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Canine Degenerative Myelopathy

Canine Degenerative Myelopathy

By Dr. Lisa Lipitz, VMD, DACVIM (Neurology)| Neurology

Canine degenerative myelopathy (DM) is a late onset, slowly progressive degenerative disorder of the spinal cord white matter. It primarily affects large breed dogs with a mean age of onset of 9 years; most patients are 8 years or older when signs of disease develop, and there is no sex predilection.

Previously DM was considered idiopathic. However, recent advances demonstrated a genetic basis in certain breeds due to a mutation in the canine SOD1 (superoxide dismutase 1) gene. The SOD1 protein is a free radical scavenger in the central nervous system and mutations lead to myelin and axonal loss. This results in demyelinating disease, a condition that damages the protective, insulating outer layer of nerves (the myelin sheath). In canine DM, unprotected nerve fibers (axons) in the spinal cord no longer transmit signals normally; as conduction of nerve impulses slows along these damaged pathways, neurological deficits appear.

The SOD1 genetic mutation has been documented in breeds most commonly affected by DM, which include the German Shepherd, Pembroke Welsh Corgi, Boxer, Rhodesian Ridgeback, and Chesapeake Bay Retriever. DM has many similarities to human amyotrophic lateral sclerosis (ALS), and mutations in SOD1 have been identified as a cause for some forms of human ALS. Therefore, dogs with DM can serve as a model for this adult-onset, fatal neurodegenerative disease in people.

Clinical Signs

DM is not a painful condition, and the clinical course is often insidious. Dogs initially present with signs of a T3-L3 myelopathy manifesting as upper motor neuron paresis (weakness) and proprioceptive ataxia (loss of coordination) affecting the pelvic limbs. Therefore, DM should be suspected in an older dog that presents for progressive spastic paraparesis and exhibits lack of paraspinal pain. As DM progresses, nerve fibers are damaged cranially and caudally along the spinal cord. This eventually leads to thoracic limb motor deficits (resulting in tetraparesis) and pelvic limb lower motor neuron signs (resulting in flaccid paralysis and pelvic limb reflex deficits); urinary/fecal incontinence and widespread muscle atrophy occur towards the end stage of disease. Ultimately many pet owners elect humane euthanasia once affected dogs lose the ability to support weight in the pelvic limbs and walk independently.


Definitive diagnosis is made only via spinal cord histopathology on post mortem examination (Figure 1). Clinical, antemortem diagnosis is best made by excluding other diseases that can cause a progressive T3-L3 myelopathy.

The neurodegenerative changes that occur within the spinal cord during the course of DM are too small to be visualized via MRI examination. On cerebrospinal fluid analysis testing, a mild protein elevation is often found in dogs with DM which is a non-specific, common finding in many types of spinal cord disease. A combination of appropriate signalment, history, and neurologic signs, in conjunction with a normal spinal MRI examination are supportive diagnostic findings for canine DM. However, performance of a spinal MRI examination is essential in order to rule out other conditions which can present similarly to DM, such as Type II (chronic) intervertebral disc disease, chronic discospondylitis, and spinal neoplasia.

Because a familial cause has been identified, the University of Missouri offers a genetic test for the SOD1 mutation; currently, an autosomal recessive inheritance is presumed and homozygosity for this mutation is considered a major risk factor for developing canine DM. Not all dogs homozygous for this mutation go on to develop clinical signs of DM later in life, which must be kept in mind when interpreting test results. It is suspected that other, still unidentified, genetic and environmental factors may also determine whether at risk dogs develop DM. Still, the genetic test is a useful tool both in supporting a clinical antemortem diagnosis of DM and also for breeders working to eradicate the SOD1 mutation from the gene pool of commonly affected breeds.

Treatment and Prognosis

The clinical course of DM usually varies from 6 months – 1 year, and sadly, treatment options are limited. Studies evaluating the effects of anti-oxidants (vitamin C, vitamin E, and N-acetylcysteine) have found no benefit. Corticosteroids at anti-inflammatory or immunosuppressive dosages have not been shown to alter the course of disease. Anecdotal reports that the antiprotease agent aminocaproic acid improves DM have not been validated in scientific studies. Therefore, to date no medical intervention is available to reverse progression of disease. The search for a cure is an active area of ongoing research at the University of Missouri.

Daily, intensive physiotherapy is the only measure thus far which has been shown to prolong survival of affected dogs by helping maintain functionality. This protocol includes daily gait exercise, massage, passage range of motion, and hydrotherapy; affected dogs which receive physiotherapy have longer survival times (255 days on average per one study) and remain ambulatory longer than dogs with DM that do not undergo physiotherapy. Unfortunately, the long-term prognosis for this condition remains guarded as most owners elect humane euthanasia once their dog’s quality of life becomes poor.

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