Hi Linmarie,

I developed RSD in June, 1995, and about a year later I got my first PC and began researching this disease on the Internet. It was the sort of research that would have been impossible until then; allowing me to read more than 3500 research abstracts (not all on RSD), and focus entirely on published research. It didn't take me long to learn that there is very little actual published research into this disease. More than 90% of the published literature on RSD is nothing more than opinion and speculation.

It took about six months of intensive (six hour per day) research before I was convinced that there is absolutely no evidence that this is a neurological disorder. It was thought to result from a peripheral nerve injury when it was discovered in 1863, but no one knew anything about nerves back then.

In 1916, French surgeon, Rene LeRiche, was invited to examine a wounded soldier (it was WWI) diagnosed with causalgia. He saw that everyplace the soldier reported pain was cyanotic, and based on an experience with a pt diagnosed with "...a rare sympathetic disorder", LeRiche hypothesized that the disease is the result of damage to sympathetic nerves, and not peripheral nerves as was first thought.

It made sense. The SNS exerts great (but not exclusive) control over circulation by contracting and dilating the smooth muscle that surrounds all of our arteries, so it was easy to imagine that damage to sympathetic nerves could cause abnormal vaso-constriction; compressing the arteries until only a tiny amount of blood could pass through them.

LeRiche introduced the surgical sympathectomy (severing sympathetic nerves into an extremity to stop them from constricting the arteries), and it worked. For the next 30 years, surgeons made lots of money cutting sympathetic nerves; The problam was (and is), that the surgeries only stopped the pain for about two years, then it returned; in the words of many patients "with a vengance". Doctors assumed the nerves had regrown and reconnected. They were wrong. There isn't space here to explain why, but they were wrong.

In the late 1940s, medical technology had advanced to the point where arterial blood flow could be measured and statistical averages could be obtained showing what was normal. To the surprise of RSD "experts", it was learned that arterial blood flow in RSD affected limbs was equal to, and sometimes greater than that in contralateral (opposite) limbs of patients, and of controls. Sympathetic vasoconstriction did not cause RSD.

All that I just said was prelude; showing how assumptions about the sort of nerve injury required to cause this disease seemed to make sense, but could not stand up to scientific analysis. In the 1940s, RSD "experts" lost their neurological explanation for cyanosis: SNS vasoconstriction did not cause the cyanosis in RSD. What was their response? They named the disease RSD (it was causalgia until then) and stopped talking about cyanosis.

I don't know why they did this. I'm guessing that after years of telling pts it was SNS vasoconstriction, they just didn't have the guts to admit they were wrong. So they stopped using the word cyanosis, and I mean STOPPED. You have a greater chance of hearing the Pope mutter "****" than hearing an RSD "expert" say the word "cyanosis".

I was brought up to drink my whiskey neat, vote the Democratic ticket and believe that doctors ALWAYS follow the Hippocratic Oath. Today, I don't drink, am a recovering Republican and know that when they continue to pretend cyanosis doesn't exist in RSD, some doctors are not following the Oath. They are lying by omission, and it is destroying the lives of RSD patients around the world; because cyanosis is the key to understanding RSD.

Cyanosis means that the cells are not getting enough oxygen (O2) [or nutrients (Nts)] to function properly. Our cells combine these two ingredients to generate the energy they need; it called aerobic (having molecular oxygen present) metabolism. Our cell mitochondria turn O2 and Nts into ATP, which is stored in the cell and used much like we eat an energy bar. Most of the cells in RSD affected tissue can't use this because they aren't getting nearly enough oxygen.

Our DNA is really incredible stuff: It contains instructions for everything the cells must do in order to survive and function, including an alternative to aerobic metabolism. Plan B is called glycolysis: (GeneratingATP without consuming oxygen and thus anaerobic).

Aldolase is a by-product of glycolysis, and thus, like cyanosis, just more evidence that RSD is the result of ischemia (blockage of arterial blood flow [to the cells]).

In my first paragraph I said that just about everything written about RSD is opinion or speculation. I should have said it is a splivit (ten pounds of horse-**** in a five pound bag). It could almost be funny if it weren't so tragic.

If the 100 or so "experts" who do most of the writing about RSD would just begin using the word "cyanosis" again, some researcher would start looking for causes. They wouldn't have to look far.

In 1963, 100 years after the discovery of causalgia/RSD/CRPS, researchers discovered a brand new disease: One in which a physical trauma begins a disease process in which tissue becomes inflammed and then cyanotic.

The disease, called ischemia-reperfusion injury (IRI), was discovered after the heart-lung machine allowed surgeons to block arterial blood flow to the heart (ischemia) in order to perform open-heart surgeries. The surgeries were successful, except that too many patients were dying. They looked for an answer and they found it.

The problem for us is that the physicians who know about IRI are cardiac and thoracic surgeons, and they believe it is caused by physician-induced ischemia (using tourniquets during surgery), which is followed by a complex series of ischemic events caused by the immune response to trauma.

(There isn't space in five posts to completely describe the IRI process, so (if God allows me the time and energy), I will have to write even more posts. Anyone who wishes can certainly look up IRI on the Internet and learn about it the way I did; and if you want to try, I'll help in every way I can).

Back to "the problem is": It makes sense that docs familiar with IRI think it only happens after physician-induced ischemia; that's the only way they have ever seen it happen. Few cardiac or thoracic surgeons have even heard of RSD, and even if they did, and looked it up, they would learn that the "experts" agree that it is a nerve injury. That would end their investigation.

If one of them read the word "cyanosis" in the context of RSD, that might cause their antennae to quiver: cyanosis is proof of hypoxia (a deficiency of oxygen reaching the tissues of the body), and they know ischemia produces hypoxia. But they aren't going to find that word in the RSD literature, and so we will continue to suffer from a disease that everyone (who counts: the doctors, not the patients), agree is a nerve injury. We're just along for a very bumpy ride until a few more RSD people begin demanding evidence...Vic