Vic...
 

I try to read all of the posts. One problem I had was that work took my laptop. I couldnt sit in our computer room for very long at all with my leg the way it is. The other problem I have is paying attention. I can only pay attenetion for a short time for some reason. But I have got my laptop back now so maybe I can read alot more! Also thank you all that post the long post with lots of info! I am trying to learn as much as I can about what I have!!!!:grouphug:

Hi Jose,

I completely agree 100% with everything you just said (is that a first :D - no, we usually do agree!). Yup, every last darn thing. It was a very thoughtful post, thank you.

So there you are, Vic, that's my input too.

First, for anyone wondering what the heck this is about, I've quoted Vic's post below. The url is:
http://neurotalk.psychcentral.com/sh...0615#post90615

OK, done that.

So Vic...well, as I have said before, I wish you'd post on a separate thread (for the more serious posts, I mean) because I, for one, hate having my own threads railroaded and try (I know, often without success!) not to do it to others. So unless someone's writing in saying "So, what about cyanosis, then?", for example, I often don't feel right about diverting attention from the specific problem or query of the poster, to whatever I might want to ask you or comment on unless it's specifically related to the original subject of the thread, which it almost always isn't.

I've told you this before, but...well, you're an ornery old cuss and seems there ain't no changing you :p. Anyway, that's why I find it hard to post back to you in situations like your first post in the Upset thread. Doesn't apply to all your posts, but it often happens.

Anyway, we do need you to keep posting, whatever you do don't stop... love ya lots!
all the best :hug:

Vic's post:
The first words in my reply on this thread were "I'm probably burning a bridge"; well, this time I may almost certainly be burning that bridge, and that bridge connects me to the people I care about more than anyone except my family.

I wrote things in my last post that I think should have caused most people to ask 'Are the experts we rely upon for accurate information about this disease actually lying to us?' But no one even hinted that they saw anything wrong in experts pretending that cyanosis doesn't even exist in RSD.

I asked you to imagine how things would be different if doctors who never heard of RSD were able to look it up and see cyanosis listed among the signs and symptoms of this disease. Do you really believe that wouldn't make any difference?

Instead, I watched this thread drop off of page one without a single comment. I'm forced to ask myself whether everyone here simply believes I'm full of ****, or whether taking this disease out of your life just isn't worth the effort of learning something about it.

I've felt this way before: At BrainTalk I wrote at least three lengthy posts about symptom migration. I talked about the science that shows that it is at least possible that oxygen free radicals (OFRs) play a role in this. I reported that taking the antioxidant grape seed extract (GSE) has almost certainly delayed any symptom migration in my life for ten years now.

I said even more: I reported that when I stopped taking GSE I developed all of the signs of inflammation in both arms and both legs within a few days. I said I couldn't prove the inflammation would have progressed to chronic RSD except by letting it happen, and I'm not going to do that, but that it is more than coincidence that the inflammation developed shortly after stopping GSE.

In the years since I wrote my first post on symptom migration I have read post after post written by people reporting that it was happening to them, that another limb had been taken by RSD. I have cried over that, then I would write another post about symptom migration, and then read more sad posts.

I don't compare myself to Dr Ignot Semmelweis, who tried to get surgeons to wash their hands; for one thing, he was reviled by the physicians of his day, while I am merely ignored, but I have some idea how he felt; knowing he had an answer that could save lives but knowing that no one would listen to him.

I'm not going to end up like Semelweis either, dying a broken man in an insane asyoum. At worst, I will die knowing I did all I could. At best, I will leave this planet knowing that my work made a difference in peoples lives. That I may be a bed-ridden cripple, but that didn't stop me from trying.

It's possible, but unlikely, that my words here will will leave some people feeling I've insulted them, and they might write replies telling me that the Forum doesn't need people like me. Enough posts of that sort, combined with no "attaboys", could drive me away. I don't even want to think of that happening and I'm sure it won't.

Meanwhile I have written thousands of words about the cause of RSD and feel that no one really pays any attention to them: like I'm pissing into the wind. You can't know how frustrating it is to know that you're right, but you can't find the right words to persuade others.

So, I'm not going to post a formal poll, but I would like to hear from others what you need to read in order to decide to take the time to find out if I'm right. It would be nice just to read that someone is paying attention, even if that someone isn't entirely convinced that I'm right.

If, as I suspect, the fact that I'm a lowly social worker arguing against experts simply outweighs anything I might write, I'd like to know that too. It probably wouldn't stop me from writing, but at least I'd know what I'm fighting.

I could understand that view, even though I've written so many words about the science supporting what I say, and made countless offers to email copies of research abstracts so you can see for yourselves that I'm not making it up. Maybe I'd just post the articles and definitions for the words I don't think most people would understand, so you could see for yourselves that I'm not peeing on your leg and telling you its raining.

I'm sure that some people here wish I would just sit down and shut up, but I probably won't do that. I would like some hints about how to make my message meaningful to you, however, because you may not believe it now but in ten years or so researchers will have proved enough to make it impossible to keep telling people this disease is the result of nerve damage.

Or maybe I'm just writing this post because I'm getting older, weaker and finding writing more and more difficult. That I'm asking for a couple of attaboys to just encourage me to keep trying. Kinda like a wife telling her husband that all she really wants is to know the he appreciates having clean socks when he needs them.

So call this whole thing a "Vic needs an attaboy" and then decide whether you really care whether I keep trying...Vic
__________________
rsd_hbot@hotmail.com

I wanted to reply to this too.
 

Vicc, you are certainly not alone in not getting post answered.

I have noticed in the last few months when people would start things that everyone scatters like a bomb was thrown in the room with all of them.

I have seen new people come on here and not get any help nor support at all. I have actually talked to several on the phone and still email with them.

As far as the oldies, they seem to have scattered also.

We need to support any and all that come on here, not just pick and choose who we do answer. If we don't know what they are talking about then yes we might skip it or come on to them and just say hi and give them some emotional support.

It has bothered me a lot about this of late and have approched it with one of the Moderators. I realize there is nothing she can do about it but I just wanted to say something about what I am seeing.

We don't all agree on everything, and that's ok. We need to be ok with what we believe in and the fact that not everyone agrees with everyone.

Jose's right. People can come on here and say the exact same thing and someone will come on and aknowledge the second or third one that said it but not the first one to say it in the same post. I don't get that part myself.

People do try to read what you have to say and we may not agree with all of it, like Jose, I can't even understand a lot of medical words and it's hard to look everyone of them up so I just try to understand what I can of the medical post at times.

I would hope I don't get any flack from how I feel about this whole issue but I just think people need to support everyone that comes on here for help and pretty quick so they don't just disappear into darkness by themselves.

Ada

I enjoy reading Vicc's posts too-
I get a bit lost on the tech jargon sometimes. But I can get the gist of it.
And my vision is goofy sometimes too- some fonts and /or colors don't have enough contrast and it makes it hard to keep my concentration.

Does anyone else have that trouble?
Are the dark fonts easier to read or keep your concentration?

I thought I posted this on one of the other threads - unless i forgot to hit the submit button.

The moderators of a forum can move individual posts to make a new thread - and it's no trouble for us to do it. All you need to do is send a PM about it to one of us.

Heya

Ada - I think one of the reasons that people sometimes get missed is that some of us that struggle with concentration/ vision rubbish automatically look for names on threads that we know - shouldn't do it I know, but I suppose it's trying to keep up with whats happening - I find that I can very quickly lose track of what has happened if I'm not careful to at least try and skim some posts.....Also, I find there are some posts that I want to comment on - but that I have nothing to say... some of your deeply personal posts about you and Bill for instance - I read them and want to offer support - but it's hard to know how to do that when I have never been in the situation you are in - and I don't want to trivialise it by comparing it to anything that's happened in my life - meaning that I can't empathise with you - and sometimes I fear that sympathy is not always useful.

I wish we could have a button that was "I am thinking of you" or something - just to say the person was in our thoughts even if we aren't up to replying or maybe haven't got anything useful to offer.

As Artist said a while ago the whole spectra of this forum seems to be changing and perhaps as members we have to try and keep up with the changes...

Thanks for your post - I didn't really think about how much I reply to people I do know etc until it.

Love

Froggsy xxxxxxxxxxxxxxx

I Also Enjoy Vic's Posts, And Although I Sometimes Get Overwhelmed With The Amount Of Information He Gives In One Post, I Am So Intrigued By The Theory He Puts Forth. One Of His Posts Was The First Thing I Read On This Sight And I Was Happy To Read Of All His Researching. I Do Not Always Comment But Do Put A 'thanks' Because I Am Thankful For His As Well As Others Input. Rsd Is Full Of 'could Be's' ... And I Am Always Open To What Doctors Do Not Say. After All I Was A Nurse And I Know Doctors Do Not Know Everything ....that Is For Sure. Joan

RSD Family
 

I am so glad to belong to this group, and truely feel like it is a family. I mean how many times do you have disagreements in a real family? In mine it is ongoing, only because we are all different, with different opinions.

I know I come here and post things my family never hears or reads, and will never know unless they find them here. They absolutely would not understand the way my RSD family understands. Sometimes I try to tell them only to see the glazed look come over their faces :p

It is good to see Vic so full of life, and I too worry when there is long silence spells. I also worry about others as well, like Condor, Gigglebabe, and really all the people I have grown to love over the years that you do not see. That list is pretty long now :(

I am also like Frogga in that if I really dont have anything to add that would help, or even sound half way intelligent, or not have the words, I will not post. Even though I do try to catch the new people, I can only sit here so long. That is why I lean on all of you, or use the great (Thanks) hot button :D

We all really do have to stick together, for there isnt very many that understand what we endure, or even really want to.

Big hugs!!

:grouphug:

vic, lowly?
 

vic.... don't try that 'lowly social worker' crap with me!....u know you've done good work researching rsd and as one who held off migration for a LONG time with antioxidants, i'm in a position to speak!

also....i posted this long ago on braintalk, when a member there questioned vic's ability and/or his "right" to do medical research....if u read it before, then skip it...if u haven't, then please note that while it may be hard for someone outside the medical profession to get their work taken seriously, that doesn't mean they're incorrect....an addition.... this was written before 2 australian doctors, who had been the laughing stock of the medical world 20 years earlier, were awarded the nobel prize in medicine for their work in CURING gastric ulcers.

Who should do medical research?

Should a Dutch merchant, who made a hobby of lenses, be given credit for amazing advances in medical science?

Thousands of scientists who have used the microscope invented by Leewenhock vote "yes".

Should an Australian women with no formal or certified training be allowed to treat children stricken with a crippling, sometimes fatal disease, in a manner opposed to the advice of neurologists and orthopedists?

Thousands of people who survived polio with no ill after effects thanks to Sister Kenny's heat and movement treatment, rather than the splint and immobilization favored at that time by doctors, vote "yes".

Should a young French chemist, whose career goals included the improvement of local wine and increasing the yield of silkworms, be allowed to work on a vaccine for a deadly disease carried by animals? or work on the public health problem of making food supplies safe?

Millions of children who grew up safe from tuberculosis carried in cow's milk, and hundreds of people whose lives were saved by Pasteur's rabies vaccine vote "yes".

Within the medical community, should researchers be allowed to investigate outside their own specialties?

Should a scientist, whose recognition is based on his work about cuckoo birds, be allowed to research and develop a vaccine for a killer, and often epidemic, viral disease?

Generations of people who have lived safe from smallpox, thanks to the work of Jenner, vote "yes".

Should a humble country doctor try to make a priceless contribution to public health and sanitation by discovering the tuberculosis bacteria? and contribute to the work of other giants in medical history, like Lister, by proving that certain germs cause certain diseases?

Millions whose lives have been saved by Koch's work on identifying bacteria, vote "yes".

Should an orthopedist be encouraged to do research in the field of endocrinology assisted only by a lab technician?

Every diabetic who has been able to lead a relatively normal life since approximately 1930, because of the work on insulin done by Dr Banting and Charles Best, votes "yes".

It seems obvious that some of the most innovative ideas come from those who are crossing disciplines, or by those looking at the facts with an entirely new perspective.

My own view is simple....anyone who is willing to struggle through medical papers and research reports looking for information that may be useful to those living with a terrible disease, is a first-class medical researcher.

Liz: An excellent post - and let us not forget that Albert Einstein worked in a patent office.

Not having a degree does not make one any less intelligent. Some members of Mensa are manual laborers. Not all are professors and doctors. People with an inquisitive mind are born that way. Not having the opportunity to get a degree hardly makes anyone less smart.

I would guess that most of us here have had to work under an "educated" supervisor who seemed to have the common sense and intelligence of a dehydrated pea. How many of us here have gone to a doctor who seemed clueless about our symptoms? Regards, Lil

Hi Liz,

It's so very good to see you back and posting in your usual perceptive and witty style
Absolutely, to both points! And, of course, the Odone's research for ALD (the Lorenzo's Oil couple).

Hope you're bearing up OK after the winter, how's that cane these days?
all the best :hug:

faulty nutrition
 

Greetings. I hadn't seen Vic's post until Sunday afternoon and had no particular inclination to enter into another round with him.

But, having been "called out" I do have one question for him. In his post, Vic says - in part - that:

It is impossible, Dr Schwartzman, to see thousands of RSDS/CRPS patients and not notice that most of them present with cyanosis; but you never mention the word.

I am frankly confused by the comment, where the disease is commonly known as Reflex Sympathetic Dystrophy and "dystrophy" is in turn defined by the [U.K. – based] “On-Line Medical Dictionary" as "any disorder arising from defective or faulty nutrition, especially the muscular dystrophies." As I understand it, these "nutritive losses can ecompass everything form a loss of oxygen to nerve signals.

Put it another way, if, by definition, we're talking about a loss of "nutrition," I don't see the issue in whether the term "cyanosis" ("a bluish discolouration, applied especially to such discolouration of skin and mucous membranes due to excessive concentration of reduced haemoglobin [sic] in the blood) is used or not, so long as the more general concept of dystrophic changes is firmly in mind. See, RSDSA, Complex Regional Pain Syndrome: Treatment Guidelines, "Introduction and Diagnostic Criteria" pp. 10-11 referencing "trophic changes" as those of the "hair, nail, skin."

The ground that’s being covered is essentially the same, and to say that it’s an area that Dr. Schwartzman has never addressed is just wrong. 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:

Autonomic nervous system and CRPS pain

. . . Several studies have provided . . . potential mechanism for the coupling of sympathetic and sensory systems. Nociceptor and mechanosensitive afferent fibers express adrenorecptors that my be activated following nerve injury. A significant increase in the number of [alpha]-1 adrenoreceptors has been reported in the hyperalgesic skin of CRPS I patients. In addition to sympathetic coupling in the periphery, CNS adrenergic neurons process and modify pain transmission as part of the diffuse noxious inhibitory control (DNIC) system. 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.

* * *

Autonomic dysregulation & edema

The autonomic nervous system is involved in other aspects of CRPS besides pain, since the diagnosis of CRPS requires that there must be, or at least have been at one time, evidence of edema, change in skin blood flow or abnormal sudomotor activity in the region of pain.

Skin blood flow abnormalities are often obvious clinically as increased redness, livedo reticularis or dusky cyantic- appearing skin. The use laser Doppler fluxmettry has enabled the quantification of skin blood flow, which is largely influenced by sympathetic innervention of the arterioles that control blood to skin capillaries. Unfortumately, an indicator of deep sympathetic control of blood flow to muscle and bone is not available.

An early study using laser Doppler fluxmetry, found that the normal reduction of skin blood flow following activation of the sympathetics by a Valsalva maneuver or cold pressor stimplation was not present in patients with CRPS, and the normal sympathetically mediated spontaneous wavelike fluctuations, known as vasomotion, were also reduced or absent in these patients. A more recent study confirms this observation by demonstrating that vasoconstriction induced by inspiratory gasp, cold immersion or mental stress was reduced in early CRPS. This sympathetic dysfunction may be transient. Evidence of reduced vasoconstriction response in very early CRPS returning to normal has been reported in a longitudinal study. The return of normal vasoconstrictor activity has also been demonstrated to coincide with recovery from acute CRPS I.

* * *

Edema is often a major component of CRPD which may be caused be sever potential mechanisms:

- Increased capillary filtration capacity, a measure of microvascular permeability, has been reported in the affected limbs of CRPS I patients;
- Increased sympathetic stimulation of the lymphatics that is under sympathetic control;
- Neurogenic inflammation.

Sensory fibers contain and release a variety of vasoactive substances from their afferent ending. Subcutaneous perfusion of one such peptide, SP, as well as transcutaneous antidromic stimulation of sensory fibers, has been demonstrated to evoke protein. extravasation. This report has been reported to be active in the affected limbs of CRPS patients. [Emphasis added; citations omitted.]

See, also, “Reflex sympathetic dystrophy,” Schwartzman RJ and Popescu A, Curr Rheumatol Rep. 2002 Apr;4(2):165-9, where the abstract reads as follows:

Reflex sympathetic dystrophy (RSD) is composed of five major features: pain, swelling, autonomic dysregulation, movement disorders, and atrophy and dystrophy. RSD is caused by an injury to a specific nerve or the C- and A-delta fibers that innervate the involved tissue. It is a progressive illness that spreads with time and may encompass the entire body. There is no psychological disposition to the problem, but all patients are severely depressed because of the constant pain, lack of sleep, and complete disruption of their lifestyle. The continuing pain is usually secondary to the process of central sensitization. The autonomic dysregulation has a major central nervous system component. Atrophy and dystrophy are partly due to loss of nutritive blood supply to the affected tissues. The movement disorder is partly due to deficiency of GABAergic mechanisms; the tremor is an exaggeration of the normal physiologic tremor. Treatment consists of decreasing the afferent pain, maintaining barrage from the underlying defect, and blocking the sympathetic component of the process. New developments include the use of neurotrophic factors to reverse the phenotypic changes that occur in the dorsal horn and the use of pharmacologic agents to block the activity-dependent NMDA channels that appear to be instrumental in maintaining central sensitization. [Emphasis added.]

Please forgive me for going on, but the point is a simple as it is fundamental. Unless I am missing something, it would appears that “cyanosis” is but a subset of the general problem of dystrophic changes, upon which much has been written through the years.

Or to recall the words of the Bard, a rose by any other name . . . .

Mike

* I will be happy to email anyone a full-text copy of the article who wants it, just send me a pm with an email address. Unfortunately, the other article cited does not appear to be available in any electronic format.

Oh, goody, Mike. I knew you wouldn't let me down.

There is a more succinct definition of cyanosis in the OMD, it reads: a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood. I like to stick to the KISS (keep it simple, stupid) model, but I know that lawyers pay the bills by confusing and obfuscating things.

The thing is, those "experts" back in the 1940s didn't want people to talk about blue to purplish skin, so they used the word "dystrophy". As I pointed out in my first reply to Bronco's thread Upset, if they used the word "cyanosis" people might ask what causes it, and they were fresh out of neurological explanations, what with the evidence showing no sympathetic vasoconstriction in the disease.

It was more convenient (expedient) to pretend the word simply ceased to exist than try to claim sympathetic dysfunction at the very moment when sympathetic dysfunction had been demonstrated to be not a factor in RSD. I can understand that: lots of people prefer pretending to facing reality

You might like to put it another way, but I'm not going to: we are not talking about a loss of nutrition, we are talking about blue to purplish skin. Blue to purplish skin means the cells aren't getting enough oxygen, and oxygen is only delivered by the arteries, which science had just proved were not being affected by sympathetic vasoconstriction. The experts back then, and doc S and you today, didn't want to talk about blue to purple skin.

The ground that's being covered is not essentially the same. Doc S and the other experts want to define the ground in terms of dystrophy, for a very good reason (and one I may have mentioned before): They have no neurological explanation for cyanosis.

And I'll be damned! Doc S actually did come close to using the C word, but in typical doc S fashion he distorts reality. The clear implication in the phrase "cyanotic-like" is that it may look like cyanosis, but it isn/t. That's just doc S, up to his usual manipulative tricks again.

In fact, the entire article appears to be nothing more that his manipulative tricks. He's either talking out of both sides of his mouth or out of both faces. The next time you two chat, you might ask him is this is the result of a sympathetic dysfunction; which his double-talk here seems to indicate, or if he still stands by his previous statements that RSD pain is caused by a peripheral nerve injury which is later assumed by the spinal cord during spinal sensitization.

You'll have to watch his lips (both sets) carefully, to see whether they are saying the same thing.

I haven't seen Coderre's presentation of this as an ischemia reperfusion injury, but I'll bet its lotsa fun to read: He is after all, the same guy who authored that silly article about ketamine therapy. (Yup, I'm baiting you again. I wasn't real happy when you tossed that in your final post during our last contratemps. You weren't obligated to honor my request that you limit your reply to topics we had already discussed, but you knew I had already said I wasn't going to make another post: that really was a cheap shot, and I'm looking forward to round two).

As to your concluding statement: The point is neither simple nor fundamental when you, doc S and the rest of the RSD "experts" want to hide cyanosis inside a box labelled "dystrophic changes".

You are correct that much has been written about "dystrophic changes" through the years. That's because these liars (doc S included) use that phrase to avoid using the C word. A rose by any other name would smell the same, but "dystrophic changes" isn't a rose; it's a splivet: ten pounds of horse **** in a five pound bag.

In both of my posts on Dana's (Bronco's) thread Upset, I asked people in our forum family to imagine how different things would be if cyanosis were listed among the signs and symptoms of this disease. I now point out how different things are because it isn't:

Instead of an agreed upon sign that leaves no doubt that an objectively identifiable disease process is going on, proof beyond contradiction that RSD is real, we live in a world where lawyers for insurance companies can argue that there is no objective evidence for this disease.

Instead of an agreed upon sign that doctors could immediatly identify and thus confirm that the pain the patient reports is indeed real, we are treated like junkies when we have to go to an ER because even our own doctors won't believe us.

I could go on, but I believe I've made my point. Doc S is a liar. He lied agan when he used the phrase "cyanotic-like". I don't know why he lies. It could be the money he makes off of ketamine; it might be that he simply doesn't have the guts to admit he was wrong all these years; or he may just be a pathological liar. Whatever his motives, he is, as I've said before, not just a liar but a damned liar...Vic

Jose, Liz, Pat, everyone; I finished my reply to Jose's post, and its a biggie: 1900 words. I was too tired to go back and edit it, and too tired to reply to other posts here, but obviously not to tired to do another thousand or so words here.

Don't be mad at me. Yeah, I'm irresponsible, but playing with Mike is so much fun

Hey Jose,

What a joy to see your post! I was instantly flooded with memories of that chat room at BT; feeling like I’m sitting around with friends at the favorite watering hole and Jose comes through the door; people calling out “Hi Jose” and “Jose’s here, we can start the party”. So many conversations about so many things, some serious, some nonsensical. We really had something good happening there.

Auntie Josie, please tell us another Bubba story. Just one more, huh? Huh? I promise we’ll go to bed right after…pleeeaaaasse.

If I had any fears that my words would burn bridges, they’re gone now. Jose’s back. And Liz came out of semiretirement to add her two cents; and Kate’s here too. I never went to high school reunion, but I have to wonder whether that would be any better than seeing so many of my good friends all posting here at the Forum on the same day.

Before I start talking about some of the things you and others have written here, I should tell everyone that I stopped taking Paxil about a week ago. I see smiles and nods of understanding; quitting the happy pills can mean major changes…so why quit?

Those of you who were here when I wrote my first post at NeuroTalk know that I was resigned to the fact that I was gonna die real soon, and that I had already decided that I would choose the time and manner of my death. I was starving myself to death; dropping from 220 pounds to an eventual low of 126 pounds, and stuffing my face wasn’t helping.

If I kept losing weight I would reach the point when I was too weak to live at home and end up in a nursing home. We know that nursing home food is not going to help anyone gain weight. I knew I wasn’t going to starve to death while enduring the indignities that go with living in one of those places, I would wait as long as I could, then I would tuck a .22 pistol under my chin.

Paxil played a significant role in making that scenario not happen, so why would I stop taking it a week ago? Paxil does other things besides help people not pull triggers: It makes the penis useless as a toy, it also makes you not care that its useless. But that was no big deal for me: my back and nerve injuries made “fun” a distant memory and I’m too homely to find anyone who wants to play with me anyway.

But Paxil also puts out the fire in the soul. I wasn’t writing about RSD anymore; I would try, but what I did write sucked. I spent ten years researching and writing about this damn disease and now, when I think I’ve finally found a way to put the words together in a way that won’t make people feel they just took too big a bite of ice cream, I’m asking “Whets the point?”

To me, the choice was between what had been making me miserable and what was making me miserable now. I’ll just have to see what happens next; I know I won’t let myself start looking at my pills and asking “Why not now?” I used to do that a lot; several times a day. I’ve gained weight, so if I see I’m not eating as much I may have to start popping the Paxil again. Maybe I’ll figure out a way to cycle back and forth so I can get something done. Right now, outside of a tendency to feel a bit sorrier for me, I’m doing ok.

I have already finished one article for the website, and I don’t think it’s a coincidence that I suddenly made three posts here after weeks of silence. And the posts on this and other threads, plus the fact that the word cyanosis appears more on page one than in the entire body of literature on written about RSD since 1950, and several “attaboys”, seem to make my decision to quit the right one.

Jose, you’re right about putting everything in one place rather than in replies to others posts. Pat (Artist) said the same thing weeks ago, and that was part of my new plan. But I can be a tad impulsive and those recent posts prove it. I guess stopping Paxil relit all the fires; I know that when I read Dana’s (Bronco’s) post I got really ******. Reading what Frogga said about it being too bad pain doesn’t turn you green was the trigger. It didn’t seem off-topic to me that pain may not turn us green, but cyanosis does turn us some interesting shades of purple. So I said it.

And I said some other things too. I thought I might get people started talking about cyanosis, but for a while it looked like I was wrong. That’s when I wrote the second post. Now people are talking about it, and as you’ve probably already guessed, that makes me feel like my words are finally accomplishing something.

And yeah Jose, I was deliberately calling Mike out. I have faith in Mike; he’s a scrapper and is intensely loyal to doc S. He could still post an interesting reply…or two…or three. So I’m prolly not gonna back away from this in the interest of peace in our time.

And you’re right about the need for long articles. If I’m ever going to convince anyone that there is a way out of this RSD ****, and there is, I’m gonna have to write a lot of words. A whole bunch of words. But this time I’m not going to over-explain until people’s eyes glaze over. I hope it works.

But before I can get anyone interested in ischemia reperfusion injury (IRI), I have to prove that it is simply impossible for any nerve injury, no matter how severe, to mediate the signs and symptoms of RSD. I just finished that article.

That’s just the beginning: ischemia reperfusion injury (IRI) is a very complex process; so complex that doctors didn’t even begin to figure it out until 1963. It begins with the immune system’s response to trauma, and I’m working on that one now. The next one will explain how this immune response goes wrong and turns into IRI.

Oxygen free radicals (OFRs) play a central role in the immune response, and it will take an entire article to explain that. Then I’ll talk about the science supporting my hypothesis that OFRs cause symptom migration and that antioxidants like grape seed extract (GSE) and DMSO can at least delay the onset of this awful complication. It will be the first article on symptom migration that doesn’t rely on things like:

Well, if this happens and then that happens, maybe the other happens, that could explain why symptoms appear in new parts of the body. I’ll write about what scientists know happens, and how putting known facts (not speculation) together really does explain it. For some really dumb speculation about how symptom migration might happen, if God has a sense of humor like Jeffrey Dahmers. email me a request for Maleki’s mostly pointless discussion of the topic. (Just click on my link at the bottom of the page and type “Maleki” in the subject line).

I hope I can fit everything about microvascular systems (MVS’) into one article, because I can’t leave that out. It is a well established fact that IRI plugs MVS, and that leads to cyanosis and tissue hypoxia. And pain and trophic changes and patchy osteoporosis and lower skin temperature.

After I write all that, I have to explain how hyperbaric oxygen (HBO) fixes exactly what IRI breaks, but only if you provide HBO at a much lower level and pressure than the industry does right now. And you can’t rush the job because HBO has to work with the body to replace millions, even billions of plugged MVS. The body can’t do that overnight. Like IRI itself, fixing the damage doesn’t happen overnight.

All of this is going to take a lot of words, and it’s going to take dedication and commitment on the part of those who want to learn. It won’t be an easy task for the reader; it took me four years of intensive study, several hours every day, before I felt I had a really good basic understanding of what is really going on.

This stuff can’t be scattered over dozens of posts, or even dozens of threads; they all fall off page one and eventually fade into oblivion. It will take a dedicated website. Good thing Allen knows how to build them.

Most people will not be willing to take the time and make the effort to learn all of this. I don’t understand why they won’t: This disease is kicking our asses, it is destroying our lives and our families. I would have thought that people would do anything to learn how to stop it, but I haven’t seen much evidence of that so far.

Hell, I’ve been writing about how to delay symptom migration for years. Others have written posts saying they haven’t had any “new” RSD since they started following my advice, and I still cry when I read new posts saying ‘it is happening to me.’ It only costs about $10.00 a month, and I spend more than that on root beer.

I do take comfort in the reasonable belief that the lies about RSD can’t survive much more than another ten years: some physicians are already talking about the possibility that RSD is IRI, and their number can only grow. Those who are still alive in 10-15 years will finally be able to get the treatment they should have begun getting tomorrow; it’s a damn shame that they will choose to suffer all that time.

Oh, and I should have dropped that part about burning bridges: If you had read the first couple of drafts, you’d have probably agreed that someone needed to take my matches away from me; but I eventually calmed down and wrote the posts all of you read. ATTABOY VIC!!! I told you you didn’t have to waste all that money on those stupid anger management classes.

Anyway, I felt kinda shot down when people didn’t respond to my words the way I hoped they would, but I got over it. Getting a bunch of attaboys from people I have loved for so many years helped a lot. And I’m a lot like a terrier: you can beat the crap out of me, but as soon as I start feeling better I’ll be right back in there, biting the Hell out of your toes.

Don’t ever feel bad about your long posts. If someone pressed me hard enough, I might be able to come up with one of your posts that could possibly not have been worth the time it took to read it. Perhaps. Most of em help more people than the one you’re talking to.

(I still remember a post from someone who loves me, a true friend. And friends aren’t people who accept you for who you are all the time; real friends tell you when they think you’re screwing up.

(Do you remember what you said when I wrote about going back to Chiapas? I do. You pretty much demanded to know what was going on in my pointy little head. You said I must be crazy to think about driving 1900 miles when I collapse in pain after just 200. You asked what I would do once I got there – if I got there. How would I find a place to live? How would I shop? Stuff like that.

(I didn’t think about that stuff. I felt so totally emasculated that all I wanted to do was go back to the place where I had proved to myself that I was a man. To the moment that I knew I was willing to die to protect my friends).

Well, old pal, I’m still here, still alive and still writing. I like to think I probably would have recovered my sanity before I drove past the point of no return, but…

Anyway, thank you for that. Thank you for the Bubba stories, thank you for this wonderful attaboy and thank you for being you…Vic

Oh, by the way, my plan to edit the Hell out of my articles is off to a roaring start. Before editing, this was about 1900 words: Now it’s 2200.

I still have things to say to my other dear friends who rushed to support me. I’m just kinda tired right now. Jeez, 1900, erm 2200 words. No wonder I’m tired. Meanwhile, I just found a toy I haven’t played with in years…

typo
 

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.)

Quote-
[This stuff can’t be scattered over dozens of posts, or even dozens of threads; they all fall off page one and eventually fade into oblivion. It will take a dedicated website. Good thing Allen knows how to build them.]

Vicc-
You can always start a dedicated thread here by adding your informational posts to the same thread each time.

Even though the thread might drop off the page in time- it will be easily search able and easy to find in the future with a link to it in the useful sticky thread.

Hey Mike, that's what some of us ratists think too, now and then ;)
all the best!

artist
 

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

Something else for you to think about...
 

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 :hug:

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