I found one of Vic's articals on a website today and decided to share it with you all, he wrote this in the year 2000. Sadly Vic is no longer with us but his knowlege and spirit live on. RIP Vicc you are sorely missed. Sandra
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M. S. Vic Collins, BSW

I have no medical education or training. I am just someone with a diagnosis of RSD/CRPS frustrated by continued reliance on treatments which have a history of frequent failures and multiple reports of symptoms migrating to treatment sites. When the RSD symptoms of my left foot began to appear on the right, my (then) doctor informed me that RSD doesn't migrate. But it did, and I decided to learn why.

Since new sympathetic nerve lesions could not explain all of the cases of migration - especially migration into internal organs - I began to focus on the circulatory system as the most likely way that whatever caused these new symptoms could travel to different parts of the body. Another reason for starting with circulation is that cyanosis (blue to purple discoloration), along with colder temperature in the affected area, are also signs of a vascular disorder..

(These two facts led me to wonder whether hyperbaric oxygen therapy (HBOT), might be helpful n treating this disease. I knew that cyanosis is evidence of hypoxia (oxygen deprivation), and wondered if HBOT might not force more oxygen into cyanotic areas. I did not pursue this line of reasoning because I felt something this logical must have occurred to others and because I felt that hypoxia would return as soon as HBOT ended).

Fortunately, someone better qualified was investigating HBOT. Heather Guhl, RN, BS, not only researched HBOT, she underwent a series of HBOT treatment. Her discussion of this therapy is included in a research proposal she posted in the Mass. General Hospital RSD forum. There has been no systematic research of HBOT and RSD, but Ms Guhl did find evidence that HBOT can be effective in treating RSD. She also reports significant improvement of her RSD and TOS (thoracic outlet syndrome), symptoms after undergoing this therapy.{1}

If you aren't familiar with HBOT; very briefly; it is a chamber where air pressure is raised to at least
twice what it is at sea level. Instead of air, the chamber is filled with oxygen. In this way, much more oxygen gets into the blood than is possible even using an oxygen tank and mask.. Much more oxygen reaches RSD affected areas and cyanosis decreases, and there is evidence the benefits of HBOT continue even after the treatment is discontinued.

But, like just about evreything else with RSD, there is a problem. Actually three problems: 1, most doctors don't know anything about HBOT, so getting your doctor to prescribe it will be difficult, 2, HBOT is not "usual and customary", so insurance companies and worker's compensation will probably refuse to pay for it, and, 3: many HBOT providers don't include RSD in their protocols (disorders which may be treated by HBOT), so you may have to travel to get access to it

Doctors and insurance companies resist change. They will have to see a lot more research about HBOT, and that is going to take more than just time. Research can cost hundreds of millions of dollars and can take years to gather enough evidence to prove the drug or treatment is safe and effective. The people who finance this research expect large profits on their investments and there aren't enough profits in HBOT to interest investors. Getting to the point where doctors who diagnose RSD/CRPS automatically think of hyperbaric oxygen treatment is going to take a lot of time

In the meanwhile we seem limited to two unsatisfactory choices: Do nothing until HBOT becomes available and hope the symptoms don't worsen or migrate, or risk migration of symptoms by accepting invasive treatment. There is a third option; it comes under the heading of alternative medicine.. A lot of people, myself included, hear those words and close our ears and our minds to anything that follows. In order to understand why you should even consider an alternative, you need to know what some researchers have learned about RSD

The alternatives I will present are based on abstracts and articles published in respected medical journals. The information is "new" only because no one has put all of them together until now. And while this report may seem pretty long, it is really a brief overview of research which may change the way RSD is treated in the future. It is my hope that after reading this you will be more able to make informed decisions about how to deal with this disease and better armed to persuade your doctor to investigate treatments now considered unorthodox..

After describing and quoting from this research I will tell you the choices I have made as a result of what I've learned. These choices are not alternatives to HBOT, but ways I feel offer the best hope of stalling the disease until I am able to begin hyperbaric oxygen therapy. I should point out that I had already decided to refuse any more invasive treatment - which only offered pain relief - even before I learned about the potential of HBOT. It is our right to make the final decision about any treatment, but you should always consult with your doctor before making any decision.

The first thing we need to understand is that if HBOT works, oxygen is a lot more important in this disease than most doctors think. I will step right into the middle of controversy by saying that damage to the sympathetic nerve may have started the problem, but it is probably not any part of a solution - at least after stage I.. Rather than call it RSD, what we suffer could be more accurately described as a peripheral vascular disease (PVD). This simply means that our circulation has been compromised (damaged), somehow. Even so, I will continue to use RSD because we are more familiar with this name.

There are a lot of different types of PVD's, and a long description of how circulation works or how and why we ended up with this problem really isn't necessary. (And since I barely squeaked through Biology 101 anything I say would only confuse you anyway). Very few of us have any understanding of what the sympathetic nerve does, nor do we need to becomes experts in periphal vascular disease. We will never know as much about the vascular system as our doctor. The most we can hope is that our doctor will be willing to examine new evidence. with an open mind.

I have already described cyanosis as a symptom of hypoxia. But cyanosis does not fit into the medical model of RSD. (Medical model just means the way health care professionals believe a disease begins, progresses and should be treated). In this medical model, RSD is an inflammatory disorder. The inflammation is the result of the sympathetic nerve being damaged and overresponding to a minor injury by flooding the area with cells designed to protect against infection.

One sign of inflammation is called rubor (the red skin color you see when the body is fighting an infection near the skin surface). You will learn that inflammation is usually seen in the first stage of RSD, but not in the later stages. Since hypoxia does not fit the medical model, many doctors still refer to rubor to describe the changes in skin color to blue and then to purple.

Under almost every circumstance where skin tone is blue to purple it is identified as cyanosis and every effort is made to restore circulation, as damage from hypoxia can be irreversable. Our situation is somewhat comparble to "The Emperor's New Clothes"; many doctors may feel it is cyanosis, but because they haven't the time to research RSD, or because they aren't inclined to dispute what "everyone knows", they see rubor even though it isn't there. Cyanosis is rarely mentionedwhen describing RSD. Some researchers, however, decided to investigate how circulation is affected during three defined stages of RSD.

A study of skin blood flow in rsd patients divided them into three stages, based on patient reports of temperature sensations. Stage I was warmth, stage II intermittent warmth and cold, and stage III was cold. They also used a control group who did not have RSD. In comparison with the control group, they found that patients in stage I had increased skin blood flow and increased skin temperature. Stage II had decreased skin blood flow and normal skin temp. In stage III both blood flow and skin temp were decreased. They also tested for nutrient blood flow (whether other nutrients could be found in the capillaries. Nutrients were decreased at stages II and III. Oxygenation at the surface skin layer was normal in all three stages. There was, unfortunately, no mention of skin color{2}

The findings in this study are significant because they show that circulation is affected differently in different stages of this disease, that it is positively correlated with skin temperatures, and, most important, the supply of essential nutrients to the cells decreases as the disease progresses. It also reports that there were some indications of inflammation in stage I, but not in later stages {2}. If inflammation isn't found in later stages, the discoloration is probably not rubor.

Another research abstract, studying phosphate metabolism in muscles of the lower legs of people with RSD, found that this metabolism was impaired. Very few of us understand what this means, but it is their conclusion that matters to us.. They found that it "...may be caused by cellular hypoxia or diminished oxygen utilization, which would agree with previous findings that oxygen extraction is reduced in extremities affected by RSD". {3}. Diminished oxygen extraction means that the cells are not doing their job - usually because they have been damaged somehow. And we already know what cellular hypoxia means.

Cells can be damaged when they don't receive enough oxygen, but they are not what produce the blue to purple color of cyanosis. It is the capillaries which change color. Capillaries are the tiny vessels which deliver fresh blood to the cells and return "used" blood to the veins. When circulation is normal our skin looks "normal". When cicrulation is compromised fresh blood doesn't get into the capillaries and the "old" blood in these tiny vessels does not pass back out to the veins. It is this "old" blood, which has passed its oxygen to the cells, that causes the discoloration. .

So what is it that is causing all this damage? It is time to introduce the oxygen free radical (OFR). Oxygen free radicals are oxygen molecules with an unpaired electron. In nature, all of the stable elements have paired electrons. An atom or molecule which is missing an electron is unstable, much the same way as a toy top with even a small amount of unbalanced weight is unstable. When you try to spin it, it wobbles and falls over. Oxygen free radicals restore their stability by bumping into another atom or molecule and stealing an electron. This also changes the structure of the "victim" molecule, causing it to become a free radical.{4}

When an oxygen free radical steals an electron from a cell molecule, the cell must divert some if its energy into containing and then repairing the damage. Some scientists estimate that billions of cells take OFR "hits" every day{4}. Any cell can be damaged by OFR's, including capillaries. When enough capillaries are damaged in an area, circulation is compromised. This means the cells in the affected area are not getting enough blood to function properly I suspect the pain we feel is from the pain sensors reacting to hypoxia. The body has several natural defenses against free radicals, but they are barely sufficient against the "normal" number of OFR's .{4}

While there are other types of free radicals, oxygen free radicals are the main type found in living organisms. Many scientists believe they are responsible for several disorders and may even be responsible for the aging process. With all these dangerous oxygen molecules you may wonder why we would want HBOT flooding our bodies with more oxygen. It seems logical that more oxygen means more OFR's. But according to Hyperbaric Oxygen Therapy {5}, a book length manuscript; it is hypoxia, not oxygen, which causes OFR's. . The text goes on to say that correcting hypoxia will limit OFR production.

--This may explain why there is nearly universal agreement that prompt treatment offers the greatest chance of success against RSD. It may be that the reduction of edema (which impairs circulation), as well as reducing inflammation (also part of the process which creates hypoxia), may prevent the overproduction of free radicals so that the disease cannot progress to stage II --

The next two articles may seem morbid to some, but they provide critical evidence of the relationship between oxygen free radicals and RSD. The authors refer to "free radicals", but since OFR's are the main free radicals in organisms, there is no reason to to believe they refer to anything else.. These studies show what happens when there are more OFR's than the body's defenses can counter.

The first abstract describes giving rats a continuous intra-arterial infusion (a transfusion into an artery) of free radicals into their left hindlimbs. The rats were observed and reported to have increased temperature and blood volume of that paw (A stage I symptom of inflammation), along with impaired function and increased pain rections. After 24 hours the rats were killed and examined. They found visible free radical damage to the muscle of the left hindlimbs, but none in any other part of their bodies, nor in any of a second group of rats which were given only saline (the control group)

They concluded that "...free radicals in the left hindlimbs of awake rats mimics the acute signs and symptoms of acute RSD....[underline added]..with alterations of pain found....in acute RSD patients" [The dots indicate parts I left out of what was said but which did not change the meaning of the sentence]. As noted already, they found OFR damage in the affected muscle. Since OFR's are also associated with inflammation, they concluded that RSD is caused by that. We have seen, however, that OFR's are created in greater numbers during hypoxia. Also, evidence from the first abstract indicated that inflammation disappeared in later stages of RSD. Blame it on inflammation or hypoxia, OFR's can create all the signs and symptoms of RSD.{6}.

The second article is so important you should read every word. Titled: Muscle Abnormalities found in Patients with Mysterious Pain Syndrome, it can Be found in the July 21, 1998 issue of "Neurology"; the journal of theAmerican Academy of Neurology.{7}:

Here, Dutch researchers examined the amputated legs of eight RSD patients. They found "...several abnormalities in the muscles, including signs of oxidative stress, or cell damage caused by free radicals" They also found abnormalities in the capillaries similar to those found in diabetic patients. They hypothesize that an increase in free radicals may may impair the body's ability to regulate its vascular system. They found some, but no consistent, abnormalities in the nerves.

This certainly appears to contract the theory that the pain results from an abnormal response to an injury by the sympathetic nerve. Unfortunately, despite evidence of damage to muscles and capillaries, and of possible inability of the body to regulate it's vascular system, they could not explain why we suffer severe pain.{7}.

I used "appears to contradict" because this is a disease of paradox'. Every treatment known has reports of success, and it is hard to imagine doctors using treatments they don't believe will work. It may be that future research will identify different pathologies which respond to differeent therapies. Until that happens, we can only choose between available options. But the hyperbaric oxygen therapy option isn't readily available to most RSD sufferers yet.

We have seen that circualtion is impaired by edema and inflammation in stage I, that hypoxia creates a favorable environment for the creation of OFR's, and that OFR's can create visible damage to muscle and capillaries.. OFR's travel through the circulatory system. As their numbers increase they migrate to other parts of the body, where they overwhelm the body's defenses and create muscle and capillary damage at a new site. Usually the new target is a hand or foot, which are furthest from the heart an blood return is the most difficult. As the van del Laan research shows, the influx of large numbers of OFR's create a site which mimics the signs and symptoms of acute RSD..

(It may be pointed out that the van der Laan study infused rats with proportionately much larger numbers of OFR's than could exist in the human body. But this study involved only a 24 hour period. Much larger numbers of OFR's in the extremities could very possibly cause the same damage over a longer period of time.. This will be further discussed in the conclusion)

If OFR's are responsible for creating an increasing number of sites with the same symptoms ascribed to RSD, they can only do so by overcoming the body's natural defenses against free radicals These defenses, called antioxidants, operate by "donating" an electron to an oxygen free radical without becoming free radicals themselves.{4}

If the body could create antioxidants in sufficient numbers to neutralize any number of OFR's, we would expect that OFR's would not be present in sufficient quantities to damage cells in the first place. If the body does not create sufficient antioxidants, we must find a way to supply the body with more.

Antioxidants are becoming recognised as significant in maintaining health. Many vitamin manufacturers now put antioxidants in their product, but the research suggests we will need much more than can be found in a multivitamin. Vitamins C and E are antioxidants, and most people can safely take 2,000mg of vitamin C and 1,000mg of viatmin E. But this dosage is recommended for everyone. and we will certainly need more. There are two products which approximately 40 as powerful as viatmin C.

Pycnogonel is made from the bark of a specific kind of pine tree found in France. It has been used since the early 1950's with no reports of side effects and no reports of damage to the liver or kidney (usually the first organs affected by toxins), or any other organ. It has been tested extensively and I have not found any reports of overdose or toxicity. A second antioxidant is grape seed extract. There has been somewhat less testing on this product, but it is roughly equivalent to the pine bark, and there has been no evidence of any of the side effects mentioned above.

Neither product has been approved by the Food and Drug Administration for much the same reason that hyperbaric oxygen therapy has not been tested for effectiveness in treating rsd: Both are generic products. This means one company cannot control the sales of these products. Therefor no pahramceutical company is interested in financing the research. They would never earn as much as testing would cost.

I have begun antioxidant therapy as a result of this research. I considered reporting the regimen I am on. but variables such as body weight and the degree of oxygen free radical damage must certainly affect dosage. It is also important you discuss this with your doctor or other health care professional knowledgable about antioxidants.

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CONCLUSIONS: It is clear that more research is necessary. Research with rats during an accelerated time frame is not going to tell us a great deal about the introduction of oxygen free radicals via hypoxia within the body. Logic, while useful, can be slippery. Many erronious conclusions have been reached through logic. The fact that there is no evidence about the effectiveness of antioxidants in the treatment of RSD must be considered - especially if you are considering refusing standard treatment recommended by your doctor.

We face the same dilemna when considering hyperbaric oxygen therapy. The research which would show whether it is or is not effective has simply not been done. Nor will it be done in time to help those of us who are fighting RSD now. It is too expensive and the potential for profits is too low to attract investors.

Antioxidants will not cure RSD. It is hoped they might slow the progress and the migration of this disease, but there is no proof they will. Having said all of this, I take antioxidants because I believe my body is being destroyed by free radicals and I want to stop as many as I can while I wait for access to HBOT. If I could find something else proven to do the job, I would be taking it.

Finally, there is no evidence that antioxidants compromise any of the treatment options currently in use to treat RSD or it's symptoms. You should, of course, inform your doctor and your pharmacist about all medications and supplements you are taking. This is your best assurance that none of your medications or supplements are dangerous when taken with any other.


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There is another powerful antioxidant on the market. It is called DMSO and right now it is not available for use on humans. It is available at health and nutrition stores and a lot of claims have been made about its effectiveness. I have begun research of the medical literature on DMSO (done mostly in Europe), and plan to report on my findings in the near future. I am not taking it now, but feel everyone should have the right to information which might help in the fight of this disease. I urge the reader to investigate this product thoroughly before making a decision to use it.

We are fighting for our lives, and while we know there have been successes with blocks, infusions, the different types of sympathectomies and pain control devices, we also know there have been failures.
We must carefully consider all of the options before making crucial decisions about our medical treatment. You and your doctor should be partners in this endeavor, but we are the ones who will have to live with the results.

I believe hyperbaric oxygen therapy offers the most promise in the fight against RSD, and plan to start therapy as soon as I can find the money to pay for it I will fight worker's compensation later for reimbursement. If HBOT works as well as it has in the few recorded cases, it will be money well spent, no matter who ends up paying for it. In the meanwhile, antioxidants seem to me the best way to fight a holding action. And I plan to continue searching for other weapons and to pass the information on to anyone interested.

This should only be one resource in your search for ways to fight this disease. All of the information found here can be found on the internet - plus a great deal more. Take the time to learn for yourself because the decisions you make are some of the most important decisions of your life. Use the words in boldface as keywords in your search. If you would like copies of the articles and abstracts mentioned here, just E-Mail me the number(s) found in the text and list of references.

This is provided for information only, and is certainly not intended to persuade you to select or reject any specific treatment. I have told you my choices, which are based on my particular situation. Yours may be different. If you know someone you think might be helped by reading this report, feel free to send them a copy. Changing the system is currently a process of changing one mind at a time



Vic Collins / Artical posted by Sandel.
R.I.P. Vic Collins

I sure miss Vic and have found some of his recommendations to be beneficial.

I would advise against the use of DMSO however. I believe more testing will show this chemical can and will do as much harm as good. There might be a means to use it beneficially but I plan to wait for the evidence.

Grape seed extract does help me and vitamin C might. I strongly suggest trying ginkho biloba and taking as much as is tolerated. I take about 150 mg/ day but wouldn't want to go much higher. That's in two doses with the larger one in the morning. Doctors want to know if you take this one.

I don't see you on here much but I am glad to see you show up off and on anyway.

Thanks for this. I still miss Vicc. Isn't it funny how one person can touch your life in a way that you don't forget him or her. We talked many times on the phone and he was very interesting to talk to and so smart. Like my Dr., when he talked to me about medical issues, he actually thought I knew what he was talking about. LOL Vicc was very smart and had to have a mind that was very aware even though he was in pain. That part I have trouble with, is keeping my mind working right.

One thing that struck me on there was the inflamation. I think he's right on about that and I do think that if the inflamation was brought down in the body, the pain goes down. When I first started with the RSD, my whole body, inside and out felt like it was inflamed. It took years for my Drs. to get all of it calmed down through blocks, triggerpoint injections and meds.

As far as the HBOT, DianaA, is very up on it. She took Vicc's advice and worked with it to get better. It worked for her.

What I am wondering is does anyone know what research if any is being done on RSDS. I see all of these websites popping up to get money together for research but I don't hear anything on where or what is being done to research it.

Thanks again for this on Vicc. Diana and I were just talking about him a few days ago. He sure hasn't left our hearts and minds.

Ada

I have read up on HBOT and I think it will help as much as any thing. A new HBOT clinic has opened that will take RSD paitents about 2 hours from me. I plan to try this next year when my son gets a apartment just a few miles from the clinic.
I am trying DMSO now it seems to help my finger tips some but not my hand. I have talked to a few people that have used it for years with no side affects for other problems not RSD.
Woody

Hi Woody

Sadly Vic has passed on.. I am sory I did not make that clear enouph in the origional post .

So sory for any confusion or hurt this may cause to anyone else as well, I will try fix this.

Woody, I am very glad you are going to get a chance to try HBOT in the future, and glad about the DMSO. Have you thought about upping your antioxidents too, I am not sure where you are at with your RSD but if you are newly diagnosed, spreading or prespread you might want to take some vitamin C.. I will post some relevant studdies later for you, I am full body and I take 1000mg vitamin C and when I stop taking it noticed I go into a flare up for a few days.

Be well,
Hugs
Sandra

Hi Ada

I miss him too, I keep up on the research studdies and they actualy get me thinking about him quite a bit.. sometimes I feel realy bad because I actualy get mad at him for leaving us before he could see that he was right in so many ways.. is that weird of me?

As for the research studdies if you like I will start posting them again as I find them.

Please feel free to post relevant material or memories on this thread.. it is time I think.. I warred with myself over this and I am glad a friend helped put it all into perspective for me.

hugs Ada I am glad they have your inflamation down, it's a big part of the whole picture.

Sandra

Just put these up in another thread (also started by Sandra) but I keep thinking how much Vicc would have enjoyed them. So here goes:

(1) Cutaneous tactile allodynia associated with microvascular dysfunction in muscle, Laferrière A, Millecamps M, Xanthos DN, Xiao WH, Siau C, de Mos M, Sachot C, Ragavendran JV, Huygen FJ, Bennett GJ, Coderre TJ, Molecular Pain, 2008 Oct 28;4:49, free full text at http://www.ncbi.nlm.nih.gov/entrez/u.../content/4//49

ABSTRACT:

BACKGROUND: Cutaneous tactile allodynia, or painful hypersensitivity to mechanical stimulation of the skin, is typically associated with neuropathic pain, although also present in chronic pain patients who do not have evidence of nerve injury. We examine whether deep tissue microvascular dysfunction, a feature common in chronic non-neuropathic pain, contributes to allodynia.

RESULTS: Persistent cutaneous allodynia is produced in rats following a hind paw ischemia-reperfusion injury that induces microvascular dysfunction, including arterial vasospasms and capillary slow flow/no-reflow, in muscle. Microvascular dysfunction leads to persistent muscle ischemia, a reduction of intraepidermal nerve fibers, and allodynia correlated with muscle ischemia, but not with skin nerve loss. The affected hind paw muscle shows lipid peroxidation, an upregulation of nuclear factor kappa B, and enhanced pro-inflammatory cytokines, while allodynia is relieved by agents that inhibit these alterations. Allodynia is increased, along with hind paw muscle lactate, when these rats exercise, and is reduced by an acid sensing ion channel antagonist.

CONCLUSION: Our results demonstrate how microvascular dysfunction and ischemia in muscle can play a critical role in the development of cutaneous allodynia, and encourage the study of how these mechanisms contribute to chronic pain. We anticipate that focus on the pain mechanisms associated with microvascular dysfunction in muscle will provide new effective treatments for chronic pain patients with cutaneous tactile allodynia. [Emphasis added.]

PMID: 18957097 [PubMed - indexed for MEDLINE]
PMCID: PMC2584041

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

and

(2) Effect of tadalafil [Cialis®] on blood flow, pain, and function in chronic cold complex regional pain syndrome: a randomized controlled trial, Groeneweg G, Huygen FJ, Niehof SP, Wesseldijk F, Bussmann JB, Schasfoort FC, Stronks DL, Zijlstra FJ, BMC Musculoskeletal Disorder 2008 Oct 20;9:143, free full text at http://www.ncbi.nlm.nih.gov/entrez/u...471-2474/9/143

ABSTRACT:

BACKGROUND: This double-blind, randomized, controlled trial investigated the effect of the phosphodiesterase-5 inhibitor tadalafil on the microcirculation in patients with cold Complex Regional Pain Syndrome (CRPS) in one lower extremity.

METHODS: Twenty-four patients received 20 mg tadalafil or placebo daily for 12 weeks. The patients also participated in a physical therapy program. The primary outcome measure was temperature difference between the CRPS side and the contralateral side, determined by measuring the skin temperature with videothermography. Secondary outcomes were: pain measured on a Visual Analogue Scale, muscle force measured with a MicroFet 2 dynamometer, and level of activity measured with an Activity Monitor (AM) and walking tests.

RESULTS: At the end of the study period, the temperature asymmetry was not significantly reduced in the tadalafil group compared with the placebo group, but there was a significant and clinically relevant reduction of pain in the tadalafil group. Muscle force improved in both treatment groups and the AM revealed small, non-significant improvements in time spent standing, walking, and the number of short walking periods. CONCLUSION: Tadalafil may be a promising new treatment for patients that have chronic cold CRPS due to endothelial dysfunction, and deserves further investigation.

PMID: 18937830 [PubMed - indexed for MEDLINE] PMCID: PMC2575214

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

regards,
Mike

He really would have liked this research, I could hear him crowing about it whilst I read it

This is a bump. There is some very good info here that I think that people that have never seen, might use.

The HBOT is one of the things that has helped many, and you dont see or hear of that much anymore.

I promise to get back in the present right after this comment

I found this writing about oxygen free radicals and RSD/CRPS absolutely fascinating. Thank you so much for sharing it with us! You're right, I had not seen this. Gosh, I hate that we lost Vic. From what I’ve read here.. we really needed him! He sounds like a wonderful man who was really trying to help us.