who used this approach. I did it in one dog because I struggled to justify daily dosing when it literally one just one bad weekend every like 8 months. (see the similar question below).

  • What do you think about adding oral alprazolam for a few days in clustering dogs?

    • I don’t have personal experience or great knowledge of alprazolam in dogs, but I can assume it would have the same functionality and purpose as clorazepate being a benzo. Using the clorazepate as a model, I can absolutely get behind the use of oral benzo as a pulsed approach to clusters!

  • Is pulse therapy (3-day protocol) with Keppra supported in a patient with novel cluster seizures that isn’t already on some form of anticonvulsant?

    • Very similar to the other question. I don’t think it is wrong if we have a situation where they aren’t clustering more than 6 monthts to a year. I think once we get below that 3-4 month threshold, we have to start asking ourselves. . . Should I be using a daily maintenance? The other thing would be if they go into status or have a super prolonged seizure, is there benefit of the daily to help try to dampen down that first severe one that won’t have any drugs on board to help? To me if they go into status (or even have a super prolonged seizure) it is justification for daily maintenance to try to help prevent that situation.

  • Midazolam in a normal syringe (for IN use) needs to be tossed after 3 months per human neuro. Is that a human thing or something we should follow in vet med?

    • Likely, as it does bind to plastic (diazepam more so!!). I saw an abstract presented once but never saw a publication about it in Vet Med, and I can’t remember their details, though it wasn’t exactly a perfect replication. I would be lying if I didn’t push it to 6 months once I couldn’t get the 2ml midazolam bottles anymore (that was perfect!!). I try to avoid sending home in plastic as best I can for these reasons, but sometimes it is hard of course.

  • Missed your best cluster buster recs, can you please reshare?