The way these sorts of trials are run is to compare large groups of people, each group on a different treatment (e.g. the DMD and a placebo, two different doses of a DMD or two different DMDs). Using large numbers cancels out individual differences - e.g. if you wanted to know the average height of 13 year olds, you would get close to the proper number if you measured 1000 random 13 year olds, but you’d probably be way out if you measured only 10 random 13 year olds.
So you start one group on a DMD and one group on a placebo and regularly monitor their relapse rates, the number of lesions on their MRI, any progression, etc. For the original DMD trials, this was done for at least 2 years. At the end of this, you compare the group data and see what difference the DMD has made, if any. Some studies go on to put the placebo group also onto the DMD - this gives the chance to see what difference starting later makes as well as what difference being on a DMD for longer makes.
Neuros refer patients to the trial based on pre-agreed criteria (e.g. newly diagnosed, EDSS less than 6 (EDSS is a measure of disability), relapsing remitting MS, etc), but they don’t know what group the patient will be assigned to - it’s done randomly by a computer programme, so no one knows who’s getting what.
The data are compared using statistics. If there was no difference between the treatments, the numbers should be the same. However, differences could happen by pure chance so there is a standard rule in all research that differences are only believed if they could have happened by chance at most 5% of the time (you’ll see this as p<0.05; smaller numbers mean less chance of it being a fluke, e.g. p<0.01). This can mean that even when there is quite a big difference in the numbers, it may not be accepted as evidence that the drug did better than the placebo.
Betaferon was the first of the currently available DMDs to publish data, I think in 1995. The research team is still gathering and reporting data - they have kept in touch with as many people as possible and are still monitoring the effects. The same goes for the other teams. So the things we know about DMDs don’t just come from the initial trials. There are more than just the initial trials too because new drugs have to do a trial against older drugs, to show if they are better or not. So, e.g. Gilenya was tested against Avonex and Campath was tested against Rebif in the past couple of years. So these kind of studies also provide data.
There’s a lot more to it than that, but the upshot is that you can believe the data: injectable DMDs reduce the number of relapses that we have by 30% on average (i.e. across all the people in the trial). That “on average” means that some people do very much better, some people do worse and everyone else is somewhere in between. Neuros generally say that a treatment has failed if someone has a “clinically significant” relapse after they have been on it for at least 6 months-1 year (they can take a while to get properly into our systems). At that point, you should be offered a stronger DMD. At the moment, if you start on Copaxone, you will be offered an interferon next. If you start on an interferon, you will be offered Copaxone or Gilenya or Tysabri (depending on MRI results).
I’m not sure why your neuro is only offering Copaxone. Perhaps he thought it would be helpful to give you a suggestion, but according to NICE, the decision about what we get is ours and we can choose from Copaxone, Avonex, Rebif, Betaferon and Extavia (which is Betaferon under a different name). Interferon is sometimes avoided for patients with a history of depression though, which is not uncommon in people with MS.
Hth.
Karen x
Kx