Dr. R. M. Clemmons, neurology professor at University of Floridaâ€™s veterinary school, feels that the peculiar syndrome seen in our breed is also seen only (and even then rarely) in the Belgian Shepherd and the Old English Sheepdog, and he has believed that what is seen in other breeds may well be a different disorder.
Those other degenerative myelopathies are probably not caused by the same immune-system-related deficiency as we have in the GSD
The president of the Kerry Blue Terrier Club
reported DM in her
breed, and there has been another indication that Auburn University
was about to publish a study of a disorder that appears to be DM in Bernese Mountain Dogs.
It had been reported that brain stem involvement eventually occurred (Clemmons, 1992) which could result in a number of signs including asymmetrical tetraparesis, cranial nerve abnormalities and altered mental status.
It had been reported that brain stem involvement eventually occurred (Clemmons, 1992) which could result in a number of signs including asymmetrical tetraparesis, cranial nerve abnormalities, and altered mental status.
The pathology in the spinal cord had been described in detail by a number of authors.
Only one author suggested that there was evidence of axonal regeneration in the spinal cord (Clemmons, 1989), the same author mentioned the possibility of changes occurring in unspecified white matter areas of the brain.Â Detailed examination of the brains of affected dogs revealed novel (not seen in other disorders) pathological changes in specific brain nuclei.
Years later Clemmons
and others claimed that 2000 IU of vitamin E daily, 500 mg of vitamin C twice a day, and a high-strength vitamin B complex twice a day was the best dosage.
More recently, Clemmons
has been quoted as saying that steroids are no longer recommended for DM dogs.
found that steroids lead to muscle wasting.
Therefore, giving steroids to a dog with DM is like pouring gasoline onto a fire.
A dog with DM that is given steroids will lose muscle mass much more rapidly than one that is not on steroids.
Hydergine, a prescription drug derived from ergot fungus, is being studied, since it seems to promote nerve regeneration.
For dogs with advanced DM, Dr. Clemmons
suggested trying 5 mg three times a day for at least three months.
The approach to treatment of DM that has been proposed by Dr. Clemmons
is what he
calls â€œintegrative treatmentâ€�.Â It combines conventional pharmaceutical treatment with â€œalternative medicineâ€� or â€œsupportive therapyâ€�.Â Paraphrasing some of his
comments might be helpful here.Â Conventional drug therapy (medicines) has been of little lasting help to patients with DM.
However, the combination of exercise, vitamins, and certain drugs (he says) has delayed the progression of DM in many dogs.
Treatment has been directed at suppression of symptoms, and since until recently the actual cause or causes of this autoimmune disease were not known, little had been done in the way of finding out how to prevent it.
We now know that the genetic component is the major factor.Â Saying that Degenerative Myelopathy is an autoimmune disease means that the animalâ€™s immune system attacks its own cells; in this case, the central nervous system.Â The myelin insulation sheath around the nerves and axons (fibers) is gradually destroyed.Â Itâ€™s worst in the thoraco-lumbar area of the spinal cord, but can also affect the brain stem and other nerve tissue.
â€œIntegrativeâ€� or supportive treatment of DM, as promoted by Clemmons
at the University of Florida
vet school, suggests the use of dietary alternatives and supplements to combat the immune system, and is derived from an approach to treating Multiple Sclerosis.Â You probably know at least one person with MS, and can recognize the similarity in symptoms.Â It has been postulated that besides the vitamins E and C, the drugs, and the exercise mentioned above, avoidance of toxins such as is found in pesticides and lawn chemicals, and perhaps in some processed foods, is possibly helpful.
Clemmons recommends â€œstress formulaâ€� B-complex containing 100 mg of most of the B vitamin components.
says that â€œOmega-3 fatty acids such as EPA
(eicosapentanoic acid) and DHA
(docosahexanoic acid) are constituents of fish oils that act as anti-inflammatory agents and may be worth trying if your dog has an autoimmune disorder or arthritis.â€� If so, fortunate is the owner who can give an afflicted dog a couple of cooked sardines or a small piece of salmon as a daily, natural source of such fatty acids.Â A 1000-mg fish oil capsule, tablespoon of ground flax seeds, or flaxseed or wheat germ oil supplement can do about the same thing.Â If you are really â€œintoâ€� the health-food store shopping, 500 mg twice a day of GLA (gammalinolenic acid), a fatty acid found in evening primrose and black currant oils, is an alternative anti-inflammatory without the side effects of most anti-inflammatory drugs.Â All of the above should be considered as optional adjuncts to conventional treatment with the drugs, vitamins, and exercise, not replacements for them.
(1992) suggested, among other ideas, the presence of an 85kDa antigen in dogs with CDRM.Â However, no other authors have mentioned such a possibility.
has also made numerous other observations and conclusions that have not been duplicated by other researchers, so one must look with care at his
â€œdataâ€� until verified in the scientific community.
treatment regimen has also been controversial, as the claims made therein have not been substantiated elsewhere.
High doses of vitamin E (2000 IU/day), high-potency B vitamin complex, and epsilon aminocaproic acid (EACA) had all been used as treatments (Clemmons, 1989 & 1992) although their efficacy appeared questionable.
Since EACA has anti-protease activity, Clemmons
considered that it would therefore be helpful in CDRM, as it would presumably block the final step in the inflammatory pathway, thus helping to prevent tissue destruction.
There was no further evidence suggesting that any of the therapies suggested by Clemmons
were beneficial in the treatment of CDRM, which was still considered untreatable.
The finding of CDRM in several littermate pairs, combined with the acknowledged high incidence of the disease in the German shepherd breed in general suggested that a genetic factor may well be involved in the aetiology of the disease, as previously suggestedÂ (Clemmons, 1989).
Due to this unusually high incidence of CDRM in one breed of dog and the discovery of at least two pairs of affected littermates, the investigation of a possible genetic factor was indicated.
Following a literature search for diseases in other species with clinical and pathological similarities to CDRM, a working hypothesis was established: CDRM is caused by a CAG trinucleotide repeat expansion in an unknown gene.