
Multiple Sclerosis (MS) Support Group
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deleted_user
I have received some great ?s about treatment for SPMS so I thought Id post an update and anyone can jump in:
BACKGROUND:
As many of you know, there is no consensus on the mechanisms underlying the evolution from the relapsing remitting to the secondary progressive phase of MS. Studies indicate that this transition can be mainly driven by the prevalence of neurodegenerative over inflammatory features which is important for treatment options.
SUMMARY of the current Medical Literature on Treatment for SPMS:
1) Interferon Beta 1-b has shown modest improvement in some large trials and no improvement in others
2) Interferon Beta 1-a (rebif and avonex trials): In the Rebif trials treatment significantly reduced the median numbers of active lesions per patient per scan and the accumulation of T2 lesion load (but had no real effect on disablility). In the Avonex trials patients did have 33% fewer relapses and there was a significant benefit of active treatment on eight of 11 MS quality-of-life inventory subscales.
3) IVIG (Intravenous Immunoglobulins): The study results showed no significant effect of treatment on disability, relapse rates, T2-lesion load HOWEVER a significantly lower rate of brain atrophy progression was observed in patients treated with intravenous immunoglobulin than in patients in the placebo group, which could warrant further investigation.
4) IMMUNOSUPPRESSIVE STRATEGIES:
a) Treatment with high-dose methylprednisolone (solumedrol) might have a modest benefit in delaying time to onset of sustained progression of disability.
b) Methotrexate and cyclophosphamide have also been reported to be effective in stabilizing disease in some studies, including patients with chronic progressive MS, but this effect has not been confirmed in other studies.
c) Novantrone essentially had modest to no effect on SPMS
d) immunosuppressive therapy followed by stem cell transplant: In one study 66% of 60 patients with secondary progressive MS had no disease progression over 3 years of follow-up which does make us want for more studies on stem cell transplant HOWEVER the short-term and long-term toxic effects associated with this treatment (including a mortality of about 5%) remain an important concern.
AGAIN:
The limited effectiveness of available immunomodulating and immunosuppressive agents (geared toward reducing inflammation) in prevention of irreversible disability in patients with Secondary progressive MS suggests that inflammation plays only a minor part in driving the dysfunction and progressive loss of neurons and axons.
I hope this helps keep us up to date....
Dr O.
BACKGROUND:
As many of you know, there is no consensus on the mechanisms underlying the evolution from the relapsing remitting to the secondary progressive phase of MS. Studies indicate that this transition can be mainly driven by the prevalence of neurodegenerative over inflammatory features which is important for treatment options.
SUMMARY of the current Medical Literature on Treatment for SPMS:
1) Interferon Beta 1-b has shown modest improvement in some large trials and no improvement in others
2) Interferon Beta 1-a (rebif and avonex trials): In the Rebif trials treatment significantly reduced the median numbers of active lesions per patient per scan and the accumulation of T2 lesion load (but had no real effect on disablility). In the Avonex trials patients did have 33% fewer relapses and there was a significant benefit of active treatment on eight of 11 MS quality-of-life inventory subscales.
3) IVIG (Intravenous Immunoglobulins): The study results showed no significant effect of treatment on disability, relapse rates, T2-lesion load HOWEVER a significantly lower rate of brain atrophy progression was observed in patients treated with intravenous immunoglobulin than in patients in the placebo group, which could warrant further investigation.
4) IMMUNOSUPPRESSIVE STRATEGIES:
a) Treatment with high-dose methylprednisolone (solumedrol) might have a modest benefit in delaying time to onset of sustained progression of disability.
b) Methotrexate and cyclophosphamide have also been reported to be effective in stabilizing disease in some studies, including patients with chronic progressive MS, but this effect has not been confirmed in other studies.
c) Novantrone essentially had modest to no effect on SPMS
d) immunosuppressive therapy followed by stem cell transplant: In one study 66% of 60 patients with secondary progressive MS had no disease progression over 3 years of follow-up which does make us want for more studies on stem cell transplant HOWEVER the short-term and long-term toxic effects associated with this treatment (including a mortality of about 5%) remain an important concern.
AGAIN:
The limited effectiveness of available immunomodulating and immunosuppressive agents (geared toward reducing inflammation) in prevention of irreversible disability in patients with Secondary progressive MS suggests that inflammation plays only a minor part in driving the dysfunction and progressive loss of neurons and axons.
I hope this helps keep us up to date....
Dr O.
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Most of the trials (and the indication for copaxone) is for RRMS
I will say a recent trial in the Lancet Neurology revealed disappointing results for copaxone and relapsing remitting MS (RRMS). There are no copaxone trials on SPMS
Dr O.
I'd try the immunosuppressive therapy followed by stem cell transplantation if there was broader access to the treatment, though -- especially if it halted the progression. The mortality rate is significant, to be sure, but at this point, it's a risk I'd be willing to take!
-Karen
Dr O.
I also would rather not have Karen take such a mortal risk.
No idea if my insurance would cover enough so I could even take it. Apparently there is a certified site in my area or the new guy wouldn't be bringing it up.
Have you heard about this sort of thins happening before DrO?
Previously, I was told that my black holes indicate SPMS. This makes sense to me. But I still have relapses so I am taking copaxone. I can no longer take interfersons and methotrexate due to low white blood count.
So in addition to the previous question, what would be the next line of defense for someone who is on copaxone?
thanks,
Jan
~Tonya