Reflex Sympathetic Dystrophy (RSD and CRPS) Reflex Sympathetic Dystrophy (Complex Regional Pain Syndromes Type I) and Causalgia (Complex Regional Pain Syndromes Type II)(RSD and CRPS)

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Old 04-24-2007, 11:08 AM #1
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By example, see, “Pathophysiology of Complex Regional Pain Syndrome,” Robert J. Schwartzman, et al, Expert Review Neurotherapeutics, 2006 May 6(5):669-81, . . . at 674-75:
* * *

The recent ischemia-reperfusion model presented by Coderre and collegues is comparible with many of the signs of autonomic dysfunction and pain noted in CRPS I. Prolonged hind-limb ischemia in the art followed by reperfusion causes:

- A hyperemic and warm extremity in 4 g that evolves into a dry and shiny extremity within 4 h;
- Pinprick hyperalgesia, cold and warm mechanical allodynia that lasts up to 4 weeks;
- Contraleteral damage.

The ischemia may sensitize and activate deep tissue noceptors of muscle joints and bones which, to date, has not been explained and, as noted above, is very important in CRPS.
Err . . . "art" should have been "rat." (That's what happens when the block and copy feature is disabled in a .pdf file: you're stuck with my typing.)
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Old 04-24-2007, 11:45 AM #2
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"art" should have been "rat."
Hey Mike, that's what some of us ratists think too, now and then
all the best!
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Old 04-24-2007, 12:15 PM #3
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oh, well done.......made me laugh out loud!

my day is made!

liz
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Old 04-24-2007, 12:51 PM #4
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Dear Vic -

It is good to hear you sounding so well. (At least when you stay away from personal attacks, which brings out a definatively darker side.) I have to say that it sounds as though you're doing something right.

And for what it's worth, I haven't been in touch with Dr. Schwartzman in a couple of years. When I had a small (non-transmural) MI - which I personally attribute to inflammatory cytokines known to be produced by RSD, among them Interleukin 6 - I was no longer a candidate to participate in his research studies, and hence there was no point in flying across the county just to see his smiling face.

No, most of what I get today is from my docs in LA, specifically the part about dystrophic changes being a function of more than just loss of oxygen. There is at least in the classical model, a loss of some nerve signal that, in and of itself, contributes to a shrinking of muscle mass.

Now I know that you feel that you have shot down every article that has tried to show some damage to nerve cells in CRPS I. That said, I think it would serve you well to carefully re-read to full text of Dr. Oaklander's article, "Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy), Pain 2006; 120:235-243, a copy of which is attached. Put it another way, I know that you feel that you've previously taken care of her thesis down in a couple of sentences, but you might want to look at the article a little more carefully, where it not only survived peer review prior to publication, but has been widely hailed since it came out. Or if you just want to develop your point in further exchange with me, that's fine too.

Having said this, never say I didn't give you anything. Please find attached "Tissue hypoxia in complex regional pain syndrome," M. Koban at al, Pain 104 (2003) 149–157. I'm pretty sure you're already familiar with it, but here it is in any case.

I guess what I'm trying to say is that I don't take issue with the fact that tissue hypoxia is terribly important here, and I've felt that way since I started experiencing debilitating leg cramps, all in the absence of any blue-ish skin. I just think it's not the only answer, not when there really is evidence of nerve damage associated with CRPS I, and not when I had a non-transmural MI with no known risk factors, but one that could be explained by an immunological model. And you are well on record as having extolled the anti-inflammatory properties of grape seed oil. So why not at least take the plunge and start checking out some of the immunological literature? (The water's fine.)

Just to see if it's of any interest, check out "Mast cells are involved in inflammatory reactions during Complex Regional Pain Syndrome type 1," Frank J.P.M. Huygen et al, Immunology Letters 91 (2004) 147–154, a copy of which is also attached.

Be well.

Mike

Last edited by fmichael; 04-24-2007 at 10:39 PM.
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Old 04-24-2007, 01:34 PM #5
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Hi there,
Just a little something for the two of you, Vic and Mike. And yes it is very good, Vic to see you doing so much better.

I'm starting to see more interest in the growing evidence of genetic disposition towards developing RSD. I have scattered links which at some point this week I'll gather into a proper post for you to take a look at.

What got me started was my interest in erythromelalgia, so similar to RSD that I couldn't see the difference. But they've isolated a specific gene for it, called SCN9A

SCN9A-Related Inherited Erythromelalgia
http://www.genetests.org/profiles/etha

SCN9A-related IEM is characterized by recurrent attacks of intense pain, redness, warmth, and swelling involving the feet, and less frequently, the hands [Drenth & Michiels 1994]. Warmth is an essential part of the syndrome. During the attacks, the extremities appear red or purple and may be swollen. Commonly, the attacks occur in the evening or at night and so may not be observed by a physician. The individual may seek medical advice for painful extremities, but neglect to mention the characteristic warmth or redness (especially if limited to the soles of the feet). The symptoms are usually bilateral and symmetric. Within a family, the manifestations of the disorder may vary considerably.

However, not all erythro sufferers have this gene.

Then, interestingly, there are other complications. They found a family of 6 kids in Pakistan with a genetic mutation of the SCN9A gene. They can't feel any pain at all.

"The mutation that takes away pain"
http://www.bioedonline.org/news/news.cfm?art=3002
The researchers compared DNA samples from the six children and found that they all share a mutation in a gene called SCN9A, which is strongly expressed in nerve cells. They report their results in Nature.
The SCN9A gene encodes a 'sodium channel': one of the structures that allows electrical charge to flow into nerve cells, triggering a signal, the researchers explain. Without this particular type of sodium channel, the brain does not receive any signal that the body has encountered a pain-causing stimulus.

You can see why I'm interested; then I saw something quite recently about the "growing evidence" for gene involvement in RSD. Can't find it this minute, but will post the missing info soon.

Anyway, something for you both to think about!
all the best

Last edited by Jomar; 04-24-2007 at 04:54 PM. Reason: spelling fix requested
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Old 04-24-2007, 01:41 PM #6
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Hi,

Artist you are so brillant. Here is a article on Erythromelalgia.

http://www.erythromelalgia.org/tea/s...ythromelalgia?

Here is a book that tooks about Hansen's and why we should be thankful for the pain. At least are whole nervious system isn't whipped out yet anyway.
http://www.amazon.com/Gift-Pain-Paul.../dp/0310221447
Hugs, Roz
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Old 04-28-2007, 04:16 AM #7
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OK, Mike,

And fair's fair: If we're free to talk about the hope and promise of Jesus, I won't (and wouldn't) complain about your talking about your beliefs.

I gotta say, though, that I personally wouldn't talk about something like the rapture controversy to an audience that never heard of it. The phrase "dependent co-origination" leaves me in the dust.

On the other hand, if I had just participated in a discussion or debate on that topic with experts I totally admired, I would probably do 2500 words on the rapture (giving members a rough sketch) then talk about some of the finer points discussed. You brief summary is probably the better route.

"Tomorrow's" today now, but good luck...Vic
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