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Differential matrix metalloproteinase expression in cases of multiple sclerosis and stroke

Multiple sclerosis (MS) and stroke pathology are characterized by blood–brain barrier breakdown, leucocyte emigration, and tissue destruction. Each process is thought to involve the matrix metalloproteinases (MMP), but little is known of their expression. We undertook to investigate whether MMP expression is dependent on the nature of the CNS lesion and whether expression would coincide with the histopathology. MS or cerebral-infarct tissue was examined for the presence of gelatinase-A, gelatinase-B, matrilysin and stromelysin-1. Gelatinases A and B and matrilysin expression was found to be up-regulated in microglia/macrophages within acute MS lesions. In active-chronic MS lesions, matrilysin and gelatinase-A expression was pronounced in the active borders. In chronic MS lesions, the expression of matrilysin was confined to macrophages within perivascular cuffs. The pattern of MMP expression in infarct lesions differed considerably. Gelatinase-B was strongly expressed by neutrophils in tissue from patients up to 1 week after an infarct, whereas gelatinase-A and matrilysin staining was much less marked. From 1 week to 5 years, neutrophils were absent and the large number of macrophages present were expressing matrilysin and gelatinase A. Only a low level of gelatinase-A and matrilysin expression was observed in normal brain controls. Thus, MMPs are expressed in inflammatory lesions in the CNS, but their individual expression is dependent on the nature and chronicity of the lesion. However, the general pattern of expression, in perivascular cuffs and in active lesions, supports a role for these enzymes as mediators of blood–brain barrier breakdown and tissue destruction, both in MS and in cerebral ischaemia.

This is the one orion linked. I don't understand it well enough to say what it means but it's interesting.

1eye, all your attacks were there in the morning? I would be afraid to lie down to sleep. I would think too that something postural or jugular was going on.

We have not talked much about reperfusion injury but it must be a part of the cycle with MS. Here's the wikipedia on it:

Presumably in CCSVI, it is low-grade oxgyen deprivation, not total ischemia, although there would also seem to be trigger events where oxygen levels are stressed (perhaps childbirth, perhaps time spent at high altitudes).

I also think about my own procedure and the dramatic brightening of colors afterwards. The assumption is that the brightening was due to a restoration of normal brain oxygen levels.

So are we at risk of reperfusion injury, either in the normal course of our MS/CCSVI or immediately after the procedure, if the degree of oxygen deprivation was relatively severe?

We have known a few patients who have gotten worse immediately after what seemed to be a successful procedure in terms of no clotting and the blood flowing properly. We haven't had a good answer for that. It's only been a few cases.

Reperfusion injury may be the name for what we've been experiencing all along, when we talk about the white blood cells attacking. Steroids or DMDs would be effective against this. It can be an excessive reaction to the injury, so that as much or more damage is done by the white blood cells' attack as it was by the initial oxygen-deprivation injury.

Cheer has been saying all along that MS may be more comparable to a series of ischaemic events.

As for if reperfusion injury might occur (particularly in more easily inflamed brains?) as an immediate result of CCSVI treatment, I don't know. Hypothermia and hydrogen sulfide are the only things listed in wikipedia as protective against reperfusion injury. Presumably most of us have low grade chronic issues rather than acute, but we also have areas of CNS damage that might be particularly vulnerable to another insult.

...... Here's the paper Dr. Dake was talking about.
Changes in Cerebral Perfusion precede plaque formation in MS
http://brain.oxfordjournals.org/content ... 1.full.pdf
cheer