That sounds like great news.

I guess if you are this far into SPMS, they wouldn't expect enhancing lesions any more . . . but no black holes or more permanent lesions sounds GREAT!

Have you lost any functionality over this two (X) years in SPMS?

Cherie

Good to hear Cin. Jim's was unchanged too but those darn symptoms keep a coming don't they?

Call your lawyers! I smell a hefty payout!

Cherie,

I don't understand your statement that SPMS people will no longer have enhancing lesions on a brain MRI. If the person is stable, or on a plateau, the MRI will not show enhancement because they are not progressing. But active lesions I thought would still enhance if a person is progressing even if SPMS.

Did I miss Radiology 101? (kidding) Just curious about your statement.

Cindy, for what it's worth - my neuro asked me why I prefer not to use a DMD and I told him I was concerned a DMD would cause more problems than it would solve.

He sat back and said he found my answer interesting. He had gone to a medical convention where one of the speakers said there is a possibility the DMDs could be making those with MS worse not better

Is that what has happened to you?

That's great news!

I am on C and just got the same report you did - no changes in 2 years. But that was only on my brain MRI. They didn't do the spine (c and T) this year.

I mentioned that because I have both the reports and quite honestly, they are almost identical with the exception of a slight change in one of the lesions. They have standard statements that they use and the transcriptionists pull it up and put it in the report. It makes you wonder, huh.

Anyhow, I hope that continues for you. Whatever you are doing, keep it up as it is obviously working for you.

It was a 'guessterlization', based on how what a enhancing/inflammatory lesion is:

It is my understanding that once someone goes from the inflammatory phase of the disease (RRMS, with enhancing lesions), into the progressive phase (SPMS), generally they have few to no relapses, and inflammatory (enhancing) lesions are far less common.

“During periods of multiple sclerosis activity, white blood cells (leukocytes) are drawn to regions of the white matter. These initiate and take part in what is known as the inflammatory response. The resulting inflammation is similar to what happens in your skin when you get a pimple.

During the inflammation, the myelin gets stripped from the axons in a process known as demyelination. The effect of this bears many parallels to the rubber insulation on wire perishing - some or all of the electricity in the wire will short out and the efficient conductivity of the wire will be reduced. When the myelin sheath is damaged, the transmission of nerve impulses is slowed, stopped or can jump across into other demyelinated axons.”

As the disease progresses, axons are also destroyed though not necessarily by the inflammatory response. During the secondary progressive phase of the disease, inflammation becomes less and less common but still the axons continue to die. This degeneration of axons is known as Wallerian Degeneration.”

http://www.mult-sclerosis.org/howms.html

“RRMS is characterised by relapses (also known as exacerbations) during which time new symptoms can appear and old ones resurface or worsen. The relapses are followed by periods of remission, during which time the person fully or partially recovers from the deficits acquired during the relapse.”

“During relapses, myelin, a protective insulating sheath around the nerve fibres (neurons) in the white matter regions of the central nervous system (CNS), is damaged in an inflammatory response by the body's own immune system. This causes a wide variety of neurological symptoms that vary considerably depending on which areas of the CNS are damaged.

Immediately after a relapse, the inflamatory response dies down and a special type of glial cell in the CNS (called an oligodendrocyte) sponsors remyelination - a process whereby the myelin sheath around the axon is repaired. It is this remyelination that is responsible for the remission.”

http://www.mult-sclerosis.org/relaps...sclerosis.html

“After a number of years many people who have had relapsing/remitting MS will pass into a secondary progressive phase of the disease. This is characterised by a gradual worsening of the disease between relapses. In the early phases of Secondary Progressive, the person may still experience a few relapses but after a while these merge into a general progression.”

http://www.mult-sclerosis.org/whatisms.html

“Secondary Progressive Multiple Sclerosis tends to be associated with lower levels of inflammatory lesion formation than in RRMS but the total burden of disease continues to progress. This is thought to be caused by higher levels of axonal loss.”

http://www.mult-sclerosis.org/second...sclerosis.html
The formation of lesions:

http://www.medhelp.org/health_pages/...show/23?cid=36

Cherie

My (newer) neuro recently asked me the same question, Snoopy. I told her that while the CRABs may reduce relapses by 30%, IMHO long-term studies have not proven them sufficiently effective in the longer run, for the majority of people.

She said "you know why?", "because they can't track down enough patients to show one way or another".

I said "exactly!". Given that those people are ALL provided free drugs to stay in the long-term studies, if they were effective, wouldn't there be a ton of people they could easily track down to see how they are doing?

I do think they are potentially effective (and tolerable) for a minority of patients . . . and when they seem to be, those patients should probably stay on them. Guaging efficacy can be difficult too though ...

Interesting that they think they might be making some people worse though. I wonder how they guage that? I know that people with Devic's/NMO are supposed to completely avoid DMD's . . . which is a good reason to be NMO-IgG tested if a person has large spinal lesions. (I'm going for a test soon ....)

Cherie

Raising hand to Snoopy...may I answer that question? Yes I believe that the DMDs may have made my MS advance faster..

I remember AMN complaining of getting worse, while using Copaxone and I believe that's why she stopped it?

Jim was also on Copax for years before he got worse. The ms was worsening since he was already spms within five years of being dx'd. He did one infusion of chemo because Copax and Beta showed no improvements and that's when he went into kidney failure. He has since tried Avonex and it sucked a big one. Now he's back on Beta.

So, yeah, it is possible the dmd's made him worse. Very interesting discussion. Too bad we can't prove it.

Thanks ms for being so darn unpredictable.