Hey Flippnut,

You didn't raise any questions I felt needed my reply, but I do have some comments about the State of the Science [on RSD] published by the National Institute for Neurological Disorders and Stroke (NINDS).

That report is more than 6 years old; here is information from the NINDS Fact Sheet on CRPS, published in 2006 [1]:

Complex regional pain syndrome (CRPS) is a chronic pain condition that is believed to be the result of dysfunction in the central or peripheral nervous systems. This confirms what I said about no agreement about which nervous system is damaged in RSD. They just don't know; but they're neurologists, so they're committed to the idea that it MUST be the result of a nerve injury.

NINDS is part of the big lie pretending that cyanosis doesn't exist in RSD; in their list of key symptoms of this disease, they include: changes in skin temperature: warmer or cooler compared to the opposite extremity. This is distinctly different from what their Fact Sheet on RSD said in 1996 [2]: One visible sign of RSDS near the site of injury is warm, shiny red skin that later becomes cool and bluish.

Their 1996 version avoided using the word cyanosis, but certainly described it, and that was obviously going too far; so they changed it to a collection of words that don't accurately describe what happens in RSD.

Even though they begin by talking about dysfunctions in either the peripheral or central nervous systems. later in the text they frankly admit: The cause of RSDS is unknown. Those who insist on believing that RSD must be caused by nerve damage do so in spite of the facts.

The Oaklander study you posted in your 2nd reply has intrigued me for some time: If you read my first post in Facts you may not know about RSD, you saw how I demonstrated that ischemia alone can cause allodynia. I reported that neurons (nerve cells) have no energy reserves, so they are the first to show signs of hypoxic stress, and would be the first to die in ischemic hypoxia.

Oaklander reported: The skin biopsies showed that, the density of small-fiber nerve endings in CRPS-I patients was reduced from 25 to 30 percent in the affected areas compared with unaffected areas. The A-fibers I discussed in Facts, are commonly referred to as small nerve fibers.

Oaklander had no explanation for what caused this huge reduction in small nerve fibers; finding no evidence of physical nerve damage, but when cells die from hypoxia, the body reabsorbs them without leaving a trace of evidence as to what killed them. Ischemic hypoxia killed those small nerve fibers, not some sort of physical injury that left no damage to tissue surrounding those fibers.

I know this won't offer much comfort for those who argue that the "experts" are right and RSD is the result of physical nerve damage, but science is science; at least when "experts" don't pretend that obvious signs of RSD aren't even there...Vic

(I don't include you in the group that believes this must be the result of physical nerve damage; it is obvious you're struggling to learn the facts).

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