This disorder is a degenerative disease of the spinal cord also known as “German Shepard Degenerative Myelopathy” based on the elevated occurrence in this specific breed. Nevertheless, the disease is also found in other breeds, especially large or giant breeds, and can be found in cats as well. The first clinical symptoms of DM appear between the ages of 5 and 14, however it can also occur in younger animals. There is sex predilection.
The cause of this disorder is still unknown.
There are several hypotheses however none have proven to be backed by reliable scientific evidence. The most reliable of these hypotheses attributes the illness to nutritional deficiencies, while others speak of degenerative problems and autoimmune mechanisms. In fact, in support of the first hypothesis, in some patients with DM they have found a concomitant chronic enteropathy associated with later abnormal proliferation of bacteria in the small intestine, poor absorption and decreasing blood levels of vitamin E and B12.
Nevertheless, administering vitamin B12 via an injection in dogs was ineffective in slowing the development of the symptoms.
Furthermore, a recent study of 25 dogs with Degenerative Myelopathy excluded vitamin B12 deficiencies as a possible cause of the illness.
The immune-mediated hypothesis, however, is based on the findings of impaired cell mediated responses and lymphocytic infiltrates in various organs in dogs with Degenerative Myelopathy.
Other authors believe that DM is a degenerative disease of late development with a genetic basis.
The proprioceptive deficits are significant, given the ataxia of the hindlimbs and mild paraparesis.
The lack of coordination is much more evident in the paralysis. This aspect enables the doctor to move towards a suspected diagnosis of Degenerative Myelopathy, as supposed to other bone marrow diseases.
The absence of a painful reaction upon touching the spine and the set of factors, such as insignificant response to treatment with NSAIDs or corticosteroids, as well as the owner’s inability to determine when the onset of symptoms occurred, support the suspicion of Degenerative Myelopathy.
In examining the spinal reflex points during the first stages of the disease, patellar normo or hipereflexia is observed while in the advanced stages, lumbar hyporeflexia is observed. Sphincter control is usually intact.
The evolution of progressive deterioration of the clinical symptoms occurs within a period of 6 to 36 months, but in average paraplegia sets in at 12 months. In this case, many patients are euthanized.
To ensure correct diagnosis, it is recommended that a myelograhy of the thoracic and lumbar spine is done in order to rule out compression illnesses as well as examine the cerebrospinal fluid.
There is no treatment protocol with proven effectiveness.
A combination of exercise, vitamin supplements and the aminocaproic acid is used.
Moderate swimming and physiotherapy are useful for preventing atrophy in the hind legs from muscle disuse.
The Vitamin B complex and vitamin E decrease the degeneration of the nervous system.
The amino-caproic acid seems to slow the progression of the disease due to its anti-protease activity.
Using corticoids, with immunosuppressive doses, is to be used only for limited periods of time and when there is recurrence of symptoms.
The prognosis for these animals is bad.
There are products on the market such as the bike brace or thermal blankets that can help improve walking, the clinical symptoms, reduce ataxia and, although they do not “cure” the disease, they can improve the symptomology.
The histopathological lesions spread to the white matter of the spinal cord. These can affect the whole bone, but generally they are concentrated in the segments of the thoracic and cranial caudal lumbar.
Some authors discard the involvement of the brain, however, isolated lesions of the brain stem have recently been observed and the clinical consideration is still unclear.
Dr. Costabile Annaluce
For more information about this treatment consult this Ortocanis article.