Treatment Aims

Whilst we all want a cure, until you get at the cause then it is going to be difficult. It is should be easier to stop damage occurring rather than repair the damage.

For many years we have focused on the immune response and if we look at the genetics of suceptibility it tells us that the immune response is a major player.  

When a damaging immune system gets in the brain it causes relapse. A damaging immune system is present in progressive disease also. However the two types of inflammation are probably different in nature and need different drugs to treat

Does one type of inflammation condition the presence of the other or are they independent of each other. I think the answer to this is that the lymphocyte-type conditions the other glial-type inflammation but with PPMS this second type of inflammation is set in motion very early. In RRMS this takes more time to set in motion, so disability takes longer to develop.

People with RRMS have different trajectories in their disease some worsen faster than others but at some point the glial-type of inflammation, also set in motion early in disease, surfaces and then disease follows a stereotyped trajectory. 

The aim of a DMT is to move that trajectory, by reducing the conditions that set the glial-type inflammation in motion so that the disabilty accummulates later or ideally not at all. 

The current DMT focus on the lymphocyte-immune response only. For RRMSers this can remove/reduce relapses but does not stop progressive MS if treatment is started late in disease course. The question is can it change the slope? Ongoing trials with Tysabri, Gilenja and Sphingolimod should answer this in progressive MS. 

Will lymphocyte-directed immunosuppression alone stop progression. In my opinion the answer is probably going to be no. So unless the drugs do something extra I predict progression will continue, because we need to target neurodegenerative elements of the disease.


If we treat agressively and early the hope it that this alone will move the tragectory sufficently such that disease is treated and that the compensation mechanisms that our brain has can deal with MS.

This is potentially good news for people just being diagnosed, assuming that the regulators can see sense and allow people access to the drugs and that the risk of side-effects is acceptable.

However for people with MS, more needs to be done. We need to target the nerve damaging elements of the disease and this requires use of additional drugs or drugs that have additional properties. But giving nerve protectors or repair agents on their own is probably not going to be the best way to stop progression in RRMS and probably early PPMS as both types of inflammation and the rest need to be dealt with.