Harry and Moom--
exactly right. This is why my husband can have 20 white matter lesions and mountain bike, while our friend has one white matter lesion and cannot walk.
The only true correlation with MS disability and disease progression is gray matter atrophy. It's not inflammation, it's not white matter lesions. It's loss of brain tissue. I write about it on Facebook, for those interested in all the studies. This has been noted for over a decade,since the advent of higher powered MRI.
https://www.facebook.com/notes/ccsvi-in ... 6696872211Sadly, the white matter lesions are what could be seen, and what the EAE-based therapies could affect. But that isn't really MS disease progression or disability. It's also not about the cortical "lesions" or immune activation highlighted in the MS Society report Tracy linked. It's about overall cortical DAMAGE.
Here's what the Yale paper says about this-
Quote:
Despite acknowledgement in the early studies of MS and that the disease includes cognitive symptoms, cortical involvement in MS has been given less attention than the characteristic white matter lesions until recently. Given that cortical damage is now recognized as a major site of disease pathology, why has this occurred? The most plausible explanation is that cortical lesions are simply not obvious by the standard means of visualization (MRI and histopathology) and early macroscopic studies suggested that they represent a minor fraction of damage that occurs in the brain [8]. Cortical immune infiltrates associated with tissue damage are often sparse [9]. In the absence of an immune infiltrate, these lesions maintain a normal water concentration and therefore are not hyperintense on T2 weighted MRI like white matter lesions [10] highlighting why they are not easily visualized. Although identification of individual cortical lesions in MS are elusive, cortical atrophy in patients with MS is apparent, particularly in the hippocampus [11]. It has been established that the cortex atrophies more rapidly than white matter in patients with MS and that the degree of cortical atrophy is independent of that which occurs in the white matter [12]. Cortical atrophy correlates with the clinical progression of the disease better than the white matter lesion load [13-15].
Jeff has had a reversal of gray matter atrophy since venoplasty for CCSVI almost 3 years ago. His gray matter is plump and normal again, as shown on MRI. He continues to feel even better than he did a year ago. More alert, energized, working from 6am-midnight, traveling around the globe, alive again. I'm wondering how many more years will pass before the McDonald criteria is updated, before the EAE model is done with. It does seem that the MS specialists will try to find a way to connect the gray matter demyelination with the immune system. We'll see. But once again, it's not about lesions (even in the gray matter) it's about atrophy.
cheer
_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS 
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