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!