Degenerative Myelopathy

Degenerative myelopathy is a slowly progressive, fatal spinal cord degenerative disease that has been linked to the SOD1 gene in German Shepherds, Corgis, Boxers, Rhodesian Ridgeback and Chesapeake Bay retrievers. The disease is currently diagnosed via histopathology which can only be performed post mortem. Degenerative myelopathy (DM) presents initially with proprioceptive ataxia of the pelvic limbs, progresses to paraparesis and then a loss of the patellar reflexes may occur followed by tetraparesis and eventually loss of respiratory and cranial nerve function. Most owners euthanize prior to the development of tetraparesis but not all. What else can present with the initial signs of a slowly progressive proprioceptive ataxia and paraparesis? Right! Intervertebral disc disease, myelitis, or spinal neoplasia. Each of these diseases has their own subtle differences but the typical history is similar among all of them. As a result, neurologist struggle to confirm a diagnosis of degenerative myelopathy.

Diagnosing Degenerative Myelopathy

The SOD1 gene mutation can be identified on a genetic test, readily available from several sources. If found to be a homozygous carrier, is that enough to diagnose DM? Approximately 78% of neurologists and 50% rehabilitation specialists thought so according to a recent study published in the Journal of Veterinary Internal Medicine (Bouche T, Coates JR, Moore SA, et al JVIM 2023). What if the dog was unlucky enough to have developed an intervertebral disc extrusion AND was a SOD1 homozygous carrier. Can they have both diseases? Can they have a disc herniation and not (yet) be clinical for DM? According to the article, 43% of neurologist always or sometimes required an MRI plus the SOD1 genetic testing to make the a presumptive diagnosis of DM. I require both to make a diagnosis. Dogs can be at risk for something but have something else and we are not doing them a good service if we assume a diagnosis without eliminating the most common other options.

Treatment
This will be a short paragraph. None. We cannot successfully treat DM as of 2025. However, a very small study (Kathmann I, Cizinauskas S, et al. JVIM 2006) found that the time to non-ambulatory status was delayed with intensive PT 3-5x daily along with weekly hydrotherapy, massage and passive ROM compared to a cohort with moderate or no treatment. For this reason, most neurologists and physical therapists recommend consistent physical therapy. This recommendation was also frequent in the 2023 study as well. The mean survival is 10-36 months, so any little bit helps! If you have a patient with a minimal progression after 36 months, reevaluate your diagnosis.

Take away message

• Diagnosing DM requires histopathology

• A presumptive diagnosis is obtained through a combination of SOD1 gene testing and MRI

• Treatment is physical therapy centered but will not eliminate/cure the disease

Happy New Year everyone! I hope you had a safe, enjoyable holiday season. January’s schedule is a little different due to my children’s schedules so, as always, please reach out if you cannot find a suitable time for a consult. The regular schedule resumes in February. One of the perks of being the owner is that I can control the schedule!

Can Paraplegic Dogs walk?

What do we know about the natural progression of thoracolumbar intervertebral disc extrusion (TL-IVDE) in dogs? We have been taught when a dog stops having voluntary movement of their pelvic limbs (paraplegia) they need surgery to recover the ability to walk, right? What about those that have lost deep pain? What if we didn’t do surgery – what happens to those dogs? A study was published in JVIM this year that looked at the natural progression of medically managed TL-IVDE in non-ambulatory dogs and evaluated not only the recovery rate, but also what the discs “did” on sequential MRI 3 months after starting medical management.

Results

Sixty-seven dogs met the inclusion criteria – 51 with deep pain, 21 without deep pain, 5 with signs of myelomalacia at presentation.

Treatment consisted of NSAIDs (steroids were discontinued and replaced with NSAIDs if started), pain management and physiotherapy.

·         Recovery

·         Dogs with deep pain: 96% regained walking and voluntary urination (49/51)

o   Median time to recovery 11 days (7-21 days IQR).

·         Dogs without deep pain: 63% regained walking and voluntary urination (10/21).

All dogs (regardless of ambulatory status on recheck) did not have signs of back pain on evaluation 3 months after enrollment in the study.

The change in compression on MRI was interesting. In some patients, the compression almost completely resolved, and for others there was less than a 5% change. This wasn’t correlated with clinical signs but looking at the figures it does not appear to have a direct relationship.

Key point:

If you have a patient presenting with acute, non-ambulatory paraparesis or plegia, surgery is a very reasonable first step. However, it isn’t the only option! Don’t euthanize unless myelomalacia is present!! Consider conservative treatment because we may end up with an ambulatory patient after 3 months! Just because an owner cannot afford an MRI or surgery, doesn’t mean we should do a neurology consult, either. 😊

Thanks for reading! I hope you’re having a good week and look forward to working with you soon.

Neuroanatomic Lesion Localization Practice Case

It's time to sharpen those pencils and put on your thinking hat. It's neuroanatomic lesion localization practice case time! 
Signalment: A 4 year old FS Mixed breed dog (along the lines of a Pitbull X)
History: The patient presented with a 24 hour history of acute onset ataxia, and weakness. The owner's noticed significant muscle fasciculations in the neck (mistaken for seizures) along with a reluctance to lift her head. The weakness was progressive from thoracic limb lameness initially, through ataxia to ambulatory tetraparesis. No medications had been given prior to the consultation. 
PE: Unremarkable other than BCS 7/9
Neurologic Examination
Mentation: QAR. Friendly, but subdued.
Cranial nerves: Normal
Gait: Ambulatory tetraparesis, worse on the left thoracic leg. She was noted to have reduced mobility in the left thoracic limb along with a lack of adequate weight-bearing on that limb. The other three limbs were weak, but she could bear weight.
Reflexes: Absent withdrawal left thoracic limb. Normal withdrawal noted in the other three limbs. Normal patellar reflexes bilaterally. Normal anal tone and perineal reflex along with c. trunci reflex. 
Postural reactions: Absent paw replacement testing all four limbs.
Palpation: Painful with cervical palpation and unable to perform cervical ROM without yelping. 

Neuroanatomic lesion localization: where should we start?

The easiest place to start is with elimination.
A. We do NOT have a seizure history, change in mentation or any cranial nerve deficits, right? The lesion therefore is unlikely to be rostral to the foramen magnum. 
B. We have evidence of disease in all four limbs therefore the lesion must be cranial to the T3 spinal cord segment. (If the lesion were caudal to T3, we would expect the thoracic limbs to be normal and without deficits.)
Okay, so far, we have now narrowed our findings to C1-T2
C. The reflex arc is C6-T2 in the thoracic limb. Do we have any evidence of reduced or absent thoracic limb reflexes? Yes - the left thoracic limb has a reduced withdrawal reflex. Animals with reduced reflexes have their lesions IN the reflex arc (C5-T2 or L4-S3 in the pelvic limb). 

Lesion localization is: C6-T2 spinal cord, more affecting the left side

What would you consider for differential diagnoses? 

In this case, the two most important historical factors that I would focus on are the "acute onset" and "painful" parts. Things like neurodegenerative disease are not painful, and rarely acute. The most common painful myelopathies I like to summarize as being "2-Ds, 2-T or an M". What are they? Disc herniation, discospondylitis, tumor (I know, I know, it's called neoplasia but it's easier to remember 2D,2T,M.), trauma and meningitis/meningomyelitis. 

Because this isn't a disease-focused TidBit I'll cut to the chase and tell you that this dog was diagnosed with a type I disc herniation and had surgical decompression. She felt much better! 

How did you do? Did you enjoy this case this week? Sometimes the simple ones are the hardest because we over think them so much! If this wasn't a simple one remember that I'm available to help you with cases. Neurologic cases aren't fun for everyone so reach out for help if you're stuck! 

Thanks for reading. I will be away at a conference and taking a little vacation time May 4-8th. I will have some access to email but please be patient with inevitable delays. Thanks for including me in your patient's care! Have a great week and stay safe.

Is there a Weekend Effect in Veterinary Medicine?

The “weekend effect” (WE) is a term used to describe poorer patient outcomes associated with treatment out-of-hours. There has been debate in the human literature if this effect is “real” or not. Specific focus has been aimed at mortality or morbidity associated with the WE. A recent study in England, looked at the WE in relation to decompressive hemilaminectomy surgery in a cohort study (comparing a poputation of dogs having surgery afterhours to those operated during business hours) and, I found it informative. (Low D, et al. Veterinary Surgery. 2024;1–10.)

You may be aware that the timing of spinal cord decompression has been hotly debated over the past…oh..100 years or so. Recently, some studies have suggested that surgical decompression for an acutely non-ambulatory dog is not an emergency and therefore can occur during normal business hours. This has been suggested for dogs with and without deep pain sensation. Additional studies have supported that in fact it DOES matter and those studies advocate for decompression of dogs with a loss of deep pain within 24 hours of documented loss of deep pain. I tend to favor the “don’t wait, cut ASAP” approach but the choice is controversial. The study by Low and colleagues from England did not address the pros or cons of timing of surgery but instead looked at outcome (did they walk, or not) and adverse events (urinary tract infections, gastric ulcers, skin infections/ulcers, post operative neurologic deterioration, etc.) for dogs undergoing back surgery within or outside of business hours.

The findings of this study were interesting. They identified a significant difference in postoperative morbidity and the recovery of ambulation in a group of dogs undergoing surgery afterhours vs those undergoing surgery during business hours. They stated that 1 in 8 dogs would not recovery ambulation when exposed to weekend surgery compared to if they were exposed to weekday surgery. Furthermore 1 in 7 dogs would experience an additional post operative morbidity when exposed to weekend surgery, compared to weekday surgery.

What contributed to the results? The variables for a patient undergoing, and recovering from, surgery are numerous regardless of the timing of the surgery. For example, there are pre-hospital variables (such as the timing and treatment provided by the referring vet), hospital variables (staff tiredness, case load, surgeon experience) and post-hospital factors (availability of aftercare support in the patient’s home, the hospital discharge process). Many of the hospital variables were evaluated in the study and not statistically associated with outcome or morbidity. The pre- and post-hospital factors are more difficult to study due to the inherently heterogenous state.

What do I do with this information? I included this study as at TidBit Tuesday to increase awareness of the possible WE in both veterinary medicine at large (yet to be fully determined) and specifically within neurosurgery. The data does not suggest that you shouldn’t make a referral if you have a nonambulatory patient, especially if they’ve lost deep pain! It also shouldn’t be used to deter a client from pursuing surgery on a weekend or afterhours. I’m not sure there is an actionable outcome by gaining this knowledge, except for the simple purpose of increasing your (and my) knowledge of the existence of a WE. By being aware, we can sometimes change our actions in subtle ways that may improve the outcome for our patients. Have you ever managed an especially difficult seizure patient? What if you had a dog develop liver disease while taking zonisamide or phenobarbital? Those cases increase our awareness of the “bad” outcomes and increase our sensitivity to treating the next seizure case, or next dog on zonisamide or phenobarbital. In fact, population statistics would suggest that a low number of dogs have resistant epilepsy but when it is 1 of your 10 or so cases that you’ve managed it feels like a high risk and may change how you discuss seizures with the next client that walks in the door with a pet with seizures. Awareness of the WE may change how we, as neurologists, operate and intern may affect the WE. Time shall tell!

Thanks for reading through this long TidBit. I hope you enjoyed the lovely weekend weather (it was in the 70s for us!) and have a wonderful week.

Managing Upper Motor Neuron Urinary Retention in Cats

An upper motor neuron bladder means that the sensory information from the bladder cannot be transmitted to the pons and that upper motor neurons from the pons cannot reach the lower motor neurons of the bladder to cause initiation of bladder expression. To cause this, the lesion is usually cranial to S1. Cats are especially difficult to manually express due to their high external sphincter tone.
Let's look at the bladder innervation for just a moment. The detrusor muscle contracts secondary to innervation that comes from the T12-L1 region via the hypogastric nerve. There are two sphincters, both innervated by nerves arriving from the pelvic plexus (S1-S3 region), that help retain urine. The external sphincter is the only one with voluntary control and that is handled by the pudendal nerve. When we say an upper motor neuro bladder (UMN) we are really talking about anything cranial to the pudendal nerve, that is S1, because that is the only nerve with voluntary control. 

We use manual expression in the acute phase of spinal cord injury to avoid separation of the tight junctions of the bladder wall muscles and, therefore, possible permanent injury to the bladder wall. Manual bladder expression works because pressure is exerted onto the urinary bladder which then forces the internal sphincter open, and eventually the external sphincter as well. Due to the high external sphincter tone occasional urinary rupture has occurred when expressing cat urinary bladders. Dogs appear to have less tone and therefore rupture is less common. A recent study (Galluzzi F, De Rensis F, et al Nov 2023) evaluated 34 cats with UMN induced urine retention secondary to acute or chronic spinal cord injury. They divided the cats randomly into two groups: group M underwent manual expression only and group MT underwent manual expression PLUS tactile stimulation of the perigenital region during expression. Tactile stimulation was described as a rapid striping motion of the perigenital region (from prepuce to scrotum or anus to vulva) over a 30 second period. This technique was copied from how female cats will lick their kittens during the first few weeks of life to stimulate urination.(As an aside - In a small study of cats less than 2 weeks of age, urinary retention occurred if this stimulation was not applied.) With this understanding, Galluzzi et al added tactile stimulation to manual expression to see if it improved bladder expression. In the M group, a urinary stream was achieved in half of cats while the MT group obtained a urine stream in 100% of the cats. Additionally, the stream was obtained in significantly less time (3.75 seconds vs 7.8 seconds). This is so simple, and yet make so much sense!

Key Point
Bladder expression for cats with UMN bladder dysfunction could have manual expression PLUS tactile stimulation applied to improve success rates! 

I hope you enjoyed this week's TidBit Tuesday!  Do you have a case you feel would benefit from a neurology consultation? Please reach out or use the online scheduler to schedule a consultation. This has been an emotional week for many veterinarians that I know; please stay safe and know that my phone and email are always available for you if you need to talk. I hope you have a good week. 

What to do with a narrowed disc space?

Narrowed Disc Spaces

It's a Tuesday morning and on your schedule is a 2 year old MC Labrador retriever with a 2 week history of back pain. The neurologic examination is normal. Without any neurologic deficits, remember that the pet hasn't been diagnosed with neurologic disease (yet), so spinal pain can be due to bone, joint, nerve, spinal cord, muscle or meningeal in origin. You elect to take sedated spinal radiographs and send them off to the radiologist. A radiologist will report what they see, which often includes "narrowed disc space(s)" on the report. What do you do with this?

Does a narrowed disc space indicate a disc herniation?
No, sorry. A narrowed disc space could be positional (often), beam angling (often), due to disc degeneration, or disc herniation. Disc degeneration occurs when hydration leaves the annulus fibrosis, thus causing the disc to shrink a little. This is a normal aging process and does not indicate a herniation. Herniation occurs when part of the disc (annulus fibrosis (AF) or nucleus pulposus (NP)) leaves it's normal position. When the NP leaves, we call it a Type I disc herniation. Type I disc herniations are common in chondrodystrophic dogs and about 30% of non-chondrodystrophic dogs. Clinical signs often include calcification of the NP which might be visible on radiographs. Remember, in situ calcification is appropriate and normal for chondrodystrophic and some non-chondrodystrophic dogs and does not indicate herniation. Calcification in the canal suggests that the disc has herniated but does not indicate that the current clinical signs are due to THAT disc herniation. This means we cannot diagnose a type I disc herniation strictly on radiographs. An MRI, CT or myelogram is needed to diagnose a type I disc herniation. 

When the AF displaces, it is called a Type II disc herniation. This is more common in non-chondrodystrophic dogs and is often part of disc associated wobblers and lumbosacral disease. No calcification occurs for this form of herniation therefore it cannot be seen radiographically. A narrowed disc space often (but not always) accompanies a type II disc herniation but is not always radiographically visible. An MRI, CT or myelogram is needed to diagnose a type I disc herniation. 

What about FCE or ANNPE?
Acute noncompressive nucleus pulposus extrusion (ANNPE) or fibrocartilaginous embolism (FCE) are two more forms of disc herniation where in a small amount of disc material leaves its normal location, often under great force. A narrowed disc space can be seen with these types of disc herniation as well but would  NOT be diagnostic for either disease. An MRI is needed to diagnose an FCE or ANNPE. 

What causes of back pain CAN you diagnose on radiographs then??
The most common causes of spinal pain are 2 "D"s, 2 "T"s and an "M" (as I teach it to students). Discospondylitis, disc herniation, trauma, tumor, and meningitis. Of these, only discospondylitis, vertebral neoplasia and fracture/subluxation can be diagnosed on plain radiographs.

The patient above could have discospondylitis on their differential diagnoses list therefore radiographs are absolutely indicated. However, please be cautious reading too much into a "narrowed disc space" and instead look for discospondylitis, vertebral neoplasia or signs of trauma. 

I hope you enjoyed this week's TidBit Tuesday! We're almost into March which, if you're a long-time patron, you know means we're approaching St. Patrick's day. My girls are Irish Dancers and, as such, usually perform in over 30 shows in the month of March. That means this proud mamma has a more limited work schedule due to all of the driving so PLEASE reach out if you cannot find a suitable time on the online scheduler. I may (often can) shift things a bit to accommodate your request! Have a great week and stay safe out there. 

T3-L3 Myelopathy in a German Shepherd Dog

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

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

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

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

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

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

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

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

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

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

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

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

Spinal Cord Neuroanatomic Lesion Localization

"DIR" Coming In

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

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

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

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

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

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

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

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

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

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

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

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

Thanks for reading! Have a great week!

IVDH Consensus Statement – Medical Management Data

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

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

Medical vs. Surgical IVD extrusion management

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

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

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

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

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

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

What is medical management?

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

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

The 5 Types of Disc Herniation (that we know of!)

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

'Tis CE season so I thought it would be fun to pull up this old TidBit Tuesday from 2020 and refresh our memories about the different types of disc herniation that may be diagnosed in dogs. I hope you enjoy this light reading on your midsummers morning!

1. Dystrophic calcification secondary to chondroid degeneration of nucleus pulposus (NP), is called 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 and extrusion.

2. Fibrous degeneration occurs when fibers of the disc split leading to accumulation of tissue fluid and plasma between the annular fibers. 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 (probably) NP that is exploded into the canal, usually during high activity. Also called a traumatic disc herniation by some folks.

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

   1. There may be 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 material histologically similar 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.


Thanks for reading! I hope you have a wonderful week. As always, reach out if I can help you, help your patients, with neurologic disease. 

Intervertebral Disc Herniation in Yorkshire Terriers

Yorkies are a popular, and common dog breed in the USA and I (we?) see them quite a bit in neurology referral practice. That said, I had never read that they were officially considered a chondrodystrophic breed. Apparently, they are! 

Intervertebral disc herniation (IVDH) occurs with high frequency in chondrodystrophic dogs, but how often do we see it in Yorkies? According to a recent article, about 10% of Yorkshire Terriers with neurologic disease are diagnosed with IVDH and undergo surgical intervention. 

How do Yorkies present with IVDH?

• Cervical hyperesthesia only 5/60 (8.3%)

• Ambulatory tetraparesis with or without neck pain (grade 2):  26/60 (43.3%)

• Non-ambulatory tetraparesis or plegia with or without neck pain: 29/60 (48.4%)

No association with recovery and presence or absence of ambulation was found in this study. This is inline with other studies that have not found voluntary motor to be a prognostic indicator. 

• Acute signs in 80% of dogs

• Chronic signs in the remaining 20%

Yorkies with IVDH instead of another neurologic disease were statistically heavier and older

How do Yorkies do with surgery?

Thankfully, quite well, according to this report. In this study, the majority (82%) had one IVDH, 15% had two and 3% had 3 IVDH site repaired. In my experience, Yorkies far exceed dachshunds for having multiple IVDH requiring surgery at the time of diagnosis. Could this be a difference in genetic pool (this study was conduced in Czechia, Slovakia and Hong Kong)? In this study, all dogs returned to ambulation at some point, post operative. Most were walking by hospital discharge, but not all. This is comparable to dachshunds. 

Key Points

• Yorkshire Terriers are chondrodystrophic and therefore predisposed to type I IVDH

• Surgical intervention is likely to improve ambulation

• Approximately 50% of Yorkies will be ambulatory, and 50% will not at the initial diagnosis. 

Thanks for reading! I am leaving for ACVIM today (Tuesday June 13th) and will be out for the remainder of the week. I'm so excited to collaborate with colleagues and bring new knowledge back to the patients we share! If you need me, email is preferred but texting is also fine. I will have limited ability to answer the phone but will do my best to return your call in a timely manner. Please excuse any unusual delays! Have a great week!
 

Cervical Disc Herniation Associated Myoclonus in Dogs

Intervertebral disc herniation (IVDH) is the most common cause of cervical pain in small breed dogs. The most common clinical presentation is cervical pain with a normal neurologic examination, however in a few dogs gait deficits, paw replacement deficits, or reflex deficits can seen. Myoclonus, or a sudden onset, repetitive muscle contraction is seen in about 4% of dogs in a recent study from France. This muscle contraction is frequently confused for seizure behavior by clients so be on the look out for it! The classic presentation is a small breed dog that stops an activity, demonstrates myoclonus, and then resumes it's activity. Other signs of cervical pain (yelping, low head carriage, reduced range of motion) are often present when clients are questioned, so be sure to ask! 

What is the Significance of Cervical Myoclonus with IVDH?

The presence of myoclonus did not change the prognosis or outcome for the 20 patients in the recent study (JAVMA 2023: 261:4: 511-516.). Surgical correction resulted in less recurrence of signs, and immediate resolution in the post operative period compared to medical management. Approximately 25% of of medically treated dogs experienced another episode of myoclonus considered to be distinct from the original presentation. Medical management consisted of NSAIDs, gabapentin and, for some, tramadol. 

What is the Take Away?

• Myoclonus can occur with mechanical or chemical irritation of cervical nerve roots 

• Myoclonus does not affect prognosis

• Surgical management remains the recommended treatment for rapid resolution of signs of pain and reduction in relapse/recurrance

• French Bulldogs were over represented in this study!! (Again - See TidBit Tuesday in March for the list of Frenchie spinal cord diseases

As always, thank you for reading! I am thrilled to see the lovely weather on the horizon this week and hope you have a chance to enjoy some of it, too. 

Pug Myelopathies

Did you know that Pugs are commonly diagnosed with T3-L3 myelopathies? There are so many to chose from I thought I'd take this TidBit Tuesday and discuss some of the more common ones. 

Intervertebral disc herniation

Dis herniation is a common etiology of a T3-L3 myelopathy in many dogs, and Pugs are no exception. Type I and Type II disc herniations have been diagnosed in Pug dogs in the thoracolumbar region. Clinical signs include acute (or chronic if type II) variably painful (but often WITH signs of discomfort in this breed), pelvic limb proprioceptive ataxia followed by paraparesis. Signs can progress to paraplegia with loss of deep pain. Surgical and medical correction have been shown to be useful for Pug dogs and depend on the severity of the clinical signs.

Subarachnoid diverticulum

Subarachnoid diverticulum (SAD) can be described as cystic accumulations of fluid in the subarachnoid space around the spinal cord. Pugs are cited as among the most common breeds to be diagnosed with SAD. Clinical signs are slow in onset and often include incontinence early in the clinical course. Dogs with SAD are not typically painful. Medical and surgical management have been tried however neither approach appears to be an overwhelming success. Medical management is typically my preferred approach. 

Meningomyelitis and Neoplasia

Any and all breeds are at risk for these two diseases and Pugs are not overrepresented in this group. That said, clinical signs would include acute or chronic onset of signs with paraparesis and proprioceptive ataxia in the pelvic limbs. Treatment is medical for meningoencephalitis and medical, surgical or with radiation therapy for neoplasia. 

Degenerative Myelopathy

Degenerative myelopathy (DM) is caused by a genetic predisposition to demyelination of the T3-L3 spinal cord segments. Pugs are over represented and either confirmed or strongly suspected to have a mutation of the SOD1 gene (I cannot remember if it has been confirmed, yet!), like  German Shepherd dogs. Clinical signs include a slowly progressive, non-painful, proprioceptive ataxia that progresses to paraparesis, then paraplegia. If not euthanized, pets can progress to tetraparesis and eventually respiratory failure. A diagnosis is made through findings of a normal MRI and CSF analysis along with appropriate clinical signs. Genetic testing can be useful but isn't a stand alone test. 

Constrictive myelopathy

This is the new kid on the block. First published several years ago, constrictive myelopathy is caused by a fibrous band of tissue that circles the spinal cord and causes a constriction to CSF flow and compression of spinal cord tracts. Constrictive myelopathy is now thought to form due to a lack of development (hypoplasia) of the articular processes of the TL vertebra. If you imagine the articular processes are the "hands" that hold the vertebra together, supported by muscles and ligaments, becomes easy to see how hypoplastic articular processes might result in vertebral instability. This instability would then result in fibrotic tissue forming to help "stabilize" the joint. Sadly, this fibrous tissue then causes spinal cord constriction. To make matters worse, SAD can also form secondary to chronic spinal cord trauma so these poor dogs can have constrictive myelopathy secondary to hypoplastic facets and SAD in their T3-L3 spinal cord segments. Yikes. A diagnosis is made on MRI. A recent study (https://onlinelibrary.wiley.com/doi/full/10.1111/jvim.16639?) evaluated the incidence of constrictive myelopathy alone, or in combination with other spinal cord diseases in a group of Pug dogs. They found only constrictive myelopathy in 3 dogs, constrictive myelopathy combined with IVDH in 17 dogs and IVDH only in 9 dogs, IVDH + SAD in 2 dogs and articular process dysplasia in ALL 32 dogs!

Summary:
Pug dogs are at risk for many causes of paraparesis and proprioceptive ataxia. A detail neurologic examination, history , and appropriate diagnostic imaging and spinal tap can help determine the underlying etiology and subsequently direct treatment most specifically. 

I hope this TidBit doesn't give you the impression that I am anti-Pug - I adore these little dogs. BUT,  I recognize their predisposition to specific spinal cord diseases when assessing them clinically. Remember, not all dogs with pelvic limb weakness have a disc herniation! 
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

Consensus Statement for Intervertebral Disc Herniation in Dogs, 2022

October, 2022... We have long known that intervertebral disc herniation type I (IVDH) affects chondrodystrophic dogs, at a young age, disproportionately compared to non-chondrodystrophic dogs. We also know that many dogs benefit from surgical and medical intervention. We also know that the neurologic examination is a major predictive factor on recovery (medical and surgical intervention). What we don't know, is how to put what we know into a digestible nugget for clients to hear and understand when in our exam rooms with a dog with suspected IVDH.

First things first... We diagnose IVDH with MRI, CT, CT-myelogram or just myelogram. We don't diagnose IVDH on plain radiographs, or on neurologic exam. (Sorry, soapbox here.) When I say a dog "with IVDH" I mean that they have undergone some sort of diagnostic imaging (MRI, CT, CT-myelography or myelogram) and have been found to have compression to the spinal cord from suspected or confirmed herniated disc material. Presumably, of type I nature for this TidBit. If we don't have diagnostic imaging, but have a chondrodystrophic dog (beagles are included in this group) with appropriate neurologic signs we can call it "presumptive or suspect IVDH". We should, honestly, discuss other differential diagnoses with clients to ensure they understand that there are other possible causes so their decisions are informed. Common diseases that can mimic IVDH could include (but are not limited to) meningomyelitis, neoplasia, Syringohydromyelia, discospondylitis, and spinal trauma/fracture.

Medical intervention... The cornerstone of medical intervention is bedrest for 3+ weeks, anti-inflammatory (typically NSAIDS, but some neurologists prefer steroids), and muscle relaxants or pain management, if the pet is painful. See below for the consensus statement recommendations for medical intervention.

Surgical intervention.... I think this one is self explanatory (mostly). One small point I'll make is that fenestration is not always included when discussing surgical intervention. I consider fenestration an important part of surgical treatment but it does NOT decompress the spinal cord and is therefore excluded in lots of literature. Fenestration means to make a "window" in the affected disc UNDER the spinal canal and remove disc through a lateral or ventral incision (TL vs C-spine). This is also performed in adjacent discs in most cases.

July 2022...ACVIM consensus statement on diagnosis and management of acute canine thoracolumbar intervertebral disc exclusion (doi/epdf/10.1111/jvim.16480). A few key points are listed below and I will have more to share with you in future weeks.

Outcome of dogs managed medically or surgically, based on severity of presenting signs

• Pain only. 80% of dogs had positive outcomes with medical management. 98.5% of dogs had positive outcome with surgical management.

• Non-ambulatory paraparesis. 81% had positive outcomes with medical management however the level of recovery was less complete with medical management. 93% had positive outcomes with surgical management.

• Paraplegia, deep pain intact. 60% of dogs had positive outcomes with medical management however this was prolonged and less complete compared to surgical management. 93% of dogs had positive outcomes with surgical management.

• Paraplegia, deep pain absent. 21% of dogs had a positive outcome. 61% of dogs had a positive outcome.

• The loss of deep pain causes the biggest shift in predictive statistics for surgical intervention. If you have any question about checking deep pain, please ask!

Medical management key points

• Strict rest of 4 weeks is recommended based on low-level evidence to allow for healing of the annulus fibrosus. Strict rest is recommended by all, the 4 weeks part has low-level evidential support in the literature.

• Corticosteroids are NOT recommended in acute intervertebral disc herniation and their use did not demonstrate superior outcomes in many studies. The exception is management of chronic signs in which corticosteroid use may show some benefit. (Not addressed in this article.)

• NSAID use is recommended for at least 5-7 days, assuming no specific contraindication exists.

• There is low-level evidential support for acupuncture or rehabilitation for dogs.

Surgical management key points

• Much of the information provided is useful if you perform the surgery. If you do, please seek out the article as I won't be presenting those points here.

• The timing of surgical decompression is hotly contested amongst neurologists (and surgeons performing neurosurgery). Conventional wisdom suggests early decompression leads to better long-term outcomes, and faster. This has not been consistently shown in the literature therefore the consensus statement elected to skirt the issue and not provide a "optimal window of time" recommendation. My thoughts (I was not on the consensus team, please note) is that if your client is able to seek surgical management please do so as quickly as possible.

That's it for this week. This is supposed to be a "TidBit" so I don't want to overwhelm you and discourage you from reading. If you perform these surgeries, or refer frequently, please consider reading the consensus statement. If you have any questions about what I've covered so far, or IVDH in general, please reach out! I will cover more from this statement paper in future TidBit Tuesdays!

Have a great week, stay warm, and enjoy these glorious sunny days of fall!

Intervertebral Disc Herniation in Cats

Intervertebral disc herniation (IVDH) does occur in cats but is reported at a much lower prevalence than dogs. Is this because the disease is less prevalent or because owners are less likely to pursue advanced diagnostic imaging to obtain a diagnosis? I don't know the answer, however a recently published article reported on 35 cases of feline TL IVDH over 21 years. That sounds like a lot fewer cases than we see for dogs!

Clinical Presentation

Like dogs, the most common presenting complaint is difficulty walking and/or pain. In this study, They found 2 cats had grade I, 20 cats were grade II, 7 cats were grade III, 3 cats were grade IV and 3 cats were grade V on presentation. (Grading scale listed at the bottom). There was no significant difference between outcome at discharge or follow up and initial presenting grade. Does that mean that we shouldn't rush to get cat's seen, imaged, and cut? Probably not. Of the 3 grade V cats (the ones that we would consider a surgical emergency), one improved, one was static and the other was lost to follow-up. What was the timeline for surgery? Unknown. Dogs have a 50% chance of improvement if they are grade V and undergo surgery within 24 hours. This is debated amongst neurosurgeons but as a general rule I subscribe to the plan of cut ASAP whenever possible if deep pain is absent.

Location of the Offending Disc

In the referenced study, thoracolumbar disc herniation was most common at L6-7. This is slightly different from the previous reports in which L7-S1 was reported to be most common, but not far off. I think it is safe to say that cats are more likely to have low lumbar disc herniation than T11-L2 disc herniation, like dogs. Why? Cats are SO MUCH more flexible than most dogs (especially the chondrodystrophic type) that the vertebral dynamics are different as well. Previous reports suggest obesity is more common in cats with IVDH (and in my experience, too) but this cannot be the entire answer. It remains to be seen, why cats are more likely to have a low lumbar disc herniation than TL. When someone knows...I'll tell you!

Key Points:

• Intervertebral disc herniation does occur in cats

• The most common presenting sign is weakness or lumbar pain

• Surgery can be done and SHOULD be done (when appropriate for the patient)

If you have a cat patient with lumbar or lumbosacral pain, reach out. I'd love to see them! Schedule a consult using my online scheduler (for veterinary use only) and let's get your patients feeling better, soon!

Grading scale:
Grade I: normal gait with hyperpathia
Grade II: ambulatory paraparesis
Grade III: non-ambulatory paraparesis
Grade IV: paraplegia with intact nociception
Grade V: paraplegia with absent nociception

Reference: https://journals.sagepub.com/doi/pdf/10.1177/1098612X211028031

Hemophilia A and Spinal Hyperpathia?

An interesting case series was published this month in Frontiers in Veterinary Science (see reference below) detailing three dogs with hemophilia A and neurologic disease. I thought we might keep with our vascular discussion this week and chat about this article. Enjoy!

Signalment and Presenting Signs
Three young, male, dogs (4 months, 11 months and 5.5 months of age) were evaluated for signs ranging from spinal hyperpathia alone, to ambulatory paraparesis and proprioceptive ataxia in the pelvic limbs to non-ambulatory tetraparesis and cervical pain. All three dogs had spinal MRI which showed changes consistent with hemorrhage. One dog underwent decompressive surgery at which point a hematoma was confirmed.
Diagnosis
Hemophilia A is an X-linked coagulation disorder that occurs due to genetic mutation and resulting abnormal function of factor VIII.  All three dogs had prolonged aPTT, and normal PT testing. Reminder: aPTT requires functional I, II, V, VIII, IX, X, XI and XII factors so it isn't highly specific when prolonged. PTT evaluates I, II, V, VII, and X. Additionally, genetic testing is now available that can measure the quantity of VIII (more like a percentage of normal) and all three dogs had reduced levels of VIII, supporting the final diagnosis of Hemophilia A in these cases.
Outcome
Two dogs underwent CSF analysis during the diagnostic process, which resulted in hematoma formation and ultimately the demise of one of the dogs. The other dog recovered, was noted to have intermittent cutaneous hemorrhage over the next 5 months at which time it sustained gastrointestinal hemorrhage which was suspected to be secondary to a foreign body and the dog was euthanized. The third dog under went surgical decompression, improved markedly after surgery, and was discharged with a normal neurologic examination two weeks after surgery. No additional follow-up was provided. In dogs requiring invasive procedures with a risk of hemorrhage, fresh frozen plasma or cryoprecipitate is recommended however there is no known cure. Gene therapy is available for humans with hemophilia A however this is not available yet for veterinary patients. A low impact life style is recommended!

Thanks for reading! I am in Michigan this week, and Chicago Vet at the end of the week speaking about super cool neurology-related topics (of course). However, I am reachable by email or telephone if you need me. I look forward to working with you next week!

Reference: Fowler KM, Bolton TA, et al. Clinical, Diagnostic, and Imaging Findings in Three Juvenile Dogs with Paraspinal Hyperestesia or Myelopathy as Consequence of Hemophilia A: A case report. Frontiers in Vet Science (2022): 9,1-9.

Zoonotic Discospondylitis!

This week I thought we could brush up on Brucella canis; an uncommon (in the northern US and Canada) cause of discospondylitis in dogs and a zoonotic disease of importance for humans. Why should we talk about this? Because I was contacted by a Wisconsin vet to help manage this case and I thought we could all benefit from this endeavor. 

What is Brucella canis?
Brucella is an intracellular bacteria that is known to be a cause of abortions and still birth in dogs. Dogs are the known reservoir for this bacterium however other Brucella spp. can be transmitted to dogs on rare occasion.

What signs does it cause?
Brucella canis is known to cause abortion and stillbirth in dogs but it's lesser known signs include discospondylitis, uveitis and fatigue/fever. Have I mentioned this is zoonotic? Wear gloves when handling the dogs, and any excrement. Avoid contact if pregnant.

When should I test a dog for Brucella canis?
Any dog with a history of chronic back pain that is diagnosed with discospondylitis should be tested for Brucella canis. The original case I was involved with had a several year history of "not wanting to be petted on the lumbar spine" that progressed to overt signs of pain over a few months. Another case was imported from Canada (not exactly a hotbed of B. canis activity!) with signs of back pain over several months duration and the most recent case I am working with the dog has a several month history of back pain, as well.

How do you treat Brucella canis in dogs?
Management is NOT recommended by experts and State Veterinarians due to the risk to human health and the poor likelihood of actual cure. No universally accepted treatment protocol is available however several choices in published literature include tetracycline-based antibiotic, aminoglycosides, enrofloxacin or rifampin. Some protocols recommend 2 or more drugs in combination, others have solo management. Repeated screening every 2-6 months, regardless of signs, is recommended. If treatment is going to be stopped, two sequential negative tests are recommended before stopping antibiotics. This is likely to be 8+ months after initiation of treatment...if ever. However, screening should continue life long to catch subclinical relapses. Again, euthanasia is recommended by the veterinary community.

What do you do if you have a suspected or confirmed B. canis infection in a dog?
If you live in in the USA, call your State Vet. This is a reportable disease and must be reported! Furthermore, the state vet can provide additional guidance on treatment, testing and culling.

Wisconsin State Vet contact information:

• Phone: (608) 224-4872, Monday-Friday, 7:45 a.m.-4:30 p.m.

• Email: DATCPAnimalImports@wisconsin.gov

• Evenings & weekends: (800) 943-0003, after-hours. Tell the duty officer you are reporting a potential animal disease.

If you live outside of the USA - contact your local veterinarian for further guidance.

If you wish to read more about B. canis the most recent article from North America that I found is: Cosford KL. Brucella canis: An update on research and clinical management. Can Vet J 2018: 59:74-81.

Thanks for reading! Have a great week and keep those consults rolling!