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 are 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. A persistent seizure disorder is possible following a CVA. Repeated seizures, without the development of other neurologic signs, could suggest a seizure disorder and NOT progression or regression of disease. 

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! With the onset of winter weather, mobile neurology consultations may become challenging at times. Remember a video consult may suit your needs if I cannot be on site due to inclimate weather! Stay safe and warm out there this week, folks!

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.

Hypokalemia Myopathy and Positioning Head Tilt in Cats?

I read an interesting article recently about positioning head tilts in cats with hypokalemia myopathy (https://doi.org/10.1177/1098612X231175761) This isn't likely to be something you encounter often in practice, but I hope you will also find it an intesting read nontheless. 

Hypokalemic myopathies are common in cats and often result in signs of weakness including cervical ventroflexion and/or tetraparesis. We can see hypokalemia secondary to renal disease, hyperthyroidism, dietary insufficency, chronic vomiting/diarrhea, and other metabolic causes. The subsequent myopathy occurs due to overpolarization of the muscle sarcolemma resting membrane potential making it resistant to depolarisation. Without depolarization, there is no muscle contraction and we see clinical weakness. 

When the head is turned, the cerebellum (specifically the nodulus and uvula) receive input from the vestibular nuclei, who in turn receive sensory information from the stretch receptors in the cervical muscles, on the whereabouts of the head and neck. This allows the cerebellum to modify the head position so that the head remains paralell to the ground as it is turned. With positioning head tilts, the head tilts to the opposite direction that the head is turning. When looking straight, no head tilt is observed. When turning right, the head tilts slightly to the left, for example.  

This article described 14 cats who had a positioning head tilt obseved on neurologic examintation AND had concurrent hypokalemia. One cat had an MRI and no cerebellar lesions were noted. Does that mean the others didn't? No, of course not. However, when the potassium was normalized the positional head tilt resolved. This would suggest cause and effect but isn't definative. The authors supposed that the muscle firing in the spindle fibers (the very small muscles located in the bigger muscles that convert stretch to neuronal impulse for sensory information) weren't able to depolarize appropriately. This lack of depolarization resulted in an absence of information about the whereabouts of the cervcial muscles (and those attached to the head, specifically) and didn't allow the cerebellum to modify head posture when turning. Pretty cool, huh? Although this is just a therory, I personally think it is pretty slick and clever. 

Take home message:
What do you do with a positioning head tilt in a cat? Look for hypokalemia and if identified, address it! 

Do you know that I'm in charge of my own schedule? I'm not corporate or owned by anyone! So if you cannot find a suitable time on the scheduler please email me! I will do my best to find an earlier time to accommodate a more urgent case. Some of you lovely, considerate, folks have told me that you hate to bother me to ask. If you're one of those, please know you're not a bother. We're both trying to work on behalf of your patient! 
Have a great week. I hope you enjoyed this little TidBit as much as I did. I look forward to working with you soon!

How to Localize a Cranial Nerve

As we sit here at the head of the year, I cannot think of a better time to review the cranial nerves. (Yes, I like cheesy jokes. I have kids. Here's another: what's the best present? See the bottom for the answer.)

First important thing to remember about cranial nerves: all cranial nerves except I and II have cell bodies associated with a specific brainstem segment. You might even argue that CN II localizes to the thalamus, which is an embryological part of the brainstem but...well, then we should have a coffee and get to know each other better!  Let's stick to the idea that CN III-XII have cell bodies in specific brainstem segments, thus making it possible (dare I say easy??)  for us to localize a lesion to either a specific brainstem segment OR the peripheral nerve. 

What are the names of the brainstem segments, again? (Mesencephalon, metencephalon, myelencephalon). Okay, whew! Now that that is over, how do you decide if a deficit is coming from the nerve nucleus in the brainstem OR the peripheral nerve?

Take the following steps:

1. Identify the cranial nerve affected (i.e. facial nerve = CN 7).

2. Identify the segment of brainstem associated with the nucleus of this cranial nerve. Don't remember what cranial nerves are associated with which brainstem segment? Midbrain = CN 3,4; Pons = CN 5, Medulla = CN 6-12

3. Are any ipsilateral long tract deficits (postural reaction deficits, hemiparesis) or mentation changes (obtunded, stupor, coma) present?

   1. If yes, the lesion is in the brainstem segment associated with the cranial nerve (i.e. medulla).

   2. If no, the lesion is affecting the peripheral portion of the affected nerve

Guess what? You can apply these steps to any deficit affecting CN III-XII. Yay!
 
Do you need help performing the neurologic exam? I'd love to help! Looking for the answer to the joke? The answer is: a broken drum! You just cannot beat it. Thanks for reading and Happy New Year!

I am Thankful For You

Thank You and Happy New Year


As we near the end of 2023, I'd like to take this moment to thank you. Thank you for welcoming me into your clinic, for subscribing to the TidBit Tuesday emails, for providing great feedback on cases we've seen together AND on the TidBit Tuesdays that spoke to you, for allowing me to help care for your patients and most importantly, for being the kind, caring and thoughtful vets that you are! It is a pleasure to work with you, see patients with you, consult with you, and learn along with you. I hope you had a good 2023 and that 2024 brings joy, health and happiness to you and those you love. 

Happy New Year! I am excited for 2024 and look forward to working with you soon!

When is Lameness not Orthopedic?

Lameness is typically orthopedic, as we know, but there are times when this isn’t true. How do we know when this is true? To answer this question, I’d love to go through a case with you today.

Signalment: 11 year old FS Labrador

History: She has a 4 week history of right thoracic limb lameness. She is a hunting dog, and signs were noted after a busy weekend in the field. On initial evaluation, mild discomfort was appreciated in her elbow therefore carprofen was started. Clinical signs did not improve; they worsened. She became intermittently non-weightbearing lame in the right limb. All other limbs appeared normal. Additionally, she started helping when laying down or rising from laying. At this point, I stepped into the game. What am I looking for to suggest this might be neurologic in origin?

Neurologic Examination:

Mentation: BAR

Cranial nerves: miosis OD, did not dilate in a dark space. Remaining CN normal.

Gait: Ambulatory, moderate right thoracic limb lameness. When toe touching, the limb was touching on tiptoe only.

Reflexes: Reduced withdrawal distal to the elbow on the right (unable to flex the carpus or elbow completely during withdrawal but able to mechanically flex both joints when I flex them), unable to detect triceps reflex on either side, remainder normal. Absent cutaneous trunci reflex on right, normal on left. Normal reflexes both pelvic limbs.

Postural reactions: Normal paw replacement in left thoracic limb and both pelvic limbs. Unable to assess paw replacement in the right thoracic limb due to non-weightbearing status. Reduced hopping on right thoracic limb compared to left thoracic limb.

Palpation: No spinal pain, normal cervical ROM.

What is the neuroanatomic lesion localization?

The first question is always, is the problem neurologic in origin? She has evidence of reduced reflexes so I would suggest, yes, it is. Essentially, our abnormalities are focused on that right thoracic limb with the addition of miosis OD and absent c. trunci right side.

Reduced withdrawal in the thoracic limb suggests a radial nerve injury/damage. Even though signs are distal to the elbow, the lesion could still be proximal, and neurodegeneration has occurred distally. Is the damage inside the spinal canal (central) or in the peripheral nerves (brachial plexus)? To answer this question, look at the right pelvic limb. Do you see any paw replacement deficits or weakness in the right pelvic limb? These are the long tracts going from the limb to the brain and the must pass right through C6-T2 and C1-C5 as they do so. If the lesion is in the canal, we should see paw replacement deficits in the right pelvic limb. We don’t, so the lesion is more likely in the radial nerves after they have exited from the canal.

What do we do with the miosis? The sympathetic pathway to the eye is as follows: thalamus à brainstem à cervical spinal cord à exit T1-T3 à join vagosympathetic trunk and ascend to the head à ganglion  à go through bulla to jump on CN 5 (trigeminal) à end in the iris for dilation. The radial nerve exits from segments C6-T2, which would cross over with T1-T3 and therefore we could make an argument that the miosis is secondary to involvement of this segment of the radial nerve.

What about the c. trunci? This one is pretty simple to understand once we refresh our memory of anatomy. Cutaneous trunci reflex is a simple spinal cord reflex that uses the dorsal sensory spinal nerves as afferent (sensory), and lateral thoracic nerve as efferent (motor). The lateral thoracic nerve arises from C8-T1. This fits with our assumption of a C6-T2 right sided neuropathy because loss of the lateral thoracic nerve on one side would cause an absent cutaneous trunci reflex.

Neuroanatomic lesion localization: Peripheral C6-T2 neuropathy/radiculopathy.

The differential diagnoses for this case were a lateralized intervertebral disc herniation, neoplasia, much less likely neuritis (infectious or inflammatory) and hypothyroidism. As it turns out this dog was diagnosed via MRI with a mass in the right brachial plexus. The owners elected amputation and it was determined to be a nerve sheath tumor. Why did the signs appear acutely? It’s not completely clear but my guess is that the dog was already decompensated slightly, and the heavy work caused inflammation or maybe even hemorrhage around the mass that resulted in an acute exacerbation.

That’s it for now! Reach out if you have any questions about this case, or any other case! I look forward to working with you soon. Have a great week!

Non-Convulsive Seizures in Dogs

Non-Convulsive Seizures in Dogs and Cats With Cluster Seizures

This week we're going to dig into non-convulsive seizures in dogs a bit before we jump off of the seizure bandwagon and back into other topics in neurology next week. (Sorry to the surgeons that read these!) A recent study out of Germany by Tastensen et al (DOI: 10.1111/jvim.16953) evaluated nonconvulsive seizures in dogs and cats with cluster seizures. A few definitions, first....

Cluster seizures: 2 or more seizures within 24 hours in which pets regain consciousness between seizures. 
Status Epilepticus (SE): Seizures lasting for longer than 5 minutes or 2 or more seizures in which consciousness is not regained. 
Nonconvulsive seizures (NCS): no visible somatic or autonomic manifestation of seizures with evidence on EEG. 
Nonconvulsive status epilepticus (NCSE): no visible somatic or autonomic manifestation of seizures, with evidence on EEG and the seizures are lasting longer than 5 minutes. (yikes!)

This study evaluated 26 dogs and 12 cats with EEG monitoring following cluster seizures and found 11 of the animals (9 dogs, 2 cats) had NCS. Of these 11 dogs and cats, 4 dogs and 2 cats (16%) had NCSE. They found repeated doses of benzodiazepine drugs and levetiracetam did not break the seizures. Only inhalant anesthesia with propofol induction resulted in a return to baseline EEG. 

Six of 11 animals had a decreased level of awareness and a few of them had mild twitching of an ear which could have represented the somatic movement of the seizure. Sadly, this group had a much higher mortality rate (73% NCS; 67% NCSE) than the general population of dogs without NCS or NCSE (27%). Overall, cluster seizures have a higher mortality rate than for dogs or cats without cluster seizures (~40%) as well. None of these patients died as a result of NCSE or NCS however several were euthanized. 

The seizure etiology was more often structural epilepsy (neoplasia, encephalitis, malformation, vascular cause or trauma) and accounted for 22/38 (58%) of the animals in the study. About 18% (7/38) had idiopathic epilepsy, 11% (4/38) had unknown epilepsy and about 18% (7/38) had reactive seizures. Does this mean that dogs and cats with structural epilepsy are more likely to have cluster seizures, or does it mean that the prognosis is inherently poorer for animals with structural epilepsy? If the prognosis is poorer, do clients elect humane euthanasia when in a situation of NCSE more readily, driving up the mortality rate, or does the disease make it harder to treat? Non-convulsive epilepsy is more common in humans with cluster seizures as well, and has a higher mortality rate than people without NCE or NCSE. I don't have the answers to these questions but pose them as a way of critically reviewing the data provided.

Take home message:
If you have a dog or cat with a history of cluster seizures and they are persistently, mentally inappropriate (obtunded, stupor or coma) after stopping the physical appearance of the seizure consider nonconvulsive seizures. Inhalant anesthesia would be recommended however without additional diagnostic testing (such as MRI or spinal tap) it would be unknown if there is high intracranial pressure from the underlying disease which could increase the risk of complication with anesthesia. So what do you do in general practice? If the owner wants a referral for 24 care - start there. If not, consider a bolus of diazepam or midazolam. OR you could monitor for 1-2 hours to determine if the change in behavior is secondary to postictal changes. 

Not sure how to manage a seizure case? Feel free to email or call me or schedule a neurology consult! Please always text or call if it is an emergency; I don't check my email very often during the day.  Have a great rest of your day!

Once Daily Phenobarbital for Cats?

A study by Dr. Mojarradi et al, out of Sweden, was recently published in the Journal of Feline Medicine and Surgery reporting on once daily phenobarbital administration for cats with seizures. The reported half-life of phenobarbital in cats is 43-72 hours which could suggest once daily treatment is possible, however based on pharmacokinetic data twice daily dosing has been the standard of care. This retrospective study questioned if this was necessary. 

This study was a retrospective review of 9 cats up to 3 years from enrollment. They tracked the number of seizures before starting phenobarbital (unfortunately for an unknown amount of time) and compared that to the number of seizures after starting phenobarbital. The cats were required to have 2 or more seizures, separated by at least 24 hours, prior to starting phenobarbital however the frequency and duration of the seizure disorder for each cat isn't known. They do comment that 6/9 cats had 1 or more per month prior to starting phenobarbital. Phenobarbital was started at a mean dose of 1.8 mg/kg PO q24h, the mean serum concentration of phenobarbital was 11 ug/ml (range 6-17) at about 1 month (range 19-54 days). All but 1 cat was seizure-free at that first follow-up. The second and third follow-up appointments, roughly 1 year apart, showed a few more seizures in the time range however overall 8/9 cats were considered to be in seizure remission (no seizures for more than 12 months) at the end of the study. Seizure remission, as defined in this study, was less than 1 seizure every 12 months. If they started at 1 seizure/month, and ended at 1 per year that is a pretty remarkable improvement! So remarkable, I wonder if the phenobarbital is responsible for that shift, or not.
My questions:

• Could such a low serum phenobarbital concentration cause such a dramatic response?

• Could this be the natural regression to the mean (shifts that are unrelated to intervention)?

• Did the retrospective nature of the study include only cats that did well on once daily phenobarbital, otherwise they would have taken twice daily phenobarbital and therefore been excluded from the study? Was this group of cats bound to do well, in other words, and it wasn't due to medication?

Another study by Pakozdy (https://doi.org/10.1177/1098612X12464627) noted that over time, most cats have a natural reduction in seizures while on anticonvulsant drugs. They tracked seizures in cats over a 10 year period and noted that most improved, some were seizure-free and some stopped medication. About 16% of the cats that stopped medication needed to have it restarted due to a return of seizures. 

The data reported in the study from Sweden suggests that we could administer phenobarbital once daily but the results are so remarkable (marked seizure improvement in a short period of time, low serum drug concentrations) that I feel compelled to repeat this study with a different, perhaps large, cohort of cats and make sure this is reliable. My advice: don't switch to once daily just yet!

Thanks for reading! I love managing seizures so please schedule a consult if you have a case that you'd like more assistance with seizure management. I'm happy to help!

Status Epilepticus in Cats

Last week we looked at the ACVIM consensus statement for the treatment of status epilepticus and focused on the different stages, and the treatment algorithm outlined by the committee. This week, I thought we should look at this statement through the lens of cat care. Please refer to the article for more details - it's a good one! (DOI 10.111/jvim.16928)
As a reminder, all available literature was reviewed and classified according to it's level of evidence. Studies with a high level of confidence for or against a specific treatment included treatments in which 2 or more clinical studies with a high quality score (more about that in a minute) evaluated this specific intervention. Moderate level of evidence for a treatment needed 2 or more studies with moderate quality score or 1 study with high quality score. A label of low evidence for a specific intervention was used in situations where 2 or more studies with low-quality score were reviewed or 1 with a moderate quality score without any high quality score articles identified. A label of conflicting evidence was used when 2 or more studies, usually with a high quality score, were reviewed and found to have results in conflict. Finally, the label "absence of evidence" is pretty self explanatory. The quality scores were numeric scores assigned each study based on clearly defined criteria such as EEG or clinical confirmation of seizure cessation for each study reviewed. 

Definitions
The definitions are the same for cats as they are for dogs. Any seizure longer than 5 minutes is considered status epilepticus (SE). Similarly, cluster seizures are 2 or more seizures within 24 hours in which consciousness is regained between the seizures. Okay, off to a good start. 

Antiseizure Therapy for Cats
Figure 3, in the aforementioned article, is a pyramid of hierarchy for therapy recommendations for cats in status epilepticus. Sadly, there are no studies with a high level of confidence for any intervention. This means that no high quality studies, evaluating seizure cessation in cats, were identified. We need to fix this! Intravenous bolus or CRI of midazolam, intravenous bolus of diazepam, intravenous levetiracetam, intravenous phenobarbital and inhalant anesthetics were considered to have moderate level of confidence for cats. This suggests that there is at least clinical evidence (if not EEG evidence) that supports these treatments for SE management in cats. Oral levetiracetam, intravenous bolus or CRI of phenobarbital and propofol had low level of evidence suggesting that giving these drugs, via these routes, to cats with seizures is not supported by the literature. Oral midazolam, intravenous CRI, oral or endotracheal diazepam were not supported by the literature. Not surprisingly, there were many drugs that were withheld from analysis due to a lack of evidence for cats. 

As I mentioned last week, the authors made the following statement:
"Although both benzodiazepine drugs are potent and safe for the management of SE in dogs and cats, midazolam may be considered a more potent or safer benzodiazepine drug than diazepam."
Based on this, and my own clinical impression, if you aren't carrying injectable midazolam yet, now is a good time to consider adding this to your cabinet!

The authors also specifically addressed CRI reduction and recommended reducing by 25-50% every 4-6 hours after a cat (or dog) has been seizure free for at least 12 hours, preferred 24 hours. It is always preferred to taper the medication, not stop abruptly, whenever feasible. 


I think that is enough for today. I hope you had a good holiday, didn't go too crazy on Black Friday, and I look forward to working with you soon!

As always, the holidays bring many challenges. If you cannot find a suitable time for a consult using my online scheduler please reach out to me via email. I will always try to accommodate your request if I can. 

Status Epilepticus Consensus Statement 2023

Status Epilepticus and Acute Seizure Management Consensus Statement 2023

The ACVIM Consensus statement about status epilepticus (SE) was published this past summer (2023) and I felt it was applicable to all of us faced with acute seizure management. They dove right in and addressed the need for a definition of a prolonged seizure as one occurring for longer than 5 minutes. The human equivalent of our International Veterinary Epilepsy Task Force (IVETF) is the International League Against Epilepsy (ILAE). The ILAE has recently also revised their definition of SE to any seizure longer than 5 minutes as well. Previously, SE was defined as anything between 5-30 minutes. Thirty minutes was the cut off because at that point, brain damage is common. The reason for adopting the 5 minute rule was to 1) minimize the risk of systemic and brain complications associated with continuous seizure activity reaching up to 30 minutes; 2) prevent worsening of the prognosis and drug resistance associated with increasing duration of uncontrolled seizure activity and 3) limit any potentially unfavorable outcomes and adverse effects associated with the prolonged administration of multiple therapeutic interventions. 

Status Epilepticus is divided into 4 stages:
1) Impending (occurs at 5-10 minutes of seizures) - there is neurotransmitter imbalance and ion channel opening/closing. Animals are likely to be responsive to first line anticonvulsant drugs (ACD) during stage 1. 
2) Established (occurs at 10-30 minutes)- Inhibitory neurotransmitters are reduced, the receptors for the inhibitory neurotransmitters are internalized and there is upregulation of NMDR and AMPAR. Some animals may still be responsive to first line ACD, but most will be responsive to second line ACD.
3) Refractory - (occurs > 30 minutes) - There is a sustained imbalance between inhibitory and excitatory neuropeptides with BBB drug transporter upregulation. Most pets will not be responsive to first or second line ACD, but should be responsive to third line ACD. 
4) (Super)refractory - (occurs > 24 hours) - There are gene expression alterations and animals are expected to be refractory to all ACDs. 

What were considered first line ACDs? IV benzodiazepine drugs were considered the most effective and safest for in-hospital use and intranasal benzodiazepines are the preferred treatment for out-of-hospital treatment. "Although both midazolam and diazepam are potent and safe for the management of SE in dogs and cats, midazolam may be considered a more potent or safer benzodiazepine drug than diazepam." There we go!

They provided a list of the steps to follow, based on the evidence reviewed, when treating SE. I have repeated it here, but encourage you to read the entire article if you treat SE regularly as there are loads of pearls of wisdom peppered throughout the paper.

Steps to follow for SE:

• Give midazolam or diazepam IV. A benzodiazepine bolus is effective if the seizure stops < 5 minutes after administration and no relapse occurs <10 minutes

• If seizure activity is controlled with a benzodiazepine drug but recurs 10-60 minutes later is considered recurrent SE

• Recurrent SE, or those that don't respond to the first bolus of benzodiazepine, should get a second IV dose of benzodiazepine drug

• If seizures persist after two bolus, administer a 3rd dose immediately followed by a CRI. Dogs = midazolam or diazepam CRI is acceptable; Cats = diazepam should be avoided. 

• If seizures still persist, administer a 4th dose of benzodiazepine and administer a second line ACD

• Second line ACD include levetiracetam IV, followed by phenobarbital IV and lastly fosphenytoin IV. Only administer the subsequent drug if the prior failed to stop the seizures. 

Note: Levetiracetam or phenobarbital IV can be started after step 2 above if long-term maintenance is desired for either medication. They do not need to be reserved for second line use only. 

I think that is enough for today. I'll go through some more data from the study in another TidBit Tuesday. I hope you enjoy the rest of this week, have a safe, relaxing holiday and look forward to working with you soon!

What is Cognitive Dysfunction in Cats?

Almost twenty years ago when I left my residency and started out as a newly minted neurologist, feline cognitive dysfunction syndrome (CDS) was not on my radar. That has changed. As we learned more about aging in cats, CDS has become a more recognized disease by yours truly, as well as many others. If you're like me and need a Tidbit-Tuesday style refresher...read on!

What is cognitive dysfunction syndrome?
Cognitive dysfunction syndrome (CDS) is a term used to describe deterioration of mental capabilities associated with age.  Clinical signs of cognitive dysfunction can also be associated with other age-related illnesses (e.g. osteoarthritis, structural intracranial disease such as neoplasia, or cardiovascular disease) which makes it difficult to diagnose. See table 1 for an outline of behavior changes seen in cats with CDS.
The underlying etiology of CDS is yet unknown. Causes such as oxidative stress/damage, neurodegeneration  and vascular changes are among the leading hypothesis for human and canine CDS, and therefore suspected to be similar in feline CDS.  Deposits of extracellular B-amyloid and intracellular accumulation of microtubule-associated protein tau have been seen in human patients with cognitive dysfunction. Similarly,  B-amyloid deposits and increased tau have been detected in aged cats with cognitive decline, however the significance remains unclear. 

What are the clinical signs of cognitive dysfunction in cats?
There is a handy article, published in the Veterinary Clinics of North America in 2020 by Dr. Miele and associates that echoes what others have been reporting in a very concise little table. (See reference at bottom) I have replicated this table, with a few modifications, here. Note: There are other signs such as decreased appetite or thirst, that don't usually drive an owner or veterinarian to seek consultation from a neurologist so I haven't included them here. 

Table 1: Clinical behavioral changes associated with CDS in cats.Increased vocalization, especially at nightAltered social interaction and relationships, either with other or other pet. Altered sleep/wake patterHouse soilingSpatial Disorientation or confusion (i.e. forgetting the location of the litter box)Temporal disorientation (i.e. forgetting if they have been fed)Altered activity (i.e. aimless wandering)AnxietyLearning and memory dysfunction

How is CDS in cats diagnosed?
Oh, this is as tangled of a web as the tau proteins we chase. (A little CDS humor here...the tau proteins can cause the "tangles" seen in human CDS!). Currently, the diagnosis is made by ruling out structural brain disease and systemic causes for diseases that mimic CDS. This may include complete blood count, full biochemistry panel including thyroid screening, urinalysis, chest radiographs, blood pressure assessment, brain MRI and possibly a spinal tap. Imaging changes associated with canine CDS include increased depth of the sulci, dilation of ventricles secondary to neuronal loss (called ex vacuo hydrocephalus) and a measurably small interthalamic adhesion. Exclude everything else, and it's probably CDS.

How can we help these cats age easier?
Currently, there are no proven treatments for feline CDS.  The addition of antioxidants (B vitamins, vitamin C, other) as well as fish oil were evaluated for use in cats in one study and showed promise. The use of S-adenosyl-L-methionine (SAMe) has been recommended for cats based on a study that identified improved performance on cognitive testing. This study only found significant improvement in cognitive function testing in the least affected cats. In addition to medical management, environmental management with ready access to food, water, litter box and areas of comfort (beds, hiding spots) is recommended. Environmental stimulation with low impact toys, or bird feeders in which the cat can choose to ignore any activity if they do not feel inclined to engage, are recommended. Finally, focused veterinary visits can be important for cat owners to feel supported through the aging process. Focus your exam to specifically evaluate body weight, urine production (to assess for signs of dehydration), behavior changes and mobility.This may help detect signs earlier in the course of disease and to identify concurrent morbidity that may contribute to, or be confused with, cognitive dysfunction.

Did I forget anything? Most of you treat and see this more than I do. What have you used (successfully, or not) for treatment? 

Reference:
Miele A, Sordo L, Gunn-Moore DA. Feline Aging: Promoting Physiologic and Emotional Well-Being. Vet Clin North Am - Small Anim Pract. 2020;50(4):719-748. 

Does the Duration of Diazepam and Propofol CRI in Dogs Matter?

Does the Duration of CRI Matter?

If you work in a 24-hour facility, odds are high that you've employed a constant rate infusion (CRI) to control seizures in dogs with cluster seizures or status epilepticus. A recent article evaluated the duration of a CRI of diazepam and propofol to see if there was a superior choice.

Why could duration matter?

On one side, the longer a pet is on a CRI (12 h or 24 h), the longer they must remain in hospital which incurs more charges. However, most dogs will have a recurrence of seizures within 12 hours of hospitalization according to prior studies, so if you run a CRI longer perhaps the less chance they have to have another one and thus return to hospitalization. 

Materials and Methods

Cagnotti et al (Frontiers, 2023) collected 73 dogs and separated them into two experimental groups. The first group received diazepam CRI for 12 hours, the second propofol for 12 hours. No standard dosing was employed for either group, just the duration. These were compared to a prior study of dogs with identical inclusion criterial in which the CRI was continued for 24 hours. 

Results

No difference in outcome, or hospital duration was noted between the 12 hour CRI group (both diazepam and propofol) and the 24 hour group. Surprisingly, the dogs receiving the 12 hour CRI still had a 56 hour hospitalization! I cannot locate any data on breakthrough seizures after stopping CRI in either group but one might suspect this occurred to result in a 56 hour hospitalization for the 12-hour group. Either that, or the CRI dose was much higher and therefore had more step down doses compared to the 24 hour CRI? Those are my suppositions, not verified by data in this study. 

Take Home Message:
It is well established that a CRI should be employed for dogs having cluster seizures or status epilepticus and that 2 step-down doses are typically recommended to avoid withdrawal seizures when stopping. That said, this paper suggests that a 12 hour CRI is comparable to a 24 hour CRI. Personally, I typically start with 0.25 mg/kg/hr diazepam CRI for 12 hours and then step down in 50% increments until the dose is below 0.1 mg/kg/hr. This data would suggest that this is an appropriate approach but I think it is 'loosely' supportive!

Reference: Cagnotti G, Ferrini S. Duration of constant rate infusion with diazepam or propofol for canine cluster seizures and status epilepticus. Frontiers in Vet Sc Aug 2023. 

Thanks for reading! I hope you have a great week and I look forward to working with you next week when we're back stateside again!

Tick Paralysis and Dogs

The ticks are still here but owners may have stopped applying topical treatments. So fall is the time to be on the look out for Tick Paralyses (okay, really anytime but now isn't a BAD time to be aware)!

What causes Tick Paralysis?

Salivary transfer from a Dermacentor (in America) and Ixodes (in Australia, for my Australian readers) will result in neuromuscular blockade. How it actually works is really pretty ingenious. (Skip this next part if you're in a hurry.) At the presynaptic terminal, acetylcholine packets must be released into the neuromuscular junction so they can then bind to the post synaptic (muscle) membrane receptors. The acetylcholine binds to the presynaptic membrane using specific proteins as well as calcium. The saliva from one of the aforementioned types of ticks will interfere with acetylcholine release at the presynaptic terminal by binding calcium. Amazing, really.  

What are the common clinical signs?

If you cannot release acetylcholine from the presynaptic membrane at the neuromuscular junction, what can you do?  Exactly...nothing. 

Therefore clinical signs are an ascending pelvic to thoracic limb flaccid paralysis. No reflexes, no motor, no paw replacement, nada. These signs begin 5-9 days after exposure to the tick saliva. Cranial nerves are RARELY affected. This is important because botulism more commonly affects cranial nerves and this can be one way to try to differentiate between these two diseases. 

How do you make the diagnosis?

1. Find the tick.
2. Remove the tick.
2.5 (Apply Frontline/Bravecto/other)
3. Clinical improvement should begin 24-48 hours after tick removal.
No specific testing is available to confirm the diagnosis. 

I once had to find a tick on an Old English Sheepdog waaaay back in the year 2000. Topical tick treatment wasn't as prevalent then as it is now, so our solution was to shave the dog. We found the tick between the dog's toes. (Insert eye rolling here!!) In 2023, I suggest applying Frontline/Bravecto (your choice of topical flea treatment) first then perform a non-invasive tick hunt and monitoring for clinical improvement. If ineffective after 48 hours you can either commence a thorough tick hunt, or search for other causes of flaccid paralysis. (Or, call me for a neurology consultation!)

How do you manage patients flaccid paralysis?

Flaccid paralysis means that the animal does not have reflexes, or voluntary motor. As such, these animals may be at risk of respiratory failure due to loss of intercostal muscle function. Frequent CO2 monitoring, respiratory watch and ventilatory support if needed can be very important in the early stages of disease. Due to the rapid recovery common with tick paralysis, most patients do not need long-term intensive nursing care or physical therapy. 

Thank you for reading!  I appreciate you, and all that you do for your patients. Please note that I'm currently in Australia and will have delays in email response and NO telephone service. You can message me through FB if you want to but otherwise email is best. Thanks!!

To Seize is to Grab, to Seizure is to Convulse

Seizures and Deficits...What to Do?

Today, we have, back by popular request, another lesion localization practice case! Enjoy!!

Signalment: 7 year old MC Pitbull-X (maybe Boxer dog?)
History: The dog presented with a history of 2 seizures, 1 day apart. Since the seizures, the dog has been walking compulsively to the left, and appears to bump into objects. Although a decreased appetite has been appreciated, the dog is still eating when hand fed. 

Physical Examination: unremarkable

Neurologic Examination:
Mentation: Obtunded
Cranial nerves: Absent menace OD, intact PLR OU, mild head turn left, remainder normal. 
Gait: Ambulatory with intermittent compulsive circling to the left. He is able to walk to the right when asked but will not continue the circles without inspiration. 
Postural reactions: normal all limbs.
Reflexes: Normal all limbs.
Palpation: no spinal pain and normal cervical ROM  and tail jack. 

Neuroanatomic lesion localization (NALL) Practice

Let's look at the examination is sequence as it is listed above. If you wish to use the table format that I prefer, please look at the tables provided in the Small Animal Neuroanatomic Lesion Localization Practice Book (publisher CABI, date 2022 by yours truly). We'll discuss it in conversation format for this TidBit Tuesday. 

Seizures: Seizures ALWAYS localize to the forebrain and are not readily lateralized (left or right side). 

Obtunded: reduced mentation is noted with lesions in the forebrain and brainstem. This is NOT a clinical sign of cerebellar, spinal cord or neuromuscular disease, nor a non-neurologic finding. This narrows our lesion localization to forebrain or brainstem.

Cranial nerves: The menace pathway, in it's most basic sense, involves CN 2, the forebrain and CN 7. PLR involves CN 2, midbrain and CN 3. The blink reflex is not states as being abnormal above (blink reflex: CN 5 and CN 7) therefore by process of elimination, the menace deficit OD is most likely due to a forebrain lesion. The second part of the story is lateralization. Only the right eye is affected. This is a crossing tract (mostly) which means that the lesion should be on the left side of the forebrain.

Gait: The compulsive circling to the left is localized to the forebrain and, rarely, vestibular system. Localization to the vestibular system is most likely when a head tilt is present. Without a head tilt, I would consider a forebrain lesion most likely and they circle TOWARDS their lesion. This would further support a left forebrain lesion. 

NALL: Left forebrain

How'd you do? Did anything surprise you with the NALL? If you enjoyed this case, thank your colleagues for suggesting a seizure NALL case for practice. :)

As a reminder, I will be out of the country starting next week through November 14th. I will be available by email ONLY (no cell phone service) and will be doing my best to keep up on emails. Please expect minor delays in my response because I will be lecturing and we'll be on different time zones but I will do my best to be as responsive as possible. Have a great week!

T3-L3 Myelopathy in a German Shepherd Dog

In July, my colleague Dr. Sam Long and I held a CE seminar on neurology for 2 days here in lovely southwest Wisconsin. During this conference, we discussed a case that I'd love to present to you today. If you were at the conference, you may recall the ensuing debate! Here we go...

Signalment: 9 year old FS German Shepherd Dog
History: 6 month history of slowly progressive paraparesis and proprioceptive ataxia in the pelvic limbs. This dog started with scuffing of one pelvic limb when walking, and progressed to scuffing both pelvic limbs, and then weakness, which had progressed to a moderately poor ambulatory state by her evaluation in clinic. 
Physical examination: mild thickening of both stifles and a history of TPLO in one stifle many years ago. 

Neurologic examination:
Mentation: QAR
Cranial nerves: normal
Gait: Ambulatory with moderate proprioceptive ataxia and mild to moderate paraparesis, worse on the right PL with mild limping on the right pelvic limb. 
Postural reactions: Absent paw replacement test in both pelvic limbs, normal in both thoracic limbs
Reflexes: Normal all limbs, normal c. trunci bilaterally. 
Palpation: Non painful spinal palpation, tail jack or cervical ROM

Neuroanatomic lesion localization: T3-L3 myelopathy. (Not sure how we got here? Please see last week's TidBit Tuesday for a review on neuroanatomic lesion localization practice for the spinal cord.)

Differential diagnoses: Degenerative myelopathy, intervertebral disc herniation (type II), neoplasia. 

Diagnostic plan: We proceeded with a minimum database, which was unremarkable. The MRI showed a mild to moderate disc herniation mid-lumbar, more on the right side. The disc herniation was felt to be a possible cause. Concurrently, the clients had submitted a SOD1 gene test, which is the genetic test available to look for one of the mutations suspected to cause degenerative myelopathy in German Shepherd dogs. The results came back as a homozygous at risk (i.e. she has the genetic mutation). So...now what? We have a dog with evidence of two possible causes for the T3-L3 myelopathy. 

On the one side...
If the clinical signs are due to the disc herniation, surgical correction may provide clinical improvement and stabilize progression. That said, there is a risk of worsening the neurologic status with anesthesia and surgical decompression, especially with chronic compression. Many dogs are worse after decompression for a week or so before then gradually improving. 

On the other side...
If clinical signs are due to degenerative myelopathy (DM), the dog is expected to progressively worsen regardless of the treatment provided. Anesthesia *might* worsen signs, but that isn't clear. Certainly surgery won't help! 

What do we do? We had a lively debate and ultimately it came down to which carries more risk - doing nothing in the face of a possible surgical disease, or doing surgery (and risking making them worse) in the face of a medical disease. What would you do? 

The clients ultimately elected not to proceed with surgery and I supported this decision, however Sam had an opposing viewpoint and would have preferred surgery. It isn't clear cut, and neurologists debate this problem in rounds around the world! I'm grateful that we have many folks working to find solutions to problems like these and will be sure to pass along any new information on diseases like chronic disc herniation or degenerative myelopathy. 

Thanks for reading! Please reach out with thoughts or opinions on the topics, recommended future topics, or questions as they arise.

Please note that I will be out of the country, doing a repeat of this CE but in sunny Australia for 2 weeks, and will not be available by telephone. My email will still work :) but please be patient with expected delays. I leave at the end of October and return mid-November so be sure to book pending consults before I go! Have a great week!

Spinal Cord Neuroanatomic Lesion Localization

"DIR" Coming In

Does anyone else use the acronym "DIR" to represent "down in rear"? I dislike this phrase but it's a soapbox rather than scientific fallacy, I suppose. Anyway, today, let's imagine that you have a patient on your schedule coming to see you for signs of difficulty walking. Today is a lesion localization practice case, so grab a pencil and dig in!

History:
Gabby is a 4 year old FS Beagle-X. She is presenting with a 3 day history of difficulty walking in the pelvic limbs with swaying, falling, and occasional vocalization such as pain. No prior medical history and normal physical examination. 

Neurologic examination:
Mentation: BAR, anxious
Cranial nerves: normal
Gait: Ambulatory, paraparesis with moderate proprioceptive ataxia in pelvic limbs only. 
Reflexes: normal withdrawal in all four limbs, normal patellar reflexes bilaterally and normal anal reflex. The cutaneous trunci reflex stops at L2 bilaterally. 
Postural reactions: Absent paw replacement testing in both pelvic limbs, normal in both thoracic limbs. Normal hopping in both thoracic limbs, absent hopping in both pelvic limbs. 
Palpation: Spinal pain at TL junction, the remainder was non-painful. Normal cervical ROM and tail ROM. 

The first questions we ask ourselves is "is this dog normal or abnormal neurologically?"
The answer, of course, is abnormal, so let's break it down.

This dog has normal mentation, no cranial nerve deficits and no history of behavior changes or seizures so I think we can safely assume the lesion is NOT intracranial. This leaves spinal cord, peripheral nerve, neuromuscular junction, or muscle to choose from. Let's start by assuming it's spinal cord in origin but if the lesion doesn't localize to ONE spot on the spinal cord you should then move on to considering the neuromuscular system. When looking at the spinal cord, you have four localization segments to choose from:

C1-C5
C6-T2
T3-L3
L4-S3

The C6-T2 and L4-S3 segments are where the lower motor neuron cell bodies are housed and where the peripheral nerves that you test with limb reflexes originate. Look at the reflexes listed on the neurologic examination. No spinal reflex deficits are noted, except for c. trunci, correct? This means you can consider C6-T2 and L4-S3 "free" of disease, or normal. This leaves us C1-C5 and T3-L3 to evaluate. To do this, we must look at the gait description. 

What is paraparesis? Paraparesis is a weakness in the pelvic limbs. Monoparesis = one limb weakness, tetraparesis = all four limb weakness. Make sense? 

What is proprioceptive ataxia? There are 3 forms of ataxia, and proprioceptive ataxia is the most common one. This gait deficit occurs when the sensory nerves running from the toes --> peripheral nerve --> spinal cord --> brainstem --> forebrain become disrupted. When the nerves are disrupted, anything "downstream" or caudal to that disruption may show ataxia. In this case, it is just the pelvic limbs, therefore the lesion is caudal to the thoracic limbs. Caudal to the thoracic limbs is T3. We've already decided that we don't have reflex deficits therefore the lesion must be in front (cranial to) L4. Voila! The neuroanatomic lesion localization for this case is T3-L3 by process of elimination (and by doing a thorough neurologic examination). 

DDx: The most common differential diagnoses for this dog with spinal pain and acute, progressive T3-L3 myelopathic signs would be an intervertebral disc herniation, meningomyelitis, and trauma. I wouldn't exclude neoplasia or discospondylitis however they are less likely based on her history. 

Plan: Spinal radiographs would rule out discospondylitis but don't diagnose disc herniations, meningomyelitis and rarely will diagnose neoplasia. 3D imaging is needed to look at the spinal cord which would be a myelogram with CT, a CT alone or an MRI (my personal favorite). 

How did you do? Was this easy-peasy or more challenging? I'd love to know! Please feel free to email me your comfort with the localization on this case so I can introduce either more or less challenging localization practice in the future. 

Thanks for reading! Have a great week!

Autoimmune Feline Encephalitis

Autoimmune encephalitis is a unique pathology, identified in perhaps up to 50% of humans with encephalitis, and recently identified in a large cohort of cats. In a study published in Vet Journal (2023), Glantschnigg-Eisl et al described the clinical, laboratory, radiological and pathological findings in 32 cats diagnosed with this specific form of epilepsy. Human autoimmune epilepsy is caused by immune attack of the voltage-gated potassium channel (VGKC), generating specific antibodies to this protein complex and the secreted protein LGI1 as well. It is now proposed that the presence of these antibodies reflect a specific form of limbic epilepsy in cats, similar to the autoimmune epilepsy noted in humans. Most importantly to us (veterinarians), cats with this form of epilepsy have a normal MRI and CSF analysis! Therefore, calling it encephalitis based on our standard testing is challenging. Is it a form of idiopathic epilepsy, or an encephalitis? Time shall tell. The authors describe this as an encephalitis, similarly to the human counterpoint. Below is a small summary of their findings. For the full study, please refer to the article link at the bottom. 

Clinical Picture

All cats in the study had seizures as their presenting complaint. All cats had positive antibodies to VGKC, with 26 cats having LGI1 antibodies as well. No clinical findings distinguished cats with LGI1 antibodies from those without. Focal and generalized seizures were almost evenly divided as a presenting seizure type with cluster seiuzres in 27/32 cats. Similar to humans with limbic epilepsy, many of the cats (22/32) had interictal behavior changes with  a history of unprovoked aggression in 12/32 cats. This was identified as a common finding but not yet pathognomonic for this form of epilepsy. Median age at onset was 3.42 years.

Laboratory Findings

.No significant laboratory abnormalities were identified. As noted above, CSF analysis was normal for all but 1 cat and that cat had only a mildly elevated protein. 

Long-term Outcome

Phenobarbital was started in 26/28 cats that underwent treatment with about 1/2 of the cats having a second AED added throughout treatment. Prednisone was administered in 10/32 cats (most of which were the LGI1 positive cats).The cats that received steroids, often received prednisone. This medication was administered to the cats with the most severe neurologic signs, including seizure frequency or severity, and was linked to poorer survival. As the authors noted, it is unclear if the prednisone is linked with poorer outcome or if the survival is linked to more severe condition and therefore prognosis.  This was interesting because the human seizure disorder associated with LGI1 antibodies is typically rapidly and markedly responsive to steroids.

Two factors were associated with prognosis in this study. The first was number of seizures at presentation. Cats with a higher seizure frequency were more likely to be euthanized. The second was the association with hippocampal pathology. Higher MRI scores suggested a lower prognosis and higher likelihood of euthanasia. The overall survival rate was 70-80%, which was similar to survival rates for idiopathic epilepsy in cats. At 1 year, most cats had a marked decrease in seizure activity from a mean of 3.6  seizures daily to 1-2 per year. This suggests that if they survive the short term, their long-term prognosis is good. QoL scores were good to acceptable in the long-term follow-up group.

What are my take away points from this study for practice?
1. Be aware that this disease exists. If you see cats with seizures, especially severe onset seizures, VGKC autoantibodies could be an underlying cause. 
2. Treat with phenobarbital - it works terrifically for most cats, regardless of the underlying cause. 
3. Steroids may not be the answer. Then again, maybe they are if we catch the disease earlier?? I don't think we can make this a take away just yet; more information is needed. 

I hope you have a wonderful week and thanks for reading! 

A gentle reminder: I've had an uptick in cancelations over the past few days. I know my schedule is getting booked out further than is typical, and I apologize for the resulting delay.  Please cancel your appointments with as much notice as possible, whenever possible. I have a waitlist and would LOVE to move folks forward if I have an opening. I am hopeful that the waitlist will diminish soon now that I able to open up a few more days for consults. Thank you!

Lastly, gut yantif to those of you celebrating! I hope you had a safe fast yesterday. 

Reference: https://www.sciencedirect.com/science/article/pii/S1090023323000254

Can You Help?

Hello fellow Veterinarians!

I am working with a company to possibly purchase a MOBILE MRI that would be small enough to literally fit into a Sprinter van. This would enable me to drive an MRI to your facility, evaluate pets and do the MRI right then for you and them. This is unique - no other small animal veterinary neurologist currently has this machine in the USA so the company has asked for my help. Consequently, I'm asking for yours.

The coil (the place the head goes when it goes into an MRI) is smaller than many other big machines and I need to make sure that the majority of my patients could fit. I'm only looking at skull size right now. 

What do I need? I need head measurements, please. Specifically, can your pet/patient/parent's dog/etc. fit inside of a 7" tall x 6" wide space? If you can measure and send me a YES or NO and the dog breed that would be terrific. The more data the merrier so don't limit yourself to just one dog. :) We know cats fit, so no need to annoy them with a measurement of their head.

How to measure: The photo above is my simple calipers that I'm using when I travel to hospitals. You can make something similar or just use a ruler and a piece of string or paper. Measure across the top of the head putting a string at "0" and 6". If the head bends the string, it's too big. Then, measure the height  using a piece of paper or cardboard at the edges of the ruler to approximate 7". If you cannot fit the paper across the top and bottom, the head is too big. Although science is precise, this doesn't need to be at this stage.

Thank you!!

Thank you for reading, and for your help!
Sincerely,
Heidi

Geriatric Vestibular Disease

Geriatric Vestibular Disease of Dogs and Cats

Geriatric vestibular disease (GVD) is characterized by an acute onset, unilateral failure of the peripheral vestibular system. The cause remains unknown, but causes such as inflammation (viral or immune mediated) or atrophy have been hypothesized. A study back in 2021 (DOI: 10.1111/vru.12893) by Sungjun Won and Junghee Yoon out of South Korea identified a significant size difference in the utricle, one of the parts of the bony labyrinth in the ear, in dogs with GVD compared older dogs without GVD. Necropsy evaluation has shown a reduction in the size of the peripheral CN 8 and the affected ganglion, further supporting atrophy as a cause. And yet, it is difficult to explain the recovery that most dogs and cats experience 1-6 weeks after onset of signs.

Common Clinical Signs

Animals with GVD are middle age to older dogs and cats that demonstrate peracute onset of signs, often proceeded by vomiting with no clinical worsening after 24 hours. These dogs and cats usually have very severe vestibular signs such as head tilt, nystagmus, ataxia (if ambulatory), positional strabismus and rolling/nonambulatory vestibular ataxia. IF you are able to have the animal stand you should not find paw replacement deficits, hemiparesis or obtunded mentation. If you do, the lesion localization is central and a different set of differential diagnoses should be considered. 

Differential Diagnoses for Peripheral Vestibular Disease
Not accounting for history, a general list of differential diagnoses for peripheral vestibular disease would be as follows:
Degenerative: none
Anomalous: none
Metabolic: hypothyroidism
Neoplasia/nutritional: Yes (lymphoma, nerve sheath tumor)
Infectious/Inflammatory/Idiopathic: Yes (neuritis and geriatric vestibular disease)
Trauma/Toxin: Topical antibiotics (Oral metronidazole SHOULD be central, but it may be difficult to tell in a recumbent animal.) Trauma - less common in dogs and cats.
Vascular: none. 

Geriatric vestibular disease is diagnosed by exclusion at this time. Although the report referenced above does provide measurements for the utricle on MRI, it is not yet a diagnostic marker for GVD. Exclude all other causes using chest x-rays, blood work including T4, brain MRI and spinal tap, if indicated. 

Treatment?

This is a self-resolving disease. The head tilt is commonly permanent, but all other signs of vestibular disease should resolve over several weeks. Signs begin to improve 24-48 hours after onset of signs but may take up to 1 week to start improving. Full resolution of clinical signs should be by 6 weeks. If signs wax and wane, or progressively worsen, GVD is not the proper diagnosis. Supportive care such anti-emetics. diazepam or meclizine for anti-vertigo effects, and nutritional support such as hand feeding (only when sternal!) , may be used. IV fluids may be needed for severe or prolonged nausea. 

Prognosis

Don't euthanize these pets in the first 24 hours! They look miserable...but they can recover with time and supportive care. This can be very difficult for clients to witness and, because the pets are elderly, may result in a triggered response to consider euthanasia. If you can, please hang in there for a few days even if that means hospitalization. Also, please note that signs may reoccur multiple times over the animals' life. 

Thanks for reading! I'd love to hear if you have any suggested topics for TidBit Tuesdays. If you have a question, chances are that other readers are interested in the topic too! I tend to pick things that I think are timely or interesting (or both!) but then again, I find everything interesting in neurology so help me narrow this down! :)

Have a great week!

IVDH Consensus Statement – Medical Management Data

In July 2022, the ACVIM Consensus Statement on the diagnosis and management of acute canine thoracolumbar intervertebral (IVD) disc extrusion was published. This is the first of two installments about this consensus statement as a TidBit Tuesday. For this one, we will discuss the expected outcomes from medical vs. surgical management and what entails medical management. Enjoy!

The recommendations by the committee were graded as being supported by high, medium and low levels of evidence. Recommendations with high level of confidence include multiple randomized controlled trials with concordant findings. The evidence strongly supports the conclusions. Medium level of confidence includes retrospective studies with concordant findings, or small placebo-controlled trials. The evidence suggest that the findings are likely to be real. Lastly, low levels of confidence include isolated or small retrospective studies or single non-controlled trials. The evidence suggests that the findings might be real.

Medical vs. Surgical IVD extrusion management

A very helpful table was presented to help guide appropriate treatment for dogs presenting with signs consistent with TL IVD extrusion. The “%” represent the % of dogs that respond favorably to medical (M) or surgical (S) treatment.

·         Pain only: M 80%, S 98.5% à lateral extrusion may lead to reduced response to medical management.

·         Non-ambulatory paraparesis: M 81%, S 93% à level of recovery was less with medical management.

·         Paraplegia with deep pain: M 60%, S 93% à medical recovery is prolonged and less complete.

·         Paraplegia loss of deep pain: M 21%, S 61%

This is based on moderate level of evidence.  The statement here is “In paraplegic deep pain negative dogs, success with medical management is largely poor with an increased frequency of progressive myelomalacia. Surgical management is recommended.” – moderate to high level evidence.

What is medical management?

“At least 4 weeks of restricted activity is recommended, putatively to promote the healing of the annulus fibrosus. This period should include confinement to a restricted area 9crate, ideally, or small room without furniture) except when performing rehabilitation exercises or outdoor toileting. There should be no off-leash walking, no jumping on or off furniture and no access to stairs during this time”. This statement was supported by low level evidence. Corticosteroids are NOT recommended (moderate level evidence). Dogs with NSAIDs had a higher quality of life score than those on corticosteroids but NO STUDIES specifically address the use (or no use) of NSAIDS. Pain management is discussed, but no recommendations were made because of the lack of studies evaluating different medication protocols. Acupuncture was noted to be good adjunctive treatment for medical management but is not a recommended substitution for surgical management. What are my typical recommendations? For an uncomplicated T3-L3 myelopathy without MRI, with a strong suspicion of IVDH, I recommend NSAIDs, muscle relaxants and most importantly, cage rest for at least 3 weeks.

I hope this was enlightening. Please reach out with questions and stay tuned for the next update on the consensus statement. I hope you have a wonderful week. I am enjoying our tiptoe into fall and hope you are too!

Limber Tail?

Limber tail, or cold tail, is known medically as coccygeal myopathy and is a poorly characterized condition associated with acute onset tail flaccidity and pain. Working dogs are more commonly associated with the disease, especially hunting breed dogs. I recently evaluated a patient with suspected "limber tail" and thought it might be fun for us all to review this unusual disease. The most recent study published was 2016, so I'll reference data from that study in this TidBit Tuesday. Reference at the end. 

What is the pathology associated with limber tail?

Limber tail is a self-resolving disease, usually within 10 days of the onset of signs, therefore very little pathology has been described for the problem. One study from Norway in 1999 identified inflammatory cells in the coccygeal muscles along with evidence of myofiber damage and elevated CK in dogs with clinical evidence of limber tail, compared to breed matched control (nonclinical) dogs. 

What are common triggers?

In a questionnaire to dog owners in the UK (2016) the following triggers were queried and the responses are as follows:

• Swimming (29 yes, 9 no)

• Exposure to cold weather ( 19 yes, 19 no)

• Exposure to wet weather (11 yes, 26 no, 1 unsure)

• Vigorous exercise (18 yes, 18 no, 2 unsure)

• Confinement (5 crate, 1 car, 31 no, 1 unsure)

Some triggers appeared to be dual, such as swimming on a cold day. Increasing latitude has been identified as a risk factor, which is assumed to be linked to colder temperatures. They determined that while swimming was not a necessary precursor to the development of limber tail, it appeared to be a risk factor. The odds ratio of a swimming case compared to control was 4.7. Furthermore, cases were more related (had common ancestors) compared to controls and this was more than is expected for random selection. Otherwise, a similar distribution between cases and controls was noted for neuter status, coat color, height, weight, exercise levels, household type, and smoking vs non-smoking in the home. 

Do you need to treat it?

The self-resolving nature has made treatment protocols difficult to evaluate. Pain management in the early phases, as needed, is appropriate. This could include anti-inflammatory medications such as NSAIDs, but probably doesn't need to rise to the level of steroids in most dogs. Pain modulation with gabapentin, narcotics if severe pain is noted, or muscle relaxants could be utilized. If clinical signs have not resolved by day 10, additional diagnostic testing such as MRI of the lumbo-coccygeal region, electrodiagnostic testing or both may be indicated. 

I hope you enjoyed Labor Day holiday and weekend and have a great week! I am in town this week but leaving for a few days over next weekend to speak at IVECCs in beautiful Denver Colorado. I will have limited email and telephone access Monday-Tuesday September 11-12th due to travel and speaking hours. Please pardon my delay in response if you reach out on those days. Thanks for reading!

Reference: https://bvajournals.onlinelibrary.wiley.com/doi/epdf/10.1136/vr.103729