[Vicc]

When we visit a doctor (except, of course, one who works for the insurance empire), we assume he/she combines science with other learned skills and experience in order to figure out whether we have a medical problem; if so, what; and find a way to treat it if treatment or an effective therapy is possible. We believe that of the doctors who treat us for our RSD.

The truth is, however, that our doctors can’t use science to understand RSD, because there is absolutely no research showing what causes this disease, how it spreads or how it progresses. There is no science telling anyone that this is a neurological disorder. Without research identifying something about the nature of a disease, speculative conclusions about it can result in attempting to tread a problem that doesn’t exist while ignoring the one that does.

Doctors talk to us as if nerve injury in RSD is a proven fact, but when we stop to think about it, we know this isn’t true: The reason there are two diagnoses: CRPS-I, where no nerve injury can be identified, and: CRPS-II, where the RSD is attributed to a nearby nerve injury, is that there is no evidence that CRPS-I is caused by a nerve injury. CRPS-I patients make up the vast majority of RSD people.

(CRPS-II is equally hampered in that no one is able to describe how a nerve injury can develop into all the signs and symptoms of this disease, which can involve dysfunctions of every one of our nervous systems. It doesn’t leave a trace of evidence, hopping from one nervous system to another without any sign of any nerve damage in its wake. Science demands evidence, and no one has yet provided any evidence that it is even possible for nerve damage to produce the signs and symptoms of CRPS-II, much less that it really does).

The fact is that doctors aren’t dumb, they know that it is unlikely that two disorders with two different etiologies would develop identical signs and symptoms; that it is much more likely that both disorders have the same cause and course. They tell us that the causes may be different, but they have chosen to assume they aren’t; that CRPS-I is also a neurological disorder even though they have no evidence that it is.

Most doctors who treat RSD patients have never investigated this disease; they are too busy treating patients to devote the time necessary for this sort of independent research into a disease that only affects a small percentage of their patients. Researching every disorder they treat would be like trying to reinvent a wheel for every use. Physicians read what the experts have written and assume the experts are right; unfortunately, history is filled with examples of experts who were wrong, and there is no reason to believe it can’t happen today.

The reason Mitchell assumed causalgia resulted from severe nerve injuries is simple: he couldn’t think of any other conceivable explanation. Physicians who followed him couldn’t find any other conceivable explanation either, and through the passage of time Mitchell’s assumption somehow became incontrovertible fact. Facts are based on evidence, however, and there is simply no evidence that Mitchell was right.

You may be thinking; “Of course there’s evidence, everyone wouldn’t agree that it starts with a nerve injury if they weren’t sure of that fact”.
There is one way to prove I’m wrong, you can read everything written about this disease in the medical literature, find documented research and post it here.

The problem is that this takes time, a lot of time. I researched RSD for two years and didn’t get close to reading even half of it. I stopped when I realized I had gone back far enough that I was reading “facts” that had later been disproved. It is much easier to confirm what I say by simply by reviewing the history of causalgia/RSD/CRPS:

RSD was first discovered during the Civil War (1863). Dr Weir Mitchell was a neurologist, but we need to keep in mind that not much was known about neurology 140 years ago. He thought it involved peripheral nerve injuries severely traumatized by high velocity impacts from gunshots and shrapnel. Either the speed of the projectile or the widespread damage it caused resulted in an unending and widening painful response by an increasing number of nerves of the peripheral nervous system (PNS). Mitchell called the disease “causalgia”.

The next major discovery came in the midst of another war: World War I. French Army surgeon Rene LeRiche noted that the painful areas of wounded soldier’s skin was cyanotic. He knew that a sympathetic nervous system (SNS) dysfunction also caused cyanosis, so he hypothesized that this disease might be the result of damage to sympathetic, not peripheral nerves.

He proposed severing sympathetic nerves entering the affected area to relieve symptoms, tried it, and it seemed to work; patients got dramatically better almost overnight. Later, other physicians more knowledgeable about the SNS explained exactly what happened in RSD: During this era everyone had RSD; not RSD-I or RSD-II.

Accoring to experts back then, the high velocity impact damaged sympathetic nerves, deeper within the tissue, without actually coming into contact with them. The SNS controls blood flow by dilating and contracting the arteries, and in this disorder it was abnormally contracting them, reducing blood flow into the affected area.

REFLEX: an involuntary response. SYMPATHETIC: self explanatory. DYSTROPHY: a word pertaining to nutrition. (e.g. cells are not getting nutrition from arterial blood.

RSD: an involuntary and abnormal SNS response (to trauma) that lowers arterial blood flow to tissue resulting in diminished delivery of oxygen and nutrients to tissue. Causalgia suddenly had a new name, a new explanation and a cure.

Well, it wasn’t a cure; for most patients the pain returned in about two years. This was easily explained, the severed nerves had regrown and reconnected; but second sympathectomies, both above and below the original surgery, failed to again reduce the pain. By all logic, they should have, since the nerves were again severed. The operation didn’t cure the patient.

Another problem appeared: sympathectomy patients had reduced SNS control of arteries in previously unaffected areas below the site of the RSD, blood would pool in the feet of patients who had undergone sympathectomies for RSD of the thigh, knee or calf. Obviously not all of the severed nerves had “regrown” and reconnected, perhaps none had.

This new explanation fell apart in the 1950s when researchers discovered that arterial blood flow into RSD affected tissue is not diminished, that it in fact is equal to, or even greater than, arterial blood flow into unaffected contralateral limbs and is generally the same as in non-RSD affected controls. Damage to sympathetic nerves is not causing abnormal vasoconstriction.

LeRiche had had enough; he publicly abandoned his hypothesis as untenable. Other doctors were unwilling to give up on the SNS. From the 1950s to the early 2000’s they confidently told patients that the SNS is the problem, despite the fact that they knew better.

Younger physicians probably read the SNS explanations that are still being written today, and may have never learned about the research showing that abnormal SNS vasoconstriction is not the problem. Only two or three researchers have recently replicated those earlier studies, achieving the same results, and you have to carefully read everything written about RSD if you are going to stumble on these studies. You won’t find them cited at the RSDSA website.

So, doctors continued merrily doing sympathectomies (and raking in money), but the popularity of this operation eventually waned as newer surgeons learned that they provided only temporary relief and caused impaired circulation below the surgical site. Today, only a few surgeons recommend sympathectomies, and then only in the most severe, intractable cases.

We can count ourselves fortunate, if the sympathectomy had only begun being introduced in 1990, most doctors today would be telling us to have one done. Our predecessors paid the price for their doctor’s mistakes. When I joined the other forum about 9 or so years ago, there were still a couple of members who had undergone that operation and, of course, still had RSD.

It took the experts 50 years after proof that the SNS doesn’t cause RSD before they finally stopped talking about it (some of them still do). Today, it is CRPS, and Schwartzmann (the RSD guru, who once wrote about permanent recoveries from sympathectomies), now tells us that indeed, CRPS is the result of a peripheral nerve injury; not just CRPS-II but CRPS-I also.

Dr S (and others of this opinion), offers absolutely no evidence showing any peripheral nerve damage in CRPS-I, but then no one has ever shown that those nerve injuries found in patients diagnosed with CRPS-II are linked to the signs and symptoms of this disease), but he is THE EXPERT today, so people assume he must know what he’s talking about.

Doc S doesn’t stop with a peripheral nerve injury, however. He tells us that the transmission of pain messages to the brain is later taken over by nerves in the spinal cord. He bases his conclusion on research into what physicians now call central sensitization or autonomous pain. Pain that continues long after an injury has healed. In this he is making a scientifically untenable link between chronic pain and RSD pain.

It is untenable because nearly all of the research into autonomous pain has involved patients with chronic lower back pain that doesn’t have an evident medical explanation. Patients with chronic low back pain who showed any evidence of any real or even possible injuries were excluded from these studies. Researchers wanted to learn why people feel pain when no cause for the pain can be found.

Aside from pain, which is described as subjective, there are objective signs of RSD: Lowered skin temperature; osteoporosis; decreased hair and nail growth, and, even though Dr S avoids using the word; cyanosis. These are objective signs of a disease that also causes pain, and are reason enough to exclude RSD patients from this research.

This leads to a third reason Doc S’ is scientifically untenable: RSD pain has never been part of any research into autonomous pain. You can’t simply lift a body of research into one thing and try to apply it to something entirely different, simply because you want to. You need to provide evidence that the research can be linked to the disorder you are trying to link, something S hasn’t bothered to do.

There is yet a fourth reason this research can’t be applied to RSD: This disease actually involves three kind of pain: burning sensation of the skin; allodynia, and; painful hypersensitivity to cold. It is nothing like the unexplained chronic low back pain that was studied.

There is a simple reason why I’ve chosen to focus on discrediting Schwartzmann’s claims: they are being quickly integrated into “theories” about RSD and they are wrong. Dr S has chosen to lead the peripheral nerve injury and central sensitization parade. He is THE EXPERT and he’s leading a parade in the wrong direction.

(I also think he’s a fraud who is doing everything he can to divert others from paying attention to the admittedly still very small amount of research pointing toward a non-neurological cause for RSD while busily lining his pockets with enormous profits from a relatively inexpensive procedure: outpatient ketamine infusions, but that’s just my opinion).

Therapies for treating RSD don’t work. Hope that ketamine would provide the panacea is not being fulfilled; the one member from the other forum who went to Germany for the “coma technique” returned without any recovery and with complications resulting from poor screening for other medical disorders.

Outcomes from outpatient ketamine infusions reported by forum members range from months of relief to none at all. Repeat infusions are being done despite the absence of any research into the safety of multiple doses of the drug, which is licensed as a surgical anesthetic and only a small percentage of the population can be expected to have as many as three surgeries in a year.

A TV commercial for a big cancer center tells people that we have to take responsibility for our recovery. RSD is destroying your life; the FDA will (hopefully) never approve the German coma method, and; outpatient infusions offer temporary relief for some, but there is no data on how many times this procedure will be effective.

Some of you know that I have written countless posts at the other forum about another disorder that is too remarkably similar to RSD to overlook, even though the medical profession has overlooked it for years. The disorder I describe wasn’t discovered until 100 years after RSD, so no conceivable explanation was even possible for a century after Mitchell discovered it.

Now there is an identifiable injury that, I believe, makes more sense than nerve damage that no one can find, or when nerve damage is nearby, no one can link directly to RSD. I can’t prove it, because the research necessary to link it to RSD hasn’t been done, but I think anyone who takes the time and effort to study will agree it is a more likely explanation than nerve injury.

I don’t think my words are going to persuade anyone to reject the neurological view of this disease. I see my role, and my goal, as finding a way to get others interested enough in what I say to decide to learn for themselves whether the disorder I describe (called ischemia-reperfusion injury [IRI]) is the most likely explanation for RSD. I try to do this by:

Describing how the IRI process begins, using words more people can understand. This involves teaching how the immune system responds to cell debris from physical trauma, how this immune response usually ends and what happens when it doesn’t end as it should.

Describing what has been shown to occur during the IRI process that leads to the destruction of hundreds of thousands and even millions of microvascular systems (the arterioles, capillaries and venules that deliver arterial blood to the cells and return “used” blood to the veins), making it impossible for arterial blood to reach the cells served by these systems.

Describing how this blockage of arterial blood flow to the cells affects soft tissue; bone, nerves and the body’s natural healing.

Since this involves teaching the reader facts you need to understand about how the immune and microvascular systems function, necessary before you can begin to understand how they malfunction, it involves lots of words. These processes are complex and the reader can’t learn them by simply skimming what I write. It may take several readings to understand each step.

It is easy to think of me as just Vic, another forum member, and not as someone who has carefully researched every word I write. I can’t do anything about that except keep writing and hope other members will decide that my dedication to this education process reflects my conviction that RSD is an ischemia-reperfusion injury, and that “my doc isn’t really helping me, the experts haven’t come up with any real solutions, I have time on my hands, so why not look further?”

In order to confirm that the facts I present are really facts, I will list citations as if there were a bibliography. When I actually posted biblios and offered copies of abstracts to anyone requesting them, no one ever asked for even one.

This time, anyone who wants to read the actual research abstracts need only press the link to my email address (on my signature line), type in the title of the post and the citation numbers you want to read, and I will reply with the abstracts included as attachments.

Please keep in mind that I’m still very weak and that I’m working on the article I plan to submit for publication. I don’t have the time or energy to reply to multiple requests for abstracts. If you wish to read that much research, and it aint easy; there will be lots of words you won’t understand, you will be better served by researching ischemia-reperfusion injury on your own.

As long as God chooses to keep me on this planet and allows me enough strength to continue writing about RSD, that is exactly what I will do. Maybe not as often as in the past, but as often as I can…Vic

[dreambeliever128]

Hi Vic,
I read most of what you have wrote and I did put this into save so I can read the rest of it and run it off also so I can have a copy to read.

We had a guy in our group that went down to see Dr. Swartzman and all I could see that he got from him was a Tshirt showing where his RSD is. The Dr. had this test done that shows the RSD areas in Red and the area that is well in green. Then this guy came home and had a tshirt made by the test results.

As far as I knew he didn't do anything medical for him. He stayed down there 2 weeks.

I watched Montel one day and he said that diseases that donot have enough people with them to warrent money going into the research was caused Orphan disease. I had never heard that term used before.

What you are saying makes sense. I was also diagnosed with Central Sensitization Syndrome and I was told because I had it a pain pump wouldn't work for me. I think that was a line of bull to save money from not putting the pain pump in. One other girl on this forum had saw the same Dr. I saw and he had told her the same.

I would say that these Drs. are doing a lot of guessing on what to do for us to help us. If the research isn't being done to find out more about this disease and what to do for it then it just stands to reason they are experimenting with the meds they do use.

When my RSD comes out full force I have no meds here that does anything for the pain. I have had ketamine and lidocaine shots and they do help for some pain but I can't say it's for the RSD pain.

Thanks for such an interesting essay to read and learn from.

I am glad to see you post and I hope you are doing better.
Ada

[fmichael]

Dear Vicc -

You will pardon me if I say that I think you are being a little hasty in knocking Dr. Schwartzman as a man who represents all in your view that is wrong with the treatment of RSD by the medical establishment in this country. I can tell you that I was his patient for a number of months in 2004. I ultimately wasn't enrolled into either the high-dose ketamine study in Germany or a low-dose ketamine study he was running at his hospital in Philadelphia, due to a couple of disqualifying physical conditions, but I can tell you that he was about as compassionate and caring a doctor as I think I've ever met, and I've known a few. (Forgive me old friend, but this discussion seems very familiar, we may have gone through it once before on BT1.)

I know you prefer abstracts to articles, but thanks to the assistance of the RSDSA Medical Articles Archive at http://www.rsds.org/2/library/articl...ive/index.html there are now a lot of important studies that we can all have free full-text access to, studies that go directly to a number of issues you've raised.

First of all, on ketamine, I think the most impressive study I've seen is "Subanesthetic Ketamine Infusion Therapy: A Retrospective Analysis of a Novel Therapeutic Approach to Complex Regional Pain Syndrome,"Correll GE, Maleki J, Gracely EJ, Muir JJ and Harbut RE, Pain Medicine, 2004; 5:263-275 (following the first course of therapy, 54% of 33 individuals remained pain free for ≥3 months and 31% remained pain free for ≥6 months, after the second infusion, 58% of 12 patients experienced relief for ≥1 year, while almost 33% remained pain free for >3 years). I don't know about you, but I find those numbers to be impressive. Especially where every suggestion of a mechanism of action is tied to ketamine's role as an N-methyl-D-aspartate (NMDA) receptor antagonist. But granted, it doesn't cure everyone.

Moving on there is the assertion that no evidence has been put for identifying CRPS-1 with any actual nerve injury, I refer you to two articles that appeared earlier this year in the journal Pain. The first article was "Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy)," Oaklander AL et al., Pain, 2006;120: 235-243 (showing a significant deduction epidermal neurite densities among CRPS-1 patients). For a short article/press release written in plain English on the significance of this study, please go to the following link to EurekAlert! dated January 30, 2006: http://www.eurekalert.org/pub_releas...-sfn013006.php

The next was "Pathologic alterations of cutaneous innervation and vasculature in affected limbs from patients with complex regional pain syndrome," Albrecht PH, Hines S, Eisenberg E, et al., Pain, 2006;120: 244-266 ("in CRPS affected skin, several neuropathologic alterations were detected, including: (1) the presence of numerous abnormal thin caliber NF-positive/MBP-negative axons innervating hair follicles, (2) a decrease in epidermal, sweat gland, and vascular innervation, (3) a loss of CGRP expression on remaining innervation to vasculature and sweat glands, (4) an inappropriate expression of NPY on innervation to superficial arterioles and sweat glands and (5) a loss of vascular endothelial integrity and extraordinary vascular hypertrophy; the results are evidence of widespread cutaneous neuropathologic changes").

Finally, in the interest of open academic debate, an editorial by two German researchers who have long been critical of any unitary theory based upon peripheral nerve disorders was also printed by in the same issue of the journal. "Is CRPS I a neuropathic pain syndrome?," Janig W and Baron R, Pain, 2006;120:227-229.

All of these articles can be accessed through the RSDSA page with the free Adobe Acrobat Reader program, and while I leave everyone to their own judgment, my reading of the Janig and Baron piece was that their criticisim of Oaklander's paper was particularly weak. Using what looks like an old litigator's trick, they direct most of their fire first at Albrecht's study [read: the straw man] not saying all that much about Oakander's article, one which I understand met a lot of excitement on it's publication, as showing the strongest link to-date between CRPS-1 and actual changes in peripheral nerve physiology.

And as far as Dr. Schwartzman is concerned, he's still out there publishing away. I put this up on another thread this evening, but it bears mention here as well: "Changes in immune and glial markers in the CSF of patients with Complex Regional Pain Syndrome," Guillermo M. Alexander, Marielle J. Perreault, Erin R. Reichenberger, Robert J. Schwartzman, Brain, Behavior, and Immunity xxx (2006) xxx–xxx [Epub November 28, 2006], abstract:

Complex Regional Pain Syndrome is a severe chronic pain condition characterized by sensory, autonomic, motor and dystrophic signs and symptoms. The pain in CRPS is continuous, it worsens over time, and it is usually disproportionate to the severity and duration of the inciting event. This study compares cerebrospinal fluid (CSF) levels of pro- and anti-inflammatory cytokines, chemokines and several biochemical factors (glial fibrillary acidic protein (GFAP), the nitric oxide metabolites (nitrate plus nitrite), the excitatory amino acid neurotransmitter glutamate, calcium, total protein and glucose) in patients afflicted with CRPS to levels found in patients suffering with other non-painful or painful conditions. The aim of the study is to determine the degree of involvement of glial cells and immune system mediators in the pathophysiology of CRPS. There was no elevation or reduction of a CSF marker that was specific for CRPS patients. However, there were several patterns of markers that could be helpful in both elucidating the mechanisms involved in the disease process and supporting the diagnosis of CRPS. The most common pattern was found in 50% (11 out of 22) of the CRPS patients and consisted of; elevated IL-6, low levels of IL-4 or IL-10, increased GFAP or MCP1 and increases in at least two of the following markers NO metabolites, calcium or glutamate. The results from this and other similar studies may aid in elucidating the mechanisms involved in the pathophysiology of CRPS. A better understanding of these mechanisms may lead to novel treatments for this very severe, life-altering illness.

As noted in the other thread, I will be happy to email a full copy of this article to anyone who want it, just send me your email address via a pm. (Personal, non-commercial use only, please.)

Lastly, I know that sometimes I come across as a trained monkey who's pretty good at stringing disparate materials together, whether or not I actually understand them. And there may be some truth to that, where that's a good part of that on a lot of the preliminarly stages of most legal research projects. Nevertheless, these articles are out there, they're free and I think it behooves us to make the most of them. In the meantime, maybe antioxidants will prove to be the Holy Grail. I'm not ruling anything out.

Be well,
Mike

[fmichael]

Bumping to highlight insertion of link to EurekAlert! - plain English - press release on Oaklander article.

[carousel]

I think that some years from now, the fact/fiction/ and rsd will meld and, perhaps, direct to the one causative factor for rsd plus some other chronic ailments. Biomedicine is complex and takes time. In the meantime, I think research on a number of things is heading down a better path than the last hundred years. More recently we have hypoxia, cytokines, proteins, genes, and all mannner of things in the fluids like blood, csf (spinal fluid) and a whole host of things. It sometimes reminds me of the research for penicillin... in that the final anaylsis will strike us as hmmmm.... that simple huh?

All the best to all of you who send your support here...
Ina

[Vicc]

Hi Ada,

It is so good to hear from you and to see this evidence that you are not being totally overwhelmed by the tragedy in your life.

Yes, RSD is an orphan disease, and because of this the research we need has not been done, is very limited in scope and progresses slowly. When we look at the history of this disease we also need to take into account that the kind of research necessary to identify the cause and process of RSD was not possible until relatively recent advances in technology began to appear.

The view that this disease is the result of nerve damage really is the result of ‘no other conceivable explanation’ or of excluding any other possible explanation as making less sense than the one selected; even though most doctors would agree that nerve damage in RSD contradicts much of what is known about nerves and nervous systems. I will have more to say about this in my reply to Mike, and in another post I plan to add to this thread.

To my mind, the near stampede to link central sensitization (CS) to RSD is a recognition of the fact that peripheral nerve injury alone doesn’t fit the known facts about nerve injuries, it isn’t necessary to defend nerve injury if it quickly becomes something involving a process in the spinal cord.

It is sad to see that CS is being used to deny one of the more effective tools in a limited arsenal against RSD pain. Many more RSD patients report significant and longer lasting relief from the pain pump that from the spinal cord stimulator or from pain medications.

This isn’t to say that the pump is a great, or even a good answer to RSD pain; it won’t help at all when symptoms begin in a leg and appear later in an arm, for example, but when pain is intolerable and the pump is the only thing that might work, it should be an option.

Ina, sad to say it is true that effective treatment for RSD, whether that involves a safe method of repeating a therapy that involves long periods of remission or an actual cure, is probably still years away. It could be much sooner if the "experts" ego's or incomes weren't so intimately connected to their explanations for this disease.

I am doing my small part in trying to speed this process by returning to work on an article I think has a fair chance of being published in an admittedly minor medical journal. I know the audience of this journal will be receptive to what I say, and believe I can even teach them something about treating RSD.

Whether published or not, my plan is to make this article the centerpiece of a website that will introduce ischemia-reperfusion injury to a wider group of RSD people than I can reach through this forum. In effect making an end run around the “experts” who almost totally dominate the literature about this disease today.

Mike, I am working on my reply to you. I feel something like a juggler because I have begun writing my article and also on a follow-up post to the one that began this thread. Going from doing absolutely nothing for months to taking on three major projects is a real challenge, but oddly enough I feel up to it (today)…Vic

[allentgamer]

Hi Vic!

Good to see you taking up this cause again, even though it must seem like a huge undertaking after all you have been through. I am starting to stabilize a bit, or am getting used to all the new pains and discomfort from the spread.

Thought I would jump in here with my support as all of my converstions with my vascular doctor seem to agree with what you are saying. I for one did get RSD from ischemia as you well know, and my doctor concurs with you that it is what caused the nerve damage I am suffering with. According to him, when you go back and study the disease's history, you will find that would be true of a lot of the way people have aquired RSD all the way back to the Civil war.

I guess once the damage is done it would look exactly like nerve and muscle damage, but that would be the after what ever it was ravaged the area to cause all that damage. Reperfusion injury actually never came up in my conversations about the cause of all my problems, but it is something I intend to bring up the next time I get to visit with the vascular doc since they did have to put back the blood in my leg after having it blocked for a solid week. It makes sense that all those nasty little things from tissue death would cause great problems through out my body since they were flushed from my leg into my body. Would even explain all the troubles with my heart, and the spread.

Keep up the good work my brother, there is always room for more than one opinion, and I believe it is healthy for the research to keep an open mind on all sides if we are ever going to find the true culprit of this monsterous disease. It is too bad that the lure of money clouds the minds of some doctors, and even jeopordizes the finding of the root of RSD.

You go bro!!
love
Allen

[moonstar]

Thank You For All The Info And All Your Hard Work..i Will Be Talking To My Drs About It All. Have Printed Out Your Research And Will Have Her Read It...maybe We All Can Learn Something About How To Help All Of Us Who Are Suffering So For Such A Long Time..

[Vicc]

Hey Allen,

We've talked a little about your RSD on the phone; you began with a classic ischemia-reperfusion injury (IRI) in which the ischemia went on for days, not just hours. The fact that RSD developed is powerful evidence that this really is an IRI.

As you know, I have written extensively about how an IRI would produce the symptoms of RSD and your case is more confirmation of that.

This means that IRI does what I said it does. You are proof of that. This means we have an explanation for the cause of RSD that doesn't require that nerves do things they just can't do.

Your doctor talked about going back into the history to the Civil War; run this past him.

During the Civil War (when RSD was discovered) and during World War I (when LeRiche -- incorrectly -- linked this disease to damage to sympathetic nerves), RSD must have occured fairly frequently if doctors like Mitchell and LeRiche focused on it.

Before RSD I read numerous books and articles about the Civil War, but it was a long time after I began researching this disease before I realized one startling fact:

The most common battlefield first aid during those two wars was the tourniquet; which creates ischemia by blocking arterial blood flow to the wounded limb.

Combat medics, and Corpsmen, were not extensively deployed until World War II; before that, a soldiers greatest fear was that he would be wounded and bleed to death on the field before anyone found him and carried him to help.

Nearly every book I've read on Civil War combat contained heart-searing descriptions of the screams and moans of the wounded, fading through the night as many soldiers lost their fight for life. The survivors heard these cries, and they carried tourniquets to improve their chance for survival if/when they were wounded.

It makes more sense to assume that these tourniquets caused their RSD than to assume that nerve damage no one can find is the cause.

More later.

moonstar, I'm human and my spirits are lifted by encouraging words, thank you.

Mike, still working on that reply. I can't tell you how much I appreciate replies that disagree with me; they force me to reread things, think and focus.

Everyone else, questions are great too; I know my explanations can't answer every question, but I can't answer questions that no one asks...Vic

Hi Vicc,
Yes, I believe their is a vascular issue going on. But it is more than that with me. I believe my CNS is involved as well. My cells are really out of whack, in other words I feel totally toxic at times.

In my opinion, their could be 4 or 5 different roots of the problem if not more for people. Maybe this could be why the DOCS are confussed. Why can some people here work? How I have heard it is because they have to. Well I could't today if we were all homeless. I have got to move back to the city in a 2 story where I have trouble waliking up the stairs.

I had a very successful business and can barely today fix my youngest son something to eat.

Why does HBOT work for some and not for others? If someone has a lung condition they should wait till they get over it to try HBO, because even if they put them down 10 feet the breathing will be 10x rougher for them.

I was first DX with type 1 now they have me DX with type 2? The nerves in the Brachial Plexus were very injured in my case, I saw the 200 pictures myself. I had plastic surgery on the nerves.

But I know someone with a full on B/P injury and they are able to work. The dermatones in my case go way beyond any neuro condition as well.

I do believe in my case Cytokine involved is going on. What kind I have no
clue. I 've heard the nerves and blood run together as well. These are from T. Vascular surgeons. But I also just see any DOC at this stage in the illness as just a consultant. Huge Hugs, Roz