Probably simply a matter of semantics, but, if the disease progression is slowing, then sx manifestation will also be slowing/changing for the better. Mind showing me the source for your statement that C wasn't developed to impact sx?

Hi ZiaSolis,

This could just be semantics. But you couldn't notice a symptom difference because you can't compare what symptoms you haven't experienced as a result of copaxone to what you would have experienced if you had been untreated since you have no idea what symptoms you WOULD have experienced without copaxone or on a different dosing schedule.

So no, you couldn't make the statement that you "saw no difference symptom wise" and attribute that to your dosing regimen unless you could expect to have had an MS attack and therefore new symptoms on a different regimen or none at all.

And since copaxone is only estimated to prevent about 1 attack every 2+ years, I am not sure you can really make any determination on efficacy based on skipping doses, doubling doses, etc. unless you've done this over the long term. And then you'd need to compare it to how you would have done either with nothing, or with regular dosing, or regular double-dosing, etc. That's why there's clinical trials, because with such a variable disease, it's almost impossible to have a reliable pattern of cause/effect for just one person.

I can't offer you evidence that copaxone doesn't affect existing symptoms except that none of the clinical trial data I've read even measured its impact on existing symptoms. So if the trials didn't measure its impact on symptoms, then I assumed that it wasn't developed to impact existing symptoms. The results talk about rates of disease progression and rates to reach certain EDSS points, but they don't talk about improvements in EDSS over and above what they were at the beginning of the trial.

But I agree with you that certainly copaxone is suppose to help prevent new symptoms from occurring. It's just not that good at it so you could still expect to see some disease activity, even if you were dosing at an optimum level. But to determine whether dosing is the cause of no disease activity, or copaxone at all, or just plain disease activity idiosyncracies, I think it would be impossible to attribute anything to one particular cause.