Canine Distemper Causing Lameness?

An interesting case report came across my desk awhile ago so I thought I might share some key points with you this week. (Green L, Cook L, et al. Distemper encephalomyelitis Presenting with Lower Motor Neuron Signs in a Young Dog. JAAH 2020)

Signalment: 4 month old spayed female dog

History: The puppy was presented to the neurology service with a several day history of right thoracic limb monoparesis. Key findings in the neurologic examination included axial pain on palpation, thoracic limb lameness, weak withdrawal of the affected limb and a paw replacement deficit in that limb. Absent cutaneous trunci reflex was also noted on the right side. Other than the neurologic findings, the only other interesting finding on physical examination was a mildly febrile state of 102.7F) and crusting of the foot pads.

She was initially managed conservatively however signs progressed to inappropriate mentation which was suspected to be due to the fentanyl patch. This was removed and signs improved however the clients elected to proceed with additional testing at that time.

Neuroanatomic lesion localization? You tell me!! (see below when ready)

Differential diagnoses listed at this time included non-infectious inflammatory conditions (MUE), infectious meningomyelitis, and hemorrhage or trauma.

Diagnostic testing

• Spinal MRI: Abnormalities in the central spinal cord

• Brain MRI: Unremarkable

• CSF: Mild pleocytosis cell count 10/ul: reference < 5/ul) with normal protein and RBC.

• Infectious disease testing: Neospora IFA was negative however the Toxoplasma IgG was markedly elevated with a borderline IgM. Parvovirus testing and cryptococcus antigen testing was negative. PCR on CSF for distemper (CDV) was positive. A whole lot of other infectious diseases were tested for, and negative.
  

Treatment with clindamycin, sucralfate, gabapentin, tramadol, famotidine, metronidazole and a single dose of dexamethasone was started.

Progression: She was discharged 4 days later, but returned due to progressive mentation changes and worsening ambulation. During evaluation she had a focal seizure. (Now we have multifocal neuroanatomic lesion localization!). She was humanely euthanized and submitted for necropsy.

Necropsy: Findings consistent with CDV were found and in addition, immunohistochemistry of the C5 and lumbar spinal cord and strong nuclear and cytoplasmic brown staining for CDV and no staining for Toxoplasma.

What is so noteworthy about this case?

• She was partially vaccinated. Did you know that 40% of dogs with confirmed distemper infection, in one study, were vaccinated? (Tipold A: 1995).

• She had hyperesthesia associated with her neurologic signs. Pain is a very unusual finding for a distemper case and the authors suggest this is the first case report of confirmed CDV in a dog with limb pain.

• The progression from limb to brain is unusual but not unreported.

Take Home Message
A young dog, with multifocal neurologic findings, or findings of spinal pain in conjunction with neurologic findings, may have CDV. I suggest adding this disease to your ever-growing-list of infectious diseases that can cause spinal pain in dogs.

Neuroanatomic lesion localization answer: C6-T2 radiculopathy or neuropathy. There is no evidence of spinal cord involvement initially so a myelopathy is less likely.

As always, thanks for reading! I hope you have a NON-PAINFUL week, that isn't LAME! (Sorry...I just couldn't help myself.)

Predicting Spinal Shock

When things go bump in the spine...

So many interesting cases happened this past week! Please join me today as we evaluate a 4 year old FS Mixed breed 10 kg dog, together. Her presenting complaint was acute onset difficulty walking in the last 24 hours.

Neurologic Examination:
Mentation: BAR
Cranial nerves: all normall
Gait: Paraplegia (no voluntary movement)
Reflexes: reduced withdrawal in both pelvic limbs, poor anal tone, and reduced cutaneous trunci reflex to T13 bilaterally. All remaining reflexes normal.
Postural reactions: Absent both pelvic limbs, normal both thoracic limbs
Palpation: Painful at T12-T13, remainder non painful.
Other: Absent nociception in both medial and lateral toes of both pelvic limbs.

Neuroanatomic lesion localization: Hmmmm....let's take a moment and think this through.
1) Does this dog have neurologic disease? Yes!
2) Are forelimbs and intracranial structures normal? I'd say, yes. Okay, the lesion is caudal to T2.
3) Our choices for lesion localization are, T3-L3, L4-S3 or neuromuscular at this point.
4) Are reflexes affected? Yes. Therefore the lesion must be L4-S3 or neuromuscular. But wait! What about that back pain and reduced c. trunci reflex? The cutaneous trunci reflex reflects a T3-L3 myelopathy and the back pain certainly supports that but could be from non-neural causes. Is this multifocal spinal cord?
5) Hold the phone, Barnes. Tell me why this isn't neuromuscular? Okay, I'll tell you. Sensory neuropathies are extremely rare and are usually congenital. Therefore, to have a loss of deep pain this animal needs to have a spinal cord lesion. Moving on then....

Neuroanatomic Lesion localization: Folks, this is an example of multifocal neuroanatomic lesion localization of T3-L3 and L4-S3 spinal cord. Primary differentials would include acute diseases affecting the spinal cord (such as FCE, disc herniation, trauma) plus spinal shock, or a true multifocal spinal cord disease (such as meningomyelitis).

What is Spinal Shock?

Spinal shock occurs when there is "reverberation" and a change of the local environment that results in temporary cessation of reflexes downstream from the injury. In most models, the injury is at the TL junction so the pelvic limb spinal reflexes are temporarily lost. This is transient! For most animals, the reflexes return in 1-3 days if not shorter. It is important to note that there is NO pathology in the pelvic plexus.

Predictive Models

How do you know when you have a pet with spinal shock or a pet with a multifocal disease when you have multifocal spinal cord lesion localization? The honest truth is you don't know until you do an MRI and show that only one lesion is present. However, there was a predictive model recently published (https://onlinelibrary.wiley.com/doi/10.1111/jvim.16352) that showed smaller breeds, with a history of less than 24 hours, are more likely to have spinal shock. As with all predictive models, this isn't fool proof, but it is a start. For the case above, I would strongly consider spinal shock with a T3-L3 myelopathy. Indeed this is what we had; we had an FCE at T12-L1 on MRI and no additional lesions in the L4-S3 segment.

Hope this TidBit was helpful to your practice! Please reach out if you have a case I can help with, or if you have an idea for a TidBit Tuesday mailer. Happy February!

Orthostatic Tremor in Dogs

How often do you hear "my dog's legs shake when s/he stands?" (Okay, perhaps not as often as I do...but I'm going to assume you hear it at least a LITTLE bit of the time!)

Etiology
Orthostatic tremors can be primary, meaning the tremor is the disease itself. This is suspected to originate from the cerebellum or brainstem but is still, as of now, unknown. The disease is progressive therefore neurodegenerative causes have been considered.
Tremors that are associated with another neurologic disease are termed OT-Plus and include an assortment of spinal cord compressive diseases such as Wobbler's or LS disc herniation. The tremors with OT-PLUS are therefore suspected to be associated with weakness driven from the primary myelopathy, not a disease process in its own right.

Description
When rising to stand, during standing, or occasionally when rising to sit, dogs will exhibit a fine, involuntary tremor in pelvic limbs (most commonly), all four limbs (second most commonly) or thoracic limbs only (rarely). These abate when recumbent, or in active motion (walking, running). Specific awake electrodiagnostic testing confirms the disease but the clinical suspicion is high with the history alone. Orthostatic tremor (OT) has been described in large or giant breed dogs only. Signs begin between 9 months and 2 years of age for OT, and a bit older for OT-plus. In fact, Retrievers and older age were associated factors with OT-plus in a recent retrospective study reporting on orthostatic tremors. (10.1111/jvim.16328.)

Treatment
Okay this is super interesting to me (and hopefully you)! This data is for primary OT, not OT-plus.

• Phenobarbital/primidone - 15/15obtained remission (2 lost to follow up)

• Gabapentin/pregabalin - 25/29obtained remission (3 lost to follow up)

• Clonazepam - 5/6 obtained remission (1 lost to follow up)

Improvement was more likely to be partial than complete resolution (7:3) but some improvement was noted. Interestingly, clonazepam is reported to be the drug of choice for human OT and yet the response to treatment is minimal compared to what we see with our canine patients.

Why do these treatments help? Unknown. It isn't a convulsive disorder therefore these medications are helping from a different angle. I'll keep you posted as we hear more!

Take away from this:
Young, large or giant breed dogs with tremors may have OT
Look for an underlying cause if signs onset at an older age, especially in a retriever breed
Try one of the treatments listed, let me know what you think!

As always, thanks for reading. Please let me know if you have any questions about OT, or any other case you are evaluating.

I appreciate your business and look forward to continuing to work with you and your team!

Managing a Pain in the Neck

Cervical pain can present with or without concurrent neurologic deficits and therefore maybe secondary to neurologic or non-neurologic disease.

Animals with neurologic deficits in addition to neck pain have a neuroanatomic lesion localization (C1-T2 myelopathy) which includes the region of pain.

Deficits noted in the C1-T2 lesion localization may include proprioceptive ataxia of all four limbs, tetraparesis (or plegia), reduced or absent postural reactions in all four limbs, +/- reflex deficits of the thoracic limbs. Postural reactions are often more severe in the pelvic limbs than thoracic limbs with a C1-T2 myelopathy therefore this finding should not dissuade you from this lesion localization. Rarely noted neurologic deficits may include unilateral Horner’s syndrome and unilaterally absent cutaneous trunci. With acute, peracute and severe cervical injury respiratory failure (lack of inspiration) can be seen secondary to damage to the phrenic nerve (driving diaphragmatic function) and/or damage to the upper motor neurons that regulate the intercostal innervation. A lesion localization of a C1-T2 myelopathy indicates neurologic damage, and therefore diseases affecting the nervous system should be considered for these patients. See the section below discussing differential diagnoses for animals with a C1-T2 myelopathy lesion localization.

Animals with cervical pain without neurologic deficits cannot have a neuroanatomic lesion localization because they do not necessarily have neurologic disease.

Therefore, the diagnosis written in the record should be “cervical pain”. These animals may have neurologic disease; however, diseases outside of the nervous system should also be included on a differential diagnoses list.

Differential Diagnoses (not a complete, textbook list...just the more common ones)
** Many differential diagnoses listed below may start with signs of neck pain ONLY, without evidence of a myelopathy and then may or may not progress to signs of a myelopathy.

Differential Diagnoses (not a complete, textbook list...just the more common ones)
** Many differential diagnoses listed below may start with signs of neck pain ONLY, without evidence of a myelopathy and then may or may not progress to signs of a myelopathy.

1. Acute/peracute onset clinical signs:

   1. C1-C2 subluxation (congenital or traumatic)

   2. Intervertebral disc herniation (type I)

   3. Traumatic fracture/subluxation non-C1-C2

   4. Meningomyelitis

   5. Discospondylitis/osteomyelitis

2. Slow/subacute onset clinical signs

   1. Discospondylitis

   2. Vertebral or neural neoplasia (note: intramedullary neoplasia is commonly non-painful. Any involvement of the meninges can result in cervical pain.)

   3. Intervertebral disc herniation type II

   4. Syringohydromyelia

   5. Cervical spondylomyelopathy (AKA Wobbler’s syndrome)

   6. Meningomyelitis

3. Acute, non-progressive clinical signs

   1. Fibrocartilagenous embolism (note: this may be painful in the first 24 hours, however most become non-painful after 24 hours.)

   2. Syringohydromyelia

What do you do?

First, a neurologic examination. If the animal has neurologic deficits, referable to the cervical region, localize the lesion. (Self promotion plug here....remember if you're not confident with a neurologic examination, please call for a consult!)

Radiographs are useful if trauma or subluxation is a primary differential diagnoses. Treatment should follow with your differential diagnoses list. If the pet is poorly or non-ambulatory a consultation or referral to a neurologist is recommended ASAP.

Thanks for reading! I hope you have a great start to 2022. Keep those consults coming!

Neurologic Cat?

Where is the Lesion?

History: Sarah is a 4 year old, indoor only FS DSH. She was obtained as a kitten and had been normal, per clients, her entire life thus far. She presented to me for acute onset (same day) weakness. No known trauma, toxin ingestion or medication exposure.

Physical examination: No abnormalities, normal TPR.

Neurologic examination:
•Mentation: BAR
•Gait: Ambulatory severe left hemiparesis with proprioceptive ataxia in all four limbs
•Cranial nerves: Normal
•Postural reactions: absent left thoracic and pelvic limbs only
•Reflexes: reduced withdrawal left thoracic limb, normal all other limbs. Cutaneous trunci absent left, normal right side.
•Palpation: Non-painful

Lesion localization? I do not see evidence of intracranial disease so automatically I localize caudal to C1. Both a front and rear leg are affect, so again, we can isolate cranial to T2. So...right away you can think left C1-C5 or C6-T2 myelopathy. Which is it? Well, the reflexes were reduced to the left thoracic limb, and the reflex arc is C6-T2, so our localization must involve C6-T2.
Up is differential diagnoses building. Here is what I came up with:
D: none, this is acute
A: None, the cat is too old for congenital disease onset signs
M: none
N: Lymphoma is possible however it is rarely acute in nature
I: Meningomyelitis (infectious or inflammatory) is possible
T: No known trauma, but cannot rule it out
V: Fibrocartilagenous embolism is highly likely due to the acute onset of signs.

Did you think of something else that I missed?
Unabashed plug for the CE August 2nd here - we will look more specifically at this case and do lesion localization in greater detail. Please consider joining us from 7-8PM. Details can be found at my website.

Diagnosis: I debated about giving this away before the talk and I have decided NOT to tell you the final diagnosis this week. I will share it on next week's TidBit Tuesday (August 3rd) so stay tuned!

Hopefully you enjoyed this case review this week. Do you have a suggestion for a TidBit Tuesday topic? If so - please send me an email. I would prefer to write about something you want to read. :)

I hope you have a great week!

Tetanus and Dogs

What is tetanus?

Tetanus is caused by the Clostridium tetani bacteria which produces a neurotoxin that causes muscle contractions. This bacterium is found commonly in soil and is ubiquitous throughout the world. After the bacterium is injected into an anaerobic environment it produces the toxin. The toxin targets inter neurons in the spinal cord, inhibiting their function.

Diagnosis?

A diagnosis is made by observation of classic clinical signs such as limb rigidity, muscle retraction on the face or periocular. Detection of the C. tetani bacterium in the wounds through culture can provide a definitive diagnosis, if obtained.

Treatment?

Wound debridement followed by appropriate antibiotics (penicillin or metronidazole) will result in recovery for the majority of dogs and cats. For severe cases, respiratory assistance with a ventilator, sedation to avoid painful sustained muscle contractions and 24-hour nursing care may be needed.

Seasonality?

An interesting article came across my view recently that identified a spike in tetanus cases in the winter months (December-February) in England. This was surprising because more cases are reported in warm, humid climate than cold ones. The authors didn't provided substantial reasoning for the odd seasonality but suggested it may be related to the exposure by walking in wet muddy environments. Here is the link to the article if you'd like to read more: https://doi.org/10.1111/vec.13068

I hope you have a wonderful, productive, safe week and I look forward to working with you soon. Thanks for reading!

Large Breed Dogs and Disc Herniation

A little background...

Dogs greater than 10 kg experience type 2 disc herniation more frequently than type 1 disc herniation. (Refresher: Type 1 = acute extrusion of the center of the disc; Type 2 = bulge of outer ring of the disc into the spinal canal.) An estimated 10-30% of the time large breed dogs have type 1, depending on the study.

How is a type 1 disc herniation different for a large breed dog?

The answer is rather obvious, but glossed over frequently. They are bigger! That means nursing care is harder, surgery takes longer and is more extensive, and as a result there can be a greater expense for some of our larger dogs.

Does the prognosis change for a medium to large breed dog?

Yes. Dr. Woelfel from NCSU recently published data from a cohort of dogs > 10 kg that had both acute disc herniation and extensive spinal cord hemorrhage.

(Spinal cord hemorrhage occurs infrequently for large and small breed dogs and was shown in a few studies to have a minimal effect on prognosis as a stand alone feature. Meaning, the prognosis was still mostly based on the presence or absence of deep pain and didn't depend on spinal cord hemorrhage identified on advanced imaging.)

Okay, back to big dogs with disc herniation and spinal cord hemorrhage. The NCSU study reported a worse prognosis, and a higher complication rate, compared to overall data for small breed and chondrodystrophic dogs.

The details in summary:

• No deep pain before surgery, recovery about 38% (general population: 50%)

• Deep pain present before surgery, recovery rate about 77% (general population:90-95%)

• Complication rate was about 24% (general population: 10-15%)

Post Operative Complications Noted in the Referenced Study

• Decubital ulcers

• Pneumonia

• Self-mutilation

• Fever of unknown origin

• MDR UTI

• Sudden death

• Progressive myelomalacia

What is the take home message?

When talking with an owner of a medium to large breed dog with acute onset paraplegia, I suggest emphasizing the need for intense at-home nursing care, possible complications (along with the higher incidence) and a realistic prognosis if the dog is diagnosed with a disc herniation on advanced imaging. Remember that other differential diagnoses can cause acute onset paraplegia! Please do not interpret this paragraph as a call for euthanasia for large breed dogs with acute paraplegia. A 38% recovery rate is not zero! But a honest, open, vet-to-client discussion is the best way to achieve an informed decision for the client.

Not sure if you are interpreting the neurologic examination appropriately? Not sure if you are doing the neurologic examination properly? Please reach out! I am happy to work with you to help guide your clients in a compassionate and informed way.

Happy Easter to those that celebrated last weekend. We welcomed spring with big smiles around my house this weekend!

Reference: Woelfel, CW, Robertson, JB, Mariani, CL, Muñana, KR, Early, PJ, Olby, NJ. Outcomes and prognostic indicators in 59 paraplegic medium to large breed dogs with extensive epidural hemorrhage secondary to thoracolumbar disc extrusion. Veterinary Surgery. 2021; 50: 527– 536. https://doi.org/10.1111/vsu.13592

Root Signature Sign: Neurologic Lameness

It's Wednesday morning and your first consult is a limping dog. You nod...you've got this. Upon examination you cannot find any evidence of joint pain, muscle or bone pain. Not deterred, you radiograph shoulder to foot. Nothing of interest is visible.

What if the lameness is neurologic in origin, you ask yourself?

The most common causes of neurologic lameness in dogs are cervical disc herniation and nerve sheath tumors. Most dogs have neurologic deficits along with their lameness so it is worth a close look at the neurologic examination. Deficits could include reflex deficits, postural reaction deficits and/or pain.
Side note: Did you know that lameness from a neurologic cause is called a root signature sign?

Cervical Disc Herniation
Cervical disc herniation with resulting nerve root impingement occurs from type I or type II disc herniation. Many dogs have cervical pain along with the root signature sign, but not all. Cervical radiographs are non-diagnostic for cervical disc herniations and therefore not often recommended. MRI or CT/myelogram are the diagnostic tests of choice with MRI providing greater detail. Treatment may be medical or surgical. My recommendations for medical management vary by pet, but typically include a NSAID, gabapentin and a muscle relaxant. Additional management with opioids can also be included. Best rest is often recommended for the first 3 weeks. Surgical management is recommended for medically resistant dogs, or if the MRI or clinical signs are severe.

Nerve Sheath Tumor
Nerve sheath tumors are typically slow growing, locally invasive (eventually into the spinal canal) tumors. These are best diagnosed with MRI. Definitive treatment is surgical removal. If surgical removal is not pursued, supportive care with pain management (NSAID or prednisone +/- opioid), muscle relaxant and gabapentin are recommended. Acupuncture may provide additional pain relief. The slow growing nature of nerve sheath tumors means that clinical signs may be present for months before the pain or debilitation becomes life limiting.

Not sure if the patient you are seeing has neurologic disease? This is one of the main functions of a traveling neurologist (me!). Sorting between orthopedic and neurologic causes of lameness can be challenging, especially if you're not comfortable doing the neurologic examination. Please reach out, you're not alone! You can find me on email, or schedule directly online using my website.

Okay, now that we got that out of the way, enjoy that Wednesday morning lameness evaluation!

Happy St. Patty's Day everyone. I have two kids that do Irish dancing so we're really missing the festivities this year, but we look forward to celebrating next year.

Stay safe, stay kind, and I look forward to working with you soon!

Prognostic Indicators for Acute Myelopathy

Acute Paraplegia: When to ship for surgery, treat medically or consider euthanasia

It happens to all of us (perhaps to me, more than you). Monday morning, 9 am, we are presented with a dachshund (Shih Tzu, Corgi...pick your top chondrodystrophic breed) after the dog became acutely non-ambulatory over night.

You perform a neurologic examination (self high-five!) and determine that the dog has a T3-L3 myelopathy with spinal pain at the TL junction.

What do you do next?

To be clear, a T3-L3 myelopathy does NOT equal a type I disc herniation. It means the dog may have a type I disc herniation or it could have a fibrocartilaginous embolic myelopathy (FCEM), acute non-compressive nucleus pulposus extrusion (ANNPE) or in rare cases meningomyelitis. (Yes, even dachshunds can get meningomyelitis!)
If we play the odds, that chondrodystrophic dog likely has a disc herniation. What, if any, prognostic indicators can you provide to the client?

Thankfully, an article out of Frontiers in Veterinary Science entitled "Prognostic Factors in Canine Acute Intervertebral Disc Disease" was published in November 2020 for just this purpose! (1) Here are some key points from the article. (The entire article is available as an open access article if you wish to read it in it's entirety. I highly recommend doing so if you are in the habit of seeing paraplegic dogs.)

Prognostic Indicator Key Points:

• Recovery following medical management (only) for dogs with paraplegia (loss of all voluntary motor) and loss of deep pain perception (DPP) is about 22.4%.

• Recovery following medical management (only) for dogs with paraplegia and intact DPP is 56%.

• Recovery following surgical management for dogs with paraplegia and loss of DPP is about 61%.

  • 25% recovered at 2 weeks

  • 42% recovered by 4-6 weeks

  • 53% recovered by 12 weeks

• Recovery following surgical management for dogs with paraplegia and intact DPP is about 93%.

*** Did you catch that?? DPP is a prognostic indicator! Dogs without DPP do worse long-term compared to dogs with intact DPP. They are also have a 10x higher likelihood of developing progressive myelomalacia which is a fatal secondary outcome from acute spinal cord injury.

What exactly does "recovery" mean? It means walking without support but it DOESN'T mean walking normally or complete continence. Dogs may (and often do) have fecal or urinary incontinence consistently or occasionally following severe spinal cord injury.

Other Key Points:

• Spinal shock can be more commonly associated with long-term fecal incontinence but does not seem to affect the ability to recover ambulation.

• Age, breed and weight are not associated with prognosis...mostly. Some studies have found heavier dogs have a worse prognosis, other's haven't. My take - bigger dogs are harder to care for but that doesn't mean they cannot recover.

• Reduced pelvic limb reflexes due to a L4-S3 lesion (not associated with spinal shock) has a higher likelihood of incontinence long-term.

When do you send a dog for surgery?

1) if the dog is non-ambulatory or paraplegic and the clients have a desire and financial ability to pursue surgery. Surgery with imaging costs $2000-5000 USD, depending on the specialty referral center.
2) Rapidly progressive signs (E.g.: dog was walking at 8 am, and is paraplegic at 10 am, with loss of deep pain by noon) and clients wish to pursue surgical intervention if indicated after imaging.

My plea...

Please don't send clients several hours to a specialist for surgery only to discover that the cost is prohibitively expensive. It is heart breaking for everyone and unnecessarily stressful for the dog. Call me and I'll happily talk with you about consult/medical management choices or sadly advocate humane euthanasia for the dog, if it is the best option.

Stay Safe, Keep Keeping On and Have A Good Week!

(1) Olby Natasha J., da Costa Ronaldo C., Levine Jon M., Stein Veronika M. Prognostic Factors in Canine Acute Intervertebral Disc Disease; Frontiers in Veterinary Science. 2020:7 p 913.

Monoparesis following Vehicular Trauma

How do you sort out a cat or dog with thoracic limb monoparesis following trauma?

This is an important question. First, let's review the innervation to the front leg. (Get back here - it's not that bad!) There are two important nerves that guide weight bearing and movement in the front leg:
1) Musculocutaneous - exits spinal cord segments C6-8. Important innervation is biceps muscle but it does a few others. The important action is flexion of the elbow and extension of the shoulder
2) Radial - exits spinal cord segments C7-T1 +/- 2. Innervates triceps and the muscles on the cranial distal limb that extend the carpus. The important action is extension of the elbow and carpus for weight-bearing.

So, to weight bear there must be an intact radial nerve. To move the limb forward there must be an intact musculocutaneous nerve. The other nerves (supra and subscapular, axillary, median and ulnar) are important too, but not as important. If you want to remember only two nerves, remember radial and musculocutaneous.

Now that we have that over with, let's put this to practice. Here is the scenario: You are presented with a 1 year old cat with a history of vehicular trauma a few days ago. The cat is presented dragging the left thoracic limb, unable to bear weight. When you watch it walk you can see advancement of the shoulder and elbow but it is minimal.
Question: What nerve is affected MOST?
Answer: Radial
Question: What spinal cord segment does the radial nerve arise from?
Answer: C8-T1 or 2.

Really good question: What is this cat's lesion localization?
Answer: Let's do a neurologic examination! :)

Neurologic exam:
Mentation: BAR
Cranial nerves: normal (note Horner's can be seen with thoracic limb injuries but isn't seen in this cat).
Reflexes: Absent triceps, absent withdrawal of the left thoracic limb. Unable to detect bicep or extensor carpi reflex (hey, it's a cat, give me a break!). All other limbs have normal withdrawal and pelvic limbs have normal patellar reflexes.
Palpation: non painful
Proprioceptive testing: absent tactile placing left thoracic limb, absent tactile placing left PELVIC limb, normal entire right side.
Gait: left thoracic limb monoparesis as previously described.

Now you can properly answer the previous question.
With absent radial nerve and diminished musculocutaneous innervation to the left leg, we KNOW the lesion must involve C6-T2, correct? (It's absent because of the missing withdrawal reflex - mediated through largely the radial nerve but also musculocutaneous too.) The real question here is this: is the injury in the plexus only or is there evidence of spinal cord involvement? To answer that question, you must look downstream from the affected segment. This means, look at the left pelvic limb. This limb has absent tactile placement so there has been disruption to the spinal cord tract going from the brain to the left pelvic limb, and back again.
Answer: This cat has a C8-T2 spinal cord lesion.

The differential list must now include things that affect the spinal cord such as avulsion and a disc herniation, hematoma or hemorrhage. Your diagnostic plan would include advanced imaging of the spinal cord. If the lesion localization had been peripheral plexus (not spinal cord) you would consider a brachial plexus avulsion only and advanced imaging would not be indicated. Knowing the lesion localization can markedly change your differential diagnoses, diagnostic plan and ultimately treatment and recovery!

Not sure about this case? Feel free to email me! This TidBit Tuesday is a slightly altered version of a real case seen recently. Keep those consults coming so we can share the knowledge folks! Please email/call/text me to schedule a consult or hop on my website and utilize the online scheduler to find the best time.

Have a good week!

C Reactive Protein and Discospondylitis

C-Reactive Protein and Discospondylitis

What is C-Reactive Protein (CRP)?

It is an acute phase protein that has been used in other inflammatory conditions such as SRMA, IMPA or inflammatory bowel disease to support or monitor the clinical response to treatment. 

Is it elevated with Discospondylitis?

Short answer: yes.
Long answer: It was elevated in most dogs in a recent study that were diagnosed with bacterial discospondylitis, but not all. In 8 dogs they measured it again 4-6 weeks into antibiotic treatment and it was normal in all 8 dogs. 

What can we do with this information in practice?

When faced with a patient with discospondylitis you can use CRP to support the radiographic evidence of discospondylitis. I would NOT suggest using this as a disease monitoring tool for dogs with discospondylitis because, as the authors point out, the intervertebral disc is a very immune privileged area of the body therefore infection could persist that is not reflected in the CRP. One of the dogs, in the study quoted above,  with normal CRP, had a recurrence of signs after stopping antibiotics. This suggests that CRP may not be a good long-term monitoring tool. 

That's all for this week! Have a safe, happy week and keep those consults coming! 

Nye G, Liebel FX, Harcourt-Brown T. C-reactive protein in dogs with suspected bacterial diskospondylitis: 16 cases (2010-2019). Vet Rec Open. 2020;7(1):e000386. Published 2020 Jul 20. doi:10.1136/vetreco-2019-000386

The Five Types of Disc Herniation

The Five Types of Disc Herniation (that we know of!)

1. Dystrophic calcification secondary to chondroid degeneration of nucleus pulposus (NP), called a Hanson Type I. This causes mechanical stress on the outer annulus fibrosus (AF), leading to rupture of individual collagenous strands of AF and eventually full failure.

2. Fibrous degeneration occurs when fibers of disc split leading to accumulation of tissue fluid and plasma between them. Over time the mechanical pressure exerted by NP causes thickening of the AF dorsally, causing protrusion. (Hanson Type II).

3. ANNPE (Acute noncompressive nucleus pulposus extrusion) - this is normal NP that is exploded into the canal, usually during activity. Also called a traumatic disc herniation.

4. AHNPE (Acute hydrated nucleus pulposus extrusion) – An apparently normally hydrated NP that is compressive and often located ventral to the cord, often in the neck.

   1. Significantly more neuro deficits and less signs of cervical pain with AHNPE compared to other causes of cervical myelopathy.

5. FCE (Fibrocartilaginous embolism): a piece of NP that becomes dislodged and finds its way into the vasculature surrounding the spinal cord. This can be into venous or arterial blood vessels. The end result is an acute shift in blood flow at the level of the spinal cord.

Match the clinical sign with the type of disc herniation

A. Chronic, progressive ataxia progressing to paresis
B. Acute, non-progressive unilateral weakness affecting one leg, or one side (hemiparesis)
C. Acute, progressive, painful ataxia progressing to paresis in a chondrodystrophic dog
D. Acute non-progressive ataxia and paresis affecting both sides of the body (paraparesis or tetraparesis)
E. Acute, rapidly progressive tetraparesis and ataxia of all four limbs with minimal cervical pain

If you answered...
Type I: C
Type II: A
ANNPE: D
AHNPE: E
FCE: B

you are correct!

Based on the clinical picture, it can be very difficult to distinguish Type I from ANNPE, and AHNPE. Typically, type I is painful (but not always), and the other two are minimally to non-painful. 

Which of these require surgery?

Any disc herniation that results in compression of the spinal cord with associated clinical signs could be considered for surgical correction. This statement would then suggest that Type I, Type II and AHNPE could be surgically corrected. Therefore, any patient with signs of a progressive or painful myelopathy should be evaluated for diagnostic imaging (typically MRI) for possible surgical intervention whenever possible.

Bonus question:
Can you name two diseases that are commonly diagnosed instead of a type I or type II disc herniation? Scroll to the bottom for the answer!

Change is coming! Starting in September I will have new fees, and new availability.  I am happy to accommodate outside of these hours whenever possible so please reach out if you cannot find a suitable time using the online scheduler. ( https://barnesveterinaryservices.com/ )

New Hours (Starting September 8th)
Monday 11a-1p, 4-5p
Tuesday 3-4p
Wednesday 11a-1p, 2-4p
Thursday 2-4p
Friday 12-1p
Saturday 9-11a

Bonus Question Answer
 Meningoencephalomyelitis (a.k.a meningitis), and neoplasia. Keep these two on your differential diagnoses list when you suspect a disc herniation!!

The Genetics of Disc Herniation

What is the deal with chondrodystrophy, anyway?

Chondrodystrophic dogs are born to have short stature, and abnormal aging of the intervertebral discs. It's what makes a Dachshund or French Bulldog look like, well, a Dachshund or French Bulldog! I'm sure it comes as no surprise that there is a genetic reason why they look this way. But, did you know that someone has sorted out the genetic mutation that has been linked to chondrodystrophy and disc herniations?

What is the genetic mutation and what does it mean?

Several studies in 2019 (and earlier) looked at copies of 12-FGF4RG and 18-FGF4RG status in chondrodystrophic dogs and found that if a dog carried at least 1 copy of the 12-FGF4RG gene they were significantly smaller, younger and more likely to have radiographically calcified discs than those without. Furthermore, 12-FGF4RG was the only factor identified in multivariate logistic regression models that contributed to needing disc herniation surgery in mixed breed dogs. Mixed breed dogs? (You ask.) Yes, Dachshunds and French bulldogs, specifically, have such a high rate of carrying 1 or 2 copies of the 12-FGF4RG gene that it's impossible to say with the relative risk of disease is for these breeds with the mutation. In other words, if every Dachshund has the mutation is it actually related to disc herniation? Not sure yet. One study found that non-Dachshund and French Bulldogs had between a 5.1-15.1 fold increase of disc herniation if they had at least 1 copy of this gene. 

What do I do with this information?

If you have a neutered animal, nothing. It might predict the risk of disc herniation in that animal but that animal is already born, and presumably loved, so this information is not actionable. If you have a client considering breeding you may be faced with the results of this genetic information and asked the question above.  My opinion? There are specific breed risks so either read the published data on risk for the specific breed in question, or reach out to me and I'll gladly pass along the information. It's in a handy table, but not my data so I don't feel comfortable including it in the TidBit Tuesday mailer. If possible, breeders should try to breed dogs with zero or 1 copy to dogs with 1 or zero copies of the mutation to reduce it's presence in the breed. *This doesn't apply to Dachshunds or French Bulldogs for the above mentioned reasons!

Keep those chondrodystrophic dogs fit, healthy, and leading low impact lifestyles! It won't eliminate the risk of a disc herniation but it may make recovery easier. 

Batcher K, Dickinson P, et al. Phenotypic Effects of FGF4 Retrogenes on IVDD in Dogs. Genes (Basel) 2019; 10(6): 435.

Do you have a case you'd like to discuss with me? Feel free to email, text, or call me! I'm still trying to see mostly video consults whenever possible but I'm gradually increasing the live consults performed. Either way, I look forward to (continuing) to work with you!