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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..


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

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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.
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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