Mydriasis in a Cat

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

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

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

Lesion localization?

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

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

Neuroanatomic Lesion Localization for Busy Vets

What is the neuroanatomic lesion localization for the following case?
Signalment: 4 year old FS DSH
History: Acute onset inability to blink one eye. No history of trauma. She is an indoor only cat. 

To answer this question, of course you must start with a cranial nerve exam. At its most basic level, the cranial nerve examination is a process of elimination. Let's start with the blink reflex. If you touch the medial and lateral canthus, what cranial nerves are you testing? (CN 5 and CN 7) How do you know which nerve is affected? To do this, we try to isolate each cranial nerve in the reflex to see which one misbehaves. How can you isolate these two nerves from each other to see which is the affected nerve? Lets's try a corneal reflex! When done correctly, the cotton swab touches the cornea and the eye retracts into the socket. Doing this tests CN 5 (sensory) and 6 (motor). Voila! If the cat does not blink when you touch the medial or lateral canthus, but DOES retract the globe when you do corneal reflex which nerve is affected? Think you know... scroll (or read!) to the bottom to see the answer. 

But wait! That is only part of the question. We have now localized which cranial nerve is affected but we don't know if this is a central or peripheral nerve lesion localization, right? To look at the brainstem we focus on the nerve pathways running towards and from the forebrain and determine if they're affected. The nerve pathways that are easiest to test are proprioception and motor/tone. Watching the animal walk you may be able to detect a toe drag or delayed placement but ultimately we have to test proprioception through paw replacement testing or my personal favoriate for cats: tactile placing. Similarly, when watching the patient walk you may see a hemiparesis (weakness on one half of the body). Often this is more obvious in the pelvic limb but both ipsilateral limbs can be affected. The last piece to the puzzle is an evaluation of level of mentation. If the animal is obtunded, stuperous or in a coma, we have an effect to the brainstem RAS. If you have 1 or more of these signs, the animal has a brainstem disease. If we DON'T have delayed proprioception, evidence of hemiparesis or a change in mentation, we are more likely to be dealing with a peripheral neuropathy.
Remember:
1) cranial nerve deficit + delayed paw replacement/tactile placing, weakness or decreased mentation = brainstem.
2) cranial nerve deficit without the above = peripheral 

Answer: Cranial nerve 7 is affected. (5 is normal in corneal reflex therefore it is not the problem in the blink reflex either.)

Thanks for reading and have a great week! Do you have a case that is puzzling you? Please reach out - I'd love to help. Did you know I also do onsite or virtual private CE for hospitals? Reach out for more details, if you're interested.

Hypothyroidism and Neuropathies

Does hypothyroidism affect the nervous system? You bet! The peripheral nerve is the most common target in the neurologic system. How does a low thyroid hormone affect the peripheral nerve (you might ask)? I'm glad you asked...

Etiology:

1) accumulation of mucinous deposits resulting in nerve entrapment
2) demyelination secondary to Schwann cell defect
3) vascular nerve damage secondary to hypothyroid induced dysfunction of BBB
4) disruption of axonal transport

Signalment:Typically older dogs, however congenital disease does (rarely) happen. NOTE: dogs are not always overweight, heat-seeking or have flaky-hair coats with peripheral neuropathy signs. 

Clinical signs:A polyneuropathy (multiple nerves affected) is most common. This results in paresis without ataxia and reduced to absent peripheral spinal reflexes. Signs may be mild, to start. 
Cranial nerve deficits such as facial nerve paralysis (VII), vestibular dysfunction (VIII), or laryngeal paralysis (X) are common signs of hypothyroidism. Of course, other things can cause damage to these nerves but don't forget to include hypothyroiism on your differential diagnoses list for patients with a peripheral neuropathy. Hypothyroidism may also cause a myopathy and/or megaesophagus.

Diagnostic tests:T4 is a good first step. If abnormal, a full panel is recommended. 

Treatment options:You guessed it...supplementation!

Prognosis:The neuropathy is likely to improve a little or a lot, after several months with therapy if the axonal degeneration is not too severe. I commonly caution owners to be prepeared for perminent deficits and rejoice when that doesn't happen!
Cranial nerve deficits may persist even with appropriate treatment.

Frequency:
Common in older dogs. Remember they don't need to be over0-weight, heat seaking or even sluggish to get a hypothyroid induced peripheral neuropathy. Cats can be hypothyroid too!

May the luck of the Irish be with you this week! Thanks for reading and have a great week! 

How do I use the Menace Response?

Picture this...You are presented with a 4 year old Pug with a history of "bumping into things" recently. You do a complete physical exam, including a fundic exam and neurologic exam (self high five!) and find the following changes:
Mentation: Quiet, alert and responsive
Cranial nerves: Absent menace OS, intact PLR, intact ocular movements, normal remaining cranial nerves
Gait: normal
Postural reactions: absent left pelvic limb, all others normal
Reflex: normal all limbs and cutaneous trunci
Palpation: non painful.

 
First question: Does this patient have neurologic disease? 

Golly, if it didn't this would be a silly TidBit Tuesday, wouldn't it?  It seems odd to ask this question but I feel it is a good habit get into, to ensure you're not trying to make a non-neurologic problem into a neurologic one. Interestingly, a recent report identified 8% of pets referred to a University Neurology service had "pretenders" disease (ex: cruciate rupture that was mistaken for a neurologic condition). 

Second question: What is the neuroanatomic lesion localization?

Start with basic anatomy. In a very simplistic sense, menace uses CN 2 (sensory) and CN 7 (motor) with a pass through the prosencephalon to connect the two CN. This is a complex pathway that we don't fully understand but the true bare basics are CN2, pass through the prosencephalon and CN 7.  Damage to 2, prosencephalon or 7 will result in a menace deficit. Now, expand the anatomy to include the pathways. The left eye uses left CN 2, crosses and uses right prosencephalon and then back to the left CN 7. 
We still don't know if it is CN 2, prosencephalon or CN 7 that is affected, right? Isolate CN 2 from CN 7 by doing PLR. 
PLR = CN 2, midbrain, CN 3. 
Deduction would say that if PLR is normal then CN 2 must be normal too, right?
Now we need to sort out if the menace deficit is due to disease of the prosencephalon or left CN 7. So, isolate CN 7 from CN 2 by looking at the blink reflex.
Blink reflex = CN 5, and 7.
If you tap the medial and lateral canthus and they blink, CN 5 and 7 must be intact! In the case above, we said all cranial nerve tests, other than the menace response, were normal. Therefore, CN 7 must also be normal. 

 
Voila! Neuroanatomic lesion localization is RIGHT prosencephalon!

What about that postural deficit in the left pelvic limb, you ask? 

That pathway goes from the pelvic toes --> up sciatic nerve -->up left spinal cord --> up left brainstem to cross in the midbrain --> ends in right prosencephalon.

This dog has a right prosencephalic lesion (aka right forebrain) giving both a left menace deficit and left pelvic limb deficit. Well done! You now know WHERE the problem is coming from and can build your differential diagnoses list for a focal prosencephalic lesion and/or refer them to a neurologist (instead of an ophthalmologist) for further testing.

Want more? I can do personalized CE at your hospital. We can go through neuroanatomic lesion localization, discuss seizure cases, or any other topic you and your colleagues might find helpful for your practice. Email me for additional details.

Have a great week and stay warm!

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!

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!

Unilateral Masticatory Muscle Atrophy

It's a Wednesday morning and you see on your schedule a 7 year old dog with unilateral temporalis and/or masseter muscle atrophy. What parts of the neurologic system could be involved?

1. Muscle: A problem with muscle function, termed a myopathy, can result in muscle atrophy. The most common cause of temporalis and masseter muscle atrophy in dogs is masticatory muscle myositis (MMM), which is caused from an immune mediated attack against the muscle fiber. This is a UNIQUE form of muscle inflammation because the proteins on these muscles are embryologically unique (2M fiber type) from all other muscles in the body. We care about that because it means that we can identify an antibody (AB) test that we can run that is highly specific AND sensitive! What else should we consider? Infectious myositis, secondary to neospora or toxoplasma infection would be my second choice differential for many dogs with this clinical presentation. In this scenario, the protozoa get into the muscle, set up a secondary inflammation (myositis) and muscle atrophy results. Sometimes you can see a mild positive on the aforementioned MMM AB titer test, but it is low, if positive at all. However, if you concurrently test for neospora and toxoplasma (serum titers) you can catch this "false" positive, and treat the correct disease.

Treatment for MMM: Immunosuppressive steroids for 30+ days, followed by a taper protocol.
Treatment for infectious myositis: clindamycin or sulfa antibiotics until negative or stable titers. This is often MONTHS of treatment!

2. Cranial nerve 5: A dysfunction of CN 5 can result in denervation atrophy of the temporalis muscles. On the exam, look closely for concurrent signs of a sensory neuropathy to the face and if present, a CN 5 dysfunction should be suspected.  This might include reduced blink reflex, reduced or absent corneal reflex, and reduced response to nasal stimulation compared to the unaffected side. The differential diagnoses list is much bigger but typically centers around a few common causes (neoplasia, neuritis, hypothyroidism, and trauma). To diagnose a CN 5 neuropathy the best approach is a thyroid panel,  CBC, serum biochemistry and then a brain MRI followed by a spinal tap, along with titers for infectious diseases (as indicated). Not all of those tests are needed for each patient so pick and choose as appropriate for your case. 

Treatment for CN 5 deficits: this varies and is dependent on the underlying cause. It is a bit hard to summarize TidBit Tuesday-style. :) 

These cases can be puzzling to sort out so please reach out if you feel a neurologic examination is helpful for your patient. Have a great week!

Horner's Syndrome and Cervical Myelopathies

Do any of you feel comfortable localizing Horner’s syndrome in a dog? If you do…skip the first section and read the data from a recent study about cervical myelopathy and Horner’s syndrome.  If not, please carry on and join us for an interesting look at Horner’s syndrome with cervical myelopathies.

 
First, Anatomy

The sympathetic pathway to the eye is a 3-neuron system. Neuron 1 starts in the thalamus, travels through the brainstem and cervical spinal cord to T1-T3 thoracic spinal cord segments where it synapses. Neuron 2 starts here and travels cranially, through the ansa subclavia along the vagosympathetic trunk (right next to that jugular vein you’re about to do venipuncture on!) to the caudal aspect of the bulla. From there, the 3rd order neuron takes a path through the tympanic bulla, along the ventral aspect of the skull (in the cavernous sinus) and hops a ride with CN 5 (trigeminal) to make a beeline to the eye. This neuron innervates the muscles of the iris, eyelids and orbit. It is the most indirect path anyone could design but I might argue that you can break it down into several key parts when localizing Horner’s Syndrome.

• Intracranial

• Cervical

• Brachial plexus

• Jugular groove

• Tympanic bulla

• CN 5

Cervical Myelopathies and Horner’s Syndrome

After reviewing the anatomy, it might be easy to see how a cervical lesion may cause Horner’s syndrome, right? The 1st order neuro travels from the intracranial structures via the cervical spinal cord to the upper thoracic spinal cord segments. Interestingly, a recent study looked at Horner’s Syndrome and cervical myelopathies* and found an incidence of only about 10% of Horner’s syndrome with concurrent cervical myelopathy. Therefore, although the anatomy makes sense, it is a fairly protected neuronal pathway and therefore a cervical lesion rarely causes Horner’s signs.

What Causes Horner’s Syndrome and a Cervical Myelopathy?

I’m glad you asked! According to this study, more dogs with Horner’s syndrome had noncompressive lesions compared to the control group (dogs with cervical myelopathy without Horner’s syndrome). Noncompressive lesions are often caused by fibrocartilaginous embolism (FCE) but hydrated nucleus pulposus extrusion (HNPE) and intramedullary neoplasia, noncompressive spinal trauma, Syringohydromyelia and inflammatory myelitis were found to cause Horner’s syndrome.  Also of note, Horner’s syndrome can be unilateral OR bilateral with cervical myelopathies.

Did having Horner’s Syndrome Affect Prognosis?

Nope. The underlying disease predicted prognosis and having Horner's Syndrome did not significantly negatively or positively influence outcome. However, seeing Horner’s syndrome on the neurologic examination would suggest that a surgical lesion is less likely to be identified.

 
Do you have a patient with Horner’s Syndrome? Do you suspect a cervical myelopathy? I’d love to help! Please reach out via email or schedule a consult online. Stay safe on these slippery roads and have a great week!

Reference from the TidBit Tuesday: https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.16588

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!

Bruxism and Forebrain Disease

Bruxism is defined, in human medicine, as repetitive, involuntary, masticatory muscle activity, often appears as grinding teeth, bracing or thrusting of the mandible. There are two types: awake and asleep. Asleep bruxism is quite commonly reported in humans and can be triggered by stress or anxiety. Awake bruxism, or uncontrolled bruxism during awake states, is a very different thing. Awake bruxism (AB) can be broken into pathologic or physiologic causes. Physiologic causes don't apply to veterinary medicine so let's dig deeper into pathologic, awake bruxism. Within the pathologic group there are idiopathic causes and symptomatic causes. Neurologic diseases such as inflammatory conditions, traumatic or congenital disease, epilepsy and a host of other causes have been reported to be associated with awake bruxism in humans. A recent article, published in the JVIM, noted that bruxism secondary to a neurologic cause is most commonly awake bruxism.

Have you seen a dog with Bruxism? The recent article by Liatis T, et al, evaluated AB in 4 dogs over a span of 11 years so don't feel badly if you've not seen one! A link to the entire report is found at the bottom. Although previously reported in dogs with congenital storage disorders, it is rare in mature adult dogs. In this study, two dogs were presented by the owners with a complaint of AB, along with other clinical signs of neurologic disease. AB was noted in the second two dogs by the attending clinicians during evaluation. AB was episodic in all four dogs, occurring throughout the day and always stopped when distracted. No post ictal signs were noted and no autonomic signs were seen during or after the event. All four dogs had forebrain lesions!

Take away: If you evaluate a dog for awake bruxism, or if you note it during the exam while evaluating the pet for other neurologic abnormalities, consider it abnormal. It is not pathognomonic for forebrain disease but, at least according to this report, is strongly supportive of a forebrain lesion. This may be an indication to get a neurology consultation and advanced imaging.

Link: https://onlinelibrary.wiley.com/doi/full/10.1111/jvim.16570?campaign=wolearlyview

Thanks for reading! I look forward to working with you again soon.

Anisocoria in Dogs and Cats

** Credit for the amazing hand-drawn image goes to my good friend, and veterinarian Dr. Pam Boutilier.
Anisocoria

Anisocoria is defined as pupil asymmetry and may be seen with ocular or neurologic dysfunction. Malfunction of the sympathetic, parasympathetic, or visual system may result in anisocoria.

Neuroanatomy

Visual Pathway
When light enters the eye, it activates the light receptors in the retina. That information then travels along CN II, crosses in the optic chiasm, and terminates in the thalamus. Optic radiations relay the visual information from the thalamus to the visual cortex in the brain. This pathway can be tested using the menace response test and/or cotton ball testing.

Parasympathetic function: Pupil constriction
The parasympathetic pathway to the eye is a short, two neuron pathway which originates in the midbrain. The two, paired parasympathetic nuclei of CN III (PSNCNIII) send fibers along with the somatic nerves from CN III to the eye. The parasympathetic pathway is best assessed using PLR. When a bright light enters the eye, CN II activates and synapses on the PSNCNIII. The parasympathetic fibers transmit this information to the eye, using cranial nerve III as a conduit, resulting in pupillary constriction.

Sympathetic function: Pupil dilation
The opposing system is the sympathetic system, which causes pupillary dilation. The sympathetic pathway is a three neuron pathway and takes a longer course to the eye compared to the parasympathetic system. In general it goes from the thalamus, through the brainstem and cervical spinal cord to exit in the upper thoracic segments. Fibers then make a U turn and head back to the eye via the jugular groove (don't poke around too much when doing those jugular blood draws!), bulla (ear infection can = sympathetic dysfunction) and then hitches a ride with CN V to make the final leg to the eye. Malfunction anywhere along this pathway will result in a failure of iris dilation in a dark room and a comparatively miotic pupil, typically accompanied with enopthalmus and ptosis.

Putting it together

Let's put this new knowledge to work. If you see a case with anisocoria, how do you decide if it is a parasympathetic or sympathetic dysfunction?
1) Assess the pet in a dark room. Does the eye dilate? If yes --> The lesion is NOT due to sympathetic dysfunction.
2) Asses PLR. Does the eye constrict? If yes --> the lesion is NOT due to parasympathetic dysfunction.

To localize to the appropriate location beyond sympathetic or parasympathetic function requires a full neurologic examination. If you aren't comfortable performing or interpreting a neurologic examination please consider a neurology consultation! I am not comfortable doing a dental...we all have our limitations! :)

If you're interested in digging into anisocoria more deeply, or you have a case with anisocoria consider checking out the following article for a full discussion and more amazing images. Note: I do not receive any royalties or financial impact from this article.
* Barnes Heller H, Bentley E. The practitioner's guide to neurologic causes of canine anisocoria. Today's Veterinary Practice Jan/Feb 2016 pg. 77- 83.

Keep those consults coming; we all get to learn a little bit more with each consult. 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

Neuroanatomic Lesion Localization for Busy Vets

Here is the case: A 5 year old cat that cannot blink one eye. What cranial nerve is affected?
To answer this question, of course you must do a cranial nerve exam. At its most basic level, it is a process of elimination. If you touch the medial and lateral canthus and the cat does not blink what cranial nerves are you testing? (CN 5 and CN 7)

How can you isolate these two nerves from each other to see which is the affected nerve? If you do corneal reflex you're testing CN 5 (sensory) and 6 (motor). Voila! So, if the cat does not blink when you touch the medial or lateral canthus, but DOES retract the globe when you do corneal reflex which nerve is affected? Think you know... scroll (or read!) to the bottom to see the answer. 

Need a little refresher on the cranial nerves and their jobs? The table below has all nerves, and their main jobs, for quick easy reference. 

Cranial nerveFunctionNeurologic examination CN I: OlfactorySmellWatch the dog sniff, ask about eating habits. * Difficult to objectively evaluateCN II: OpticSightMenace, PLR, Cotton ball test, trackingCN III: OculomotorSomatic: eye movement.
Innervates all extraocular muscles except lateral rectus and dorsal obliqueAutonomic: Parasympathetic function to the pupilPhysiologic nystagmus (medial movement), Strabismus (if present this indicates an abnormalities of CN)
 
PLRCN IV: TrochlearEye positionStrabismusCN V: Trigeminal

• Ophthalmic

• Maxillary

• Mandibular

Sensory to the face, cornea
 
Close the jaw (muscles of mastication)Sensory: Corneal reflex, blink reflex, sensory assessment of the nares and lips
Motor: ability to CLOSE the jawCN VI: AbducentSomatic eye movementPhysiologic nystagmus (lateral movement), StrabismusCN VII: FacialSomatic: muscles of facial expression
Autonomic: parasympathetic innervation to the lacrimal gland, 3rd eyelid gland, palatine and nasal glands, taste rostral tongueMenace, blink reflex, lip and ear twitchCN VIII: vestibulocochlearSensory: balance and hearing
Innervates: vestibulospinal tracts, MLF (eye movement), reticular formation, cerebrum and cerebellumPhysiologic nystagmus, pathologic nystagmus,  positional strabismus, head position (tilt), ataxia, hearing test (BAER)CN IX: GlossopharyngealSensory to pharynx
Motor to pharynx
Autonomic: parasympathetic function – taste from the caudal tongueGag reflexCN X: VagusMotor to pharynx
Parasympathetic: taste to pharynx, larynx, heart rate, GI motility, otherGag reflex
CN XI: Spinal accessoryMotor: trapezius, sternocephalicus, brachiocephalicusPalpation of associated musclesCN XII: HypoglossalMotor: tongueMove tongue left and right, visually assess for symmetry and movement.

Answer: Cranial nerve 7 is affected. (5 is normal in corneal reflex therefore it is not the problem in the blink reflex either.)

Thanks for reading and have a great week!

 Do you have a case that is puzzling you? Please reach out - I'd love to help. Did you know I also do onsite or virtual private CE for hospitals? Reach out for more details, if you're interested.

Temporalis and Masseter Muscle Atrophy

It's Tuesday at 10 am and you're about to see a 7 year old dog with unilateral temporalis and/or masseter muscle atrophy. What parts of the neurologic system could be involved?

1. Muscle: A problem with muscle function, termed a myopathy, can result in muscle atrophy. The most common cause of temporalis and masseter muscle atrophy in dogs is masticatory muscle myositis (MMM), which is caused from an immune mediated attack against the muscle fiber. This is a UNIQUE form of muscle inflammation because the proteins on these muscles are embryologically unique (2M fiber type, if you must ask) from all other muscles in the body. We care about that because it means that we can have a an antibody (AB) test that we can run that is highly specific AND sensitive! The second myopathic disease of the head muscles, that I see commonly, is myositis due to neospora or toxoplasma infection. Simply put, the protozoa get into the muscle, set up a secondary inflammation (myositis) and sometimes you can see a mild positive on the aforementioned MMM AB titer test. However, if you concurrently test for neospora and toxoplasma (serum titers) you can catch this "false" positive, and treat the correct disease.

Treatment for MMM: Immunosuppressive steroids for 30+ days
Treatment for infectious myositis: clindamycin or sulfa antibiotics until negative or stable titers.

2. Cranial nerve 5: A dysfunction of CN 5 can result in denervation atrophy of one (or both) temporalis muscles. On the exam, look closely for concurrent signs of a sensory neuropathy to the face and if present, a CN 5 dysfunction should be suspected. The differential diagnoses list is much bigger but typically centers around a few common causes (neoplasia, neuritis, hypothyroidism, and trauma). To diagnose a CN 5 neuropathy the best approach is a brain MRI followed by a spinal tap, along with titers for infectious diseases, thyroid panel and routine CBC, serum biochemistry. Not all of those tests are needed for each patient so pick and choose as appropriate for your case.

Treatment for CN 5 deficits: this varies widely and is dependent on the underlying cause. It is a bit hard to summarize TidBit Tuesday-style. :) Stay tuned for another email detailing all of the possible causes and treatments for cranial neuropathies.

I hope this TidBit Tuesday helps you focus your exam, and thoughts, when faced with a case of unilateral atrophy of the muscles of the head. This report was stimulated from recent conversations about this presentation so please reach out if you have a case, or questions about a case, with unilateral muscle atrophy. The more we talk with each other, the more we learn from each other!

Have a great week!

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 idiopathic, but causes such as neuritis (viral or immune mediated) or atrophy have been hypothesized. A recent study (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 and demonstrate peracute onset of signs, often proceeded by vomiting with no progression 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: 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 needed.

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 show improvement. Full resolution of clinical signs should be by 6 weeks. If signs wax and wane, or progressive 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. Signs may occur multiple times over the animals' life.

Thanks for reading! This TidBit Tuesday was prompted by one of you so keep those suggestions coming! If there is something you'd like to read about, chances are that someone else is also interested too.

My hours are changing the last week of August due to school starting. As always, please let me know if you cannot find an appointment time through the online scheduler.
Have a great week!

Time for a Tongue Twister!

Signalment: 12 year old MC Mixed breed dog, 45 kg
History: 1 month history of change in bark, with a 1-2 week history of difficulty eating and drinking. The owners also identified difficulty walking in the last few days and a decrease in the dog's interaction with them.
Physical Examination: Grade II/VI left heart murmur, previously noted and not progressed. The remainder of the exam was unremarkable.

Neurologic Examination

Mentation: Mildly obtunded. The pet interacted when asked, but otherwise seemed content to stare at the floor.
Cranial nerves: Decreased to absent gag reflex, tongue atrophy (see the photo above), all remaining cranial nerves were normal.
Gait: Ambulatory mild proprioceptive ataxia in all four legs
Reflexes: Normal spinal reflexes including c. trunci and perineal.
Palpation: Non painful spinal palpation however pain elicited with cervical ventroflexion
Postural reactions: absent right thoracic and right pelvic limb paw replacement test, normal left paw replacement thoracic and pelvic.

Neuroanatomic Lesion Localization?? To do this, we need to break it down and identify all of the possible anatomic localizations each neurologic deficit could be noted. Unfortunately the table does not copy to this blog very well so please email me or join our TidBit Tuesday mailing list to get all of the details.
What I did was list all of the possible locations that the affected deficit might involve and then narrowed down the lesion localization two ways:

1. Find the common denominator. In this case, the medulla. OR

2. Find the cranial nerve(s) affected and determine if the pet also has: a) abnormal mentation, b) hemiparesis ipsilateral to the affected cranial nerve or c) paw replacement deficits ipsilateral to the affected cranial nerve. If they do, it is central. If not, it is a likely a peripheral neuropathy.

Neuroanatomic Lesion Localization: Medulla, right side.

Differential Diagnoses: Neoplasia, meningoencephalitis (infectious or inflammatory)

Case Conclusion

This dog had normal CBC, serum biochemistry, UA, chest radiographs and abdominal ultrasound. Brain MRI identified a discrete contrast enhancing extra-axial mass in the right caudal fossa affecting the right side of the medulla. This finding was most consistent with a meningioma. A spinal tap was not performed due to the proximity of the mass to the cerebellomedullary cistern. Based on the working diagnosis surgical decompression, radiation therapy or supportive care were discussed with the owners and they elected supportive care.

You may recognize this case if you have been a loyal TidBit Tuesday reader. This was repeated from February 2020 because I felt like it was a good time to review cranial nerve lesion localization with a very interesting cranial nerve deficit. Thanks for reading (again)!

I hope you have a great week!

Idiopathic Facial Nerve Paralysis

Idiopathic Facial Nerve Paralysis

I thought we'd continue our theme from last week about peripheral neuropathies and talk about a neuropathy that we all (I think) see fairly regularly: Idiopathic facial nerve paralysis.

What is it?
Idiopathic facial nerve paralysis (IFNP) happens for, ahem, unknown reasons. There is some type of synaptic block that, as of now, has an unknown cause. The facial nerve is a motor nerve that starts in the medulla (brainstem), courses through the skull and bulla on it's way to the face. Other causes of facial nerve paralysis such as hypothyroidism, neoplasia, otitis media, polyps, and rarely neuritis. Remember: you must localize the lesion to the peripheral CN 7 to include IFNP on your list of differential diagnoses!

What does it look like?
The facial nerve innervates the muscles of facial expression in dogs and cats as well as providing innervation to the lacrimal eye glands. Clinical signs are typically unilateral and, result in an inability to move the eyelids (inability to blink), inability to move the lips (dogs may accidentally chew on their lips), lack of ear movement (especially noticeable in cats), and a dry, red eye with possible ocular ulceration.

Clinical Course
Signs are typically acute in nature with rapid progression to full clinical manifestation. Spontaneous resolution occurs in 3-6 weeks. Yay!

Management
Supportive care, such as eye lubricant, and ensuring lip injury is minimized by limiting chewing toys/bones, is the mainstay treatment. Antibiotics, steroids, NSAIDs and other medications do not improve the recovery time!

It's short and sweet this week. Please let me know if you have a specific topic of interest! Have a great week, and keep those consults coming.

Consults are available Monday-Saturday at various times. Check out www.barnesveterinaryservices.com (press the schedule button in the upper right corner) to schedule. Note: Only veterinarians or veterinary staff may schedule a consult.