Hi Sandra,

Interesting stuff, and one surprise that tells me that you really do need to try every possible option when using keyword searches in Medscape and PubMed: I never saw the 2nd article in your most recent post. I haven’t done any really intensive research into the literature in the last five years, but at least once a month I scan those resources using keywords like cyanosis; inflammation; central sensitization and IRI in combination with CRPS, and Berthelot’s article never came up. Thanks for bringing it to my attention.

I probably read the first abstract on that post within a year of it being published, but I almost certainly read another Goris’ abstract (the one you posted on Carose’s thread addressed to me), even sooner, I know that because he was the only one writing about DMSO back then, and I had already decided to begin using an antioxidant in the hope that it would prevent symptom migration.

I was taking 100mg of GSE daily, but after a while I began to notice some signs of inflammation on the inside of my left wrist, so based on that Goris article, I bought some DMSO and applied it as he discussed. It would relieve the redness and burning, but a month later it would return and I would have to start smearing DMSO again.

I won’t go into the full story here, but I reached the wrong conclusion about how well DMSO works, stopped taking GSE and relied on DMSO to treat the inflammation, and soon developed inflammation in all four limbs; I learned that a topical antioxidant (DMSO) is not enough to delay symptom migration; that I needed a systemic (oral) precaution. Since 100mg of GSE still allowed inflammation to recur, I increased it to 200mg daily, and since then have noted no RSD related inflammation, not have I had any new RSD symptoms anywhere over the last ten years.

Before I began taking antioxidants, the RSD had migrated from my left to my right foot, so I know I am susceptible to migration. I attribute my 10 years of no new symptoms to grape seed extract, and urge everyone to begin using it now. It’s safe, efficacious, and others have told me that they have not developed any new symptoms since they began using it. Vitamin C didn’t protect me, I was taking it along with the GSE (I had to stop taking it after ibuprofen damaged my esophageal sphincter, as any sort of acid further damages my esophagus).

About the question in your latest post: So whets with some of us with RSD getting it systemically (full body, organ etc) and some to just one limb.
Maybe it is just that our other systemic symptoms are called other things like carpal tunnel and cardiac syndrome X.

I looked up systemic inflammatory response syndrome (SIRS) soon after I read Goris’ abstract, and quickly learned that it is an extremely rare, and often fatal disease/ This is why he wrote, asessment methods may be utilized, such as nuclear magnetic resonance spectroscopy, which cannot easily be performed in ICU patients. People with SIRS often end up in ICUs, where they usually die.

It is different from RSD in that our disease changes from inflammation to the 2nd stage symptoms we’re all so familiar with, while the inflammation in SIRS continues. I’d rather have RSD than SIRS, it sounds like a really terrible way to go.

It was interesting to read support for Goris’ view that this is a regional inflammatory response, but my problem with all three articles in your previous thread, is that they are still hung up on finding a firm neurological link to RSD; no one has found such a link in the 145 years since this disease was discovered, but they keep trying. I keep trying to persuade people to learn about IRI, because it explains every sign and symptom of our disease in both stages.

Inflammation is the key to understanding the first stage, but then it ends and warm, red skin becomes cool and cyanotic, IRI tells us exactly what happens, and how.

I’m afraid I didn’t see the eclipse, I only leave my room to use the bathroom and only leave the house to go to doctor appointments. (I used to say that if there was ever a nuclear war, I would sit outside and watch; the idea of staying around to clean up the mess never appealed to me. Had the eclipse been Christ’s return, I probably would have gone outside to watch it happen).

I’m going to reply here to your post on Carose’s thread because the article you cited there was also written by Goris: As I said earlier, DMSO alone is not a good precaution against symptom migration (it’s very messy, it can irritate the skin, and you would have to apply it every day. A systemic antioxidant like GSE doesn’t carry these problems, and, as I said, since I began urging people to take it, no one who has has reported new symptoms.

Goris used it in trials with patients still in the first (inflammatory) stage, and his results persuaded the Dutch Government to mandate that physicians make DMSO available to all RSD patients.

Van der Laan, who worked with Goris at the time, was experimenting with the systemic antioxidant NAC on rats that had been injected with OFRs, and he reported two experiments with phenomenal results. It was his research that led me to begin taking GSE; I don’t remember whether NAC was unavailable at the time, or too expensive, but I did some research into antioxidants and decided GSE was the better option for me.

Van der Laan used injected OFRs into rats to produce stage I symptoms, but OFRs alone can’t lead to 2nd stage RSD; that requires white blood cells called neutrophils, because those thingies have two jobs: They first release OFRs to destroy almost everything they touch, then they become adhesive so they can capture and consume all of they debris they create. They are supposed to die after picking up the litter (apoptosis).

In IRI (and RSD), some of them don’t die. They remain adhesive, and when two or three of them pass through OFR damaged capillary walls they enter the venule, adhere to it, and completely plug it forever. Blood enters the capillary through the arteriole, and returns to the vein through the venule, so when the venules are plugged, blood stops flowing; resulting in cyanosis and tissue hypoxia.

(If anyone isn’t familiar with some of the words I used here, don’t worry; I will talk about them in much greater detail in my upcoming posts about this disease)…Vic