Re: epsilon aminocaproic acid

CatherineThomas — Tue, 12 Apr 2011 12:52:36 GMT

Thanks

Thats brilliant, just what I was looking for. I was suspicious that it would be a load of rubbish but couldn't find anything to back that feeling up.

Re: epsilon aminocaproic acid

Alex Gough — Tue, 12 Apr 2011 11:58:49 GMT

I have seen that website before. At a client's insistence, I tried acetyl cysteine from the list, but it made no difference and made the dog unwell. Was also extremely hard to source as I recall. The website lists an enormously long list of supplements, I pity the dog owner trying to give their dog all of those. Interesting to note they recommend grape juice - wonder if that causes renal failure? Bottom line is there doesn't appear to be any evidence that any of that stuff works. At best it's experimental, at worst it's quackery. I went to BSAVA lecture on degenerative myelopathy by Joan Coates who discovered the mutation that causes the disease. The only thing she thought made a difference was physio/hydro to maintain muscle mass. Interestingly the website gets the pathogenesis wrong too - they describe it as autoimmune akin to multiple sclerosis, whereas in fact it is degenerative, akin to Lou Gehrig's disease.

Note that the original source of the information on that website is a 1998 page which doesnt appear to have been updated since:

http://neuro.vetmed.ufl.edu/neuro/DM_Web/DMofGS.htm

Paper below on an evaluation of the protocol:

Evaluation of a proposed therapeutic protocol in 12 dogs with tentative degenerative myelopathy

Acta Vet Hung. September 2008;56(3):293-301.

Zoe S Polizopoulou¹; Alexander F Koutinas; Michael N Patsikas; Nektarios Soubasis

¹Diagnostic Laboratory, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki, 546 27 Thessaloniki, Stavrou Voutyra st. 11, Greece. poliz@vet.auth.gr

Article Abstract

The objective of this work was to evaluate the long-term efficacy of a proposed therapeutic protocol in 12 dogs with a tentative diagnosis of degenerative myelopathy, followed-up for a 6-month period. Twelve dogs fulfilling the antemortem inclusion criteria (breed, age, adequate vaccination, history of progressive posterior ataxia and/or paraparesis, no radiographic and myelographic abnormalities in the spinal cord and vertebral column) were allocated. All these dogs presented signs of thoracolumbar syndrome (T3-L3), scored as grade I (mild to moderate ataxia and paraparesis) in 10 and grade II (severe ataxia and ambulatory paraparesis) in 2 cases. Treatment included the use of epsilon-aminocaproic acid and N-acetylcysteine, supplemented with vitamins B, C and E. Prednisolone was given for the first two weeks and upon worsening of neurological signs. Daily exercise, performed as walking or swimming, was strongly recommended. Clinicopathological evaluation was normal in all 12 dogs, and survey radiographs and myelograms did not show spinal cord compression. Magnetic resonance imaging (MRI), performed only in 4 dogs, did not disclose compressive disorders or intramedullary lesions. Neurological signs were progressively worsening in all 12 animals, eventually resulting in severe paraparesis (grade III) or paraplegia (grade IV). The applied medications do not appear to be an attractive alternative to conservative management (physiotherapy) or euthanasia in canine degenerative myelopathy, irrespective of its chronicity.

Alex