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Vicc · 12-30-2006, 03:51 AM

Hi Roz,

It would have been nice to see these articles posted while I was still trying to teach everyone what ischemia-reperfusion injury (IRI)
is, and using the words found in your posts; they would have shown that I at least knew what words to use and how to spell them.

It is impossilbe to understand RSD without understanding IRI, but it is possible to understand explanations of what IRI does, and to see the connection between that and what takes place in RSD; all you need do is trust that the person explaining IRI is scrupulously accurate.

In order to show that I'm being scrupulously accurate, all future major posts I make will cite research that anyone can read, and offer copies of that research to anyone who requests a copy. Everyone is also free to search IRI on the Internet and reach their own conclusions.

About the pig heart research: IRI was discovered after open-heart surgeries led to high patient mortality following apparently successful surgeries. Finding an answer was critical, so lots of researchers jumped onto the problem, and found the answer.

Once they found out what was killing patients, the search focused on how to prevent IRI. Researchers found that simply applying vitamin E to the heart-wound itself resulted in a dramatic reduction of post-surgical IRI. Vitamin E is an antioxidant and this has been confirmed many times as the mechanism that prevents IRI.

Since then, researchers began looking in two directions:

They began to investigate whether IRI occured in other internal organs following surgeries. They found that it does in nearly every organ in the body. More recently, they have found that IRI is found in skeletal muscle; so far they have only investigated this disorder as something that follows a surgical intervention (transplant, surgical flaps, etc).

They have not looked into the possibility that non-surgical trauma (blunt force trauma) can cause IRI because they have no reason to look; they have never heard of an instance in which this sort of trauma caused IRI. A vascular surgeon did begin to look at the possibility that RSD is actually IRI, but he is underfunded and his preliminary findings ignored by the RSD experts. I read what he wrote and began investigating IRI. I became convinced that this is an IRI, and since then have been writing about what I learned.

The second direction IRI research took was to find more effective ways to prevent IRI; vitamin E works much of the time, but it can't be applied until the end of the surgery. The pig heart study is focused on finding a medical intervention that begins this preventive process earlier. I don't believe that preventive measures against IRI will be of much use in RSD, because this disease is so rare there is no point in trying to prevent it; it won't happen to the vast majority of the population anyway.

Mike, I had planned to let our debate end with your reply; I said what I wanted to say, you replied, let everyone decide for themselves. I would have done exactly that except you misrepresented my words twice, and while others may not have noticed, I did.

Your misrepresentations did not involve questioning my accuracy in reporting medical facts, but they did distort what I said about doc S.

You wrote: To suggest without any evidence that Dr. Schwartzman was/is receiving kickbacks from these hospitalizations is, in my opinion, not only outrageous but actionable.

I said that S is a fraud who is making enormous profits from a questionable procedure. I did not suggest that he is getting kickbacks. I don't know who gets what, but I know that $25,000.00 for a relatively inexpensive procedure is too damn much money.

You wrote: On the other hand, if your point is that no effective work can be done so long as one man or group of men lives, then I don't know what to say.

I wrote that doc S and his cohorts were barriers to understanding the real nature and etiology of RSD, that he's old and should die soon and this will remove a significant barrier. I also wrote that I didn't plan to sit idly by waiting for his death; that I felt the barrier he presents is not impossible to overcome, and if the truth emerges despite him, he would be irrelevant.

But now that I'm here, there are a couple of other comments I'd like to make. The enterepenurial doctors are a straw man; they have nothing to do with the main thrust of my post, which was that there is no evidence of traumatic nerve damage in RSD (CRPS-I or CRPS-II). This forum does not, and should not, limit the introduction of extraneous ideas, but what does this discussion have to do with what I was talking about?

I would like to see you challenge the major points that I raised here; present evidence showing that RSD is the result of nerve damage. I don't know why you offered Oaklander or Albrecht, since neither of them claimed their findings showed a neurological etiology for this disease. If you can't do that, perhaps you could argue that I was wrong in saying the SNS view has been discredited; or maybe refute my reasoning in rejecting central sensitization as applicable to RSD.

I could go on, but I've previously presented research showing why sympathetic blocks affect normal -- not abnormal -- SNS functioning, and we all know that blocks don't substantially affect the future course of RSD; it gets worse with or without them.

Hoping for a more focused discussion related to the actual material found in my original post...Vic