Like so many of life’s firsts, first dogs have a special place in our hearts. Patch, the handsome and powerful German Shepherd of my youth, was no exception. I was a teenager when Patch’s healthy body began to deteriorate. At the time, I resigned myself to our family vet’s opinion that my 13-year-old dog was suffering from the chronic effects of hip dysplasia. However, with hindsight (and a veterinary education), I realize that Patch must also have been suffering from degenerative myelopathy (DM), a debilitating neurological disease of the spinal cord, which robbed him of his dignity during his final year of life.
From his belly forward, he was a normal dog—bright, eager to please and utterly without pain, defying time gracefully. Not so the back half, which was progressively turning into Jell-O. It was as though his body was controlled by two actors in a dog costume: the guy at the front was alert and coordinated, the guy at the back was falling-down drunk. I watched my best friend become trapped inside a dying body, the absence of pain making it worse, somehow. His heart was perfect. Mine was breaking.
Fast-forward 30 years, and it’s a clumsy Newfoundland named Tonka who has me thinking about Patch again. That’s because Tonka displays similar signs: stumbling and progressive weakness of the back end.
“Her spinal MRI was clear,” said her owner, “and that new test for DM was negative. So this has to be about her hip problems, right?”
As it happens, I agreed, but my confidence that Tonka could not be suffering from DM was based on more than the “new test,” a DNA analysis recently offered by the Orthopedic Foundation for Animals (OFA), working with the University of Missouri.
As a 2009 study* revealed, DM has an associated genetic marker, SOD1. To simplify the process, let’s say the abnormal gene influencing DM is A, and its normal equivalent is N. Since every dog gets one copy of each gene from each parent, there are three possible combinations—N/N, a dog who is highly unlikely to contract or pass on DM to its offspring; A/N, a dog with a low risk for contracting DM but the capacity to pass on an abnormal gene; and A/A, an at-risk dog who will always pass on a mutated gene to its offspring.
The test is simple, requiring only a saliva swab from the inside of the dog’s cheek and payment of $65, which covers the cost of the test kit, processing and registration in the OFA database.
Without doubt, this is a wonderful tool in the fight against DM, but as the University of Missouri takes pains to point out on its website, having two copies of the mutated gene does not necessarily result in disease. Many A/A dogs are completely normal, although they may develop DM later in life. Other now-unknown risk factors may also be involved.
The list of DM-affected breeds is extensive; among those on it are Golden Retrievers, Boxers, Corgis, Chesapeake Bay Retrievers, Bernese Mountain Dogs, Pugs, Poodles, Rhodesian Ridgebacks and, of course, German Shepherds.
To date, there is no scientifically proven treatment for DM. The best hope is prevention via responsible breeding programs guided by knowledge and understanding of an individual dog’s genetic makeup.
To be absolutely certain a dog has DM, the affected part of the spinal cord must be examined under a microscope, something that unfortunately cannot be done on a living dog. Barring that, the gold standard diagnostic tool is an MRI of the spine, says neurology specialist Dr. Avril Arendse, my colleague at MSPCA-Angell.
And this brings me back to Tonka and why I felt confident that all I had to worry about were her poor hips. Yes, her DM genetic test was normal, but more importantly, her spinal MRI ruled out the possibility of disk disease, tumors and other neurological causes of her clinical signs. Looking forward, Tonka has plenty of options, unlike my much-loved Patch, who, to this day, gave me my first and best lesson for owners nursing dogs with disabling diseases: empathy.