|
Discussion of Vicc's Hypothesis on RSD
I have edited a great deal of this post as even though I have very valid reasons I realise there are many people who feel I should not be quering what VICC says. Come on Tayla, there weren’t any complaints about your asking me questions, and you even got an “attagirl” for your last post.
One person complained: Me; and I didn’t complain about questions, I asked you to quote me correctly, and that if you insist on summarizing my views, do it accurately. Flippnout’s reply demonstrates exactly why I must remain vigilant about misrepresentations of my words: He replied to what you said I said, not what I actually said. I am sorry for any distress I have caused any of the members. It is not my intention to upset this wonderful forum. This little tempest in a teapot didn’t cause anyone any distress: We’re like NASCAR fans, going to the race in the hope of seeing a spectacular wreck so long as no one is killed or seriously injured. (The NASCAR safety rules, like the mods here, do their best to insure no one is badly injured or even mildly hurt, so it’s all good fun). I do not agree with your theory about RSD being an IRI, however I do agree that IRI may occur as a result of RSD. This contretemps began after my reply to a question directed at me; now I’ll ask you one: In light of the fact that IRI is defined as only occurring AFTER iatrogenic tourniquet ischemia in order to perform surgery, how can RSD possibly cause it? I would really appreciate your answer here, because my hypothesis that this is an IRI is based entirely upon my argument that tourniquet ischemia followed by surgery is not the only way IRI can develop; that the ischemia caused by the immune response to trauma is all that is necessary. I know that few, if any, members here understand that argument, but that’s because no one has taken the time to read even a little bit about the immune response to trauma. They haven’t done it because I haven’t given anyone a good enough reason to read about it. I intend to give everyone a reason by showing how HBO can lead to significant remission from RSD at a relatively low cost. I’ll explain HBOs mechanism of action against RSD, but the only way that mechanism can be understood is by understanding the immune response to trauma. I’m confident that if I can show exactly how HBO works to repair the damage from RSD, some people will have a reason to finally take the time and effort to look for themselves. If learning about it can help you beat this disease, that’s a pretty good reason to learn. I would be very interested in reading any links you may have that support your hypothesis if you can provide them. Tayla, I’ve said many times (and even on this thread), that there is no research to support my hypothesis. The only reason I found the link is that I know the signs and symptoms of RSD, and when I compared them with those of IRI, everything fit. No one, except a tiny number of physicians who know something about both disorders, is even looking at a possible connection between the two diagnoses. There is no research demonstrating a link between RSD and IRI. That seems like a dumb thing for me to admit, but it’s the truth; and I don’t try to hide from the truth. I wish RSD “experts” would be this honest. If they were, they would stop pretending that cyanosis doesn’t even exist in RSD and admit it is the most likely cause of our RSD. They would tell the truth. Right now, they are lying to us, and it’s hurting us. But back to the “no research” thing: Did you know that there is absolutely no research showing how any nerve injury, anyplace on the body, can cause RSD? Absolutely none. How do I know this? Because RSD “experts” can’t even figure out which nervous system is involved, much less which nerve. Some say it’s peripheral nerves; others argue it’s in the spinal cord, and; some still insist that sympathetic nerves are the cause. If there was any research at all linking nerve damage to RSD, there would be no debate: We would know. RSD “experts” want to believe this disease is caused by a nerve injury, but they can’t prove it. They have done a damn good snow job on us, though; we think they’ve proved it. Think about it. If they can’t even figure out which nervous system is involved, much less how any kind of nerve damage can cause the signs and symptoms of RSD, is it really wise to reject IRI -- which can cause every sign and symptom of this disease – without even looking at it? I don’t mind queries. I beg for them. But asking questions I’ve already answered on this thread isn’t helpful; nor is misrepresenting what I said. If you can avoid these two pitfalls, I welcome further exchanges…Vic Desi, you asked some really good questions and I need to look up some things before answering a couple of them; just to make sure I'm still up to date. |
Vicc,
I would respectfully like to inform you that I HAVE had complaints about me asking you these questions----They have come in the form of PM'S so I would like to correct you when you said " COME ON TAYLA, THERE WEREN'T ANY COMPLAINTS ABOUT YOUR ASKING ME QUESTIONS" Addressing your statement " IN LIGHT OF THE FACT THAT IRI IS DEFINED AS ONLY OCCURING AFTER IATROGENIC TOURNIQUET IN ORDER TO PERFORM SURGERY, HOW CAN RSD POSSIBLY CAUSE IT "? I said to you that I had asked my team about your theory and their reply was that it may occur as the result of RSD following the use of the tourniquet for Bier blocks! Not common but apparently they had heard of it occuring. Thank you for your offer to explain the mechanism of the action of HBOT for RSD but as I thoroughly research all treatments I have, I was well informed before I started my 50 dives. In response to "RSD EXPERTS WANT US TO BELIEVE THAT THIS DISEASE IS CAUSED BY A NERVE INJURY BUT THEY CAN'T PROVE IT. THEY HAVE DONE A DAMN GOOD SNOW JOB ON US, THOUGH, WE THINK THEY HAVE PROVED IT. THINK ABOUT IT" Vicc I think the fact that nerve blocks, ketamine, mirror imagery amongst many other treatments have proven to be helpful in RSD is proof enough that this is an injury of the nervous system. They simply wouldn't work otherwise. In reference to your quote "DID YOU KNOW THAT THERE IS ABSOLUTELY NO RESEARCH SHOWING HOW ANY NERVE INJURY, ANYPLACE ON THE BODY CAN CAUSE RSD?--ABSOLUTLEY NONE" I would like to refer you to any article by world reknown German experts in the treatment of RSD---Wifred Janig and Ralf Baron. http:/www.springerlink.com/content/kegj8bb2v4Iuhd/. This is a wonderful article explaining how RSD/CRPS is a neurological disease. Also the book I recommended "Explain Pain' by Lorimer Mosely and David Butler as it is an easy to read, well illustrated book which explains very well the process of the pain of RSD. I would now like to refer to your quote " I WISH RSD 'EXPERTS" WOUULD BE THIS HONEST. IF THEY WERE THEY WOULD STOP PRETENDING THAT CYANOSIS DOESN'T EXIST IN RSD AND ADMIT IT IS THE MOST LIKELY CAUSE OF OUR RSD. THEY WOULD TELL US THE TRUTH. RIGHT NOW THEY ARE LYING TO US AND IT'S HURTING US" Vicc, who are these doctors? You say 'they' as though it is all of them. It maybe those you have come in contact with but I have never had a doctor who has not recognised that cyanosis may indeed be a part of RSD. I have had many tests to ascertain what oxygen levels I have in my RSD areas. I had to have one before I qualified for HBOT. I have also had a total body thermogram to see what vasoconstriction has occured and how it is related to my cyanotic areas. Vicc, my fellow RSD sufferers here in Australia are most grateful for the knowledge and commitment our doctors show to research and treat our RSD, there are no complaints from me regarding their lack of knowledge and they have the results to give them encouragement to continue. I think I have addressed all the issues you brought to my attention. Wishing you well Tayla |
Vicc and hypothosis
Good to hear from you Vicc and I'm sorry if I misplaced your words. I agree we should not say we are doctors but I believe we should not fool anyone I believe you have the right to your opinion as well as everyone here does too, but your studies or research is based on reports or hypothosis from studies around the world.
My dear friend you have a wealth of information and you may hold the key to RSD or not but we should not blame Docs for not really knowing about RSD do we know how much they study this in med school? probably not much. Research I'm sure is being done but not fast or with 100's of millions of dollers so the information right now is going all in diffrent directions so we are all delt with what if's. for example this from NINDS Reflex Sympathetic Dystrophy/ Complex Regional Pain Syndromes (CRPS): State-of-the-Science December 15, 2001 Washington, DC Meeting Summary On December 15, 2001, the National Institute of Neurological Disorders and Stroke and the NIH Office of Rare Diseases convened a workshop on RSD/CRPS chaired by Dr. Jon Levine (UCSF) and Dr. Cheryl Kitt (NINDS). The participants included neurologists, neuroscientists, patient advocates and NINDS staff. The goal of the meeting was to bring together leading pain researchers to consider RSD/CRPS in the context of their own research paradigms, determine the state of the science and identify new directions for research on this disorder. Top Background Reflex Sympathetic Dystrophy (RSD), also known as Complex Regional Pain Syndrome (CRPS) Type I (here called RSD/CRPS), is a chronic condition characterized by burning pain and abnormalities in the sensory, motor and autonomic nervous systems. The syndrome typically appears after an acute injury to a joint or limb, though it may occur with no obvious precipitating event. In most cases, regardless of the site of injury the symptoms begin and remain most intense in the distal most extremity. In the initial stages of RSD/CRPS, pain and swelling from the injury do not subside but actually intensify, spreading from the site of the injury to other parts of the limb, to the contralateral limb or to remote regions of the body. The skin in affected areas and particularly deep somatic tissues are painfully sensitive to touch, often red and abnormally warm due to alterations in regional blood flow. Changes in sweating patterns, hair growth, subcutaneous tissues, muscles, joints or bones and difficulty moving the joint or limb are other hallmarks of the disorder. In addition to the evidence of inflammation and abnormal autonomic nervous system function, there are changes in motor systems including tremor, weakness and dystonia, which strongly suggest a central nervous system component to the disease in a subgroup of patients. The syndrome may evolve through three stages (acute, dystrophic, atrophic), although this is very much debated, each marked by progressive pain and physical changes in the skin, muscles, joints and bones. RSD/CRPS can affect both genders and all ages (including children), although it is thought to be more common between the ages of 40 and 60 and may be more frequent in women. The cause of RSD/CRPS is unknown, and current treatments are not effective for many patients. Top Scientific Presentations Experts from a wide variety of clinical and basic research areas, including neuro-imaging, pain, neural plasticity, the sympathetic nervous system and the immune system were invited to bring their knowledge and research approaches to bear on the difficult clinical problem of RSD/CRPS. The participants considered the current knowledge about RSD/CRPS in the context of the state-of-the-art research tools used in their laboratories and proposed ways to apply these approaches to RSD/CRPS. It is hoped that new opportunities for innovative research into the mechanism(s), epidemiology and treatment of RSD/CRPS will be fostered by their cross-disciplinary discussions. During their presentations, the participants suggested that the mechanism(s) that cause RSD/CRPS are elusive, primarily because of the number of complex systems affected. It became obvious that a single mechanism can barely account for all of the changes seen in patients with RSD/CRPS. Several innovative hypotheses were presented at the workshop and it was agreed on the notion that several mechanisms interact to produce the symptoms of RSD/CRPS.
Top New Research Directions The workshop participants identified several critical needs in our basic understanding of RSD/CRPS, as well as potential directions for basic and clinical research on new treatment strategies. These needs were in the areas of 1) diagnostic criteria, 2) epidemiology, 3) RSD/CRPS model systems, 4) disease mechanisms, 5) integration between basic research and clinical research, and 6) therapy:
Top Participants
References
all invloves hypothosis so vicc I'm sure you are withen your rights to read all the studies already done to come up with your own hypothosis, again Vicc a wealth of info..keep up the good work as we all will I hope study this and find answers and questions for our doctors. |
More info for every one have a great day.
BOSTON – Researchers at Massachusetts General Hospital (MGH) have found the first evidence of a physical abnormality underlying the chronic pain condition called reflex sympathetic dystrophy or complex regional pain syndrome-I (CRPS-I). In the February issue of the journal Pain, they describe finding that skin affected by CRPS-I pain appears to have lost some small-fiber nerve endings, a change characteristic of other neuropathic pain syndromes. “This sort of small-fiber degeneration has been found in every nerve pain condition ever studied, including postherpetic neuralgia and neuropathies associated with diabetes and HIV infection,” says Anne Louise Oaklander, MD, PhD, director of the MGH Nerve Injury Unit, who led the study. “The nerve damage in those conditions has been much more severe, which may be why it’s been so hard to detect CRPS-I-related nerve damage.” Complex regional pain syndrome is the current name for a baffling condition first described in the 19th century in which some patients are left with severe chronic pain and other symptoms – swelling, excess sweating, change in skin color and temperature – after what may be a fairly minor injury. The fact that patients’ pain severity is out of proportion to the original injury is a hallmark of the syndrome, and has led many to doubt whether patients’ symptoms are caused by physical damage or by a psychological disorder. Pain not associated with a known nerve injury has been called CRPS-I, while symptoms following damage to a major nerve has been called CRPS-II. Because small-fiber nerve endings transmit pain messages and control skin color and temperature and because damage to those fibers is associated with other painful disorders, the MGH research team hypothesized that those fibers might also be involved with CRPS-I. To investigate their theory they studied 18 CRPS-I patients and 7 control patients with similar chronic symptoms known to be caused by arthritis. Small skin biopsies were taken under anesthesia from the most painful area, from a pain-free area on the same limb and from a corresponding unaffected area on the other side of the body. The skin biopsies showed that, the density of small-fiber nerve endings in CRPS-I patients was reduced from 25 to 30 percent in the affected areas compared with unaffected areas. No nerve losses were seen in samples from the control participants, suggesting that the damage was specific to CRPS-I, not to pain in general. Tests of sensory function performed in the same areas found that a light touch or slight heat was more likely to be perceived as painful in the affected areas of CRPS-I patients than in the unaffected areas, also indicating abnormal neural function. “The fact that CRPS-I now has an identified cause takes it out of the realm of so-called ‘psychosomatic illness.’ One of the great frustrations facing CRPS-I patients has been the lack of an explanation for their symptoms. Many people are skeptical of their motivations, and some physicians are reluctant to prescribe pain medications when the cause of pain is unknown,” says Oaklander. “Our results suggest that CRPS-I patients should be evaluated by neurologists who specialize in nerve injury and be treated with medications or procedures that have proven effective for other nerve-injury pain syndromes.” She adds that the next research steps should investigate why some people are left with CRPS after injuries that do not cause long-term problems for most patients, determine the best way of diagnosing the syndrome and evaluate potential treatments. “Investigations that identify the causes of disease are only possible if patients are willing to come to the lab and allow researchers to study them,” she adds. “We are tremendously grateful to these CRPS patients, whose willingness to let us study them – despite their chronic pain – allowed us to make an important step in helping those who suffer from this condition.” Oaklander is an assistant professor of Anaesthesia and Neurology at Harvard Medical School. The study was supported by grants from The Mayday Fund, the National Institute for Neurological Disorders and Stroke, and the American Federation for Aging Research. Coauthors are Julia Rissmiller, Lisa Gelman, Li Zheng, MD, PhD; Yuchiao Chang, PhD; and Ralph Gott, all of the MGH. Massachusetts General Hospital, established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of nearly $500 million and major research centers in AIDS, cardiovascular research, cancer, cutaneous biology, medical imaging, neurodegenerative disorders, transplantation biology and photomedicine. In 1994, MGH and Brigham and Women’s Hospital joined to form Partners HealthCare System, an integrated health care delivery system comprising the two academic medical centers, specialty and community hospitals, a network of physician groups, and nonacute and home health services. Updated 1/31/2006 |
Vicc..
I am bringing this here because you asked me too... Where here have you said that you agree that RSD has a warm stage?? I have reread.. and either my eyes are bad or im just not seeing it, i see where you say that cold limb is RSD.. and warm is prob not RSD..?? Just want to set things staight and not be all confused aobut what you are saying@!! Thanks! Amber |
Anber,
Here is what I have said in my replies on Steff's thread; PN Board suggested I post here: In my first reply, post 2; (08/24 at 7:17 PM), I wrote In RSD, the inflammatory stage can last anywhere from a few weeks to a few months In post 12 (09/01 at 3:50 AM), I wrote this corresponds exactly with the time when warm RSD goes cold. In post 16 (09/01 at 11:32 AM), I wrote: By saying that the bottom line is that all of us have "cold" RSD. I was putting myself among those who believe that when RSD turns cold, it enters a new and much more difficult to treat stage; that even if one alternates between warm and cold, it is the cold that defines this new stage. In post 17 (09/03 at 10:06 AM) I repeated what I wrote in post 16. In that post I cited Tayla as saying: I suppose that Vicc's presumption that RSD is the result of IRI is what leads him to believe that all RSD affected areas must be cyanosed and cold. and I replied: I didn’t and wouldn’t say that. I try to avoid saying really dumb things In post 22 (09/04 at 4:43 PM), Flippnout out said I do not agree that RSD must only be cold and in your view if it is warm than it is not RSD and I replied: Your reply is based on what Tayla said that I said; not what I actually said. Please go back and read exactly what I said about warm v, cold RSD and the warm/cold RSD you describe. I am not going to repeat them again. I don't know how many times I have to repeat it, but I'll do it once more: RSD begins with the warm, red skin of inflammation, which later becomes cold (and usually cyanotic). I hopt this clears up any questions you have...Vic |
Tayla,
I think your different style of debate will make our discussions much more interesting and enjoyable. I love to debate because people do get caught up in them and winning isn’t about points or money but about helping people in the best way each side knows how, I’m sorry if there were complaints about questions; everyone knows I beg for questions. The only reason I can think of that would cause anyone to complain is that they are tired of reading my answers. They want you to stop asking me questions so that I will stop answering them. I said to you that I had asked my team about your theory and their reply was that it may occur as the result of RSD following the use of the tourniquet for Bier blocks! If I understand your answer correctly, your team is saying that a tourniquet followed by a block can cause IRI. If they believe that, I wish they would publish it. IRI experts don’t agree on exactly how long the tourniquet must be applied, but I don’t recall anyone estimating less than 15 minutes. Evidence that tourniquet ischemia (TI) for the brief period when blocks administered could lead the experts to reconsider how long an ischemia must exist before IRI develops. Still, this would only show that briefer periods of TI are necessary to develop IRI, NOT that the RSD plays any role in causing it. Physicians don’t blame the underlying condition that required the TI and surgery as in any way causing IRI. I’m curious about the role the vascular surgeon plays in your RSD treatment team. I would imagine it would be finding the cause of the cyanosis/hypoxia, so what does she/he have to say about that? Is he/she working to identify that cause? Does she/he have any opinion? Thank you for your offer to explain the mechanism of the action of HBOT for RSD but as I thoroughly research all treatments I have, I was well informed before I started my 50 dives. Sorry I didn’t make myself perfectly clear: I intend to write a post on the mechanisms of action so others will have a reason to read more about the immune response to trauma and IRI. I have never seen anything in the literature about the mechanism of action of HBO in RSD; it is the mechanism of action in skeletal muscle IRI, so whatever you learned in your research probably has nothing to do with what I will write about. I want to make it clear that I believe that standard protocols for HBO are inappropriate for RSD, and that special precautions (the same ones used for IRI) are essential. Many RSD people have tried HBO because they learned it helped someone else, and when these precautions were not taken, a lot of them reported initial improvement followed by catastrophic relapse; sometimes coming out even worse than they went in. All of this will be discussed at length in my upcoming post on HBO. I wrote: RSD “experts” want to believe this disease is caused by a nerve injury, but they can’t prove it. They have done a damn good snow job on us, though; we think they’ve proved it. And you replied: Vicc I think the fact that nerve blocks, ketamine, mirror imagery amongst many other treatments have proven to be helpful in RSD is proof enough that this is an injury of the nervous system. They simply wouldn't work otherwise. I don’t dispute nerve injury; I argue that it is the result, not the cause of RSD. The fact that drugs can provide temporary pain relief doesn’t prove that nerve damage causes RSD; it only proves that drugs can relieve neuropathic pain. I stand by what I said in many previous posts: There is absolutely no research linking any nerve injury, any place on the body, with RSD, Hell, they can’t even find any nerve damage in what they call CRPS-I. If you want to prove me wrong, find some research. I would now like to refer to your quote " I WISH RSD 'EXPERTS" WOUULD BE THIS HONEST. IF THEY WERE THEY WOULD STOP PRETENDING THAT CYANOSIS DOESN'T EXIST IN RSD AND ADMIT IT IS THE MOST LIKELY CAUSE OF OUR RSD. THEY WOULD TELL US THE TRUTH. RIGHT NOW THEY ARE LYING TO US AND IT'S HURTING US" First, if you change the font from lower to uppercase, most people follow the quote with the words (emphasis added). That way the reader knows I didn’t use caps. Vicc, who are these doctors? You say 'they' as though it is all of them. When I say “they”, I mean every RSD “expert” who has published a list of diagnostic criteria for this disease and left out cyanosis. That means just about all of them; Including R Schwartzmann of Dexter University and A Kirkpatrick, Chair of the Scientific Advisory Committee and Director of Research of the Reflex Sympathetic Dystrophy Syndrome Association (RSDSA). They are two of the big guns in RSD in this country, and they are not telling us the truth. I have had many tests to ascertain what oxygen levels I have in my RSD areas. I had to have one before I qualified for HBOT.I’d sure like to learn what those tests were; I’m not aware of any tests needed before someone undergoes HBO, so if there is something useful, I sure want to know about it. Vicc, my fellow RSD sufferers here in Australia are most grateful for the knowledge and commitment our doctors show to research and treat our RSD, there are no complaints from me regarding their lack of knowledge and they have the results to give them encouragement to continue. Really? Every one of them? No dissatisfied customers at all? We complain all the time here in the States…Vic |
Vicc.,
This isnt fun for me to do and rather be reading stuff from the boards and getting my mind off my own pain. And dont be concerned about how i feel.. but i just wanted to say for my own part that i wasnt takin stabbs at you. I just want this all ironed out and put in easy terms so the others can understand and also join in the disscusion.. i think thats what is keeping alot of people from saying anything bc they dont know what IRI stands for or what it involves or anytihng.. they are just understnading how RSD works, and add this in convestation.. you have to look at it that way.. and im NOT asking you to repeat your self over and over!!! I would love to know why you say that.. but honestly dont care anymore.. this is getting outta hand andgetting personal i think! And i dont want to be caught up in this when it hits the fan.. I wish my post wasnt removed and thought the end of it had alot of legit questions adn for the life of me right now cant remember what i said.. but what ever.. :Soapbox: Amber PS here is my end part of my post that was removed.. Curious gave me the end part and think it needs to be said!! I am not harping on you either.. but you are saying 2 different things and even admitted to haveing "warm" stage RSD when you say that RSD is only cold?? (or in your opinion). I have a hard time reading your posts and making sense of them... expecially in the IRI issue.. and would love to see along with Tayla links to show stuff that you say exists. I researched IRI and i only find stuff on ishecmic bowl and liver disease.. nothing about RSD or any peripheral disase. I agree with everyone that you need to find a doctor that you trust and agree with , in your treatments!! but why go on a crusade or what ever and say its IRI when even the docs right now dont know IRI... Alot of us are lucky to get the diagnosis of RSD.. there are alot that dont and get blamed for making the pain up in thier heads.. why make it harder and say it could be IRI and haveing people seek out help with this and no one know about this disease.. thats what doctors and researches are for.. and im happy that you found something to research and look into helping you!! i really am.. but dont get all ..... i dont want to say preachy but thats all i can come up with right now, but preachy about something and not take any considerations or back it up... Is the treatment for IRI the same for RSD? i mean if the diagnosis is IRI... is the treatment the same as RSD? and what is the difference other then you saying its a spinal cord issue not a brain issue..??? confused... and hope you can straighten out things you said and why u feel soo strong aobut this and for me not to get to frustrated about it begin said .. i guess.. |
Vicc,
I shall address your question regarding the testing for oxygen that I underwent before I had HBOT, you say you haven't heard of it's existance but it is routine here as if oxygen levels prove to be satisfactory then often HBOT is denied as there is little proof it will an already well oxygenated body. The test is called 'TCOM' ot transcutaneous oxygen measurement! Now for some documentation on the use of HBOT in RSD. Effectiveness of Hyperbaric Oxygen Therapy in the Treatment of Complex Regional Pain Syndrome Authors: Kiralp, M.Z.; Yildiz, .; Vural, D.; Keskin, I.; Ay, H.; Dursun, H. Source: The Journal of International Medical Research, Volume 32, Number 3, May 2004 , pp. 258-262(5) Publisher: Field House Publishing < previous article | next article > | View Table of Contents Key: - Free content - New Content - Subscribed Content - Free Trial Content Abstract: In this double-blind, randomized, placebo-controlled study we aimed to assess the effectiveness of hyperbaric oxygen (HBO) therapy for treating patients with complex regional pain syndrome (CRPS). Of the 71 patients, 37 were allocated to the HBO group and 34 to the control (normal air) group. Both groups received 15 therapy sessions in a hyperbaric chamber. Pain, oedema and range of motion (ROM) of the wrist were evaluated before treatment, after the 15th treatment session and on day 45. In the HBO group there was a significant decrease in pain and oedema and a significant increase in the ROM of the wrist. When we compared the two groups, the HBO group had significantly better results with the exception of wrist extension. In conclusion, HBO is an effective and well-tolerated method for decreasing pain and oedema and increasing the ROM in patients with CRPS. Keywords: COMPLEX REGIONAL PAIN SYNDROME; HYPERBARIC OXYGEN THERAPY; REFLEX SYMPATHETIC DYSTROPHY; RANGE OF MOTION; PAIN; OEDEMA Document Type: Research article The full text is free. ----------------------- I find that most information is much easier to access and more frequently available under the name of CRPS which is the name that all modern pain specialists call RSD. Tayla |
i have to point out that the summary of the NINDS conference includes the following:
" Only such an interdisciplinary and multidisciplinary approach has a realistic chance of uncovering the pathophysiology and improving treatment of RSD/CRPS. " doesn't that sound like they're admitting they really DON'T understand the pathophysiology?.....and that seems to me like admitting they really don't know the cause, the course, or the cure for this disease??? a reminder: we once did a survey (not terribly scientific, but informative) on the number of people who developed rsd after tourniquet use, and the numbers were shockingly high....does anyone else remember that?.......i think i'd like to see someone do a thorough evaluation of this issue, to settle the chicken/egg dispute. and many blessings on the aussie docs....they seem far better informed about rsd than their yankee counterparts! liz |
Hi Liz,
It certainly is a 'chicken and the egg' situation. For me my RSD/CRPS was well and truly established before I ever had a tourniquet applied and certainly know many who have RSD/CRPS who have never had a tourniquet anywhere near them:confused: I am certain that the use of a tourniquet is surely going to complicate matters ( apart from the fact it hurts like crazy ):( The interruption of blood flow to already compromised tissue can't be good in the long term even thought the resultant pain relief from a bier block may make it seem to be a successful procedure. Cheers Tayla:hug: |
Well im a bit biased lol, but only because I know how I got RSD, and it was from ischemia.
Besides that, I do remember that survey but I think it was waayy back on BT1. At least I think it was. If you look at the history of RSD you will find alot of reference to tourniquets resulting in what we now call RSD. There even is some inference about RSD following low to no blood surgeries. My vascular surgeon told me that every vascular surgeon knows that RSD follows certain ischemic conditions, but usually dont start treatments for it, or even tell the patient it may happen to them. They are more intent on fixing the problem at hand, not something they cant fix. |
I'll post replies to some of the replies on this thread, but won't begin trying for at least a few hours, but I've been waiting for an opportunity to talk about this:
Hey Liz, I don't know if I talked about this here at NT, but I think I mentioned it twice at BT: I have been a history buff since jr hi school, and over the years began to focus on U.S. Military history and the Civil War. The soldiers back then had it really rough; bad food, harsh discipline and about half the military deaths during that war came from disease. Civil War medics were mainly cooks and bandsmen with no medical training at all; they would scour the battlefield for the wounded and carry them back to aid stations where they would wait hours (often without shade) until a doc could treat them. Because battles sometimes went on for two or three days, many of the wounded died alone in bloody fields. They couldn't do anything about most of that, but they eased their fears a little by carrying tourniquets into the battle and this might help preventing them from bleeding to death. The tourniquet was the most common form of battlefield first aid in that war. Realizing this makes it a little easier to understand how Weir Mitchell was able to treat enough causalgia patients to write a book about it. He had lots more RSD patients than most docs have seen. It is obviously much easier to develop RSD following a tourniquet ischemia (TI), which is why I took a bold leap and posted on another thread that anyone who develops RSD following surgery has an diagnosable ischemia-reperfusion injury (IRI). Nobody seemed to pick up on that. Explaining how RSD develops without TI is much more difficult, since IRI experts believe it is an essential factor, but they know that once blood flow is restored, the patient continues to suffer from waves of compression ischemias (CI) as inflammation swells the tissue, which compresses the tiny arteries that feed the microvascular systems. They know that the bulk of ischemic damage is done following CIs, as the disease continues to spread throughout all or part of an organ. I know that no one really understands what I'm saying when I talk about IRI, but I hadn't intended to begin a major discussion on it; all of this is the result of my reply to a question about whether a person might have RSD. I haven't managed much work on the second post to my thread titled Facts you may not know about RSD. That post will describe how ischemia is the most practical and logical explanation for cold RSD, I don't mind being diverted, because I think debates like this allow me to offer information in bite-size packets rather than my long and relatively dry "educational" posts. Still, I didn't expect this sort of sustained response to a few simple words: All I can say is that you would be a real exception to the rule if your warm, red skin is RSD; 16 months is just too long. Anyway, I can't complain: I wanted the opportunity to talk about why I believe RSD is an IRI, and I have had plenty of opportunities to do that here...Vic |
what about surgical touniquets?
would you even know if they were used? Surgical tourniquets prevent blood flow to a limb and enable surgeons to work in a bloodless operative field. This allows surgical procedures to be performed with improved precision, safety and speed. Tourniquets are widely used in orthopedic and plastic surgery, as well as in intravenous regional anesthesia (Bier block anesthesia) where they serve the additional function of preventing local anesthetic in the limb from entering general circulation. http://en.wikipedia.org/wiki/Surgical_tourniquet i only copied part of the post on wiki. |
Hey Flippnut,
You didn't raise any questions I felt needed my reply, but I do have some comments about the State of the Science [on RSD] published by the National Institute for Neurological Disorders and Stroke (NINDS). That report is more than 6 years old; here is information from the NINDS Fact Sheet on CRPS, published in 2006 [1]: Complex regional pain syndrome (CRPS) is a chronic pain condition that is believed to be the result of dysfunction in the central or peripheral nervous systems. This confirms what I said about no agreement about which nervous system is damaged in RSD. They just don't know; but they're neurologists, so they're committed to the idea that it MUST be the result of a nerve injury. NINDS is part of the big lie pretending that cyanosis doesn't exist in RSD; in their list of key symptoms of this disease, they include: changes in skin temperature: warmer or cooler compared to the opposite extremity. This is distinctly different from what their Fact Sheet on RSD said in 1996 [2]: One visible sign of RSDS near the site of injury is warm, shiny red skin that later becomes cool and bluish. Their 1996 version avoided using the word cyanosis, but certainly described it, and that was obviously going too far; so they changed it to a collection of words that don't accurately describe what happens in RSD. Even though they begin by talking about dysfunctions in either the peripheral or central nervous systems. later in the text they frankly admit: The cause of RSDS is unknown. Those who insist on believing that RSD must be caused by nerve damage do so in spite of the facts. The Oaklander study you posted in your 2nd reply has intrigued me for some time: If you read my first post in Facts you may not know about RSD, you saw how I demonstrated that ischemia alone can cause allodynia. I reported that neurons (nerve cells) have no energy reserves, so they are the first to show signs of hypoxic stress, and would be the first to die in ischemic hypoxia. Oaklander reported: The skin biopsies showed that, the density of small-fiber nerve endings in CRPS-I patients was reduced from 25 to 30 percent in the affected areas compared with unaffected areas. The A-fibers I discussed in Facts, are commonly referred to as small nerve fibers. Oaklander had no explanation for what caused this huge reduction in small nerve fibers; finding no evidence of physical nerve damage, but when cells die from hypoxia, the body reabsorbs them without leaving a trace of evidence as to what killed them. Ischemic hypoxia killed those small nerve fibers, not some sort of physical injury that left no damage to tissue surrounding those fibers. I know this won't offer much comfort for those who argue that the "experts" are right and RSD is the result of physical nerve damage, but science is science; at least when "experts" don't pretend that obvious signs of RSD aren't even there...Vic (I don't include you in the group that believes this must be the result of physical nerve damage; it is obvious you're struggling to learn the facts). A [ ] with a number inside means I will email you a copy of the article cited. Just click the “rsd_hbot” link at the bottom of the page and type in the title of the post and the number(s) you want to receive. |
Amber,
In your last post (#8, dated 09/05 at 7:54 PM). you're probably talking about my remark that this is all good fun: This isnt fun for me to do and rather be reading stuff from the boards. Please consider the possibility that my words were my way of hiding my frustration at having to repeatedly say "I didn't say that" in response to your and Tayla's repeated misrepresentations of what I actually said. I would much rather be working on my post about cold pain than constantly repeating "I didn't say that". I thought my reply (#6 09/04 at 4:30 PM). in which I cited six times when I referred to the warm or inflammatory stage of RSD, {which was in direct response to a post you made), would finally put an end to your accusations that I said RSD pain is always cold pain. I went even further, stating that: RSD begins with the warm, red skin of inflammation, which later becomes cold (and usually cyanotic). I hopt this clears up any questions you have...and then you repeat your accusation again in your last post: I am not harping on you either.. but you are saying 2 different things and even admitted [on another forum] to haveing "warm" stage RSD when you say that RSD is only cold?? Then you say; and im NOT asking you to repeat your self over and over!!! I would love to know why you say that.. I say it because you continue to misrepresnt what I've said. and I don't want people to remember your representations of my words as my actual words. Every time you misquote me, I'm forced to repeat "I didn't say that", and then repeat what I actually said;.again and again. I researched IRI and i only find stuff on ishecmic bowl and liver disease.. nothing about RSD or any peripheral disase. Medline shows that there are 19,007 documents matching IRI; PubMed shows 20,980 (almost all of them duplicating those found at Medline). I have more than 100 abstracts on IRI in my computer files, and I estimate I read five for every one that I saved. You have to dig for the facts, not give up because the first couple of abstracts don't seem to fit what you're looking for. ...why go on a crusade or what ever and say its IRI when even the docs right now dont know IRI [?] IRI experts know what IRI is, but they don't know anything about RSD. I'm on a "crusade" because I knew about RSD when I began investigating IRI, and I concluded that they are one and the same. but dont get all ..... i dont want to say preachy but thats all i can come up with right now, but preachy about something and not take any considerations or back it up. I don't understand exactly what you're saying here but I don't need to back up what I say by citing research: I say things that are found in commonly known facts about science and medicine; anyone can go online and look for science that contradicts what I say. I'm "preachy" because I know that RSD is IRI and I know that properly administered HBO can bring significant relief for almost everyone here. What should I do? Keep silent when I know something will help someone? Can't do that. I guess that's all I have to say for now...Vic |
Vicc,
I am guessing that when you feel up to it you will comment on my post and if you do I was wondering if you could comment on what you mean by 'properly administered HBOT"? Have you experienced improperly administered HBOT? HBOT as you know is a complex treatment that requires highly trained technicians, doctors and nursing staff to firstly to assess you for the treatment, to ascertain the timing and depth of the dive and then to medically supervise the dive. There are far too many restrictions in place here to allow for anything other than properly administered HBOT so I am wondering whether perhaps you work to completely different guidelines in the US? Our medicare here requires each patient to have a proven hypoxic illness or wound caused by hypoxia or infection before they will ok the payment of treatment. I know people who have been assessed with me who were knocked back for treatment as their TCOM (Trans cutaneous Oxygen Measurement) revealed no hypoxia in their tissue yet they have been diagnosed as having RSD/CRPS. Can you possibly explain how you feel that this can be the case? Thank you Regards Tayla |
Hi Curious,
I'm not surprised that you missed the one time I mentioned that tourniquet ischemia (TI) is surgical tourniquet ischemia. I just looked for that reference and couldn't find it; guess it got buried in the mass of words these three thread have become. I didn't actually use the words surgical tounrniqueat ischema: I simply said something like iatrogenic ischemia followed by surgery. I was pointing out that IRI experts currently believe that TI, followed by surgery, is the only way one can develop this disorder. My argument with this view is that the known signs and symptoms of IRI and the predictive signs for RSD are identical, and the only the idea that TI is a prerequisite for an IRI stands in the way of linking the two. IRI experts know that compression ischemia (CI) is the reason the disease spreads, and I take the position that CI (a part of the immune response to trauma), not only spreads IRI, but that it can cause it; that TI is NOT a prerequisite. I probably shouldn't have even mentioned TI here, but I guess I felt it was necessary at the time. It is just a distraction at this point...Vic |
Tayla,
Thank you for your diascussion of TCOM, I suspect it is known under another acronym here as I seem to recall a similar sounding test used in an experiment involving RSD patients. (Now I will have to look it up and learn whether it measures arterial or microvascular oxygenation: If it is the former, it isn't useful in understanding what is happening in RSD, but if it is the latter I might be a good diagnostic test for this disease). The abstract you posted isn't really very useful as it doesn't contain any information about the dosage of oxygen or the atmospheric pressure (ATA) at which it was delivered. Both are critical in treating RSD. I know that all modern folks call RSD, CRPS. but I think both taxonomies are unrealistic: RSD representing the discredited view that damage to the SNS causes this disease, and CRPS implying that this is only a pain disorder. Given that neither are accurate, I prefer the one that involves typing fewer letters. Referencing your last reply: I am not prepared to get involved in a protracted discussion about HBO at this time, preferring to present my views in an organized manner in a single post. Anyway, these discussions have already travelled far from their starting place: Steff's question to me and my reply to her. I don't want to get involved in another long discussion of something else. I'll try to limit my replies here to questions about what has already been introduced or to provocations I must refute. I want to get back to work on posts I've already promised...Vic |
Vicc,
I respect the fact that you do not wish to answer my queries now but l look forward to when you can take the time. I agree we have strayed somewhat from Steff's original post but as you have a new thread devoted to your hypothesis then I thought this was the most appropriate place to discuss things with you. I do have one more query--you mentioned that the dose of oxygen and the ATA are critical in the treatment of RSD, I was wondering that seeing as the dose is always 100% oxygen the only differential being the ATA by what criteria do the doctors choose what ATA to use? Here, unless you are lucky enough to have a chamber to yourself then that ATA is one that will suit the majority of the patients in the chamber. I have had varying pressures for my dives depending on whether I was being treated for infection or my oedema and hypoxic tissue damage of RSD. The most usual being 2ATA. Look forward to your response Regards Tayla |
Tayla,
If you're interested in what I have to say about HBO, please read Buckwheat's thread Vascular Issues. In it you will find nearly everything I will say in my intended post: They involve replies to questions and clarifications where necessary, and they aren't well-organized structurally, but the answers to the questions you ask are there...Vic |
Thank you Vic,
There was something you mentioned that really concerned me and that was that in some states people could be flipping burgers then running HBOT :eek: I find it unimaginable that your AMA could allow this to occur when this treatment in the hands of unqualified personel could be lethal. Our HBOT centres do not run unless there is a physician qualified in hyperbaric medicine, 4 qualified nursing staff and a hyperbaric technician all in attendance. I would recommend that anyone considering HBOT do not proceed unless these staff are present to handle any emergency that may occur. Cheers all Tayla |
Tayla,
As I recall, I wrote about why I believe the FDA does not impose stricter standards on HBO chamber operators, and I'm sure I urged anyone considering it to only choose chambers accredited by the Undersea and Hyperbaric Medical Society. I don't however, believe that chambers need all the people you believe are absolutely essential -- anymore than I believe that every patient who fills a prescription for a med they have never used before needs nurses following them around in case of an adverse reaction (a far greater risk than death by oxygen). There is a middle ground between these two extremes, and I described it in that thread...Vic |
Vicc,
I must disagree with you. The HBOT chamber I attend has 12 people in it. All patients are carefully monitored and observations done before and after their treatment. Diabetics especially are prone to hypoglycaemia as a result of the treatment and can slip into a coma if not observed carefully over the 2 hours of treatment. Have you ever been witness to someone collapse with oxygen toxicity? I have actually been extremely grateful for the medical staff who were able to resuscitate me. Many patients have problems equallizing their ears and need a member of staff to assist them to do so so as not to risk blowing out their eardrums and some pateints can very quickly develop pulmonary embolus, this is, as you know a life and death situation. As you have repeatedly said, it is imperative to get the treatment just right in terms of oxygen and ATA levels and this requires a team of well educated and skilled practitioners to achieve. Many of the patients having treatment are actually critically ill with major infections and other severe illnesses. HBOT chambers are filled with unwell people and these patients must have the same level of care in the chamber as they would in a high dependency unit. Hyperbaric oxygen therapy is not a treatment that I would liken to getting a prescription made up for the first time---the risks factor is far greater and your analogy of having a "nurse follow them around" is greatly underestimating the complexity of the treatment. Tayla |
Now that everyone is scared ********, let me give you the really bad news:
We don't get all worked up about "worst case scenarios" at our nuclear power plants either...Vic |
Quote:
Vicc, You can't have it both ways. I believe you have often descibed "worst case scenarios" particularly in your thread posts about the use of anti psychotic drugs! Every patient who has HBOT must read and sign a release form that makes them well aware of all the risks but with the knowledge that there are well trained nurses and doctors available if something does go wrong, they usually choose to give it a try. Have you ever had HBOT? Tayla |
I didn't realize that so many are in a HBOT treatment chamber at one time.
I thought { assumed:o} it was a one at a time personalized treatment. I could see if so many with varying dx's were in one chamber for a tx - that many more attendants would be required to monitor everyone. |
decided to look up a bit more on HBOT centers-
http://www.hbotofaz.org/ http://www.hyperbaricrx.com/home.html this site lists many with contact and/or website links http://www.kid-power.org/hbo.html http://www.hbot.com/frontpage.htm |
Hi Jo,
The Undersea and Hyperbaric Medical Society is made up of phsyicians who learned HBO treating deep-sea divers with "the bends" and learned a little more when it was discovered that HBO saves lives following carbon monoxide poisoning, and even later that it could prevent amputations in end-stage diabetes. It is also made up of physicians who were attracted to HBO's potential beginning in the 1970s. With funding similar to that of RSD, their research has produced some really stuff and/or showed that the counter-intuitive can sometimes be right. Right now it is about as dead-end as you can find in medicine: Specialize in HBO and tell your wife you'll have to wait a while before paying cash for that Beemer. You can still buy one, but not for cash. Everybody know's they're doomed, because the pharmaceutical empire can't figure out a better replacement they can market and make billions on. It has been derisively referred to as "a cure in search of a disease"; the FDA and HHS have so severely restricted its use in accredited hospitals that it never amortizes itself but must be kept on because people sometimes suffer from carbon monoxide poisoning. Yet HBO has achieved incredible popularity among the public. Enough so that specularors see it as a way to make a fast buck. FDA standards outside of accredited hospitals are as similar as 1870s Boston and 1870s Dodge City. I suspect FDA hopes for some sort of disaster so that it can shut down every chamber in the country. The FDA is totally owned by Pharma. Oxygen toxicity may be a bad way to go, but I imagine it's quick. More important; it is rarer than hen's teeth. Even assuming my extreme example of someone coming over from MickyDee's, he she has to know how to read and follow directions. Even the greediest speculators know they will lose thier *** if they kill someone. I believe the Undersea and Hyperbaric Medical Society have established standards for accreditation that make sense; they are the medical professionals best able to set these standards because they know what the risks are. If I were able to do the physical activities necessary to access HBO, I would not consider a chamber that wasn't so accredited. I will talk about cost v profit for chanber operators and about cost v benefit for the consume, and lots of other stuff, on my upcoming HBO post, but I wanted to ease any potential fears of anyone living near a free-standing (non-hospital) chamber that they don't need to fear poisonous clouds of oxygen, and if people started showing serious problems following HBO at whatever current staff levels exist, we would have at least heard about it...Vic |
So are you saying you are for it or against it??
|
Quote:
Hi jo, There are some mono chambers around here but they are usually hired out by elite sports teams who can afford to have the appropriate staff on standby for just one person however the greater number of centres have chambers that take 6 or more people at once. As this is the case the variance of needs from one patient to another in the chamber is often great. I have been in a chamber with an unconscious intubated accident victim at one stage so we actually were in longer to accommodate his needs. No harm done except from extreme boredom.:( This is a costly treatment for sure so unfortunately the multiple use is by far the most common and because of that there are the appropriate staff available to treat any side effects that may occur. I had oxygen toxicity on my first dive and in my months in the chamber I have seen 2 others. This problem resolves as soon as the patient is removed from the chamber but if there is nobody there to recognise or treat the seizures then there can be catastrophic problems. I guess it is like any of our treatments where we must decide whether we are willing to take a risk no matter how miniscule it is to perhaps improve our situation. Despite my first experience I continued my treatments with no other major problems other than a little claustrophobia and earache. Regards Tayla:hug: |
Just been catching up on this thread and have a real interest in one of the topics discussed in particular
Tayla, yourself and Vicc had a lengthy discussion about IRI / RSD and tourniquets Am I right in thinking that there are studies that suggest that the use of tourniquets are not useful for RSD patients and may also lead to further IRIs If that is the case, then I am seriously wondering if the tourniquet used during Alisons bier block is somehow directly linked to the worsening of her symptoms and the fact that her motor skills have been severley impeded in that leg since the block four months ago and have yet to recover I always said at the time it was as though the RSD jumped from the sympathetic to the motor nerves whilst she was in theatre, although her PMT suggest that this is a confidence issue which is somehow a psychological and protective reaction to the fact that the block did not relieve the pain Any thoughts....? Andrea |
Hi again, Andrea,
I hope you are prepared for another lengthy Vic reply, because here it comes. First, it slipped my mind that bier blocks involved tourniquets, which are the worst possible procedures for people with RSD (assuming, of course, that this is an IRI), because current belief about IRI is that it always and only begins with the use of a toruniquet. My hypothesis that RSD is an IRI rests entirely on my contention that this view is incorrect, and that the ischemia mediated by the immune response to trauma is sufficient; that tourniquet ischemia is not necessary to initiate IRI. I will have much more to say about this in my long-promised series of posts on IRI, so I'll limit my discussion here to saying that that it is folly to beleive everything is known about anything: That there is more to learn about IRI. The disease was discovered in 1963, a century after Weir Mitchell reported the new disease he called causalgia. The discovery came about after the heart-lung machine made open-heart surgery possible by maintaining circulation while stopping the heart. But open-heart surgery required that arterial blood-flow into the heart be blocked, creating ischemia. Not long after the first successful open-heart surgeries, patients began dying following apparently successful surgeries. Researchers began looking for the cause and discovered that the microvascular systems (MVS), the arterioles, capillaries and venules that deliver arterial blood to the cells and return "used" blood to the veins, were being plugged by white blood cells in the venules. (If you dip a straw into a liquid and then remove it, the liquid drains out, but it you plug one end, the liquid is trapped in the straw. This is similar to IRI, in that blocking blood from leaving the MVS prevents fresh blood from entering). The cells of the heart muscle died from oxygen deprivation (hypoxia), and when enough cells died, the heart stopped and the patient died. Later researchers discovered that other internal organs were also affected by IRI following surgeries (which always involve tourniquet ischemia). In the late 1980s, other researchers discoverd IRI in skeletal muscle (including arms and legs), but again, tourniquet ischemia was involved: Limb transplants in which ischemia lasted for hours, and surgical procedures, which can last minutes to hours. No one involved in IRI research has ever learned of a disorder like IRI in which tourniquet ischemia isn't involved, and they won't learn about it by reading the literature on RSD, because the only clue for ischemia is cyanosis, and that word simply can't be found in the literature. (I'll explain why this is so in that series I keep promising). So, we have one group of experts who know about RSD, but not IRI, and another group who know about RSD, but not IRI, and me. I've studied both disorders and believe than anyone familiar with one who learns about the other will agree with me. I haven't come across anyone who has studied both, but it will happen All that is necessary for the diagnosis of RSD to be changed to one of IRI is recognition that tourniquet ischemia is not essential. That is more difficult to prove than you might imagine, since I can't tell IRI experts that cyanosis is common in RSD. They would rather trust the literature than a bed-confined social worker in rural Kansas. RSD "experts" are so dedicated to the view that this is a neurological disorder, they aren't going to listen to me either. So I talk to RSD people, who know all about cyanosis, but must be taught about IRI. I understand your frustration with Ali's physicians, and I'm beginning to understand their frustration with you: You ask too many questions they can't answer. According to what is known about IRI today, every surgery that results in signs of tissue hypoxia: Cyanosis; lower skin temperature; painful hypersensitivity to cold; inhibited hair and nail growth; etc, should be viewed as a potential IRI. This includes RSD following carpal tunnel surgery or any other surgery in which blood flow to the surgical site is blocked. Here is an interesting fact: When Weir Mitchell identified high-velocity impact wounds as the cause of causalgia, he knew that every soldier in that war carried with him a tourniquet: Thousands of soldiers bled to death while waiting for someone to carry them to surgeons, and they were determined not to die that way. I would bet that every causalgia patient Mitchell saw had used a tourniquet after being wounded. Had he known about tourniquet ischemia and IRI, the history of RSD might be completely different, but he couldn't know that, of course: IRI wouldn't be discovered until a full century had passed. Allen's RSD began when a surgeon inadvertantly looped a suture around an artery, where it blocked blood flow until the pain forced surgeons to re-enter the site and find that suture. It is entirely possible (probable, certain), that any symptoms that followed that tourniquet on Ali were caused by it. That wouldn't be the case for worsening symptoms in her leg, however, as the tourniquet would not affect the leg. I'm afraid her worsening symptoms there are solely the result of the disease's progress. IRI does not follow every surgery involving tourniquet ischemia; it is relatively rare. RSD does not follow every physical trauma, and is rarer than IRI, but both are preceded by the immune response to trauma (IRT), because it follows every trauma, no matter how minor. There is clearly some sort of pre-conditioning for both; it could be genetic, it could be environmental (lots of chemicals in our air), or it could be something else, but both disorders clearly require more that trauma and initial ischemia. We may never know what that is, but that isn't necessary; all we need to know is how to treat it. I'll talk about that in my upcoming series too. I will have much more to say about IRI in the future, and after reading your question here, I suspect you will be reading those posts...Vic |
Thanks for the quick response Vicc - Much appreciated as always!!!
Just to clarify - you say It is entirely possible (probable, certain), that any symptoms that followed that tourniquet on Ali were caused by it. That wouldn't be the case for worsening symptoms in her leg, however, as the tourniquet would not affect the leg. I'm afraid her worsening symptoms there are solely the result of the disease's progress This confuses me as the tourniquet was used on the leg and that is the area where we have seen marked loss of balance immediately after the block was completed. Am I right in thinking you belive the two are not connected??? As you have far more knowledge an research under you belt than myself I await clarification on this with interest Yu are right that I must annoy the doctors as they never can answer my questions, though I mainly ask about there experiences with other patients and how this may be applied to helping Ali recover Thanks again and I await you response with interest Andrea |
Hi Andrea,
The reason for your confusion is clear: I got confused. Instead of refreshing myself about what you wrote on another thread, I relied on my faulty memory and assumed that Ali's block involved her arm. When I wrote the passage in question, I erred. Now that I actually reread what you wrote on that other thread, all I can say is that it is possible that the tourniquet aggravated the symptoms that were already present, but it doesn't appear likely. The reason I must revise my remarks is that it would take a certain amount of time (days, at least, and possibly weeks), before an IRI caused by the tourniquet would develop symptoms. The stages of IRI are well defined and there is no evidence that I know of that would suggest that they would be bypassed even when the IRI had already begun to develop. I'm afraid that you will probably never know why Alison suddenly worsened after the block, but I suspect that it was more likely the block itself rather than the tourniquet. It is possible that the well-intended weight bearing exercises were a factor, but there doesn't seem to be a way to confirm that either. I know this doesn't answer any of your questions -- either here or on the other thread -- but, like her doctor, I have never heard of anything like this happening before. There is more that is unknown about IRI than is known, especially in the way the brain and body responds to microvascular ischemia, and the role of blocks in this disease. It is known that sympathetic blocks act to inhibit normal sympathetic function, as research has shown that injecting norepinephrine below the site of the block results in an instant resumption of symptoms [1], [2]. Research has also shown that production of adrenalin (aka: norepinephrine), is increased in RSD affected limbs (not sure if I have a copy of that research, so I haven't cited it). This is because the body's response to tissue hypoxia is to increase adrenaline, which is a vasodilator and increases blood flow in the affected limb. Increasing blood flow is useful in arterial ischemias such as late stage diabetes. Since these blocks inhibit production of adrenalin while the body is increasing it, pain relief from blocks is understandable, but no one can explain why they often suppress visible cyanosis. There is still much to learn. But I digress. All that I can add to what I've said is that the overwhelming evidence is that blocks only provide temporary relief, and they eventually stop working entirely. If my RSD became unendurably painful, I would present for blocks, but with the understanding that they would only provide a brief vacation from that pain. I suppose I should add that before I conluded that my time would be better spent watching daytime TV than studying the professional literature on RSD, I learned that some "experts" believe that all of the relief provided by blocks are placebe effect [3]. [4]. I find it hard to believe that they are right, as too many people have reported remarkable (but temporary) relief from these procedures. I wish this reply could have been more useful to your immediate needs, but as I said before, there is just not much research into any aspect of RSD, so answers just aren't there...Vic |
To those who may have read this entire thread today:
The first several posts on this thread were originally posted on another thread, then transferred here by KimmieDawn, so when you read references to previous posts, those posts are on the thread from which this was transplanted. Post #16 here was originally posted on that other thread, so the posts I referenced in it are actually found in Steffs thread, PN board suggested I post here, As I reviewed this thread today I saw how my references to those posts would lead anyone reading it today to wonder what in the Hell I was talking about. Sorry for the confusion; Kimmie wanted to restore the original thread to focus on the issues Steff raised there...Vic |
Stirring the pot . . .
Alright, I am a newbie here, but I have had RSD since I was 11. (Gymnastics is an evil sport!) But beyond that, I am a neuroscientist. Fancy degree and all. So my understanding of the nervous system doesn't quite match a lot of what I am hearing in this post. Norepinephrine is not produced in reaction to only hypoxia- in fact this would not be the first neurotransmitter produced in response to hypoxic conditions. NE is produced in response to any noxious stimuli as detected by the Sympathetic division of the ANS. Nitric oxide would actually be the NT of choice in response to a hypoxic condition- its your primary vasodialator. That and histamine, which is a hormone. There are very compelling and highly tested reasons as to why this is a disorder of the peripheral sympathetic nervous system. It's probably a cop out not site a lot of highly reputable studies, but there are literally thousands of papers that establish a body of work that points in this direction. Science in never infallible- we should remember that- but all of these papers and studies are equivalent to a giant arrow pointing in this direction. (Sympathetic causation.) I have honestly never heard of any process through which the coagulation cascade recruits the nervous system as part of its pathology. And randomly enough I have suffered from major ischemic events- my first pulmonary embolism was 4 years ago. I'm now on coumadin and have clots here and there. But this really isn't based upon my personal experience. I just don't think that the science supports hypoxia as being the cause of RSD.
In its early days RSD was known as causalgia- literally meaning "on fire". But to jump from the original trauma to tourniquet application as the causal factor is a big jump. This used to be the disorder of gun shot victims- that is how it was known. These are big traumatic events, and it is the job of the Sympathetic nervous system to mediate the response to such an event. This is the primary injury and the primary response. At least this is what my scientific endeavors have shown me . . . :) Linnie (I may have to pull out the 2000 page neuro-bible!) |
"But to jump from the original trauma to tourniquet application as the causal factor is a big jump."
There is more in the literature which suggests lack of blood flow in the initiating event; specifically ice application is associated. It seems from suffering from this condition that it is a result of infection. Of course this is hardly scientific and evidence still is weak. |
deleted because edits appear in smaller font. reply follows
|
Quote:
Hi Andrea, IRI occurs when there is tissue damage to an area that is reperfused after a period of ischaemia--whether it be from trauma or possibly a tourniquet. IRI is extremely rare and as Ali had already been diagnosed before her Bier Block it is unlikely that there is an IRI cause to her RSD. The damage tissue area from an IRI is quite obvious to see and whilst Ali has very obvious oedema and dystonia she does not appear to have trophic skin changes due to a substantial hypoxic event. I must admit I do believe there may have been some mismanagement with regards to her Guanethidine block and her aftercare but it is so hard to pinpoint and even harder to find out from the doctor if he did the procedure correctly:( Wishing you and Ali well Tayla:hug::hug: |
| All times are GMT -5. The time now is 09:18 PM. |
Powered by vBulletin • Copyright ©2000 - 2025, Jelsoft Enterprises Ltd.
vBulletin Optimisation provided by
vB Optimise (Lite) -
vBulletin Mods & Addons Copyright © 2025 DragonByte Technologies Ltd.