http://www.jbjs.org.uk/cgi/content/abstract/89-B/8/1069

This abstract is completely consistent with what I've been saying for years: Stopping inflammation during the first stage of this disease offers the best hope of stopping it from entering the 2nd (and much more destructive) stage.

As time goes by, I notice more and more research suggesting what I've been saying for this long time. I hope others here will remember that seven years ago, I was the only person talking about inflammation in RSD. (I'll be happy to provide anyone with abstracts by "experts" that "proved" inflammation doesn't exist in this disease.

Ok, not many people are talking about inflammation -- yet. But 7 years ago, no one was talking about it...Vic

Hi Vic
http://www.level1diet.com/157158_id
I see alot to support ischemia bud, more answers just means more questions, almost time to put the puzzle pieces together methinks.

http://www.level1diet.com/147091_id

http://www.level1diet.com/91001_id


Sandra

Did you go out and see the lunar iclipse tonight? I have been awaiting this night and we are fogged in..
it'll be a full red moon.. go look

Reflex sympathetic dystrophy: model of a severe regional inflammatory response syndrome.

http://www.ncbi.nlm.nih.gov/sites/en...arch&db=pubmed

So whats with some of us with RSD getting it systemicly (full body, organ etc) and some to just one limb.
Mabie it is just that our other systemic stmptoms are called other things like carpal tunnel and cardiac syndrome X.

Here is another interesting one too, on recent treatments:

http://www.ncbi.nlm.nih.gov/sites/en...arch&db=pubmed

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

Hi Vic..
Thank you for responding

For the most part I do not agree with everything in the articals I post..
But the IRI effects and the fact that inflamation is involved with the starting of RSD to me becomes more obvious the more I read, and I read alot.

As I read articals I watch for terms and wording to use in my searches for more info on what is striking my interest at the time.. I find myself lost in articals going deeper and deeper and it distracts me from pain the deeper I go.. yes I find some interesting stuff and alot of time I do not add CRPS or RSD to my search term but find it because of the direction of the search.
I have also set google to alert me of any new articals that include certain search words.

I totaly understand about the GSE too, and have done my best to make sure new members know of it's benifits.. hmm seems like such an insignificant term "benifits" when we now know antioxadents can infact stop RSD from happening when taken early enouph and can stop spread from happening..

Alot of people I think just can't seem to grasp the idea of antioxadents because it seems so insignificant and too simple a remedy to help enouph to actualy make a diffrence, but in reality if inflammation is the root of RSD then antioxadents are treatment needed and perhaps the lack of antioxadents is actualy a large contributer to the developement of RSD in the first place.

BINGO! My thoughts have been thus for along time and that question was looking for your answer.. it seemed so obvious to me so I started my searches without RSd and CRPS in them. Searching terms like "microvascular inflamation" etc.. being that I have symptoms full body I just compared "my" symptoms with what I was reading about and hello they are talking about my symptoms.. not very scientific but ok for a start.. helps being the one with the symptoms less confusion this way.

I am not quite ready to concede to the lack of nerve involvement yeat my friend, and that may be that I just do not have enouph information, but how do you explain the fact that the small nerve fibers are 50% less in people with RSD? and and the sensations like water dripping down my calf when anything bruskes against my leg? ishemia and cyanosis alone would not I think cause some of the symptoms we have like referred pain, electrical jabs etc however I tend to think that the inflammation causes small fiber nerve dammage, how can it not damage the nerves?

Ok lets ignore whether we feel the symptoms are nerve related and look at the whole IRI picture and what it has done to say a leg early in stage 1 or 2.. how can all that damage being done not effect our nerves and our nervous system? and what about dystonia?

I need to study this alot more before I can explain my thoughts well, but right now lets say I am starting to understand that the sympathetic system is not the culprit here, I think the reason sympathetic blocks work so well for some is that it works like a reperfusion to the ichemic condition while at the same time numbing the pain of the reperfusion action (mabie)

My first block brought momentarily an extreme pain for a minit when I lowered my legs the first time after the procedure then gone in the hot numb swollen feeling from the block. For a minit I thought they made it way worse then it fadded into a buzz of warmth.

No suprise there ALOT of treatments are so much more effective for RSD at such an early stage because at that earliest stages RSD is treatable, later antioxadents as some other treatments just staves off progression if you are lucky, and some treatments (ketamine) can put the condition to sleep for a few years or untill reinjuring it.

My recent searches are into the latteral medullary and microinflammation and norepinephrin.. interestin stuff.

However I find I have neglected the work I need to be doing right now and that I am afraid is WCB.. chronic pain and LOE's, I have till the end of this month to get a report into WCAT telling them why I feel their loss of earnings (LOE) is so patently unreasonable that it is not capible of being supported by the Canadian workers compensation act.. there are over 300 apeals here in BC that are waiting this decision by our WCB. this one is very important.

Hugs bud I hope you are well today and as always I look forward to your responses.

Sandra

This is a very interesting and stimulating topic. It sure shows that there is a lot going on here, even more than everyone realizes.

One of the things I have learned from my doctors on the subject of nerve damage and bloodflow, is that the nerves are actually the first to feel the effects of ischemia. They are much more sensitive than all the other tissues in our limbs.

What Vic is explaining right here is that the blood stops flowing, and when that happens...so does the oxygen. Plus these ofr's are traveling through the bloodstream. Wouldnt this help to spread the RSD symptoms throughout the body?

It also would explain why in most cases it stays in the limbs, as this is where there are more venules to plug.

I know Im not a doctor, but I sure can follow a map

Great stuff Sandra!

Ditto here.

Google alerts for just RSD/ CRPS so far hasn't been a great help though.

At the risk of going OT I spend a lot of time chasing down the pyramids and their builders. I find it very therapeudic to be googling the various things and the results. There is a little problem, though, if I concentrate for more than a few minutes. I guess I forget to supress the pain and it comes roaring back. It's still a godsend to have things to stay occupied and the computer accounts for more than a little of that.

Hi Allen,



This is what occurs in Peripheral vascular disease when there is permanent damage to the small vessels in the periphery. The skin becomes cyanosed and stays cyanosed as the vessels rarely improve their status.
As most of us with CRPS have TRANSIENT cyanosis accompanied often by a myriad of all clours of the rainbow then we do not have permanently plugged vessels as they do not have the capacity to suddenly unclog and get a blood supply.
The transient changes are a typical autonomic nerve response.
Some people with CRPS may also have peripheral vascular disease and thus permanent cyanosis and sometimes with worsening CRPS as vasoconstriction becomes more of an issue then cyanosis maybe there much of the time.

I have as severe CRPS as can be had, I have cyanosis sometimes but more often I am bright red and burning---a sign of vasodilation and not of clogged peripheral veins.

This is a highly discussed and often emotive topic but it must be continued to be discussed .
Cheers and hope you are doing OK
Tayla

Tayla,
I also am more like you in that I have the bright red & burning happening more than any cyanosis. In fact my feet are cold only when they become cold due to being down or on the floor or out in the car but especially shopping. I haven't had the actual bluish/purplish colors even mildly since the first LSB's were done. And most of the swelling is gone also. Except for them becoming too tight after wearing them for long periods I still need to wear size 11 wide width shoes. But early in the day can wear size 10 med width shoes. And I have RSD in both feet, and it happened at the same exact time, altho the left is worse.

In the beginning years, been at this for 5 yrs, altho only 4 have been DX'ed, they never became cold no matter the weather conditions. Just each yr now in winter becomes worse, & even some summer days they can become cool to cold feeling.

DebbyV