Canine degenerative myelopathy (DM) is a spontaneously occurring, adult-onset, progressive spinal cord disease. Degenerative myelopathy was first described by Averill as a spinal cord disorder that predominates in German Shepherd dogs. If decreased pelvic limb reflexes are observed, nerve root involvement is presumed and the disease termed chronic degenerative radiculomyelopathy. Initially thought to be specific to the GSD, it also was designated German Shepherd Dog myelopathy. This disease is not uncommon in some pure bred dogs with an overall prevalence rate of 0.19%. Although the German Shepherd Dog is the most commonly affected breed, DM has been reported in other breeds and most recently in the Pembroke Welsh Corgi (PWC). Higher disease prevalence has been determined in a number of other purebred dogs, such as the Boxer, Rhodesian Ridgeback, and Chesapeake Bay Retriever.
Signalment and disease duration
There is no sex predilection. Age of onset of neurologic signs is usually 8 years and older in large breed dogs with DM. A study in PWCs reported a mean age of onset of 11 years. The clinical course of DM can vary up to 3 years after the suspected diagnosis with a mean time for disease duration to be 6 months in larger breeds of dogs (Figure 1). The pet owners often opt for euthanasia when their dogs lose the ability to support weight in the pelvic limbs. Breeds of smaller size allow the pet owner to give the appropriate care for their pet over a longer time. The median time of disease duration in the PWC was 19 months. Longer survival times in DM affected dogs may also be attributed to increased access to physical rehabilitation facilities for companion animals.
Progressive, asymmetric upper motor neuron (UMN) paraparesis and lack of paraspinal pain are key clinical features of DM. Physical examination findings include loss of muscle mass in the caudal trunk muscles, pelvic limb weakness, and worn nails. Descriptions for severity of loss of muscle mass have differed. Most reports attribute this loss to disuse but flaccidity has been noted in the later stage of disease which suggests neurogenic muscle atrophy. Gait deficits at time of onset show spastic paresis and general proprioceptive ataxia (loss of joint position sense as described for domestic animals). Asymmetric weakness at disease onset also is frequently reported. Most large breed dogs progress to nonambulatory paresis or paraplegia within 6 to 12 months from time of diagnosis. If the disease progresses over a longer duration, clinical signs will ascend to affect the thoracic limbs. If euthanasia is delayed, the clinical signs will cause flaccid tetraparesis/plegia and other lower motor neuron (LMN) signs. Due to its smaller size and longer disease duration, this was a more common scenario in the PWC.4 At disease onset, descriptions of spinal reflexes correspond with UMN paresis. Decreased reflexes noted with the patellar and withdrawal reflexes occur in the latter disease stage. Urinary and fecal continence usually are spared until the latter disease stage.
Figure 1: Breeds representing mean age at onset, mean age at death and mean duration of clinical signs for Pembroke Welsh Corgi (PWC), Chesapeake Bay Retriever (CBR), Boxer, and Rhodesian Ridgeback (RR) with a diagnosis confirmed by histopathology or presumptive based on normal imaging