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Canine Degenerative Myelopathy - Overview

Dhicon_thumb By DogHeirs Team | February 15, 2010 | Comments (5)

Overview | Symptoms | Treatment | Management

Degenerative Myelopathy (DM), sometimes referred to as CDRM (Chronic Degenerative RadiculoMylopathy), is a fatal, neurodegenerative disease characterized by a general lack of coordination of muscle movements in the pelvic limbs. Dogs diagnosed with DM have axonal (a part of a nerve cell, or neuron) and myelin (an electrically insulating layer around an axon, also known as the myelin sheath) degeneration at all levels of the spinal cord.

As motor neurons degenerate, they can no longer send electric impulses to the muscle fibers that normally result in muscle movement. When muscles no longer receive the messages from the motor neurons that they require to function, the muscles begin to atrophy (become smaller). Limbs begin to look "thinner" as muscle tissue atrophies. In the later stages of the disease, limbs may become totally paralyzed.

Degenerative Myelopathy in a Pembroke Welch Corgi


Age at Onset: DM affects adult dogs typically over the age of 8 years. DM has been detected in dogs as young as 3 years.

Breeds Affected: The German Shepherd dog (GSD or Alsatian) is the breed most commonly affected however it is also seen in many other breeds.

  • Alaskan Malamute
  • American Eskimo Dog
  • Belgian Sheepdog
  • Bernese Mountain Dog
  • Boxer
  • Cardigan Welsh Corgi
  • Chesapeake Bay Retriever
  • German Shepherd Dog
  • Golden Retriever
  • Great Pyrenees
  • Kerry Blue Terrier
  • Lancashire Heeler
  • Old English Sheepdog
  • Pembroke Welsh Corgi
  • Poodle
  • Pug
  • Rhodesian Ridgeback
  • Shetland Sheepdog
  • Soft Coated Wheaten Terrier
  • Weimaraners
  • Wire Fox Terrier

Symptoms: DM progresses slowly, so sudden onset of disease symptoms may indicate another cause for these signs. Although variable in presentation and course, generally, Dogs with DM typically require mobility assistance within 9 months of the first onset of symptoms. Symptoms can progress to paralysis in 3-6 months when untreated. 

  • hindquarter weakness
  • lack of coordination of muscle movements in the limbs
  • loss of balance
  • difficulty rising or laying down
  • knuckling under while walking
  • limp tail
  • rear legs crossing under body
  • rear leg drag
  • lack of coordination of muscle movements in the spine
  • hoarseness of bark
  • paralysis
  • incontinence

Genetics of DM: To date, a single gene called SOD1 (superoxide dismutase 1) is associated with DM. One study showed that dogs that had mutations in both copies of their SOD1 genes were strongly associated with the clinical diagnosis of DM. Although all dogs clinically diagnosed with DM under strict guidelines had mutations in both SOD1 genes, not all of the dogs carrying two copies of the mutated SOD1 gene displayed symptoms of DM. Thus, DNA tests analyzing the SOD1 gene alone cannot definitively determine whether a patient will present with degenerative myelopathy.

Canine DM is similar to Amyotrophic lateral sclerosis (ALS) in Humans: Similar to DM in dogs, ALS, also known as Lou Gehrig's Disease, in humans refers to a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Early symptoms of ALS often include increasing muscle weakness, especially involving the arms and legs, speech, swallowing or breathing. With voluntary muscle action progressively affected, patients in the later stages of the disease may become totally paralyzed.

ALS is directly hereditary in only a small percentage of families. Although there is likely a genetic predisposition involved in 90% of adult-onset ALS, no family history of ALS exists with these patients, and they present as an isolated case. This is called sporadic ALS (SALS) because of the lack of direct inheritance in a family. In 10% of persons with ALS have a close second family member with ALS, which is referred to as familial ALS (FALS). Currently the best tool to distinguish between SALS and FALS is the family history.

The SOD1 gene in dogs and humans: Just as the SOD1 gene plays as role in canine DM, the human version of the SOD1 gene has been implicated in FALS. Changes in the SOD1 gene on chromosome #21 have been found in about 20% of families with FALS.


Please contribute to this article! If you have a dog affected by DM, please send us your photos, videos and feedback so we can include them in our article. Videos and photos are particularly useful for demonstrating symptoms to new owners who may have to face this disease. Send us materials by uploading them to DogHeirs or by sending them directly to us at Team@DogHeirs.com


Awano et al. Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2794-9. Epub 2009 Feb 2.

Rosen et al. Nature. 1993 Mar 4;362(6415):59-62  Erratum in: Nature. 1993 Jul 22;364(6435):362.

Dion et al. Nature Reviews Genetics 10769-782 (November 2009) 

ALS Association 

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Comments on this Article

Does the SOD1 gene mutation also travel in wild dogs, or is it specific to the domesticated dog? Because the disease travels more prominently in certain breeds, does this suggest that human manipulation through breeding has caused the disease to present more often in domesticated breeds?or is the gene mutation possible in the canine species in general. Humans carry a similar gene mutation, do other animals also carry similar mutations?

Sorry for all the genetic details, Naomi. We have a couple of other articles on DM in the works which focus on symptoms, treatment and management.

You're right in that there may be many more breeds affected other than those listed above (~43?), we've only listed the breeds that scientists and veterinarians agree are significantly affected by DM. It's a great idea to add all of the breeds suspected to be affected too, so we'll work on this. Thanks Naomi. :)

For neurodegenerative disease specialists in the UK, one place to start asking questions is Stone Lion Veterinary Hospital: http://www.veterinary-neurologist.co.uk/degenerative_myelopathy.htm

Please keep us updated on your DDB's condition and progress, and let us know if there's anything else we can do to help.

This information goes way over my head and way beyond my understanding.  I have a breed of dog not mentioned as being an at risk breed - a DDB and she is displaying all the symptoms associated.  She does not appear to be in pain.  Her problems are not arthritic - which I thought they were originally as I was expecting arthritis to set in as she has both cruciate ligaments operated on years ago.  Her first symptom was hoarse barking, then wobbly walking, she is now collapsing, has severe leg tremors and worn down nails on the inner nails on her back leg.  She was seen by a vet in January who manoeuvered her legs and found no pain or resistance - so no treatment was prescribed.  Is there someone similar to Dr Clemmons in the Uk ?


There seems to be at least two different genetic tests for DM: The DM Flash Test and the DM test offered by the OFA. Although both tests claim that they are testing for DM, because the genetics of DM are not completely understood, it's important to know what exactly genetic tests analyze.

The DM Flash Test appears to be based on DR. R.M Clemmons, DVM PhD work, which tests for a single change in allele*1101 (allele*1101J) of the DRB1 area of the DLA gene which is responsible for the MHCII function. MHCII stands for Major Histocompatibility Complex Class II molecules present on certain white blood cells, which are key factors in our immune systems. This is quite different from the SOD1 gene described above; I searched through Dr. Clemmons' publications on PubMED and I haven't been able to find any papers that show conclusively that DM is an autoimmune disorder. Does anyone have any papers on this work?

On the other hand, the OFA site doesn't describe what gene their DM test analyzes. Does anyone know what test the OFA analyzes for DM? Has anyone had any experience with either test?

Interesting post. Thank you!

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