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Vicc · 02-27-2007, 10:26 PM

Hi HWRSD,

I read the Veldman article and saved it, but after two computer failures that I thought I had prepared for, I can't find it today. I think I remember it well enought to show how Oaklander misused it.

Veldman has been a "voice in the wilderness" for years, pointing out that Sudek was right when he reported evidence that this disease begins with widespread inflammation. The community of RSD "experts" were still locked into the view that the disease results from some sort of abnormal sympathetic nervous system activity but could not refute Sudek, so they claimed what he found represented a rare variant of RSD and began calling it Sudek's Dystrophy; making it irrelevant to "the real" RSD.

RSD appears to be a significant problem in Holland and a fair amount of the literature comes from that country. It is such a problem that early diagnosis is important there, where red, warm skin and edema are among the primary diagnostic criterion.

Using this criterion, Veldman showed that a large number (approaching 50% as I recall) of RSD patients recovered spontaneously within six months of diagnosis; during the inflammatory stage.

At that time he was clearly unfamiliar with ischemia-repefusion injury (IRI), so he wasn't able to explain how this became what many call "cold RSD"; when skin becomes cyanotic and skin temperature drops significantly. He could only say that 28% of that sample did enter this second stage, and that this stage is usually long-lasting.

Two years after this study was published, a new researcher (van der Laan) had joined his research team and published his first article on the role of oxygen free radicals (OFRs) in acute (inflammatory) RSD. van der Laan is a vascular surgeon and is familiar with IRI.

(It was van der Laan's article that led me to begin researching the literature of OFRs that then led me to IRI, which explains every sign and symptom of this disease).

Anyway, Veldman's article emphasized that RSD begins with inflammation, and the body is better able to deal with inflammation that with the second (ischemic/hypoxic) stage. He has since published research showing that antioxidants (specifically DMSO), improve the chances of remission at the front end (the first few months).

Oaklander does use his numbers, but with the implication that they support her view that spontaneous remission is also common in ischemic/hypoxic RSD, which simply isn't true.

(By the way, the Dutch govt has mandated that antioxidants be made available to RSD patients. It can't mandate that patients use them, of course, and use of antioxidants during the second stage is too late to stop inflammation that is now hypoxia.

(I plan to begin a series of posts on IRI, and one of them will talk about symptom migration. I will talk about the science that supports the hypothesis that antioxidants can delay [if not prevent] the onset of new symptoms in other parts of the body]).

That 28% represents us; those who continued into the second stage, where spontaneous remission is so rare as to be insignificant. Oaklander's deliberate misuse of these numbers to justify her claim that people recover from second stage RSD is a major disservice to us. If we're going to get better, why bother?

Her minimizing of suicide among RSD patients is, I believe, another distortion of the numbers. My pain from nerve injuries is much more severe that the RSD pain, but it is relatively well controlled by opiates. I'm severely limited physically, but I am not tormented by uncontrolled pain. Opiates do nothing for my RSD pain, at least at the dosages I take.

Many who suffer the severe pain of full-body RSD, poorly controlled at best, who see no hope for improvement, are more likely to take their lives in a moment of despair or after deliberately planning it.

In a recent post I found myself suddenly thinking of people I have known during the past nine to ten years; I wondered how many of them had stopped posting because they chose death over living Hell. My recent posts about HBOT are the direct result of that first post.

It was wrong of me to withhold what I knew about HBO simply because I couldn't cite research confirming it. My hope now is that people contemplating suicide will first consider HBO.

Sorry, I went off on another tangent, but I was talking about suicide among RSD people, and I am convinced that many of my friends took that route.

Oaklander cites Smith's findings among nonfatal pain patients, but most pain patients don't have RSD, their pain is usually fairly well controlled, and they still see hope in the future.

Her comments about weakness in all four extremities betray a poor awareness of the fact that those who experience symptom migration suffer identical symptoms in the newly affected limbs. Atrophy is a primary sign of retrogression in RSD, and anyone who has suffered from secondary symptoms will experience weakness in affected limbs in very short order.

Her claim that RSD is often a misdianosed small fiber polyneuropathy is patently false. So far as I know, the only two disorders that present with cyanosis, severe hyper-sensitivity to cold and lower skin temperature are RSD and diabetic neuropathy. Diabetic neuropathy is the result of arterial damage that gradually diminishes blood flow to the point that nerves begin telling the brain that something is seriously wrong: the pain nerves can only send pain messages.

"Accurate diagnosis is the foundation for effective treatment". What effective treatment? Why not tell us what works, Dr Oaklander?...Vic