[Vicc]

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.

[tayla4me]

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

[flippnout]

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.
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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.
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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.

• Drs. Ralf Baron and Wilfrid Jänig presented clear evidence of sympathetic nervous system dysfunction in their experimental studies of human patients with RSD/CRPS. Activating the sympathetic nervous system by lowering body temperature results in increased pain in the affected area in a subgroup of RSD/CRPS patients, whose pain is relieved by sympathetic nerve block or sympathectomy (destruction of the sympathetic innervation to the affected area). However, this sympathetically maintained pain (SMP) mainly involves the deep somatic tissues. While it is not known how autonomic dysfunction relates to the myriad tissue pathologies in RSD/CRPS, this evidence led the participants to generally agree on the following key issues: 1) RSD/CRPS is a neurological (rather than psychological) disorder, and 2) RSD/CRPS is likely to be a disorder of the central (in addition to the peripheral) nervous system.
• Dr. Clifford Woolf provided evidence that some types of neuropathic pain are related to changes in pain signaling pathways, including in the neurons of the spinal cord. Such modifications could distort the signaling process so that normally painless stimuli begin to produce pain, and stimuli that should be slightly discomforting actually produce severe, long-lasting pain. New technologies in gene and protein expression profiling should permit researchers to explore these issues further. However, it must be kept in mind that RSD/CRPS in most patients is triggered by traumas without nerve lesions. Thus the pain in these RSD/CRPS patients is not neuropathic pain in the strict sense.
• Dr. Linda Watkins suggested that the immune system might play a role in the disorder since signs of inflammation (redness, swelling, increased blood flow and tissue accumulation of immune cells) in the painful region are common in RSD/CRPS patients. The release of pro-inflammatory cytokines in response to neural and glial activation may be one connection between the abnormal regulation of the sympathetic nervous system and the characteristics of inflammatory immune reactions seen in the disorder. These thoughts connect to the idea that peripheral inflammatory processes are involved in the pathogenesis of early RSD/CRPS. However, the exact mechanisms of the initiation and maintenance of these inflammatory reactions, their connection to the sympathetic and afferent (peptidergic) innervation of the affected tissues and their relation to the central changes (e.g., the spinal cord, as addressed by Dr. Watkins) are far from clear. Dr. Levine, who presented several similarities between RSD/CRPS and autoimmune inflammatory diseases such as rheumatoid arthritis, provided support for this idea.
• Dr. Wilfrid Jänig approached the problem from a systems level and proposed that the inappropriate integration of sensory, autonomic and motor components at several levels in the central nervous system could be a cause of RSD/CRPS. The initial insult mostly occurs in the periphery and triggers changes in the central representations of the sensory, motor and sympathetic systems which are reflected in the changes of the respective output systems observed in the RSD/CRPS patients. Subsequent interactions with the immune, endocrine and vascular systems could lead to changes in the long-term responsiveness of the central nervous system that finally determines the disease symptomatology in the chronic state.
• Dr. Catherine Bushnell applied her expertise in neuroimaging to the question of nervous system activation in RSD/CRPS. She presented comparative imaging of pain in the brain after cutaneous or visceral stimuli to identify brain regions that are uniquely responsive to a particular type of painful stimulus. Similar comparisons between "normal" pain and pain in RSD/CRPS patients should help to clarify which regions of the nervous system are abnormally activated in this disease state. This is a very attractive and promising idea in view of the finding that many chronic RSD/CRPS patients have generalized sensory deficits (cold, warm, pain, touch perception) that can be quantified. If this is a CNS abnormality, functional imaging could suggest CNS sites that should be explored.
• Dr. Stephen Bruehl presented clear evidence that psychological distress in patients with CRPS is not a causative factor but might evolve secondary to the chronic pain syndrome. Furthermore, statistical factor analysis of multiple signs and symptoms in CRPS shows that the diagnostic criteria that have been defined so far should be extended by particular signs (e.g. by motor symptoms) in order to increase diagnostic sensitivity and specificity.

In summary, based on evidence from clinical observations, experimentation on humans, and experimentation on animals the general hypothesis has been put forward that RSD/CRPS is a disease of the central nervous system. RSD/CRPS patients exhibit changes which occur in somatosensory systems processing noxious, tactile and thermal information, in sympathetic systems innervating blood vessels, sweat glands and possibly other targets, and in the somatomotor system, indicating that the central representations of these systems are changed. The way these central changes are triggered by the peripheral trauma, which is often minor compared to the dramatic expression of the clinical phenomena, remains an enigma. Furthermore, the way these central changes connect to the peripheral inflammatory/immune changes is entirely unclear. Finally, we cannot explain why pain and the other changes associated with the sympathetic nervous system (including swelling), the motor system and the somatosensory system may disappear, in RSD/CRPS patients with sympathetically maintained pain (SMP), after sympathetic blockade (e.g., with a local anesthetic or with guanethidine). It was agreed that, based on the clinical changes observed in the RSD/CRPS patients which can be measured quantitatively, it should be possible to formulate hypotheses about the underlying mechanisms. These hypotheses should be tested by using a multidisciplinary approach, which includes clinical experimentation and human models. Such an approach is imperative to reach to a mechanism-based diagnostic classification of the RSD/CRPS patients and ultimately to the development of a mechanism-based therapeutic strategy.
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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:

1. A consensus definition of RSD/CRPS with standardized diagnostic criteria. There is practical agreement among neurologists, anesthesiologists and others about the minimal clinical criteria (signs and symptoms) that define RSD/CRPS. However, without a universally accepted definition and diagnostic criteria and a further validation and extension of the present clinical criteria, it is difficult to accurately identify RSD/CRPS patients, select patients for clinical trials, validate experimental human and animal model systems for research, and last-but-not-least to formulate testable hypotheses. The participants suggested that an expert meeting to specifically define the clinical and diagnostic criteria, based on what is known, should be a high priority for the field. Once determined, these consensus criteria should be disseminated to the medical, research and advocacy communities, in particular to those groups involved in the epidemiological studies, design of appropriate models for symptoms in RSD/CRPS, research on underlying mechanisms and the design of RSD/CRPS therapies tested in prospective clinical trials.
2. Epidemiological studies of RSD/CRPS using well-defined diagnostic criteria. Epidemiological studies to identify characteristics of patients at high risk for developing RSD/CRPS, to better define the relationship between certain clinical signs and disease onset, progression and distribution on the body, and to find out the incidence of patients with RSD/CRPS were considered a high priority. Patients with RSD/CRPS exhibit different combinations of symptoms. Does the individual RSD/CRPS patient progress through the three stages of the disorder as described in the literature. Most patients do not seem to go through different stages, although this has not been thoroughly investigated. Currently the symptomatic variability among RSD/CRPS patients makes it difficult to draw firm conclusions about mechanisms of the disorder based on clinical profiles, and could contribute to unclear findings in clinical trials. Strict patient selection based on defined clinical criteria could help to resolve this problem. Epidemiological studies may also help to clarify the anecdotal evidence regarding different incidence rates between women and men and the differences in the disease state between children and adults with RSD/CRPS. Finally, epidemiological studies may serve to work out prospective studies in order to find predictors for the development of RSD/CRPS.
3. Validate the existing models of CRPS and generate new models that recapitulate the unique features of RSD/CRPS. Appropriate experimental systems in which to study RSD/CRPS are required to advance the field; current model systems do not accurately reflect all of the symptoms experienced by patients, such as the potential gender disparity. We have models to study mechanisms operating in CRPS II (which may develop after trauma with nerve lesion); however, as noted by Dr. Gary Bennett, we almost totally lack animal models to study mechanisms operating in RSD/CRPS. Further, there are few simple in vivo or in vitro experimental model systems available to study potential RSD/CRPS disease mechanisms or to predict the efficacy of potential therapeutics.
4. Define disease mechanisms that give rise to RSD/CRPS in susceptible individuals. Several theories about disease mechanisms were presented at the workshop, but most questions addressing mechanisms clearly remain open. The participants felt that further research efforts focused on determining underlying mechanisms that cause RSD/CRPS are absolutely necessary to make progress in the design of a more appropriate (mechanism-based) diagnostic classification of RSD/CRPS patients and in the design of better therapeutic strategies. In the past, research efforts relevant to RSD/CRPS have generally focused on one component of the syndrome, such as pain, or blood flow, or bone/joint changes, but very little or not at all on central nervous system components related to the sensory, motor and sympathetic systems. Because RSD/CRPS affects multiple body systems, it is important to investigate the interactions between these peripheral and central components.
5. Integrate research on animal and human models with clinical research on patients. The workshop participants found it essential (and attractive) that research on animal and human models and clinical investigations of RSD/CRPS should be closely aligned. Thus research on mechanisms performed on different models must be interactive with clinical research. Any model, even the human one, is only an approximation to the clinical situation. Research on mechanisms in the models should concentrate on symptoms but not on syndromes.
6. New RSD/CRPS therapies tested in prospective clinical trials. To date, there are no clinical trials on the efficacy of various treatments of RSD/CRPS available that used evidence-based-medicine criteria (Dr. David Borsook). The participants presented preliminary anecdotal evidence for therapeutic approaches, such as long-term sympathetic and/or spinal cord blockade and physical therapy that could be tested in controlled, prospective clinical trials. Trials designed to treat patients at risk for developing RSD/CRPS (e.g., those undergoing knee-replacement surgery) would help to standardize the patient populations and may contribute to more reliable clinical results. As suggested by Dr. Howard Fields, a collaborative, multi-disciplinary, multi-site translational research program on RSD/CRPS may help to facilitate the development and testing of new therapies for this disorder.

In summary, there was a consensus amongst the participants of the workshop that future research on the mechanisms of RSD/CRPS must be much better integrated with the observation on the human patients, i.e. with the clinic. Design of both animal and human models must be more closely integrated with each other and with the clinic in order to focus the scientific questions, the formulation of hypotheses and the experimental approaches. Only such an interdisciplinary and multidisciplinary approach has a realistic chance of uncovering the pathophysiology and improving treatment of RSD/CRPS. Such an approach should be optimal to use and focus the different methodological techniques that are available to reach these aims. The best way to achieve this overall aim is to create research programs in association with the clinic in which the RSD/CRPS patients are diagnosed and treated.
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Participants

• Dr. Ralf Baron (Germany)
• Dr. Gary Bennett (McGill)
• Dr. David Borsook (Harvard)
• Dr. Stephen Bruehl (Vanderbilt)
• Dr. Cathy Bushnell (McGill)
• Dr. Howard Fields (UCSF)
• Dr. Wilfrid Jänig (Germany)
• Dr. Cheryl Kitt (NINDS)
• Dr. Jon Levine (UCSF)
• Dr. Audrey Penn (NINDS)
• Dr. Linda Watkins (University of Colorado)
• Dr. Clifford Woolf (Harvard)

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43. Wasner G, Heckmann K, Maier C, Baron R. Vascular abnormalities in acute reflex sympathetic dystrophy (CRPS I): complete inhibition of sympathetic nerve activity with recovery. Arch Neurol 1999; 56:613-620.
44. Wasner G, Schattschneider J, Heckmann K, Maier C, Baron R. Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value. Brain 2001a; 124:587-599.
45. Wasner G, Drummond P, Birklein F, Baron R. The role of the sympathetic nervous system in autonomic disturbances and "sympathetically maintained pain" in CRPS. In: Complex regional pain syndrome. Harden RN, Baron R, Jänig W, eds. Progress in Pain Research and Management, vol 22. Seattle: IASP Press, 2001b; pp. 89-118.
46. Wenzelburger R, Schattschneider J, Wasner G, Raethjen J, Stolze H, Deuschl G, Baron R. Grip Force coordination in CRPS. In: Complex regional pain syndrome. Harden RN, Baron R, Jänig W, eds. Progress in Pain Research and Management, vol 22. Seattle: IASP Press, 2001; pp. 129-134.
47. Woolf CJ, Bennett GJ, Doherty M, Dubner R, Kidd B, Koltzenburg M, Lipton R, Loeser JD, Payne R, TorebjÖrk E. Towards a mechanism-based classification of pain? Pain 1998; 77:227-229.

Published meeting report from December 2002 issue of Anesthesia & Analgesia (subscription required): (http://www.anesthesia-analgesia.org/cgi/content/full/95/6/1812)

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.

[flippnout]

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

[RSD_Angel]

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

[Vicc]

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

[coachV]

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

[tayla4me]

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
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

[allentgamer]

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.

[Vicc]

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