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Hi,
I was wondering whether y'all could anwser a quick question I have?...

Why do some people present with inflammation on MRI's and others don't, even from the start of their disease?

Even if its the jugulars that are effected like in myself, no enhancement has ever shown (although ESR levels are high)


L

Dear L,

I can only give a hand-wavy answer to this. It seems to me that there are very roughly two modes of destruction of brain matter in MS: a) the-lack-of-oxygen-and-iron deposition mode, and b) the immune-system-doing-more-damage-while-it's-just-trying-to-clean-up-a-little-mess mode. Some people are more a) and others are more b). Why, I don't know. Maybe some people have more aggressive immune systems than others. In any event, within CCSVI theory the root of the problem is always lack of venous outflow and overall "ventilation" of the brain with oxygenated blood. This leads to attacks on the endothelium (lining of blood vessels), there is micro-bleeding, i.e. blood comes in contact with brain tissue, then the immune-system cleans up and in some patients (those with RRMS) freaks out a lot and causes much more damage than just the lack of "ventilation", then it calms down again starting a remitting phase.

Radeck

radeck wrote:Dear L,

I can only give a hand-wavy answer to this. It seems to me that there are very roughly two modes of destruction of brain matter in MS: a) the-lack-of-oxygen-and-iron deposition mode, and b) the immune-system-doing-more-damage-while-it's-just-trying-to-clean-up-a-little-mess mode. Some people are more a) and others are more b). Why, I don't know. Maybe some people have more aggressive immune systems than others. In any event, within CCSVI theory the root of the problem is always lack of venous outflow and overall "ventilation" of the brain with oxygenated blood. This leads to attacks on the endothelium (lining of blood vessels), there is micro-bleeding, i.e. blood comes in contact with brain tissue, then the immune-system cleans up and in some patients (those with RRMS) freaks out a lot and causes much more damage than just the lack of "ventilation", then it calms down again starting a remitting phase.

Radeck

What he said....

Good one Rad

Thanks Rad

LR1234 wrote:Thanks Rad

Unfortunately it only work as a description for you if you're PPMS.
And even if you have PPMS, you still have to explain why the immune system doesn't kick in in your case. I asked a similar question here:

http://www.thisisms.com/ftopic-8185-15.html

and understood the answer to be that there is less communication between the IS and brain in PPMS as well as SPMS patients. This makes the next question "why the lack of communication?"...

Wierdly, I am RRMS despite no enhancement

8 relapses in 9 months...that is a lot. Have you tried antibiotics? I had 3 in a row and that broke the cycle for me.

radeck wrote:8 relapses in 9 months like me

Good grief. Well at least if you end up getting treatment for CCSVI, you should know pretty soon if it's helping you.

redundant post

Gd goes where the blood goes and it leaks out at the places where the BBB is open. It doesn't just go to the brain or just to the injured areas.

It'll be good when SWI imaging is standard and they can look at the grey matter in addition to the white matter lesions. I suspect it will be very telling.

I had been dx'd RRMS for years with no inflammation, my neuro was of the opinion that I still had relapses but they were so mild because the copaxone was keeping them in check that I did not feel them.

Over that time, I progressed a lot. I am convinced it is really all about the grey matter.

I do not know why it is not showing as inflammation on some of us when CCSVI models suggest there is BBB disruption and leaking.

Bob has offered many times that there might be subtle inflammation that is missed.

I do know that double or triple Gd doses can show inflammation that was missed on smaller doses

OTOH Jamies mel used their experimental high tesla MRI and she had no inflammation on that either after hicy as I recall...but still progressed.

In other words the tools we've had to work with til now, MRI, Gd, white matter lesions images, do not tell the whole story..............

I was under the impression that when lesions were forming, it was because there was active inflammation and those are the lesions that will 'glow' when the contrast is used. Once the inflammation has subsided, it leaves scarred tissue or a lesion that doesn't 'glow' but still shows up but is not active (inflamed) any longer.

So, ALL the lesions were, at one time, active (inflamed) and if you had the MRI with contrast during that time, they would show up as active (or inflamed...and glowing).

I thought they glowed while inflamed because there was a lot more blood there, thus, the inflammation.

So, couldn't it be that the reflux blood agitates the brain tissue (and causes immune system response)...it becomes inflamed and when the inflammation subsides, you are left with the scar (lesion).

This is just the way I have always thought of it...but I would like to know if this is correct or not, hopefully, one of the "Old TIMers" or the "Poopers" will be able to corroborate or not....

Lisa aka CNClear

So, couldn't it be that the reflux blood agitates the brain tissue (and causes immune system response)...it becomes inflamed and when the inflammation subsides, you are left with the scar (lesion).

that is it!

scar tissue stays visible but is not repairable, a hyperintensity on MRI can be scar, inflammation or demyelination. The second two can reverse and repair. Scars require brain plasticity to work around..so if the nerve that used to work your hand is scarred near by nerves will try to take over the job. The brain is good at that and can be plastic up to a point.

That is supposed to be true but...I had 2 MRI's one at the start of my relapse and one band smack in the middle of it.....no enhancement.

Maybe more Gd needed to be used.