Fewer cortical lesions may explain benign MS
Here's more evidence that loss of gray matter is a significant factor in MS disability: the reason why some people have a benign course of MS may be because they have fewer lesions in their cerebral cortex. This finding comes from an Italian MRI study which compared 48 people with benign MS to 96 with early relapsing-remitting MS. The benign group had EDSS of 3.0 or less and disease duration of 15 years or more; the early RRMS group also had EDSS of 3.0 or less but a disease duration of 5 years or less. All were imaged with a new type of MRI called double inversion recovery (DIR) that can show cortical lesions.
Not only did the benign group have fewer cortical lesions and lower cortical lesion volume at the beginning of the study, but a year later only 8% had new cortical lesions compared with 40% of the early RRMS group. White matter lesion volume, on the other hand, was higher in the benign group both at the beginning of the study and at the follow-up.
i'm a little confused about
i'm a little confused about something regarding this. I understand the basics of what is being reported, but i'm not sure how lesions in the corpus callosum figure in this. I think (although i am a bit ignorant of the biology) that the cc is considered white matter, yet my understanding is that it is the path for communication between the two halves of the brain, which is why i was always told cc lesions were not good at all and caused significant problems. Does anyone who is smarter than me in this area have any ideas about this?
One of my earliest results
One of my earliest results (with corresponding symptoms) was that I had an atrophic corpus callosum. In cases of definite MS, isn't atrophy more a measure of (permanent?) disability than lesions? I think I have definite left/right problems which have worsened, but as far as I know this has never been measured (even by me except that I notice I seem to use the backspace key more). Is there no way to quantify it from one MRI to a later one? Might they not be electronically (or mathematically) superimposed? I know the older film ones are being digitized. I would think there might be a pattern of atrophy even as recognizable as the pattern of the lesions. If they are not random, what causes the pattern? Its presence was one of the first facts about MS I learned, from my radiologist. He was the first to give me a diagnosis, after a few gazillion blood tests that showed only hyper-normalcy.
You can probably test for it by counting the times you get digits or letters reversed, in typing them, or dialing them, or repeating them back to someone.
I would think that might be a good measure of driving disability. It is not being tested there either, as far as I know. I am pretty sure it was not tested on me for that. I drove a golf cart into the weedy drink when I stepped on the gas instead of the brake. I know that happens to others (especially older people?), sometimes with more dire consequences.
-Chris Sullivan
Chris, I believe you are
Chris,
I believe you are echoing everything I have been told over the years. The left-right issue and issues with driving are quite familiar to me. Additionally, i believe i have read literature about people who have had their corpus callosum severed or at least partially severed and it results in some dramatic symptoms. Maybe i should regard this study with the same skeptisism as most of the others. If I am remembering correctly, just a short time ago grey matter wasn't even considered to be an issue in MS. So, go figure.
JB
I know that a lot of
I know that a lot of research is being done about Multiple Sclerosis and new evidence is being found everyday. Will the new evidence about the “loss of gray matter” help the doctor determine when a Multiple Sclerosis patient will become disabling. Also, is there anything that can be done to slow the process down or any medication that will help?
I'm not sure whether
I'm not sure whether clinicians are currently using gray matter MRI metrics in determining how to treat their patients. It seems like a good idea but I would bet tracking gray matter atrophy is harder than identifying new white matter lesions or measuring overall brain atrophy. Finding gray matter lesions is difficult due to the fact that they don't show up well on MRI. New MRI techniques (such as 7T MRIs currently used in research) may change this in the future.
As for slowing the process down, I don't think very many treatment studies specifically assess effects on gray matter loss. However, I did find one such study on PubMed -- a small study suggesting that IFN-b may reduce gray matter atrophy.