Dr. R. M. Clemmons, neurology professor at University of Florida'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.
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.
Dr. Clemmons recommends the vitamin E be dropped temporarily to about 100 IU if the dog has to be given aspirin for any reason during the treatment, and recommends that daily DEC (diethylcarbamazine) replace the monthly heartworm medications ivermectin (Heartgard, Heartgard Plus, Ivomec brands) and Interceptor (a different antifilarial drug) because these increase immune responsiveness; also use the DEC in place of styrid caracide or Filaribits, he says.
, it appeared the best treatment is a combination of all three approaches (these two and the vitamin therapy), along with exercise.
According to some, alternate-day dosage with a steroid such as prednisone, plus acetylcysteine, added to the aminocaproic acid and vitamin formula, is enough to keep the dog owner very busy and tied to the home, but it might offer a chance at reducing progression, thus prolonging life considerably more than in the past.
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 "integrative treatment".
"Integrative" 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.
Clemmons says that "Omega-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.
(1992) suggested, among other ideas, the presence of an 85kDa antigen in dogs with CDRM.
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
"data" 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.
All authors agreed that maintenance of regular exercise and optimal body weight seemed beneficial to affected dogs.
has been the only author in the scientific literature who suggested a treatment regime would be effective which included vitamin E, vitamin B, and EACA; this was not confirmed by other workers in the field.
in 1989 and 1992 suggested that a combination of vitamins, evening primrose oil, and essential fatty acids might slow the rate of neuro-degeneration in cases of CDRM.
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 suggested (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.