MS Meds

[surth]

I just want to know does a person have to be on MS Meds cos im not ifi get a attack i go on a cortozone drip for 3 days. And is MS inherrited?

[daisy.girl]

What I have read and been told by Neurologist is that once we experience symptoms of a relapse, the entire damage has already been done. It may take a while for the full extent of the damage to reveal itself.   The steroids only help you to feel better.  The steroids have no effect at all on the overall progress of the disease

[COBOB]

Not sure they are front runners, but they are they best we have today.  For a large cohort, they will overall have a better outcome on DMDs while treating flairs with an IV steroid.  One of the problems is that many people miss flairs and the opportunity to stop that damage in its tracks with IVSM.  So just taking a DMD is really not good enough.  You have to treat flairs.  One flair on an optic nerve can leave you blind.

IVSM has direct anti-inflammatory and immunologic effects on the body.  It doesn't stop paralysis or paresthesias.   It suppresses parts of the immune system.  Hardy just treating a symptom. It stops the demyelination and reduces the inflammation. Those effects stops the paralysis or paresthesias.   Dexamethasone can also be used.  It is so powerful as an anti-inflammatory, it is used to treat cerebral edema and altitude sickness. I don't think I would call them palliative.

To be fair, I take Copaxone.  I know more about it than the other DMDs.  I know it is 4 amino acids found in myelin that make various combinations of protein segments designed to be a "false target" for the immune system.  That being said, it was designed to work against EAE, not MS.  TEVA got lucky.  It takes 6-9 months to become effective.   I have also been treated with IVSM.  

I try to pick words carefully, but sometimes my MS brain misses something,

Bob

[sllowe]

I got a lot out of this discussion.

Two strong points being steroids and DMDs are still the frontrunners in treating our MS and the attacks that come along with it and the track record to prove it. Especially when we are RRMS.

Thank you all!
-shell

[daisy.girl]

It is 25% not 50% of patients, that may not benefit from beta interferons, and treatment may actually make you worse. The study is from Stanford....very interesting read.

http://www.medicinenet.com/script/main/art.asp?articlekey=114947


The study strongly suggests that there are two major types of MS and that a simple blood test can tell one from the other. By itself, that would be a major finding. But that's not all.

One type of MS responds to beta interferon, generally considered the best treatment. The other type does not -- and beta interferon treatment may even make it worse, find Stanford University researcher Lawrence Steinman, MD, and colleagues.

[daisy.girl]

Good information Ren.....
The ABCR meds are the ones 28-30 percent effective, and only Ty makes it to the 68%. And I believe a recent study has shown that there is actually around 50% of MS patients that do not repond at all to any DMD.

It really makes it difficult for us patients to know what to do, it is so frustrating!

While looking for this data, I came across these very disturbing studies:

Unfortunately, because MS develops very slowly, it takes years before the
effectiveness of a drug can be properly assessed and hence it is only
now that we have some good data on whether or not the CRABs are
effective or not.
The clinical trials which tested the drugs and led to their approval were
only two years in duration and it was impossible to determine if the
drugs had an effect on disability progression over such a short time
interval. Instead, the researchers used relapse rate and MRI-detected,
lesion development to evaluate drug effectiveness. It was simply
assumed these two variables were valid “proxies” for disease
progression although the researchers had no hard evidence to support
such an assumption.
Notably, subsequent studies have shown that neither of the applied
proxy measures correlate to disability progression so it appears that
the drugs were approved on erroneous assumptions. Because of these
false assumptions, the clinical trial data for the CRABs do not tell us if
the drugs have any real effectiveness.
To find out if the CRABSs are actually effective, we will look at the results of the three recent studies which directly examine the question of the effectiveness of the CRABs for slowing the accumulation of disability.

The Boggild et al (2009) study compared the disability progression of over 3000 British MS patients who started receiving the CRAB drugs in 2002 versus the established natural
progression of untreated patients. This study was done to determine if the British National Health Service was getting acceptable value for the high cost of the drugs. The main
finding of this study is “The outcomes so far obtained in the prespecified
primary analysis suggest a lack of delay in disease progression for all disease modifying treatments”. In fact it was found that “Disease progression was worse than that in the untreated control group” although it must be noted that there was not a statistically
significant difference between the two groups.
Boggild M, Palace J, Barton P, Ben-Shlomo Y, Bregenzer T, Dobson C, Gray R.,
Multiple sclerosis risk sharing scheme: two year results of clinical cohort study with
historical comparator. BMJ. 2009, 9 pages.


A recently published study done in Nova Scotia, Canada (Veugelers et
al, 2009) looked at the effectiveness of the CRABs on the basis of data
from 1752 patients. This was accomplished by examining the time it
took to reach disability level EDSS 6 (requires a cane) for both
untreated patients and those on one of the CRABs. They found it took
untreated persons 14.4 years with a 95% confidence interval of 12-
17.4 years whereas the treated patients were estimated to reach
EDSS 6 at 18.6 years with a 95% confidence interval of 15.9-21.9
years.
The authors trumpeted these findings as proof the CRABS actually
slowed progression but unfortunately they seem to have missed the
meaning of confidence intervals for statistical findings. Because the
95% confidence intervals of the two findings overlap, this means there
is no real statistical difference between the two results and thus their
data really demonstrate that the drugs have no statistically significant
effect on progression.
Veugelers PJ, Fisk JD, Brown MG, Stadnyk K, Sketris IS, Murray TJ, Bhan V.,
Disease progression among multiple sclerosis patients before and during a
disease-modifying drug program: a longitudinal population-based evaluation. Mult
Scler. 2009 Nov;15(11):1286-94

The third study by Ebers et al (in press) very nicely complements the
other two studies in that it compares the current clinical outcomes of
the persons who got betaseron during the original betaseron trial done
16 years ago (181 subjects) with the persons who were on placebo in
the same trial (79 subjects). The basic finding was “No differences in
outcome between original randomization groups could be discerned
using standard disability measures”.
Looking deeper into the data, we see findings such as everyone got to
EDSS 6 by about the same time, 12.8 – 16.1 years. This finding is
important because these values agree very closely with those of the
Veugelers et al study. Also of importance is the finding that 38.6% of
untreated patients (those on betaseron for less than 10% of the time)
reached EDSS 6 within the past 16 years. This compares with 35.7%
of treated patients (those on betaseron for over 80% of the time)
reaching EDSS 6 in the same time interval. Once again no significant
statistical difference was detected so we can say with some confidence
that using betaseron for 16 years will not decrease your chances of
declining to EDSS 6 within that time period.
Because the results of any single study can always be questioned,
given imperfections in design and data collection, it is important that
we now have three independent studies which look at the effectiveness
of the CRABs in slightly different ways. Notably, all three studies
show that the CRABs have no statistically significant effect on
the long term progression of disability.
Ebers, G, Traboulsee A, Li D, et al., Analysis of clinical outcomes according to
original treatment groups 16 years after the pivotal IFNB-1b trial. J Neurol
Neurosurg Psychiatry, in press, 6 pages.

[rendean]

C:\Users\Brenda\AppData\Local\Temp\12.3.7_DiseaseModifyingDrugs-1.pdf

"Benefits of the Disease-
Modifying Medications


All of these medications have been shown to reduce the
frequency of MS relapses and the development of new lesions.
In individual clinical trials comparing a drug versus an inactive
placebo treatment, MS attacks were reduced by 28–68 percent
by different agents. In the clinical trials, most people were also
found to have fewer, smaller, or no new lesions developing
within their central nervous system as visible in MRI scans.
Preventing permanent damage
Permanent damage to nerve fibers (called axons) occurs
early in MS in association with the destruction of myelin.
Overall brain shrinkage (or atrophy), can occur early in the
disease, and damage can be ongoing even when the person
has no symptoms of an attack and feels well. Therefore, MS
specialists advise the early use of a medication that effectively
limits lesion formation and brain atrophy, or shrinkage. In
the opinion of the National MS Society’s Clinical Advisory
Board, limiting lesions may be a key to reducing future
permanent disability for many people with MS.
None of these medications is recommended for women
who are pregnant or plan to become pregnant. Physicians
should be consulted. Most women will be advised to avoid
using these medications during pregnancy."


This but an excerpt that I found in a great source, the National Multiple Sclerosis Society Foundation website. It discusses each of the DMD, including the newly released pill / Gilenya, in some degree but does not cover all possibilities.

Hopefully, this will help to clear up any misconceptions about their use.

Ren