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

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.

• 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.
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:

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.
Top
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)

Top
References

1. Ali Z, Raja SN, Wesselmann U, Fuchs PN, Meyer RA, Campbell JN, Intradermal injection of norepinephrine evokes pain in patients with sympathetically maintained pain. Pain 2000; 88:161-168.
2. Baron R, Blumberg H, Jänig W. Clinical characteristics of patients with CRPS Type I and Type II in Germany with special emphasis on vasomotor function. In: Reflex Sympathetic Dystrophy - a Reappraisal. Jänig W, Stanton-Hicks M, eds. Progress in Pain Research and Management, Seattle: IASP Press, 1996; pp. 25-48.
3. Baron R, Jänig, W. Human experimentation. In Harden, R.N., Baron, R. Jänig, W. (eds.) Complex regional pain syndrome. Progress in Pain Research and Management, Vol. 22. IASP Press, Seattle, pp. 239-246 (2001)
4. Baron R, Levine JD, Fields HL. Causalgia and reflex sympathetic dystrophy: does the sympathetic nervous system contribute to the generation of pain? Muscle Nerve 1999; 22:678-695.
5. Baron R, Schattschneider J, Binder A, Siebrecht D, Wasner G. Relation between sympathetic vasoconstrictor activity and pain and hyperalgesia in complex regional pain syndrome: a case-control study. The Lancet published online April 23, 2002.
6. Bhatia KP, Bhatt MH, Marsden, CD. The causalgia-dystonia syndrome. Brain 1993; 116: 843-851.
7. Blumberg H, Hoffmann U, Mohadjer M, Scheremet R. Clinical phenomenology and mechanisms of reflex sympathetic dystrophy: emphasis on edema. In: Proceedings of the 7th World Congress on Pain. Gebhart GF, Hammond DL, Jensen TS, eds. Seattle: IASP Press, 1994; pp. 455-481.
8. Blumberg H, Jänig W. Reflex patterns in postganglionic vasoconstrictor neurons following chronic nerve lesions. J Auton Nerv Syst 1985; 14:157 - 180.
9. Blumberg H, Jänig W. Clinical manifestations of reflex sympathetic dystrophy and sympathetically maintained pain. In: Textbook of Pain, 3rd edition. Wall PD, Melzack R, eds. Edinburgh: Churchill Livingstone, 1994; pp. 685-697.
10. Bonica JJ. Causalgia and other reflex sympathetic dystrophies. In: The Management of Pain. Bonica JJ ed. Philadelphia: Lea and Febinger 1990; pp. 220-243.
11. Butler S. Disuse and 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. 141-150
12. Deuschl G, Blumberg H, LÜcking CH. Tremor in reflex sympathetic dystrophy. Arch Neurol 1991; 48:1247-1252.
13. Dickensen AH, Wiesenfeld-Hallin Z. Does central sensitization contribute to experimental neuropathic pain? In: Neuropathic Pain: Pathophysiology and Treatment. Hansson PT, Fields HL, Hill RG and Marchettini P, eds. Seattle: IASP Press, 2001
14. Drummond PD, Finch PM, Smythe GA. Reflex sympathetic dystrophy: the significance of differing plasma catecholamine concentration in affected and unaffected limbs. Brain 1991; 114:2025-2036.
15. Galer BS, Butler S, Jensen M. Case reports and hypothesis: a neglect-like syndrome may be responsible for the motor disturbance in reflex sympathetic dystrophy (complex regional pain syndrome I). J Pain Sympt Management 1995; 10:385-392.
16. Galer B, Harden RN. Motor abnormalities in CRPS: a neglected but key component. 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. 135-140.
17. Harden RN, Baron R, Jänig W. (eds.) Complex regional pain syndrome. Progress in Pain Research and Management, Vol. 22. Seattle: IASP Press, 2001.
18. Harden RN, Bruehl S, Galer BS, Saltz S, Bertram M, Bakonja M, Gayles R, Rudin N, Bhugra MH, Stanton-Hicks M. Complex regional pain syndrome: are the IASP diagnostic criteria valid and sufficiently comprehensive? Pain 1999; 83:211-219.
19. Jänig W. Causalgia and reflex sympathetic dystrophy: in which way is the sympathetic nervous system involved? Trends Neurosci 1985a; 8:471 - 477.
20. Jänig W. Pain and the sympathetic nervous system: pathophysiological mechanisms. In: Autonomic Failure. Mathias CJ, Bannister R, eds. Oxford: Oxford University Press, 4th edition, 1999; pp. 99-108.
21. Jänig W, Baron R. The role of the sympathetic nervous system in neuropathic pain: clinical observations and animal models. In: Neuropathic Pain: Pathophysiology and Treatment. Hansson PT, Fields HL, Hill RG, Marchettini P; eds. Seattle: IASP Press, 2001; pp. 125-149.
22. Jänig, W., Baron, R. The values of animal models in research on CRPS. In Harden, R.N., Baron, R. Jänig, W. (eds.) Complex regional pain syndrome. Progress in Pain Research and Management, Vol. 22. IASP Press, Seattle, pp. 75-85 (2001).
23. Jänig W, Baron R. Complex regional pain syndrome is a disease of the central nervous system. Clin. Auton. Res. (2002).
24. Jänig W, Häbler H-J. Organization of the autonomic nervous system: Structure and function. In: Handbook of Clinical Neurology Vol. 74 (30), Chapter 1. Vinken PJ, Bruyn, GW, eds. The Autonomic Nervous System, Part I: Normal Functions. Appenzeller O, ed. Amsterdam: Elsevier Science B.V. 1999; pp. 1-52.
25. Jänig W, Häbler H-J. Sympathetic nervous system: contribution to chronic pain. In: Nervous system plasticity and chronic pain. SandkÜhler J, Bromm B, Gebhart GF, eds. Progr Brain Res 2000; 129:453-470.
26. Jänig W, Koltzenburg M. Plasticity of sympathetic reflex organization following cross-union of inappropriate nerves in the adult cat. J Physiol 1991a; 436:309-323.
27. Jänig W, Koltzenburg M. What is the interaction between the sympathetic terminal and the primary afferent fiber? In: Towards a New Pharmacotherapy of Pain. Basbaum AI, Besson J-M, eds. Chichester: Dahlem Workshop Reports, John Wiley & Sons, 1991b, pp. 331-352.
28. Jänig W, Levine JD, Michaelis M. Interaction of sympathetic and primary afferent neurons following nerve injury and tissue trauma. In: The Polymodal Receptor - a Gateway to Pathological Pain. T. Kumazawa T, Kruger L, Mizumura K, eds. Progr Brain Res 1996; 112:161-184.
29. Jänig W, McLachlan EM. The role of modifications in noradrenergic peripheral pathways after nerve lesions in the generation of pain. In: Pharmacological approaches to the treatment of pain: new concepts and critical issues. Fields HL, Liebeskind JC, eds. Progress in Pain Research and Management, Vol 1. Seattle: IASP Press 1994, pp. 101-128.
30. Jänig W, Stanton-Hicks M, eds. Reflex sympathetic dystrophy - a reappraisal. Seattle: IASP Press, Vol. 6, 1996.
31. Levine JD, Dardick SJ, Basbaum AI, Scipio E. Reflex neurogenic inflammation. I. Contribution of the peripheral nervous system to spatially remote inflammatory responses that follow injury. J Neurosci 1985; 5:1380-1386.
32. Livingston WK. Pain Mechanisms. A Physiological Interpretation of Causalgia and its Related States. New York, London: Plenum Press, 1943/1976.
33. Merskey H, Bogduk N. Classification of chronic pain: description of chronic pain syndromes and definition of terms. Seattle: IASP Press, 1994.
34. Price DD, Long S, Wilsey B, Rafii A. Analysis of peak magnitude and duration of analgesia produced by local anesthetics injected into sympathetic ganglia of complex regional pain syndrome patients. Clin J Pain 1998; 14:216-226.
35. Rommel O, Gehling M, Dertwinkel R, Witscher K, Zenz M, Malin JP, Jänig W. Hemisensory impairment in patients with complex regional pain syndrome. Pain 1999; 80:95-111.
36. Rommel O, Malin J-P, Zenz M, Jänig W. Quantitative sensory testing, neurophysiological and psychological examination in patients with complex regional pain syndrome and hemisensory deficits. Pain 2001a; 93:279-293.
37. Rommel O, Thimineur M. Clinical evidence of central sensory disturbances 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. 193-208.
38. Schattschneider J, Deuschl G, Baron R. Kinematic analysis of the upper extremity 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. 119-128.
39. Schwartzman RJ, Kerrigan J. The movement disorder of reflex sympathetic dystrophy. Neurol 1990; 40:57-61.
40. Stanton-Hicks M, Jänig W, Hassenbusch S, Haddox JD, Boas R, Wilson P. Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain 1995; 63:127-133.
41. TorebjÖrk E, Wahren LK, Wallin BG, Hallin R, Koltzenburg M. Noradrenaline-evoked pain in neuralgia. Pain 1995; 63:11-20.
42. Wahren LK, Gordh T Jr, TorebjÖrk E. Effects of regional intravenous guanethidine in patients with neuralgia in the hand; a follow-up study over a decade. Pain 1995; 62:379-385.
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.

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..


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..