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The following article appeared On the Boston Cure Project website today. Based on MRIs, it categorises those with MS into four groups:

- low inflammation / high atrophy
- low inflammation / low atrophy
- high inflammation / high atrophy
- high inflammation / low atrophy

As most of you know 'atrophy' (brain tissue loss) - scares the pants of me. If there is a God - please let me be in the low inflammation / low atrophy group!

http://www.bostoncure.org:8080/article. ... =nocomment

atrophy : How do they tell if this is present as no one has mentioned it in connection with hubby As to inflammation how do they rate that as once again I've read on natural ways to reduce it but the neurologist has never mentioned it other than to answer my questions. As to atrophy I never mention that in front of hubby as it is one of those things we have shoved in the denial pile where I hope it stays. The only time he has ever discussed it was to say he'd rather be in a chair rather than to loose his thought process. I'm all for - low inflammation / low atrophy but would rather a new heading if they'd hurry up with a cure of NO inflammation / NO atrophy. The inflammation I believe is controllable in hubby's case as allergens were I believe the major cause of that (in hubby).

Melody,

In terms of measuring atrophy - it's a case of what's not present. They can measure the volume change in the brain (as they do with Alzeimers). There's also that horrible term 'black holes'.

I agree with you about no inflammation / no atrophy. But the pessimist in me thinks that even if inflammation is eliminated atrophy may continue.

This is a bit of a chicken and egg scenario. Is inflammation the cause of the tissue damage or atrophy or is the inflammation just the body's reaction to the disease (something else going on)? Some researchers believe that inflammation may have a role in saving axons / nerve tissue!

Primary Progressive MS has relatively little inflammation (unlike RR) and that is why steroids have no benefit. However, atrophy is a feature of this variant of MS. Likewise with SP.

Until the researchers can work out the process they're unlikely to start identifying effective treatments.

Bromley

Bromley wrote:

As most of you know 'atrophy' (brain tissue loss) - scares the pants of me.




I'm totally with you on that. If I would have know about my MS in college, I probably wouldn't have "pruned back" so many brain cells on Friday and Saturday nights...

Primary Progressive MS: seems to be almost a different disease in the people I've met. We have a couple of our members(PPMS) starting with a naturopath and I'm interested to see if they will get a positive response. One thing I have noted is so many of our group give up after a few weeks or months into a game plan and will not go the distance to see if they will benefit from a few simple changes.

Some researchers believe that inflammation may have a role in saving axons / nerve tissue!

That statement could be a tad scary as I'm totally committed to reducing inflammation I'd hate to find later I'd done more harm than good. I also am not frightened of boosting the immune system although I've read so much that says that is not a good idea. I guess once again it's back to how well you know your own individual system or in my case (hubby's) to know if something should be eliminated or if you see benefit from it being added. I have both MRI's done 7 years apart can I be taught how to read them to see if I feel there is any atrophy occurring . Here is what Dr. O'Connor said for the MRI. The MRI in 1998 showed a possible lesion at (Actually have to check which) which has now been confirmed. Just as a note we are seeing Dr. Lee at Sunnybrook now and he seems to feel lesions aren't indicative of progression and goes more on what hubby is feeling.

Dr. O'Connor:His MRI is of interest in that he has only one TS hyperintensity in the white matter (June 6 2005) adjacent to the left posterior horn of the lateral ventricle. However, he has lesions at C2, T2-3, T10 and T11. He therefore has a multifocal cord disease. There is a C6-7 right paracentral disc herniation with some compression of the cord but no abnormality in the cord signal.

I don't know how the radiologists determine whether atrophy is present, but I remember a notation about lack of volume changes on the one MRI I had. The way I understand it, there is some level of volume loss with normal aging, so how they determine whether the volume is less than it should be for the age of the person, I don't know.

Black holes are not cheerful to think about, but I think those are different than atrophy - they can be pretty small dead spots in the middle of old lesions. Unfortunately my neurologist pointed some out to me and it made me quite queasy.

I'm not totally clear on the enhancing versus non-enhancing lesions, either, I figure that the enhancing lesion (with the gadolinium) is showing active inflammation, and non-enhancing are older lesions. I don't know whether older nonenhancing lesions, once present, ever go away or if they hang around forever as a spot on the MRI. I assume black holes are permanent.

The radiology side and its interpretations are unexplored territory for me (it's that queasiness factor).
Maybe someone has some good explanations or can suggest some links.

LisaBee

Melody wrote:However, he has lesions at C2, T2-3, T10 and T11. He therefore has a multifocal cord disease. There is a C6-7 right paracentral disc herniation with some compression of the cord but no abnormality in the cord signal.

This is interesting. I had a lesion at the exact site of a disc bulge in my neck. I'm wondering if the inflammation induced by the disc bulge led to the formation of the lesion, i.e., it may have attracted myelin reactive T-cells to that site.

NHE