This Is MS Multiple Sclerosis Community: Knowledge & Support

...came across as quite condescending and insulting. Most of us here are struggling with MS in some way: either as sufferers or those who watch, (and also suffer), their loved ones falter and fail against this relentless onslaught hour after hour, year after year. One of the few things we can do to maintain a sense of control is to try and understand this disease, and also to try and translate the bits of research we hear about and fit the pieces together into a jigsaw that spells out "hope". Still, at least it keeps us busy.

No great surprises except this: I was astounded to read
So in other words: whatever your EDSS score is, it would have been exactly the same no matter what type of MS you've got -- that's a new one on me: I'd always been led to believe that certain forms of MS were "worse" than others, (not counting the rapid, aggressive subtypes). But it sounds as if the speed of deterioration is set within each individual, no matter what form their MS takes.

Dr Coles,

I follow MS research closely and much recent research has suggested that in addition to damage to White Matter (myelin) there is also a substantial amount of damage, from the earliest stages of the disease, to Grey Matter. Some research suggests that different mechanisms may be responsible for the damage to White Matter and Grey Matter. Is there any evidence as to whether treatments such as Tysabri or Campath are having an effect in terms of reducing damage to both White Matter and Grey Matter, or are these treatments only having an effect on the damage to White Matter, which is believed to be caused by inflammation?


Thank you for this very informed question.

I would imagine that both Tysabri and Campath-1H reduce grey matter plaques, because I personally think these are also due to inflammation. But I know that this has not been directly studied in the case of people treated with Campath-1H, and I would guess the same is true for people who have had Tysabri.

Alasdair

The issue of reversible and irreversible disability damage / disability has also been raised in this thread. Given that we can't do anything about the latter (yet) we should concentrate on the former. Hopefully some interesting research relating to reversible disability will be highlighted at the AAN conference at the start of May.

Dr Coles,

I am a recipient of Campath 1-H (last November) and am so far thrilled with the results. I would be grateful for your thoughts on the following:

(i) Campath 1-H appears to offer most advantage early in the disease for those with Relapsing / Remitting MS. How long will it be before any conclusions can be drawn as to whether or not Campath 1-H offers long-term benefits to these patients (as when Campath 1-H was used on those with Secondary Progressive MS, relapses and inflammation were reduced but, over time, the progression of disability continued)?

(ii) Much research is being undertaken into neuro-protective agents, such as minocycline and cannabis extracts. If agents offering neuro-protective benefits are identified, might these offer a sensible add-on therapy to Campath 1-H, given that the latter primarily targets the inflammatory process in MS?

(iii) Some MS researchers have suggested that inflammation is a secondary response rather than the initiating process in MS. Is the research into Campath 1-H going to provide some insights as to whether MS is an inflammatory disease which results in neuro-degeneration, or a neuro-degenerative disease which (for some patients) then leads to an inflammatory response?

Many thanks

Ian


Thank you for your post.

i) As with all drugs in multiple sclerosis, it takes a “long time” to get “long-term” data! But it is this information that is so important. We have already published anecdotal data on people with multiple sclerosis who had Campath-1H up to five years ago. But we only have rigorous clinical trial data for two years of Campath-1H treatment. Later this year we will have three-year data… and so it goes.

ii) I agree. I think the ideal treatment strategy for multiple sclerosis will be drugs that are safe enough to take really early on in the course of multiple sclerosis and that combine both anti-inflammatory and neuroprotective actions.

iii) A good point. I think that the long-term effects of drugs like Campath-1H will tell us whether inflammation is the driving force behind multiple sclerosis (in which case we should see a good outcome) or just a secondary response (in which case there will be no long-term benefit).

Hope that helps

Alasdair

There's not enough clinical evidence of the ability of minocycline to delay the progression of permanent disability, but if it was a novel molecule, I bet there already would be. The first clinical study made with it was published at the AAN conference three years ago, but very little has happened since.

I contacted one of my neuros (not Dr Coles) following the publication of the research and asked if this meant that very powerful immuno-suppressants were a waste of time in treating MS. His response was:

In the inside–out model, the axon is injured by viral infection, direct attack by autoreactive T or B cells, and/or glutamate toxicity, etc.,

Autoreactive T and B cells are regular components of the healthy immune system. It has been proposed that some of these cells might have a protective function. Recent studies support this notion by demonstrating that a) myelin-autoreactive T cells show neuroprotective effects in vivo, and b) activated antigen-specific human T cells and other immune cells produce bioactive brain-derived neurotrophic factor (BDNF) and other neurotrophic factors in vitro.

"The whole system is like a giant feedback loop. The nervous system controls inflammation and can even initiate inflammation without activation of the immune system. The immune system, in turn, communicates with the nervous system through its own chemical messengers. With a constant two-way communication between the nervous system and the immune system, inflammation can be escalated unless the endless loop communicating the need for inflammation is broken.

Three possible causes for the increase in asthma and rhinosinusitis are being investigated: the chemical hypothesis, which holds that air pollution is responsible; the viral hypothesis, which claims that viral infections might be to blame; and the hygiene hypothesis, which proposes that our high standards of cleanliness are doing us in.