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!