Vestibular

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

A cat with a tilt

Welcome! Today is a going to be a busy day! First on your case list is a sick cat so let's dive in. Here is the story:
The cat was presented for a 2-month history of a left head tilt. She was noted to have effusion from the left ear when signs started and was treated with amoxicillin (dose unknown) for 14 days. Clinical improvement was initially noted, but signs relapsed after medications were discontinued and now the owner's are noting a head tilt to the right, with wide head swinging movements (think Stevie Wonder) bilaterally, especially when she first wakes up. She is an indoor only cat, with a history of indoor-outdoor lifestyle over 5 years ago.

Physical Examination


General: T: 99.4 °F/37.4 C Pulse: 180 bpm Resp: 20 breaths/min
Wt.: 3.4 kg BCS: 4/9 MM
Eyes: Corneas are clear, no ocular discharge, normal conjunctiva.
Ears: Mild waxy debris noted in both external ear canals.
Oral cavity: Patient did not allow evaluation
Teeth: Did not evaluate.
Lymph nodes: Normal, no peripheral lymphadenopathy noted.
Heart: No murmurs or arrhythmias, pulses strong and synchronous.
Respiratory system: No nasal discharge, no tracheal sensitivity. Lungs clear on auscultation.
Abdomen: Normal, soft, non-painful, no masses or organomegaly noted.
Musculoskeletal: Not evaluated
Skin and hydration: dry flaky hair, no ectoparasites noted

NEUROLOGIC EXAMINATION


Palpation: No paraspinal pain elicited on palpation
Postural reactions: normal tactile placing and hopping all limbs.
Reflexes: Normal.
Gait: Ambulatory with mild vestibular ataxia and falling left.
Cranial nerve abnormalities: Wide head swinging with an occasional right AND left head tilt, positional rotary nystagmus, mild miosis OS, remainder normal.
Mentation: BAR, occasionally hissing

What is the neuronatomic lesion localization for THIS cat?

This cat has evidence of vestibular disease based on the presence of a head tilt and nystagmus. Cranial nerves 8 are affected by loss of function of the peripheral nerve, brainstem or cerebellum. To differentiate between these three localizations, it is important to evaluate the remaining neurologic examination for clues. Animals with brainstem disease will exhibit a loss of function of the upper motor neurons and ascending proprioceptive pathways which is demonstrated as evidence of ipsilateral hemiparesis and reduced ipsilateral proprioceptive testing. Furthermore, reduced level of alertness (obtunded, coma, stupor) may be noted. If paresis, proprioceptive deficits or reduced mentation are noted the lesion is most likely in the brainstem. Cerebellovestibular disease will manifest with signs of vestibular disease plus evidence of hypermetria, intention tremors and/or truncal sway, suggestive of cerebellar disease. Absence of these findings suggests a peripheral CN 8 neuroanatomic lesion localization. This cat does not have evidence of brainstem or cerebellar disease therefore the signs were localized to the peripheral component of CN 8.
Reduced sympathetic innervation to the eye may occur through damage to the sympathetic pathway. This pathway starts in the hypothalamus, courses caudally through the brainstem, cervical spinal cord, and exits the T1-T3 spinal cord segment and travels cranially in the jugular groove to the cranial cervical ganglion. From the cranial cervical ganglion this pathway runs through the middle ear and along the trigeminal nerve to end in the periorbital muscles, 3rd eyelid and dilator muscle of the iris. Dysfunction anywhere along this pathway will result in miosis in dim light. The lesion in this case is likely in the region of the middle ear due to a lack of neurologic disease noted in the intracranial structures, spinal cord, or along CN 5.

You may be tempted to call this a central lesion because the head tilts BOTH directions but don't! Without signs of hemiparesis, proprioceptive placing deficits or mentation changes a central lesion is unlikely.

Differential diagnoses: The history suggests that we now have a bilateral otitis media/interna but you couldn't rule out a polyp or neoplastic process with a secondary infection.

What did we do?
CBC and serum biochemistry were normal. Thoracic radiographs were unremarkable. The brain MRI showed bilateral debris in the bulla with ring enhancement.

Final diagnosis: Bilateral otitis media/interna. A myringotomy was performed, with ear flushing, cultures and cytology. Unfortunately no growth was noted (this is uncommon!) so marbofloxacin was started and clinical signs improved. She had a left head tilt on presentation for 30 day recheck, and this is expected to be permanent. All other signs of vestibular disease had resolved!

Happy first week of Fall everyone! I hope you and your family had a wonderful summer and look forward to working with you as we dig into what I hope will be a lovely Wisconsin fall.

Are we any good at a neurologic exam when pets are vestibular?

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, 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).

My current work days are...well, all of them except Sundays. I'll post on FB or my website if I'm closed on a random day so feel free to check those spots if you're not sure. Otherwise, feel free to call, email or hop online to schedule a telephone, live or video consultation with me. Remember, all live consults are still curbside!