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I asked what immune-supressants completely halt MS because I truly believe that as imaging technology continues to improve that we will find the answer to truly be 'none'. I feel a long enough time span will also show that to be the case.

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Lyon wrote:
With that in mind, out of curiousity, were you referring to immune suppressants being used as long term suppressants or rebooting agents, or both?
Bob

Rebooting would of course be better than infinitely long suppression, however a period of intense suppression of some months may be necessary (and the campath trials suggest this) to allow pre-existing lesions/micro-bleeds to heal enough so that further relapses are prevented.

Radeck-I know you state this is a theory...but are there any papers or research on this? Just wondering if you've read anything to back up the circulating t-cell theory.

There is no mention of immune suppression or the immune system in relation to CCSVI research that I've seen so far, or from the presentations of the docs in Bologna....only that is doesn't seem to make a difference. Every MS patient tested has CCSVI. Even those who have had revimmune, tysabri, copaxone, (don't know about campath) etc. They still have reflux, stenosis, iron deposition, and hypoxia in the brain.
cheer

cheerleader wrote:Radeck-are there any papers or research on this? Just wondering if this is supposition, or what?

There is no mention of immune suppression or the immune system in relation to CCSVI research that I've seen....only that is doesn't seem to make a difference. Every MS patient tested has CCSVI. Even those who have had revimmune, tysabri, copaxone, (don't know about campath) etc. They still have reflux, stenosis, iron deposition, and hypoxia in the brain.
cheer

Hi Cheer, all I'm saying is that the immune system must be involved in all of this, otherwise intense immune-suppressants wouldn't keep progression away (be it for a limited time) from people who still have the stenoses.

I'm hypothesizing (therefore the title of the thread) that the immune-system could cause new lesions in other parts of the body. Stenosis as I see it creates the necessary conditions for the immune system to freak out and create havoc in multiple distinct areas of the CNS within a few weeks. We know from the phase II campath trial, which basically put relapse rate and progression to zero for years after the last IV, that you can either take away the immune system (at the risk of serious auto-immune issues and opportunistic infections), and from Zamboni's study that you can alternatively take away the stenosis (at the risk of re-stenoses). Obviously the latter is the much wiser approach in principle.

Let me know if this isn't clear. Thanks

And again, I already admitted that Marie's statement, that lesions are 99% at veins, would kill this theory for the spreading of lesions. Also, if indeed all symptoms in people with MS originate from an area affected by stenosis, this would also make immune system involvement in the spreading (though not in the causing of symptoms) unnecessary.

radeck wrote: It was just a thought I had to explain my explosion of over ten different symptoms (some of which my neuro says are spinal) within a few weeks, with no previous history of problems.

Radeck, you are not alone. This is how MS presents for many (not all, but mainly RRMS)...a dramatic flare of new neurological and motor deficits, seemingly overnight. My Jeff spent a week at high altitude and came home with numbness, tingling, bladder problems, fatigue, difficulty walking. In retrospect, we believe he had an hypoxic event (almost like a stroke) that pushed his CSSVI over the edge. Some people get a virus or bacterial infection, some give birth, some have a stressful time or physical accident as the precipitating events leading to their first MS flare. These events create endothelial disruption, increase hypoxia, strain the CNS and worsen CCSVI.
cheer

cheerleader wrote:
Radeck, you are not alone. This is how MS presents for many (not all, but mainly RRMS)...a dramatic flare of new neurological and motor deficits, seemingly overnight. My Jeff spent a week at high altitude and came home with numbness, tingling, bladder problems, fatigue, difficulty walking. In retrospect, we believe he had an hypoxic event (almost like a stroke) that pushed his CSSVI over the edge. Some people get a virus or bacterial infection, some give birth, some have a stressful time or physical accident as the precipitating events leading to their first MS flare. These events create endothelial disruption, increase hypoxia, strain the CNS and worsen CCSVI.
cheer

These symptoms suggest involvement of different areas of the brain. Since Jeff's and stenosis and mine (assuming here for a sec I have one) presumably didn't grow significantly over a week, my question is: what pushed us over the edge, i.e. why was there simultaneous "popping up" of various symptoms/i.e. involvement of several areas of the brain at the same instant? It must be a significant shock to push all these areas over the edge at the same time. I don't know if the immune system's involvement can explain this spreading.

I have a question. It is known that the MRI-visible areas of involvement in MS are around or close to veinous outlets. I don't know much about blood vessels, so I hope you, cheer, can help me out. Is the molecular structure of the vessels in the area where the "lesions" are found (are they there called capillaries, or still veins?) different than the molecular structure of similarly sized vessels that are closer to the arterial inlets of blood to the brain, which do not typically have lesions?

I'm asking because if the molecular structure is similar, increased pressure and reflux could explain the location of lesions. If the molecular structure is different, additional reasons can be considered.