Mydriasis in a Cat

It’s time for another case! This time, we’re going to talk about cat eyes – it’s almost Halloween, right? This case was taken from a case report presented in Vet Record August 2024 (https://doi.org/10.1002/vrc2.956). I thought it was interesting, and quite similar to another case I worked with one of you on…with the exception that we haven’t made it to MRI yet.

Signalment: 12 year old MC DSH.
History: 3 month history of mydriasis, photophobia and avoidance of jumping.

On examination, the cat had an unremarkable PE. Neurologic exam was as follows:
Mentation: normal
CN: Dilated pupils OU, no PLR (direct or indirect) OU, remainder normal. (Yes, even oculocephalic reflex!)
Gait: normal
Reflexes: not reported but assumed normal.
Postural reactions: normal

Lesion localization?

Let’s take a step back and remember that the parasympathetic innervation to the eye comes from midbrain (Parasympathetic nuclei of CN III), piggybacks with CN III to the eye where it then enters the iris muscles, causing constriction (normally). A lesion in the brainstem (midbrain in this case) should produce a change in mentation, paw replacement deficits, and/or hemiparesis along with the CN deficit. Bilateral peripheral parasympathetic damage hadn't been reported yet, but it would stand to reason that damage to CN III should result in strabismus and a loss of oculocephalic reflex (physiologic nystagmus). These somatic changes would/should be in conjunction with the parasympathetic changes expected. 

This case was localized to bilateral peripheral parasympathetic nerves because there wasn’t evidence of a brainstem lesion. This is reasonable!
MRI and CSF, along with bloodwork were normal. Unfortunately, they could not collect enough blood for infectious disease testing. Based on these findings, the cat was diagnosed with an idiopathic bilateral peripheral neuropathy of the parasympathetic nerves. So cool! No signs of progression have been noted over 9 months.
 
I hope you enjoyed reading about this interesting case report. If you have any questions about the lesion localization, or anything else, please let me know! Have a great week!

Idiopathic Head Tremors

Wow, a lot of you have been seeing head tremors lately! I thought we could use this TidBit Tuesday to look more closely at Idiopathic Head Tremors and compare/contrast to seizures. 

What are Idiopathic Tremors?

Good question!

• Tremors are action-related in veterinary medicine. 

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

• Postural tremors happen NOT AT REST. Meaning, if the body part that is tremoring is supported, the tremor stops. 

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

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

We're going to focus on postural tremors, and specifically head tremors. There are structural head tremors and idiopathic head tremors. Structural tremors are caused by something we see on MRI or CSF. These cases often involve pituitary lesions and are typically older pets, with neurologic deficits on neurologic exam. Contrast this with idiopathic head tremor. Animals with idiopathic head tremor can be of any age but are typically younger dogs, with a normal neurologic examination and normal MRI/CSF. So, what causes idiopathic head tremors? We...ahem...don't know. They are classified as a movement disorder but that means it could be from CNS or PNS lesion localization. Movement disorders are a huge box of diseases that are lumped together but may be anything associated with specific movements, or not. There is a really nice, slightly older article by Dr. Mark Lowrie that outlines the different types of tremors if you'd like to read more. 
 (https://bvajournals.onlinelibrary.wiley.com/doi/epdf/10.1002/inpr.3)

How do you differentiate tremors from seizures?

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

How do you diagnose idiopathic head tremors?

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

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

One of the tenants of idiopathic head tremors is that they don't respond to anticonvulsant medications but please read this line cautiously. Up to 30% of dogs and cats with seizure disorders do not respond to anticonvulsants (1 or multiple) either so a lack of response to anticonvulsant drugs still does not rule out a seizure disorder. Furthermore, rapid head movement in a bulldog is a COMMON presentation for a focal seizure so don't just disregard the information. Do a neurologic exam!! 

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

DATA COLLECTION

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

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

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

Rabies : It's still out there

I read some sobering data recently, produced by the CDC, pertaining to Rabies. They published a table of Human Rabies virus infections in the USA and Puerto Rico between 2000-2022. No cases were reported in 2022. Over the remaining 21 years, 57 cases were identified ranging in age from 7 to 87 years old. The source of infection was listed as "contact", "bite", "unknown" or "organ transplant" (Yeah, this one was unexpected to me!). One individual survived but the remaining 56 cases were, not surprisingly, all fatal. Reading this table reminded me that we haven't talked about Rabies on TidBit Tuesdays for awhile (actually since 2022!). As your friendly neighborhood neurologist, I feel strongly that we should have this conversation so please read on. 

Etiology

Rabies is a neurotropic rhabdovirus that causes fatal infection in dogs, cats and (usually) humans. Infection is caused by inoculation from saliva by means of a bite.  The virus then spreads into the CNS via peripheral nerves.  Once the brain is infected, the virus spreads back out through peripheral nerves to the salivary glands – at this point, the animal can transmit rabies.

Signalment
Any dog, cat, horse, cow, HUMAN

Clinical Signs

Two syndromes are described:

• Furious syndrome (forebrain signs)

• Paralytic syndrome (lower motor neuron signs ascending from the site of the bite). This means a paraplegic dog could be considered for rabies observation if they are NOT vaccinated. Be aware! 

Once neurologic signs are present, progression is rapid, and most animals will be dead within several days. Most of the individuals on the CDC table were deceased within 3 weeks of their noted infection date. 

Rabies should be considered as a differential diagnosis in any animal with acute onset, rapidly progressive neurologic disease especially if there is a poor vaccination history or exposure to wild animals.

Diagnostic Tests

  Key point: A definitive diagnosis can only be achieved postmortem, and requires fluorescent antibody staining of brain tissue to demonstrate rabies antigen. A serum RFFIT (Rapid fluorescent foci inhibition test) can be performed to evaluate for evidence of previous vaccination however it should NOT be used to make a diagnosis of active rabies infection. One of the cases I evaluated had a negative RFFIT test and was confirmed to have the rabies virus on necropsy. Due to the neurotropic nature of rabies it can remain undetected by the immune system and therefore cause a negative (false negative) RFFIT result.

What do you do if you've been exposed? Contact your local heath department immediately. 
What do you do if you have a patient that you suspect has a rabies virus infection? Contact the State Veterinarian (Dr. Yvonne Belay at 608-516-2664)

Further reading
If you're interested in reading about a case of Rabies virus infection please check out this article. https://doi.org/10.5326/0390547. I saw this case a number of years ago, but the disease hasn't changed much in 20 years!

Thanks for reading! A rabies virus infection is something worry about for those of you out there on the front lines. Be aware, be cautious, and when in doubt - put on PPE!! Please reach out if you have any questions.

Other good resources:
The Wisconsin Rabies Algorithm: (for exposure or sick animals) https://www.dhs.wisconsin.gov/rabies/algorithm/algorithmcategories.htm
Illinois Rabies information: https://www.ilga.gov/commission/jcar/admincode/008/00800030sections.html

Can Paraplegic Dogs walk?

What do we know about the natural progression of thoracolumbar intervertebral disc extrusion (TL-IVDE) in dogs? We have been taught when a dog stops having voluntary movement of their pelvic limbs (paraplegia) they need surgery to recover the ability to walk, right? What about those that have lost deep pain? What if we didn’t do surgery – what happens to those dogs? A study was published in JVIM this year that looked at the natural progression of medically managed TL-IVDE in non-ambulatory dogs and evaluated not only the recovery rate, but also what the discs “did” on sequential MRI 3 months after starting medical management.

Results

Sixty-seven dogs met the inclusion criteria – 51 with deep pain, 21 without deep pain, 5 with signs of myelomalacia at presentation.

Treatment consisted of NSAIDs (steroids were discontinued and replaced with NSAIDs if started), pain management and physiotherapy.

·         Recovery

·         Dogs with deep pain: 96% regained walking and voluntary urination (49/51)

o   Median time to recovery 11 days (7-21 days IQR).

·         Dogs without deep pain: 63% regained walking and voluntary urination (10/21).

All dogs (regardless of ambulatory status on recheck) did not have signs of back pain on evaluation 3 months after enrollment in the study.

The change in compression on MRI was interesting. In some patients, the compression almost completely resolved, and for others there was less than a 5% change. This wasn’t correlated with clinical signs but looking at the figures it does not appear to have a direct relationship.

Key point:

If you have a patient presenting with acute, non-ambulatory paraparesis or plegia, surgery is a very reasonable first step. However, it isn’t the only option! Don’t euthanize unless myelomalacia is present!! Consider conservative treatment because we may end up with an ambulatory patient after 3 months! Just because an owner cannot afford an MRI or surgery, doesn’t mean we should do a neurology consult, either. 😊

Thanks for reading! I hope you’re having a good week and look forward to working with you soon.

Shock Index and Head Trauma

How many of you see pets with head trauma in your practice? Okay, that’s good. There are several ways to look at prognosis following head trauma but the key feature of any of the measurements is serial evaluations. One singular measurement doesn’t seem to correlate well with prognosis in such a dynamic disease. A recent retrospective study evaluated the shock index (heart rate divided by systolic BP) to determine the correlation with mortality in a population of dogs with head trauma. A second part of the study was to determine if it was predictive of survival to discharge or improvement in signs during hospitalization.

Results

 A total of 86 cases and an unknown number of control dogs (normal dogs) were included. There was quite a list of possible ways these poor dogs were traumatized and an even longer list of breeds affected. See the study for full details on that.  The mean SI for the control group was 0.75 (range 0.62-0.92 with not normal distribution). The mean SI for dogs with head trauma was 0.91 (range 0.34-3.33, also not normally distributed). SI was significantly (0.0014) higher in the trauma group compared to the control group. However, the SI was not significantly different between dogs that diet or were euthanized compared to those that lived until discharge. There was also no significant difference in SI between dogs with a normal neurologic examination at discharge and those that were improved or static, but not normal, at discharge.

So, what does this tell us? My take away is that the SI is higher in dogs with head trauma, but it doesn’t prognosticate (using the data from this cohort of dogs) regarding survival or neurologic outcome. Why is SI higher in pets with head trauma? Following trauma, if the intracranial pressure (ICP) goes UP (hemorrhage, edema) the mean arterial BP goes up to keep blood flowing to the brain. The HR will concurrently drop due to a feedback loop. This SHOULD result in a lower SI (HR/systolic BP). The authors noted that in one case they had a dog with significant hypovolemia at the initial evaluation which resulted in a very high SI but due to a swing in pressure dynamics in the brain, the dog oscillated between hypo and hypertension over time. The authors suggest that SI may be an unreliable measurement in post-head trauma patients for this reason. So, I return to all of you smart people out there. Why is the SI higher in head trauma than in control dogs? This has also been reported in humans post head trauma so there must be a very good reason, but I can’t figure it out and would love your thoughts!

Thanks for reading this TidBit Tuesday! I hope you have a wonderful week and look forward to seeing you soon!

Reference: McConnell BM, Cortes Y, Bailey D. Retrospective evaluation of shock index and mortality in dogs with head trauma (2015-2020): 86 cases. DOI: 10.1111/vec.13411

How do MRI lesions affect survival for MUE?

 
A study was published this week that looked at the survival times between dogs with and dogs without MRI lesions and diagnosed with meningoencephalomyelitis of unknown etiology (MUE). MUE is diagnosed if a dog has evidence of CNS inflammation (meningitis, encephalitis, myelitis or a combination of these) without evidence of infectious etiology. Signs can be focal or multifocal, and age is irrelevant. To make this diagnosis an MRI, CSF tap, and infectious disease testing are performed. There is a subset of dogs that are diagnosed with immune mediated CNS disease that do not show evidence of disease on MRI but have all of the other markers of MUE. The purpose of this paper was to determine if there is a difference in survival between the two groups of dogs.
Results
A total of 73 dogs with MUE were included in the study. This included 19 dogs with a normal MRI and 54 with an abnormal MRI. The survival time was >107 months in both groups with a significantly longer survival in the normal MRI group. Neither group reached median survival in Kaplan-Meier survival, however. Death was secondary to MUE in 1/19 dogs with a normal MRI, and 18/54 in dogs with an abnormal MRI.
Below is the breakdown comparison between the two groups:

• Remission – 68% of the normal MRI group; 53% of the abnormal MRI group.

• Death within 3 months due to disease – 5% in the normal MRI group and 13% in the abnormal MRI group.

No difference was found between dog groups regarding remission, disease-free interval, or relapse while on prednisone. The two groups received similar treatment protocol, for which corticosteroids were included in all dogs and a variation of additional immunosuppression. The total nucleated cell count (TNCC) was higher in the dogs with the abnormal MRI however this did not correlate with higher rates of death after multivariate analysis. The only significant factor associated with death was the presence of an abnormal MRI.

Why don’t they have lesions on MRI?

Perhaps we’re catching these cases early in the course of disease. This would stand to reason why they might have a lower death rate than those with more progressive disease at the time of diagnosis. Another option is that this is a different form of inflammatory brain disease. MUE is a “catch all” for inflammatory brain disease that isn’t infectious, or a specific form such as SRMA or EME. It likely includes all of the previously diagnosed cases of GME and NME.
Take away: If you have a dog with spinal pain, seizures, vestibular signs or multifocal CNS signs remember MUE! This disease can cause all of those signs, and a collection of other signs, in dogs. Early detection may = improved outcomes. So, if your patient is showing neurologic signs, please reach out to get a consult ASAP and to proceed with additional testing when able. We might just save their life!

Thanks for reading! I hope you are scratching out the very best that summer has to offer. I look forward to working with you soon!

Reference: Survival in dogs with meningoencephalomyelitis of unknown etiology with and without lesions detected by magnetic resonance imaging. Ostrager A, Bently, TR, Lewis MJ, Moore GE.
 

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

Levetiracetam vs. Phenobarbital for Neonatal Seizures

Thankfully, neonatal seizures are not something that we identify frequently in veterinary medicine. Unfortunately, neonatal seizures are one of the most common reasons for presentation to the ER in human medicine. Among full term infants, seizures account for 1-3.5% of the cases for infant presentation to ER. To date, phenobarbital (PB) has been the anti-epileptic drug (AED) of choice, however levetiracetam (LEV) was evaluated in a meta-analysis in 202. (REF) The findings are interesting…read on to learn more!
 
Some Background
Human infants with seizures generally have a good prognosis. Phenobarbital has been reported to control 43-80% of electrical seizures, with the added benefit of reducing brain metabolism. The downside is that it has been shown to cause neuronal apoptosis in animal models (aka our patients). LEV has a seizure control rate of 35-86% for neonatal seizures and has been shown to have a neuroprotective effect without evidence of neuronal apoptosis or synaptic development. As we well know, LEV also has a lower side effect profile in our patients. This is true for human infants however the adverse effects monitored are slightly different. In this population, blood pressure and respiratory depression are more significant and are what are reported in studies evaluating adverse effects.

The Results
Most studies reported no significant difference in efficacy between LEV and PB however 1 study showed that LEV was more effective for clinical seizures (seizures we can see) and not significantly different with electrical seizures (those we can only see on EEG). Another study reported that high dose (20-40 mg/kg/d) PB was more effective than LEV, but regular dose (20-30 mg/kg/d) was inferior to LEV. The seizure control rate in 1 study was 86% with LEV, and 62% with PB. However, the meta-analysis identified that overall, no significant difference was found between the two drugs.
Levetiracetam was the winner in terms of adverse effects! In most studies, LEV had a lower incidence of hypotension and respiratory depression than PB. Neurodevelopment scores (motor, cognitive and language scores) were similar among the two groups with a slightly higher language score in infants that had been treated with PB.
Despite all of this, PB is still the first-line treatment for neonatal seizures according to the WHO (2021) because it controls most seizures, from most etiology, and also decreases the metabolic rate. This might seem trivial, but reduced metabolic rate can improve outcome fairly strongly due to a lack of “work” that the brain must do during the post ictal phase.
 
What do I think? Based on this data, I would favor intravenous LEV at 30-60 mg/kg single dose for neonatal seizures in our patients FIRST, followed by diazepam + phenobarbital second if seizures aren’t controlled.
Thanks for reading! I hope you have a wonderful week and I look forward to working with you soon.

Age, The Neurologic Examination and Seizures

Age isn't a disease, right? No, it isn't but disease is associated with age. The older pet with seizures is more likely to have structural disease (i.e. neoplasia instead of idiopathic epilepsy), compared to the younger pet. That said, none of us want to diagnose a terminal disease in an older patient simply because the patient is older!

Can the Neurologic Examination Help Vets differentiate disease in Older Patients?
Let's look at the two most commonly performed parts of the neurologic examination and see how they related to disease. The menace response and paw replacement testing (previously called conscious proprioception) both assess the forebrain and are some of the most commonly performed parts of the neurologic examination. Here is what a recent group from Australia found in reference to finding evidence of forebrain disease on MRI:

Menace response
Sensitivity: 72%
Specificity: 47%
Odds ratio:  2.26

Proprioception
Sensitivity: 54%
Specificity: 72%
Odds ratio: 3.08

If age is then factored into the analysis, dogs greater than or equal to 6 years of age were more likely to have a forebrain disease detected by MRI if they had a menace or proprioceptive deficit. 

As a "field" neurologist (without a pocket MRI...yet) this tells me that I should encourage diagnostic imaging in patients with menace deficits, and possibly for those with proprioceptive deficits depending on concurrent findings. The chances (or Odds) of a patient having underlying forebrain disease is higher if they have these deficits than if they don't. Seems intuitive, but proprioceptive testing isn't as sensitive as assessing the menace response.
What's the take-away message here? If you have an older pet with seizures, and the neurologic examination is NORMAL, you might miss underlying structural brain disease if you do an MRI but, then again, you might now. If you have an older pet with seizures and a menace or proprioceptive deficit is noted you'll LIKELY MISS a structural brain disease if you skip the MRI. 

Although this TidBit is a repeat from 2020, I liked this study and thought it was worth repeating...again. 

Chan MK, Jull P. Accuracy of selected neurological clinical tests in diagnosing MRI-detectable forebrain lesion in dogs [published online ahead of print, 2020 Jul 15]. Aust Vet J. 2020;10.

Thanks for reading! I look forward to working with you soon. Have a great week!

Myasthenia Gravis in Cats

What is myasthenia gravis?

Myasthenia gravis (MG)  has two forms: 1) congenital and 2) acquired. Acquired myasthenia gravis is more common and results from the development of antibodies against the nicotinic acetylcholine receptors on the muscle membrane. 

What is the clinical presentation?

Cats present commonly with the generalized form which includes a wide variety of clinical signs and progressions. This may include weakness (the "floppy cat"), cervical ventroflexion, or pharyngeal weakness. Signs may be slowly or rapidly progression and even result in waxing-waning clinical signs. 

What causes the acquired form of myasthenia gravis?

Most cats have an idiopathic MG however up to 30-50% of cats will develop paraneoplastic MG for which thymoma are commonly implicated. Spontaneous remission of idiopathic MG within 6-8 months is common in dogs, but was previously thought to be uncommon in cats. A 2019 article found remission within 6 months in ALL 8 cats evaluated. (Mignan T, et al. JVIM Nov 2019) Remission even occurred in several cats that didn't have any form of immunosuppression or acetylcholinesterase inhibitors prescribed (see treatment below). 

How should I diagnose myasthenia gravis?

1. A thorough neurologic exam for appropriate lesion localization (yay!), and
2. An acetylcholine receptor (Ach-R) antibody titer through a reputable lab. Here in the states, I recommend Dr. Shelton's lab (http://vetneuromuscular.ucsd.edu/). This titer can be repeated to document biochemical remission along with the neurologic exam to document clinical remission. 

What is the ideal treatment?

Oh, the million dollar question! Based on experience I'd say cats respond less favorably to acetylcholinesterase inhibitors (think pyridostigmine or edrophonium) and therefore immunosuppressive steroids have been my go-to treatment. Having seen the data on spontaneous remission, I might consider no treatment in a minimally affected cat.

What is the long-term prognosis?

Idiopathic myasthenia gravis carries a good prognosis in cats. Should pharyngeal weakness become a clinical problem, aspiration pneumonia may result in increased morbidity or mortality. The 2019 study by Mignan et al reported a 100% survival at 6 months, without signs of relapse up to 4 years after treatment. Cats with paraneoplastic myasthenia gravis have a poorer short and long-term prognosis. 

Key Points:
1. Cervical ventroflexion, or a "floppy" cat on examination should prompt an Ach-R antibody titer for myasthenia gravis diagnosis. (Maybe even a neurology consult!)
2. Treatment could be immunosuppressive steroids OR no treatment at all if clinically mild
3. Prognosis is good if a thymoma or other neoplastic process is not identified. 

Thanks for reading! Happy 4th of July to US folks reading and Happy July 1st to Canadian folks! The rest of ya - hope you're having a good week!
Also, I'm looking for a location that can hold up to 20 people for a possible CE event in February 2025 in the middle of the state (Portage/Dells/Stevens Point). Do you have a hospital conference room I could rent or do you have a reocmmenation for a conference center that you thought did a good job in that area? Please reach out if you do!

What Role Does the BBB Play in Epileptogenisis?

The blood-brain-barrier is an important player in epilepsy, even if it is an unsung hero. You may (or perhaps may not) recall from veterinary school that there are 3 parts to the BBB. 1) the tight junction (TJ) proteins between endothelial cells 2) the highly specialized and restrictive transport system in the cellular walls and 3) the capillary wall which utilizes a basement membrane, astrocyte feet (I love that they have feet) and little pericytes. The BBB is one of the best bouncers in the system and it takes extreme caution allowing molecules to pass. Over the years we have learned that the BBB plays an important role in epilepsy. For example, disruption of the TJ proteins, most notably upregulation of MMP9 (if you want to know everyone’s full name, please refer to the article) has contributed to the generation of seizures. Conversely, stabilization of the BBB can prevent seizures in experimental models. Leakage of serum albumin, through a dysfunctional BBB, has been shown to bind to TGF-beta on astrocytes and cause astrogliosis (an increase in astrocytes, or upregulation of their function). The development of astrogliosis, followed by some changes in the extracellular matrix causes a DECREASE in the inhibitory protein GABA and INCREASE in excitatory synapses in the brain. Decreasing the inhibitors and increasing the excitatory proteins. Yikes! Bring on the seizures. 

A study was published outlining some novel ways to look at the BBB using MRI (Hanael E, et al from Israel. JVIM 2024). There are parts of that article that I will be skipping for this TidBit Tuesday because they aren't applicable unless an MRI is part of your practice. However, the parts that I think are good for general discussion relate to the location in the brain. Seizures are frequently generated in the piriform lobe, so the researchers looked at that lobe using MRI, histopathology and CSF. They found a significant increase in albumin and MMP9 proteins in the piriform lobe in dogs with idiopathic epilepsy, along with evidence of damage to the BBB on MRI in this region. CSF albumin was increased AND serum MMP9 activity was increased in dogs as well. All of this supports evidence that we are finding damage to the BBB, causing consequences to the brain (specifically the piriform cortex) which is then manifested physically as a recurrent seizure disorder (epilepsy). Perhaps the future will hold some therapies directed at "patching" the BBB as a treatment modality - you'll have to stay tuned!

This week's TidBit Tuesday was a bit heavy on the sciences so I hope you'll forgive me on this first full week of summer. Epilepsy is an ever changing area of study that I find fascinating and hope you don't mind coming along for the ride with me sometimes. Have a terrific week and I hope you can get out and enjoy the sunshine!

Zonisamide Use in Dogs

Guess what? Another study evaluating zonisamide was published recently (this one out of Japan: Saito et al. JVIM 2024). A historical paucity of data about zonisamide has made me hesitant to use this antiepileptic drug (AED) so I’m pleased that times are a changing!
On to the important stuff… This was a prospective multicenter, open-label uncontrolled study in 56 dogs. Several dogs dropped out, so the end result was that 53 dogs were assessed for efficacy and 56 dogs were included for evaluation of tolerability.

Results

To determine an appropriate dose and the target plasma concentrations, many researchers will calculate the mean drug dose and concentration for 50%, 90% and 100% of the responders. They found the following:
50%: dose range was 2.7-4.9 mg/kg PO q12h; no mean trough plasma concentration provided.
90%: mean dose 4.8 mg/kg PO q12h; mean trough plasma concentration 18.9 ug/ml
100%: mean dose 5.5 mg/kg PO q12h; mean trough plasma concentration 21.9 ug/ml
Putting all of this together, the starting dose recommendation by the authors was 2.5-5.5 mg/kg PO q12h for most dogs (reduce this for dogs with renal disease). The recommended therapeutic range is 10-40 ug/ml. However, there are a couple of things to be aware of when using this therapeutic range. First, the study design stated that the dose would be increased incrementally every 1-2 weeks for dogs with persistent seizures until adverse effects were noted OR they reached 15 mg/kg dosing. They did not exceed 15 mg/kg which could affect what is considered an appropriate therapeutic range. Secondly, the dose did not predict the serum concentration, suggesting non-linear PK. What this means is that if you start a dog on zonisamide at 5 mg/kg PO q12h, you cannot necessarily predict the plasma drug concentration. Phenobarbital in cats has predictable PK, but it doesn’t in dogs, for example. Because of this, it’s not completely clear what an “acceptable” starting dose may be for a given individual. How do you decide? It is recommended that you start with the given dose, measure drug concentrations and evaluate adverse effects. If the animal is displaying unwanted adverse effects, the dose is probably too high (regardless of drug concentration). If the animal is continuing to have seizures at an undesirable frequency, without adverse effects, the dose is likely too low. We know that adverse effects happen at higher concentrations AND that organ disease is more likely to occur at higher drug concentrations so do be cautious above 40 ug/ml plasma concentration.
Adverse effects noted in this study were minimal. They reported at least 1 adverse effect in 7 of the 56 dogs. Several dogs were withdrawn from the study due to perceived poor efficacy and adverse effects as well. Adverse effects noted include reduced activity, reduced appetite, vomiting, pelvic limb weakness, soft stools and constipation. All were mild and transient. No elevation in liver values were noted. Remember that this drug is a sulfa derivative so a patient with known sulfa sensitivity should avoid zonisamide. No renal disease or renal tubular acidosis was noted however it has been reported in other dogs receiving zonisamide. 
Seizure control was obtained in 76% of the 53 dogs. A further 55% of dogs obtained seizure freedom. These results are better than the prior study evaluating zonisamide in which about 60% of the dogs were reported to obtain seizure control. The improved results are possibly due to different dosing, or a different genetic epileptic population.

Take home message:
Zonisamide is a viable alternative for dogs either as a primary or as an add-on AED. Start at 2.5 – 5.5 mg/kg PO q12h and measure plasma drug concentrations (yay!!) at 2 weeks.
 
Thanks for reading! I hope you have a great week. Remember to check FB for last minute updates to my schedule through out the summer. Happy Father’s day to all of the dads, dads-to-be and pet-dads out there!

Use of Zonisamide for Cats

Use of Zonisamide in Cats

Zonisamide has been recommended for use in cats and dogs with seizures for almost 20 years despite a lack of efficacy studies. Not that this is surprising -we love to extrapolate from human and canine medicine to cats – but it was frustrating to say the least. Well, that has been improved recently after a study evaluating the effectiveness of add-on zonisamide OR single agent zonisamide in a population of cats with seizures. (https://doi.org/10.1111/jvim.16984). This was a retrospective study of 57 cats, with seizures of any etiology that were prescribed zonisamide as part of their treatment plan. Of this group, 16/57 were diagnosed with idiopathic epilepsy (Tier II level confidence), 4/57 neoplasia, 4/57 had congenital brain disease, 2/57 head trauma and 1/57 with metabolic encephalopathy. The remainder (30 cats) did not under go diagnostic testing to obtain a diagnosis and were treated for presumptive disease based on the clinician’s assessment.

Results

Prior to treatment, the majority of cats were reported to have generalized seizures with both focal and generalized seizures taking second place. Focal only seizures were a distant third place with only 12 cats. The cats in this study demonstrated a significant reduction in seizure days (number of days having a seizure) and seizures (total count) per month following administration of zonisamide. Within the confirmed idiopathic epilepsy group, this group had a reduction in seizures/month of 1, with a total of 69.2% of cats with idiopathic epilepsy responding to zonisamide treatment. This equates to 9 of 13 cats for whom they had efficacy data. Add-on zonisamide was noted in 33 cats for whom 56% responded to treatment. Lastly, for cats whom zonisamide was the only AED, a 70% response rate was noted. A few cats had an increase in seizures after starting zonisamide. This may have been related to disease progression or resistant epilepsy. The retrospective nature, along with the lack of diagnostic testing in all cats, makes assumptions difficult.

The median daily dose of zonisamide was 7.55 mg/kg (range 3.8-17.7 mg/kg) and it was given q12h most commonly (36/57 cats). This drug can be given q12 or q24h based on the PK available.

Adverse effects were noted in 15/57 (26%) which is relatively low compared to the reported adverse effects for, say, phenobarbital. The adverse effects included inappetence (n=10), transient sedation (n=6), ataxia (n=4), vomiting (n=3). The adverse effects appeared dose related therefore higher doses resulted in more frequent adverse effects. The adverse effects lasted for variable amounts of time but typically 2-4 weeks. Mild changes to CBC were noted but significance was unknown due to concurrent disease. Liver enzyme elevation including ALT, ALP and ASK was noted but increases were mild.

What’s the take home message?
Zonisamide appears to control 56- 70% of seizures for cats, regardless of etiology. This number is closer to 70% for idiopathic epileptic cats.
Zonisamide has a low incidence of adverse effects, however the nausea/vomiting/anorexia adverse effects should be closely monitored.
Zonisamide is metabolized through the liver and is a sulfa derivative so use caution in patients with a known sensitivity.
 
I hope you enjoyed this week’s TidBit and will join me in celebrating the publication of solid data about zonisamide! I hope you have a great week and look forward to working with you soon.

Neurodisability Score for MUO

As discussed last week, a neurodisability score (NDS) has been proposed for use in dogs with meningitis of unknown origin (MUO). The goal is to help grade the clinical signs more objectively and, hopefully, prognosticate more accurately. The score was developed by Drs. Goncalves et al (https://doi.org/10.1111/jvim.16717) from the UK and published in 2023.

A retrospective evaluation of medical records was performed to identify common clinical signs at presentation. Subsequently these signs were grouped in to the following categories for prospective use: seizure activity, ambulatory status, posture and cerebral, cerebellar, brainstem and visual signs. For the prospective part, the score was tested on 31 dogs diagnosed with MUO. Table 2 of the published article has an outline of the scoring system which I would suggest you look at if you have time. As an example, under the “ambulatory status” section the options are “normal, mild paresis or ataxia but ambulatory without falling, moderate/severe paresis or ataxia with frequent falling, and nonambulatory”. Each of these options is given a numeric score from 0 (least severe) to 3 (most severe). As the categories are worked through, points will be accrued based on their neurologic exam. The maximal score is 21, indicating he most severe disease. According to the article, the mean score at presentation was 8 +/- 2.85 points. All of the things that you imagine would affect this score such as concurrent disease, treatment prior to referral, and evaluator skill must be considered here (which the authors did consider, for the most part). In the end, they found a significant difference in dogs that survived to discharge (median 8; range 3-14) and those that did not (median 12.3; range 8-13). You can see as well as I can that there is marked overlap between the ranges which makes it difficult in a clinical patient to draw conclusions. Furthermore, the study did not evaluate validity (did the test measure what it was supposed to be measuring) and did not find an association at a specific cut-off value related to long-term outcome. The study presented in last weeks TidBit Tuesday suggested a cut off value of 7 would be used to predict death by 6 months for dogs with MUO. I’m ecstatic that this work is being done but caution you to use it with care. Euthanizing a pet simply based on this score feels inappropriate at this time. Predicting a poorer possible outcome at 6 months and relaying this information to a client would be an appropriate use of the NDS. It IS encouraging that we may have a universally available tool for ALL VETS (i.e. not a specialty tool like an MRI, or a neurofilament in CSF) that we can use to talk about MUO in objective terms. As with most of the TidBit Tuesdays there will be much more to come on this topic over time so stay tuned!
 
Thanks for reading! Changes to my schedule are once again upon us as the summer sets in. My schedule varies WEEKLY so please reach out if you have a case that needs to be seen but cannot find a suitable time on the schedule; I may have more flexibility than what is listed, so please ask. I will be closed at the end of June for a few days for a family wedding, and mid-July for the Dane County Fair but otherwise anticipate high availability for you this summer. Enjoy the beautiful spring weather and the delicious smells of blooming things this week!

The Prognosis Meningoencephalitis of Unknown Origin

Meningoencephalitis of unknown origin (MUO) is a frequent diagnosis for dogs with multifocal neurologic signs. The name should tip you off that we’re still figuring out this interesting disease amd do not know the underlying cause yet.  It is thought to be immune mediated, and therefore treatment often includes an immunosuppressive dose of steroids +/- an additional immunosuppressive such as cytarabine, azathioprine or cyclosporine. Despite decades of awareness of this disease we are still working out the prognostic indicators. Back in my academic days, a resident of mine and I tried to sort out this question by evaluating brain MRI results, with little success. A recent study took another crack at the elusive prognostic indicators and published their findings in JVIM (Goncalves R, et al. JVIM 2024).

Materials and Methods

447 dogs were included in this retrospective study from 2 institutions. Did you see that giant number of included cases?? Go vet med, go! Anyhoo, the authors included dogs with signs of inflammation (brain MRI, spinal tap) and because it was a retrospective study, there were a number of different treatment protocols included. Perhaps this creates too much variability to carefully evaluate outcome or prognosis. I might argue that  there is no other way to accrue a large number of cases of MUO. A neuro disability score (NDS) was assigned to these patients (score developed by the author and several others and published in 2023). Survival was reported.

Results

I’m going to list some of the key results below but if you wish to learn more about the results, please refer to the article. It is well written and comprehensive.

• Median age at presentation was 48 months

• 
  The majority of breeds represented were small breeds, but a few Labs, spaniels, and larger dogs were also included.

• 
  The season of diagnosis was equal across all 4 seasons

• 
  Common presenting complaints were proprioceptive deficits (77%), ataxia (65%), obtunded mentation (62%), seizures (32%).

• 
  The most common neuroanatomic lesion localization was multifocal (43%), followed by forebrain (29%)

• 
  Median follow-up time was 11 months. 82% of dogs survived to discharge and 63% were alive at 6 months.

• 
  A significant difference in survival was noted for dogs WITH a NDS compared to those without and a score of greater than 7 resulted in a sensitivity of 61% and specificity of 67% for predicting death at 6 months after diagnosis.

• 
  Relapse occurred in 50% of dogs that survived to discharge

• 
  Of those that relapsed, incomplete resolution of neurologic disease during the 6 month follow-up period, a higher NDS and neurologic signs >7 days duration before intervention were statistically associated with relapse.

What should we do with this information?

The take home message should be that we should perform a NDS on patients with suspected or confirmed MUO to help provide a prognosis AND that a more rapid referral may provide a better long-term outcome.

Stay tuned next week for a review of the NDS! Thanks for reading and I Hope you have a great rest of your week!

How Well Do We Communicate?

How Do We Communicate?

An article recently came across my desk that I found enlightening and hope you will too. The topic today is about communication, specifically, communication with owners and vets about neurology. I find myself using a LOT of words in my consultations with owners and often wonder if those words are having an effect. You are not alone if you find neurology daunting – many clinicians do – and that innate worry can lead to communication barriers, too!  Prior to COVID I used a white board and wrote key points on the board as I spoke to owners. The COVID pandemic resulted in a large percentage of telephone based conversations and the white board wasn’t there. Now that I’m back to in person consulting, the white board is back too and I think, highly subjectively, that I see a difference in client comprehension. That is why this article sparked my attention. I am always trying to figure out ways to communicate as effectively as possible with you, my actual client, and your client (aka the pet’s owner) so that the pet gets optimal care.
The article I’m referencing is by Dr. Thomas Flegel (a German neurologist) and his colleagues (JVIM 2024 1-4). In this article Dr. Flegel and his team evaluated the client’s recall of the discharge and compared that to the clinician’s recall of the discharge. There were 3 parts of the study. Part 1 and 2 were only answered by the client and they pertained to demographic questions of the owner and atmosphere/comfort level during discharge. Part 3 was about the diagnosis, treatment, and long-term plan. A raw percent agreement was then calculated for different questions. Part 3 was repeated 2 weeks later.

Results

I had preconceived ideas that age, maybe native language speaking and level of education would influence these results. I was wrong! The only statistically significant difference was the client’s age; increasing age lead to a decreased raw percent agreement. This meant that clients over 50 years old had a more difficult time recalling the specifics about the case compared to the clinician. I don’t believe they accounted for clinician age in the study, but they did evaluate clinician experience.

The three questions that had significantly lower raw percent agreement 2 weeks later. Those questions were
“Should you give the medication before feeding your pet?”
“What are potential adverse effects of the medicine you have to give your pet?”
“If your pet has to live permanently with signs of the disease, which are those?”

Their conclusion was that we should emphasize the most important parts of a pet’s medical care when we discharge them (or finish a consult, in my case). The researchers also commented that many clients could refer to the discharge instructions to answer the questions therefore resulting in similar answers but their response was “who cares?” In a practical sense, if the client wants to remember the side effects of the medication, for example, we HOPE they will refer to the discharge paperwork!

After each consult I summarize the findings for both the attending clinician (you) and the client. I know many of you write summaries for your clients as well. Some parts of my written summaries will be over the heads of some owners because it is intended for you (my client) and some of the discharge will be too simple for you because it is intended for the client. But having all the information available to all parties can only improve understanding and follow through. Hopefully this limits the number of clients coming back to you with questions after my consult, and I have been told it helps many of you recall my BILLIONS of words when the client calls with questions. I know they’re long but hopefully they’re not unapproachably long. If you have a suggested change to the summary forms, I’d really love to hear from you!
 

Thanks for including me in your patients’ care. I look forward to working with you (and writing down my findings) soon!

Sciatic Nerve Injury in Dogs and Cats

Dogs and cats commonly present for brachial plexus injury, usually after a trauma, but what about sciatic nerve injury? The sciatic nerve is composed of the peroneal and tibial nerves and makes up a lot of the L6-S3 nerve roots. It's a big one! So, how easy is it to damage all or part of this workhorse? Damage can take on 3 forms. First, and most severe, is neurotmesis which means transection of axion and myelin and perineural tissues. Second, is axonotmesis, which suggests damage to the axon with preservation of the myelin and perineural structures. Finally, and least concerning, is neurapraxia, which results in functional damage but minimal to no structural damage. Neurapraxia could be like a "stretch" or loss of minimal myelin. A recent study, published by Dell'Apa, et al from Italy, outlined the signs, etiology and prognosis for 38 dogs and 10 cats diagnosed with a sciatic nerve injury. 

What are common clinical signs of sciatic nerve injury?

According to their study, Dell'Apa et al found that the majority of dogs (~80%) had either a loss of hock flexion, or a lack of hock extension. Along with this, about 75% of dogs had a loss of proprioception in the affected limb. There was variable sensory loss (deep pain) and about 13% of dogs had evidence of a root signature. All cats demonstrated a loss of hock extension (i.e. showed dropped hock) and 90% showed a loss of hock flexion. No cat showed signs of a root signature and only 5 cats (50%) showed changes in sensory. Remember, these cases are MONOparesis or plegia! No paraplegia/paresis would be expected for this disease. 

Which nerve was commonly affected?
Tibial nerve: dogs - 16%; cats 20%
Peroneal nerve: dogs - 37%, cats - 60%
Sciatic nerve (common trunk): dogs - 47%, cats - 20%

What are the most common etiology?

The most common cause of sciatic nerve injury in dogs was bite wounds (24%) followed by surgery (TPLO, TPO, DPO, Modified retinacular imbrication, or removal of an intramedullary pin; 18%), and then trauma. I must add here that the bite wounds were caused by wild board. Wild boar! It's Italy, remember? The most common cause of sciatic nerve injury in cats was pelvic trauma (50%), followed in equal amounts by surgery for a femoral fracture (20%), and an IM injection (20%). Only 1 cat sustained a bite, and it was from a dog. Apparently, cat's aren't tasty to wild boar. Or they're faster. (Or not used for hunting wild boar??)

What was the outcome?

A poor prognosis was deemed one that resulted in euthanasia, arthrodesis of the joint or amputation of the limb due to poor function. A good prognosis did not necessarily mean a return to normal, but instead indicated limb function had improved. Animals that were able to flex and extend their tarsus had a significantly better long-term prognosis than those that couldn't. Furthermore, loss of deep pain was NOT a prognostic indicator in this study. This is different than spinal cord studies in which the loss of deep pain is a strong prognostic indicator. Peripheral nerves can regenerate and therefore this loss wasn't useful for predicting recovery. Overall, 9 of 32 dogs (28%) and 1 of 9 cats had a negative outcome. This suggests a favorable long-term outcome for this population of animals. 
 
Thanks for reading! A quick reminder that I am away until Thursday (May 9) so you may experience a delayed response to emails, texts or phone calls. Happy Mother's Day to all who celebrate! 

Neuroanatomic Lesion Localization Practice Case

It's time to sharpen those pencils and put on your thinking hat. It's neuroanatomic lesion localization practice case time! 
Signalment: A 4 year old FS Mixed breed dog (along the lines of a Pitbull X)
History: The patient presented with a 24 hour history of acute onset ataxia, and weakness. The owner's noticed significant muscle fasciculations in the neck (mistaken for seizures) along with a reluctance to lift her head. The weakness was progressive from thoracic limb lameness initially, through ataxia to ambulatory tetraparesis. No medications had been given prior to the consultation. 
PE: Unremarkable other than BCS 7/9
Neurologic Examination
Mentation: QAR. Friendly, but subdued.
Cranial nerves: Normal
Gait: Ambulatory tetraparesis, worse on the left thoracic leg. She was noted to have reduced mobility in the left thoracic limb along with a lack of adequate weight-bearing on that limb. The other three limbs were weak, but she could bear weight.
Reflexes: Absent withdrawal left thoracic limb. Normal withdrawal noted in the other three limbs. Normal patellar reflexes bilaterally. Normal anal tone and perineal reflex along with c. trunci reflex. 
Postural reactions: Absent paw replacement testing all four limbs.
Palpation: Painful with cervical palpation and unable to perform cervical ROM without yelping. 

Neuroanatomic lesion localization: where should we start?

The easiest place to start is with elimination.
A. We do NOT have a seizure history, change in mentation or any cranial nerve deficits, right? The lesion therefore is unlikely to be rostral to the foramen magnum. 
B. We have evidence of disease in all four limbs therefore the lesion must be cranial to the T3 spinal cord segment. (If the lesion were caudal to T3, we would expect the thoracic limbs to be normal and without deficits.)
Okay, so far, we have now narrowed our findings to C1-T2
C. The reflex arc is C6-T2 in the thoracic limb. Do we have any evidence of reduced or absent thoracic limb reflexes? Yes - the left thoracic limb has a reduced withdrawal reflex. Animals with reduced reflexes have their lesions IN the reflex arc (C5-T2 or L4-S3 in the pelvic limb). 

Lesion localization is: C6-T2 spinal cord, more affecting the left side

What would you consider for differential diagnoses? 

In this case, the two most important historical factors that I would focus on are the "acute onset" and "painful" parts. Things like neurodegenerative disease are not painful, and rarely acute. The most common painful myelopathies I like to summarize as being "2-Ds, 2-T or an M". What are they? Disc herniation, discospondylitis, tumor (I know, I know, it's called neoplasia but it's easier to remember 2D,2T,M.), trauma and meningitis/meningomyelitis. 

Because this isn't a disease-focused TidBit I'll cut to the chase and tell you that this dog was diagnosed with a type I disc herniation and had surgical decompression. She felt much better! 

How did you do? Did you enjoy this case this week? Sometimes the simple ones are the hardest because we over think them so much! If this wasn't a simple one remember that I'm available to help you with cases. Neurologic cases aren't fun for everyone so reach out for help if you're stuck! 

Thanks for reading. I will be away at a conference and taking a little vacation time May 4-8th. I will have some access to email but please be patient with inevitable delays. Thanks for including me in your patient's care! Have a great week and stay safe.

Is there a Weekend Effect in Veterinary Medicine?

The “weekend effect” (WE) is a term used to describe poorer patient outcomes associated with treatment out-of-hours. There has been debate in the human literature if this effect is “real” or not. Specific focus has been aimed at mortality or morbidity associated with the WE. A recent study in England, looked at the WE in relation to decompressive hemilaminectomy surgery in a cohort study (comparing a poputation of dogs having surgery afterhours to those operated during business hours) and, I found it informative. (Low D, et al. Veterinary Surgery. 2024;1–10.)

You may be aware that the timing of spinal cord decompression has been hotly debated over the past…oh..100 years or so. Recently, some studies have suggested that surgical decompression for an acutely non-ambulatory dog is not an emergency and therefore can occur during normal business hours. This has been suggested for dogs with and without deep pain sensation. Additional studies have supported that in fact it DOES matter and those studies advocate for decompression of dogs with a loss of deep pain within 24 hours of documented loss of deep pain. I tend to favor the “don’t wait, cut ASAP” approach but the choice is controversial. The study by Low and colleagues from England did not address the pros or cons of timing of surgery but instead looked at outcome (did they walk, or not) and adverse events (urinary tract infections, gastric ulcers, skin infections/ulcers, post operative neurologic deterioration, etc.) for dogs undergoing back surgery within or outside of business hours.

The findings of this study were interesting. They identified a significant difference in postoperative morbidity and the recovery of ambulation in a group of dogs undergoing surgery afterhours vs those undergoing surgery during business hours. They stated that 1 in 8 dogs would not recovery ambulation when exposed to weekend surgery compared to if they were exposed to weekday surgery. Furthermore 1 in 7 dogs would experience an additional post operative morbidity when exposed to weekend surgery, compared to weekday surgery.

What contributed to the results? The variables for a patient undergoing, and recovering from, surgery are numerous regardless of the timing of the surgery. For example, there are pre-hospital variables (such as the timing and treatment provided by the referring vet), hospital variables (staff tiredness, case load, surgeon experience) and post-hospital factors (availability of aftercare support in the patient’s home, the hospital discharge process). Many of the hospital variables were evaluated in the study and not statistically associated with outcome or morbidity. The pre- and post-hospital factors are more difficult to study due to the inherently heterogenous state.

What do I do with this information? I included this study as at TidBit Tuesday to increase awareness of the possible WE in both veterinary medicine at large (yet to be fully determined) and specifically within neurosurgery. The data does not suggest that you shouldn’t make a referral if you have a nonambulatory patient, especially if they’ve lost deep pain! It also shouldn’t be used to deter a client from pursuing surgery on a weekend or afterhours. I’m not sure there is an actionable outcome by gaining this knowledge, except for the simple purpose of increasing your (and my) knowledge of the existence of a WE. By being aware, we can sometimes change our actions in subtle ways that may improve the outcome for our patients. Have you ever managed an especially difficult seizure patient? What if you had a dog develop liver disease while taking zonisamide or phenobarbital? Those cases increase our awareness of the “bad” outcomes and increase our sensitivity to treating the next seizure case, or next dog on zonisamide or phenobarbital. In fact, population statistics would suggest that a low number of dogs have resistant epilepsy but when it is 1 of your 10 or so cases that you’ve managed it feels like a high risk and may change how you discuss seizures with the next client that walks in the door with a pet with seizures. Awareness of the WE may change how we, as neurologists, operate and intern may affect the WE. Time shall tell!

Thanks for reading through this long TidBit. I hope you enjoyed the lovely weekend weather (it was in the 70s for us!) and have a wonderful week.