Discussion of Vicc's Hypothesis on RSD

Vicc · 11-20-2007, 05:54 AM

Hi Linnie,

I think you may have misunderstood my explanation of norepinephrine reversing the effects of sympathetic blocks: I wasn’t suggesting that it, or adrenaline were primary vasodilators; only citing research showing that the former does reverse blocks and that adrenaline levels are increased in RSD affected limbs. From these two facts its safe to infer that the body is reacting to tissue hypoxia by increasing arterial blood flow and that this response is at least in part responsible for some of the pain we experience.

Next, you wrote: There are very compelling and highly tested reasons as to why this is a disorder of the peripheral sympathetic nervous system. As I understand the SNS view of this disease, damage to sympathetic (autonomic) nerves causes them to abnormally mediate severe vasoconstriction, suppressing arterial blood flow so severely as to result in tissue hypoxia. This was the view almost from the moment Rene LeRiche noted cyanosis in a causalgia patient (1916) and saw that as a dysfunction of sympathetic nerves.

Even the most diligent researcher can miss something, and I suspect that you may not be aware of research first done in the 1940s that led LeRiche to publicly abandon his hypothesis: Measures of arterial blood flow showed no difference between RSD affected and contralateral (opposite) limbs, or the limbs of unaffected controls. This research was later performed with more sophisticated instruments and confirmed those findings: Sympathetic vasoconstriction is not a factor in RSD.

The only difference between my hypothesis and that of LeRiche is the cause of tissue hypoxia. He believed it was the result of sympathetic vasoconstriction while I postulate that it is caused by ischemia-reperfusion injury (IRI).

You mention your experience with blood clots and pulmonary embolisms, and since blood clots in the brain are known to cause ischemic strokes it is easy to see why you might conclude that is what I’m talking about: It isn’t.

Neuroscientists would not be expected to know a great deal about the immune response to trauma, or anything about how it can go wrong and result in IRI, but once you investigate it I’m sure you’ll see that it would explain every sign and symptom of RSD in exactly the same way as sympathetic vasoconstriction. The only difference between the two is the loci of the ischemia. In IRI it takes place in microvascular systems.

My problem with what you’re saying is here: I just don't think that the science supports hypoxia as being the cause of RSD. If you reject hypoxia, you reject the SNS view of this disease, at least as I understand it. What sort of abnormal sympathetic activity do you think takes place in RSD?

In its early days RSD was known as causalgia- literally meaning "on fire". But to jump from the original trauma to tourniquet application as the causal factor is a big jump. Again, I have to suspect this comes from not understanding IRI, which today requires tourniquet ischemia and a wound as prerequisites to the disorder.

I explained why I don’t believe tourniquet ischemia is necessary in posts at the BrainTalk forum, but those posts were lost when BT crashed last year. I plan to replicate them here at NT in the near future, but I’m confident that with your research experience it would not take you long to read enough about IRI to understand my argument that the ischemia caused by inflammation and edema is sufficient to initiate the process.

I am taken aback by what you wrote next: This used to be the disorder of gun shot victims- that is how it was known. These are big traumatic events, and it is the job of the Sympathetic nervous system to mediate the response to such an event. You must know that even minor trauma is cited as the initiating event in RSD, so big traumatic events aren't necessary.

I know that vasoconstriction is a part of the sympathetic response to trauma, yet your previous statements seem to reject vasoconstriction, and the hypoxia it mediates, as causal: What sort of sympathetic dysfunction do you believe is responsible?

I don’t believe debate between us is necessary at this point; we both need to understand the other’s view first. This may be the first time you’ve heard of IRI, but as I said, your ability to understand research should allow you to learn all that is necessary in little time; it will probably take me longer to understand your view, but I’m willing to try…Vic

Vicc · 11-20-2007, 06:12 AM

Hi Imahotep.

I certainly agree that ice aggravates RSD affected tissue and may even damage it, but I don't think it is involved in most instances of this disease. It is true that a lot of people do apply ice to reduce the swelling, but edema doesn't appear until some time after the injury that leads to this disease, so it doesn't seem likely that it is a causal factor.

It seems from suffering from this condition that it is a result of infection. Of course this is hardly scientific and evidence still is weak. I haven't yet explained it in any detail, but the first post in my upcoming series will show that the signs of IRI are identical to those of an infection, because the immune response to trauma is exactly the same as its response to infection or other pathogens.

I wrote about this in posts at BrainTalk, but I wrote in more detail than necessary and no one could wade through my words; I hope my next attempt will make it easier on the reader...Vic

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