Vestibular Disease in Cats

As we reflected on our familys, and leaned back in our chairs last week around the Thanksgiving table (sorry, Canadians, I know yours was last month) I thought - wait - vestibular disease in cats! (That, and why did I eat so much pie?) First, I have been asked "Do cats get vestibular disease?" The answer is: yes. They have the same anatomic structures and roughly the same neural pathways that influence the vestibular pathways as dogs do. Let's look at a case:

Signalment: 4 year old FS DSH
Neurologic Examination:
Mentation: normal
Cranial nerves: right head tilt, horizontal nystagmus FF left, positional strabismus OD, remainder of the cranial nerves are normal. 
Reflexes: normal
Postural reactions: normal tactile placing all four limbs
Gait: ambulatory with mild vestibular ataxia and staggering right when turning.
Palpation: Non-painful spinal palpation and cervical ROM

Peripheral Vestibular Disease

The basic players in the peripheral system are 1) The receptors, 2) cranial nerve VIII or vestibulocochlear nerve. Cats with peripheral nerve disease may have a head tilt, nystagmus, positional strabismus, vestibular ataxia and falling/rolling. The head tilt is towards the side of the lesion. The nystagmus are a bit trickier. In the old days we used to track the direction of the nystagmus as a localizer. Remember when we said horizontal nystagmus indicated peripheral disease, vertical nystagmus indicated central disease and rotary was either? Welllll..... that isn't strictly true anymore. While it is true that horizontal nystagmus are typically associated with peripheral disease, they can be seen with central disease, too. The same is true for vertical nystagmus. Nystagmus that develops only when the head is placed in a specific position (positional nystagmus) are more common with central disease, but unfortunately are no longer strictly associated with that neuroanatomic lesion localization. So how do we localize peripheral disease?? We localize based on the lack of specific findings on the neurologic examination. What they won't have is ipsilateral paw replacement deficits, ipsilateral hemiparesis and/or reduced mentation (obtunded, stupor, coma). These last three findings are identified with brainstem vestibular disease ONLY. 

Brainstem Vestibular Disease

The players in brainstem localization are the paired vestibular nuclei in the rostral medulla oblongata. The tracts for proprioceptive function, descending upper motor neuron and level of alertness (mentation) are also nearby. Therefore, if a disease in the brainstem is affecting vestibular function, it is also very likely to tick off one of those nearby pathways, therefore creating deficits. They don't need to have all 3 deficits, just one will do. So, a cat with a head tilt, nystagmus AND an ipsilateral tactile placing deficit is more likely to have a brainstem localization than peripheral disease. 

Cerebellar localization
The last group of neurons influencing or being influenced by the vestibular system are the cerebellar nerves. In the cerebellum there are "marionette" nerves that exert their influence on the brainstem vestibular system. By "pulling strings" the cerebellar influences the output from the vestibular nuclei.  Without this influence signs such as hypermetria, intention tremors and truncal swaying are noted. To localize to the cerebellum, signs of vestibular disease (head tilt, nystagmus, positional strabismus) are present PLUS hypermetria, truncal sway and intention tremors. When localizing to a specific side, follow the hypermetria. If an animal has hypermetria on the right front limb, the localization is right cerebellum. Occasionally delayed paw replacement is present, but this will be due to difficulty repositioning the limb rather than a solid paw replacement loss. 

Have you figured out the neuroanatomic lesion localization for the case? That's right - peripheral vestibular disease! Differentials for cats are very similar to dogs with the exception that we see more polyps in cats, and more PSOM in dogs. Therefore, I would consider otitis media/interna, polyps, neuritis (infectious or inflammatory), hypothyroidism (yes, in a cat!), diabetes, and peripheral neoplasia. These differential diagnoses are then tailored to the specific case based on the history. 

That wasn't too painful, was it? Let me know if you have a topic you think should be covered in a TidBit Tuesday!

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

Case Based Practice

Lesion localization is one of those things that can be lost, if not practiced. This week, we’re going to work out those muscles.

Maria, is a 13 year old FS Lab
History: Presented to me with a 24 hour history of acute onset difficulty walking. 

Neurologic examination:
Mentation: BAR
Cranial nerves: right head tilt, rotary nystagmus, remainder normal.
Gait: Moderate vestibular ataxia, falling right. No hypermetria or intention tremors noted. 
Postural reactions: absent right thoracic and right pelvic limbs, normal other limbs
Spinal reflexes: Normal all limbs, normal c. trunci and perineal
Palpation: non painful, normal cervical ROM

You know what you've got to do now, right?

What is the Neuroanatomic Lesion Localization?

There are several ways to go through lesion localization.

OPTION 1:
I like to make lists. Start by listing all of the abnormalities and ALL possible locations that could result in an abnormal finding. For example:
1) Right head tilt - peripheral CN 8 (right), medulla (right), cerebellum (right or left)
2) Rotary nystagmus - same as above
3) Vestibular ataxia - same as above
4) Reduced paw replacement right side - right C6-T2, right C-C5, right medulla, right pons, right or left midbrain, left prosencephalon.

Now, we start to clump things. Well, for starters any animal with cerebellar disease is expected to have hypermetria and/or intention tremors and Maria did not. We can cross out cerebellar disease. What else? What is the one spot where all of the signs can be explained? That's right - medulla on the right! Voila, lesion localization. 

OPTION 2:
The other way to work through this is to identify the cranial nerve affected on the exam (in this case, cranial nerve 8), identify the brainstem segment associated with this cranial nerve (in this case, medulla) and then ask yourself if you can identify if she has a) paw replacement deficits b) hemiparesis and/or c) mentation changes. . If not, it is peripheral and if so, it is brainstem. 

Differential Diagnoses

Brain stem vestibular disease in an elderly dog without an important prior medical history would suggest the following differential diagnoses:
Degenerative: none
Anomalous: none
Metabolic: Hypothyroidism
Neoplastic/nutritional: Neoplasia of the brainstem
Infectious/inflammatory/idiopathic: meningoencephalitis (infectious or inflammatory)
Trauma: no supportive history
Vascular: Cerebrovascular accident (stroke)

Final diagnosis: cerebrovascular accident (stroke). 

Please reach out if you have a case that is troubling you, a client that needs reassurance that you're doing all you can, or simply have a question. I hope you have a great week!

Idiopathic Geriatric Vestibular Disease of Dogs

Idiopathic Geriatric Vestibular Disease

If I had a dime for every time a client told me their dog had a stroke (usually "several years ago") and that they suddenly were dizzy, and then, suddenly got better, I'd be rich. Or at least I could by myself a soda. :)

Idiopathic Geriatric Vestibular Disease is Not Caused by a Stroke

Human strokes happen suddenly, and can cause signs such as hemiparesis, hemifacial weakness, and often resolve over time so it is reasonable that a stroke would be confused with the canine idiopathic geriatric vestibular disease (IGVD). But they are different! Strokes occur at the level of the brain, brainstem, or cerebellum, and IGVD localizes to the peripheral vestibular system. 

What is Idiopathic Geriatric Vestibular Disease?

As the name implies, we have yet to find the etiology. Several proposed causes have been postulated but none confirmed. Clinical signs include:
1) Acute onset vestibular signs (head tilt, nystagmus, vestibular ataxia, positional strabismus)
2) NO evidence of ipsilateral hemiparesis (weakness on the same side as the head tilt)
3) NO evidence of ipsilateral paw replacement deficits. Some older dogs have unrelated or preexisting paw replacement deficits. If the deficit involves both pelvic limbs, equally, or a contralateral limb to the head tilt, the odds are strong that the deficit is unrelated to the vestibular signs. 
4) NO mentation changes (obtunded, stupor, coma).
5) NO evidence of hypothyroidism, otitis media/interna, neuritis or peripheral/ear neoplasia 

Options 2-4 above help you localize the lesion to the peripheral system, but that is just a localization. Options 1 and 5 help you eliminate the other differential diagnoses that could also cause peripheral vestibular disease and thus, narrow the diagnosis to idiopathic geriatric vestibular disease. 

Treatment

Treatment for IGVD is supportive. Steroids, antibiotics and NSAIDs do not improve clinical signs. Signs typically begin to resolve within 48 hours of the onset, and have reached a state of stability by 30 days. The most marked improvement typically occurs in the first 14 days. Supportive care with anxiolytics (diazepam, trazodone, other), antivertigo drugs (meclizine, ondansetron), and nutritional support may allow the animal to be more comfortable during the recovery process. Clean, dry bedding with frequent comfort checks are important for non-ambulatory dogs to minimize bed sores and other complications. 

Prognosis

Dogs with IGVD have some of the most severe clinical signs but have a very good long-term prognosis! Intensive supportive care is important in the first few days. Most dogs will recover to a functional state within 1 week and return to baseline within 30 days. Importantly, the head tilt is often permanent!! Please be sure to inform clients of this, otherwise they may think the dog is still clinically affected months and years after the signs have otherwise resolved. 

Please let me know if you have a dog with vestibular disease that you feel would benefit from an evaluation. I look forward to working with you soon.  Have a great week!

Ondansetron for Nausea in Vestibular Disease

Vestibular disease, whether it is central or peripheral in origin, can result in nausea and vomiting. The exact mechanism is unclear, but it is suspected to be via neuronal projections to higher centers (forebrain) and associated with activation of 5-HT3 receptors. Ondansetron is a selective 5-HT3 receptor antagonist (blocker). It has been shown to be effective on subjective observation, in controlling nausea in vestibular patients, but a recent double-blind placebo controlled study took it one step further. In addition to observation of signs of nausea, such as lip licking, facial expression, behavioral clues and hypersalivation, they evaluated blood levels of arginine vasopression (AVP) which has been positively correlated with nausea scores. 

Materials and Methods

Eighteen dogs were enrolled, 14 were included in data analysis. Six dogs received placebo first, followed 2 hours later by ondansetron (0.5 mg/kg IV, diluted 1:1 with 0.9% saline). Eight dogs received ondansetron first, followed 2 hours later by placebo. Dogs were observed at hourly time points for signs of nausea (pre and post treatment) and had serum samples for AVP measurements taken at pre-treatment, 2 and 4 hours post initial treatment. 

Key Results

• Dogs given ondansetron, showed a rapid, significant reduction in nausea compared to dogs given placebo. 

• Only 4 dogs vomited, in addition to signs of nausea. ** Vomiting should not be the only sign you watch for to say a pet needs an anti-nausea medication!

• Serum AVP concentrations decreased significantly after administration of ondansetron, compared to placebo. 

Based on the data presented, it is reasonable to assume any dog with recent onset vestibular signs should be administered ondansetron if signs of nausea and/or vomiting are noted. It would be helpful to educate clients on the signs of nausea (not just refusing food or vomiting!) when performing at-home observation of their pets with vestibular disease.

Interested in learning more about the nausea scores? Please consider this reference:
1. Kenward H. Development of an objective means of assessing nausea in dogs. London:EThOS British Library; 2015. 

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

 Reference for article discussed above: 0.1111/jvim.16504

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