NeuroTalk Support Groups - View Single Post - Vicc is this what you have been telling us

Vicc · 02-19-2008, 02:57 AM

Hello again Linnie,

Its beginning to look like we disagree about a lot of stuff, but my wife and I disagree a lot too. but she still says she loves me, so I guess disagreements don't always make enemies. I disagree with you, and here's why:

Para 1: The abstract by doc S, et.al., makes it sound like he's a molecular biologist too; I would like to see some research supporting his claims, but he doesn't cite any in the full article either. I think he's making that stuff up.

Para 2; Research has shown that injection of norepinephrine below the site of a sympathetic block results in instant pain [1]. A ton of research has shown that adrenaline levels aren't high in RSD. This means the most logical reason why blocks work is that they block normal SNS activity, and they stop working when the brain finds another way to route its messages. And blocks always stop working.

Also, spinal cord stimulators have been shown to stimulate production of GABA at synapses, and to interrupt organically-caused pain messages (such as Diabetes and Raynaud's syndrome), but one shouldn't assume it also affects sympathetic nerves, unless tbere's research confingming that, and I've never run across any.

Para 3: I don’t endorse LeRiche hypothesis (which he later renounced), I was reporting what all the “experts” believed. In the 1940s, when they learned they were wrong, they just started mumbling “sympathetic dysfunction”, without ever showing evidence that it happens in RSD. Then, soon after the IASP totally rejected sympathetic dysfunction as a cause of this disease, the “experts” stopped talking about the SNS completely.

Now they talk about the brain and the central nervous system doing everything. But they don’t offer any research at all showing how the brain is doing it. They cite research into CS and apply it to RSD, but the CS hypothesis is only intended to explain pain when no disease process is present. Cyanosis is a disease process, so CS doesn’t apply.

And I don’t have time to skim through all those journals, so why don’t you cite a couple so I can take a peek. As I said, I don’t espouse LeRiche, nor am I stuck in 1916; I’m stuck in 1964, when ischemia-reperfusion injury was discovered; they didn't know about it when Mitchell diagnosed causalgia 100 years earlier. I think I'm "modern".

Para 4: It’s true that the SNS usually controls vasoconstriction, but as I pointed out earlier, research has shown that sympathetic vasoconstriction is not a factor in RSD [2].

Also, I would like to see any research at all into cold sensation in RSD. You say it always come first, followed by cyanosis, but I have never seen that claim before. The “experts” won’t talk about cold pain and never ever mention cyanosis, so I I’m not sure where you could have read this..

Also, if you had read my posts on IRI, you would have seen that in IRI, the cyanosis is the result of plugged capillaries. The fact that our limbs remain cyanotic so long is proof that it isn’t sympathetic vasoconstriction; if our arteries were so severely constricted (and not even arterial blood clots cause such severe cyanosis), gangrene would result.

Paras 6 and 7: I know one thing the brain doesn’t control. It doesn’t control what a white blood cell (WBC) does when it encounters a pathogen in a capillary. DNA controls that. In fact, DNA is a 100,000 page owners manual that tells the cells everyting they're supposed to do (from converting glucose into energy to dividing), without the brain doing at all.

DNA tells the WBC to do, and it tells every cell what it should be telling other cells (and they do talk to each other). DNA tells the body how to end the immune response too, and 99.999% of the time it works. When it doesn’t end properly, it’s called IRI.

I injured my foot and it turned a bright (maroon) red, and then bright, splotchy cyanosis. IRI has an explanation for that. People like doc S tell us stuff that no one except a microbiologist (or something) could possibly understand; and perhaps argue against. He talks about it, but he doesn't cite any research; we're supposed to just believe him.

Central sensitization is meant to offer a possible explanation for chronic pain (pain with no other discernable cause – mostly low-back pain). It was never intended to explain any pain with an ongoing disease process; and cyanosis is an ongoing disease process.

You apparently want to believe our brains somehow take over from a physical injury and then causes physical symptoms; I want to believe that a well-understood disease process that explains every sign and symptom of this disease is responsible. I hope others decide to find out who's right.

I write about (and debate), RSD because I believe that anyone who listens to me will eventually see that it all makes sense. The biggest barrier to understanding RSD is that we talk about cyanosis here, but the “experts” never mention it. If I can get someone to understand why cyanosis is so important, they may be willing to learn something about IRI. So I won’t mind if this turns into an exchange of abstracts. Anything to draw a crowd…Vic

A [ ] with a number inside means I will email you a copy of the abstract cited. Just click the “rsd_hbot” link at the bottom of the page and type in the title of the post and the number(s) you want to receive.