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

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

Hi again Mike,

Temporal and spatial distance can have a significant impact on debates here; people must either open two screens and keep switching back and forth to keep up with every point or hope their memories of what has been said before will help them understand how the words they read at the moment relate to earlier remarks.

You and I have a tendency toward complex and minute point and counterpoint that makes the latter choice an excercise in memory worthy of a Mensa contest and even switching back and forth is a challenge. So, I'm gonna try it this way and see how things work out.

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.

I try to avoid making personal attacks, but imperfect humans sometimes slip. I suspect, however, that you are referring to my frequent use of the words "liar" and "damn liar" in discussing doc S and others and those are not personal attacks. They are accusations which I support with facts when I use the words.

In addition, when I use such words in conjunction with supporting evidence, I am performing a public service. People have a right to know the truth about docs who write (or don't write) words that can have a substantial effect on their lives. Especially when potential victims may not be aware of important facts.because the people I accuse of lying are guilty of hiding those facts.

If you knew a young lady who was planning to marry a violent brute who had never given her any hint as to his real nature, and if you had a picture of his ex-wife in the hospital with a bruised and distorted face, wouldn't you consider it your duty to show her the picture?

...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.

Does "classical model" refer to the current model of RSD: i.e. that it is the result of physical damage to nerves? If so, I would point out that CRPS-I (which makes up the vast majority of CRPS diagnoses) is defined by the absence of any evidence of nerve injury. Advocates of this view of RSD tend to avoid talking about this inherent contradictions within their model.

And there you go again with the "dystrophic changes" nonsense. Write it down, Mike, I keep saying "cyanosis". If you're going to argue that I'm over emphasizing cyanosis to the detriment of other aspects of this disease, you're going to have to stick to discussing cyanosis. At this stage we're only talking past each other.

But talking directly at you: have your LA docs ever told you whether such loss of nerve signal is the cause, or a consequence of RSD? I suggest the latter.

There are dystrophic changes in RSD, and they are the result of more than the absence of adequate oxygen. Specifically; they are the result of the absence of adequate nutrients. Both oxygen and nutrients are delivered in our blood. When we see cyanosis, we see proof of inadequate oxygenation; from this we can infer inadequate nutrition.

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.

Now Mike, that's simply not true. There are just too many articles claiming that RSD is the result of nerve damage. I haven't read, much less refuted, most of them. More important, however: I have never argued against nerve damage in RSD. In fact, I write about it all the time. It's real. But it's a consequence, not the cause of this disease.

Dr. Oaklander [sic] ..... 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.

I don't argue with her evidence of missing small fiber neurons in RSD; I just don't believe she has proved that those missing neurons caused the RSD. The fact that they're missing suggests that the disease did something to make them disappear; unless you want to suggest that they did it then made their escape to avoid capture.

I suggest that "peer reviewed" is a vastly over-rated phrase. Every stupid, and every incredibly stupid article I've read about RSD was "peer reviewed"; and got published anyway. I further suggest that those who have widely praised her work have just as much stake in misinforming patients and clinicians about RSD as she. It's like calling in co-defendents as character witnesses.

I'm a bit confused by the words "develop your point further". If they refer to my conclusion that the missing fibers didn't cause RSD, it needs no further development. It stands as I phrased it.

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...I just think it's not the only answer, not when there really is evidence of nerve damage associated with CRPS I...

Tissue hypoxia is the direct result of ischemia. So is patchy osteoporosis; inhibited hair and nail growth; lowered skin temperature; painful hypersensitivity to cold; neuropathic pain; nociceptive pain; skin and subcutaneous lesions; impaired production of white blood cells and any signs and symptoms I failed to mention here. Cyanosis is the direct result of ischemia.

That's why I argue that RSD is ischemia reperfusion injury. It fully explains every aspect of this disease. It should: it is this disease and this disease is it.

I argue that both cyanosis and nerve damage in RSD are the result of a disease process called ischemia-reperfusion injury (IRI). Onc can argue my conclusions are wrong, but the only way to prove that is to know enough about IRI to show me flaws in my understanding of the disease.

Of course there's evidence of nerve damage in RSD. Any cell that isn't getting adequate oxygen and/or nutrients is going to suffer damage. In RSD, they aren't getting enough of either.

...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.)

It's grape seed extract (GSE), and the virtue I extoll is it's antioxidant properties. Oxidants (specifically oxygen free radicals (OFRs)), play a crucial role in the development of IRI: without them (or something like them) it couldn't happen. GSE neutralizes OFRs.

I'm a bit surprised you would suggest I "take the plunge" and learn about the immune system. Mike, I teach people about the immune system. It was my study of the immune system that led me to my personal discovery of IRI.

When I combined what I'd learned about the immune system, IRI and cell metabolism, my "aha" moment about symptom migration: that OFRs released during cell metabolism might explain this terrible complication. I wrote several posts on this topic at BrainTalk and plan to write another for here and for my website.

I wrote about my decision, nearly ten years ago, to begin taking GSE as a precaution, a possible way of delaying symptom migration, and I suggested that others do the same.

Over the years I have raised the fact that I haven't experienced new symptoms in other parts of my body for a decade now. Others have posted that they took my advice and have not yet experienced new symptoms. Liz said that on this thread.

I can't prove it works, it's a hypothesis that can only be proved by scientific research, but I can say that I've invited forum members who took GSE to tell us whether new symptoms have happened to them. To date, not one person has reported new symptoms after beginning a regimen of GSE. That beats the Hell out of the record for those who don't take it.

There are other, more powerful and probably more effective antioxidants out there, but I talk about GSE because it's inexpensive (about $10.00 per month), and the most widely available antioxidant on the market. And it apparently works!

Don't tell me the water's fine: I've been in it so long some fish think I must be a distant relative...Vic

Dear Vic -

Okay. I'm really trying to understand what you're saying but am having an exceptionally hard day: we're approaching the closing stage of escrow on a house that my hard working wife disparately wants and in the middle of everything late this afternoon I could just feel this tsunami of an attack overtake me and eventually drive me to bed with incredible spasms.

So my question is this - and I won't hold it against you if you don't have an answer - under your disease model, how is it that 1,200 well-placed mgs. of Neurontin really help keep this beast in check?

And then again, why is it, do you think, that external stress so often exascerbates RSD? If anything, this is the point which suggests - at an intuitive level - a significant neurological component in the underlying mechanism. I am curious as to your views on the subject.

Mike

Not fair, Mike.

Asking essay questions is a lot easier than having to answer them. Kinda like loading up the kids with homework just when they're thinking of spending Spring Break at Padre Island.

It just happens that I've addressed both topics at BrainTalk, where they were lost in an incident strikingly similar to the one the White House says resulted in the sudden disappearance of five million emails.

I've posted requests here a couple of times, hoping that someone saved my thread Why RSD Pain is Different, and that they will forward a copy of it if they did. It's the one that describes the experiment with the blood pressure cuff and talks in some detail about the role of GABAergic drugs in modulating pain.

My only faint remaining hope is that it might be on one of the disks which I routinely burned, from time to time in anticipation of the sudden demise of my old computer. It was really old in people years. It should have been on one of the more recent disks, but wasn't.


Had you raised this question a couple months ago I would probably have tried to replicate the information from memory, simply because I think its worth reading, but that was before I began to develop my concept of a website. Now I'm in the midst of writing articles intended for that site, and am busier than a one-legged man in an ***-kicking contest.

That particular material won't be introduced until several pre-requitie articles have been written and posted, however, so I won't promise to try to answer your first question in any timely manner right now.

Your second question is more easily answered, but I'm far too tired to even think of outlining it tonight. It, too, is something I think will be necessary in the website if I'm to explain every significant aspect of this disease; as contrasted with things like hyperhydrosis, which is always mentioned among the signs and symptoms of RSD despite the fact that it is a relatively rare sign of a relatively rare disease.

I'll try to collect and review all those disks in the next couple of days, then decide whether I can spare the time to write about GABAergics for this thread if it isn't found. I'll probably whip up something in response to your second question within a couple of days.

Meanwhile, want to consider doubling down? I know I've just finished complaining about time constraints, but I've really been eager to begin round 2 over that ketamine article you're so fond of. I can be pretty impulsive when it comes to having fun, so temporarily dropping everything else in favor of going toe-to-toe on this wouldn't be a problem.

Normally, this would require me to respond to what's found in that article, but you'd need to come up with something we can debate. No fair offering a long post made up entirely of excerpts: You'll have to come up with something similar to oral arguments before an appeals court; perhaps anticipating what I will say.

You're a good lawyer, I'm sure of that; bad lawyers can't afford to live in Santa Monica. I know you can come up with something interesting.

How 'bout it? Want a rematch with the kid? Well, the old guy who tries to look like a kid by wearing Willie Nelson hair...Vic

Vic, what is the best web site to read the symptoms of IRI? I am quite fascinated with all your posts and would like to read on this and I figured you would know where to begin. Keep writing .... joan

I think external stress is a BIG offender in many conditions- plus many people will internalize the external stress thus doubling the effects of it.

Vic -

No worries. I'm in S.F. with my brother catching a two day teaching of the Dali Lama on a text by this incredibly brilliant early Buddhist philospher - Nargajuna - on a topics called "dependent co-originaton" and "emptiness." Now Nargajuna is one of my favorite guys ever and I'm majorly invested in both topics, but I hate to say it that this one left me in the dust. Probably too much oxycodone. I'm hoping for better luck tomorrow.

Mike

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

Hi Joan,

I don't think there is a website on IRI that would be helpful to us. There are several reasons for this, the most important being that the symptoms we experience aren't really discussed in the context ot IRI.

Lest you, or anyone else, be tempted to wander away, wondering if I just made all this stuff up, I'd like to point out that while I am, to my knowledge, the first to talk about RSD as an IRI, some physicians have recently joined my church; even though they never heard of me or my church.

If figuring RSD out was easy, someone would have already done it, and if making the link between RSD and IRI was easy, I could read what others discovered and spend my days more profitably watching Days of Our Lives and Jerry Springer.

I have already written several posts about why RSD "experts" would never talk about IRI: They are so invested in the neurological model that they are willing to lie to hide the glaring flaws and defects in that view. I don't think experts should lie, but there really is no other explanation for their refusal to discuss why they can say CRPS-I is not the result of a nerve injury, while telling us that all CRPS is the result of same. They wouldn't lie by omission and refuse to even mention the word "cyanosis" either.

The problem with IRI experts is that they're still learning about the places it can develop. When it was first discovered, it was thought that it only affected the heart (that is, after all, where they discovered it).

Later, they learned that it can appear in nearly every internal organ (liver, pancreas, etc). Much later, researchers identified IRI in skeletal muscle (where RSD is also found).

From the beginning, they have believed that it can only occur following surgery in which ischemia (blockage of arterial blood flow) is induced by the surgeon. That's because surgeons almost always induce ischemia by tourniqueting the surgical site. They do it to stop the patient from bleeding to death while they're busy cutting things. Bleedy things.

In their view, this original ischemia is followed by a delayed immune response because the white blood cells (WBCs) can't reach the surgical site right away (the damned tourniquet is in the way). Once blood flow is restored (reperfusion) the WBCs come charging in and initiate the ischemia mediated by the inflammation that accompanies the immune response.

I argue that it is uncontested fact that trauma of any sort initiates the immune response. Hit your thumb with a hammer in it will turn red and swell up (it'll get warm, too, but nobody ever takes their thumb's temperature and you don't want to touch it while its red and throbbing). The swelling compresses nearby tiny arteries which causes ischemia.

Sooo, it boils down to this: Right now they think that the initial ischemia has to be caused by them blocking arterial blood flow, while I argue that ischemia is ischemia, no matter what the cause.

They have never, ever, heard of a case where physical trauma alone has lead to IRI. The only thing close to IRI is RSD, and the IRI experts are mostly thoracic surgeons who never heard of RSD. If they happen to have an RSD patient referred for liver surgery, and take the time to look up what RSD is, they will read what the RSD "experts" write; that it is a nerve injury. End of story.

Also, IRI researchers are only interested in stopping it. They don't want to know how bad it can get, so they don't let it get worse and watch what happens. When it was first discovered in skeletal muscle, I sorta hoped that some lab assistant would forget about one of the critters for a while, then come back a few months later and discover that the IRI had migrated to another limb. That would have caused a Hell of a commotion! But lab assistants are too efficient to forget an animal for months.

Ischemia produces hypoxia: a deficiency of oxygen reaching the tissues of the body. Cyanosis is visible evidence of hypoxia, but cyanosis is only seen in oxygen depleted blood close to the skin surface. Thoracic surgeons never see hypoxia in the organs they operated upon: too far from the skin surface.

I suspect, however, that if cyanosis were listed among the signs and symptoms of RSD, some IRI expert might someday notice the word and wonder how a nerve injury could cause cyanosis. She/he might be tempted to look further. That wouldn't work either, though, since lots of articles still talk about the sympathetic nervous system (SNS).

Those articles never mention that researchers proved the SNS isn't involved in RSD 60 years ago. People would wonder exactly how many brain cells those authors still had if they wrote that the SNS was to blame and admitted that it isn't; all in the same article. (BTW; IRI wasn't discovered until 50 years ago).

So, all that needs to happen before RSD is linked to IRI is the discovery by IRI researchers that RSD in skeletal muscle looks just like IRI in skeletal muscle. Well, there is another way: some RSD "expert" may find Jesus and develop an aversion to lying. It could happen.

There is a third way. Vic the SUPERHERO finishes his RSD/IRI website, where he posts an article intended specifically for insurance company medical review boards.

People read the stuff on the site, send the article to their insurance companies, and wait until some doc on a board somewhere reads is, sees that it might be cheaper to fix RSD people than fight us. God help Robert Schwartzmann if that happens while he's still alive.

You see, insurance companies may actually be more powerful than God. If they see its cheaper to fix us than to fight us, they will force RSD/IRI patients to undergo hyperbaric oxygen therapy (HBOT), and doc S and his ilk won't make anymore money hawking ketamine infusions.

That is my fantasy. It would make me very happy, even if no one ever mentions Vic the SUPERHERO. You see, I'll most likely be dead by then, so fame and fortune won't be a big deal for me. Being able to pass away knowing that I helped people overcome this ****ing disease; well, that would be nice.

Meanwhile, Joan, it looks like I won't be able to refer you to the website you're looking for until Allen and I finish building it...Vic