Hi. I haven't gotten into this thread thus far, but it seem that there is one point of clarification that I can offer.
Mommy Jen, there is as you must be aware a lot of information suggesting that RSD has an immunological component. By way of example, take a look at the following articles:
1. "Increased endothelin-1 and diminished nitric oxide levels in blister fluids of patients with intermediate cold type complex regional pain syndrome type 1," J George Groeneweg, Frank JPM Huygen, Claudia Heijmans-Antonissen, Sjoerd Niehof and Freek J Zijlstra, BMC Musculoskelet Disord. 2006; 7: 91. (demonstrating a relationship in human CRPS patients between cytokine production and diminished NO levels leading to vasoconstriction: as close to the Holy Grail as anyone is likely to come in a while, for my money at least);
2. "Evidence for local inflammation in complex regional pain syndrome type 1," Frank J P M Huygen, Anke G J De Bruijn, Martha T De Bruin, J George Groeneweg, Jan Klein, and Freek J Zijistra, Mediators Inflamm. 2002 February; 11(1): 47–51;
3. "Intermediate Stage Complex Regional Pain Syndrome Type 1 Is Unrelated to Proinflammatory Cytokines," Renate J. M. Munnikes, Christel Muis, Martine Boersma, Claudia Heijmans-Antonissen, Freek J. Zijlstra, and Frank J. P. M. Huygen, Mediators Inflamm. 2005; 2005(6): 366–372 (as described in their most recent article, this study looked at "patients with an intermediate duration of CRPS (median 20 months) and . . . found a significant elevation of IL-6 and TNF-a in the involved extremity compared with the uninvolved extremity"); and
4. Frank J.P.M. Huygen, MD, et al, "Successful Treatment of CRPS 1
with Anti-TNF", J Pain Symptom Manage. 2004 Feb;27(2):101-3.
All of which I have previously provided links to at:
http://neurotalk.psychcentral.com/sh...p?t=247&page=3
There's also another article from the Huygen's group that I've come across and will work into a thread of it's own, along with some potentially very interesting tie-ins going far afield, which I will try and post in the next couple of days. In the meantime, here's the article, Frank J.P.M. Huygen,
et al, entitled "Mast cells are involved in inflammatory reactions during Complex Regional Pain Syndrome type 1,"
Immunology Letters 91 (2004) 147–154. A copy of the full text of the article is attached hereto.
The whole point of this is to say that a lot of us have been convinced for some tome that CRSP-1 is, at lest in part, in origin, and very possibly auto-immunological as well. I know that there have been a number of thread on this and BT1 in which people were shared for information regarding their autoimmune conditions. (You may have lupus, I have some sarcoidosis.) But perhaps the most telling thing to me was a widely reported pattern of RSD remission during pregnancy. You haven't mentioned this one way or another, but perhaps it happened to you. In any event, researchers looking at an autoimmune thyroid disorder not only found a remission of symptoms during pregnancy, but a mechanism to explain it: chemical mechanisms the body produces in order to block attacks on the fetus (with it's own genetic structure) in the immune system's ongoing struggle to distinguish self from other. See, “Postpartum Autoimmune Thyroid Disease: The Potential Role of Fetal Microchimerism,” Takao Ando and Terry F. Davies,
J. Clin. Endocrinol. Metab., 88: 2965–2971, 2003, the abstract for which follows:
Fetal microchimerism is defined as the presence of fetal cells
in maternal tissues established during pregnancy. Immune
suppression of maternal immunity during pregnancy by the
placenta may play an important role in allowing the establishment
of such fetal microchimerism. However, peripheral
blood fetal microchimerism that persists in the postpartum
period is considered a natural event and implies the induction
of tolerance during pregnancy. Identification of fetal cells
that persist preferentially in maternal tissues subject to autoimmunity,
such as skin and thyroid, has also suggested the possible immune
modulation of the autoimmune response at the target tissue by fetal cells.
Accumulating evidence suggests that fetal immune cells may
be reactive to maternal antigens and, therefore, have the
capacity to trigger graft vs. host reactions. This would provide
a mechanism for the initiation and/or exacerbation
of autoimmune disease.
The course and severity of autoimmune thyroid disease
have long been known to be profoundly influenced by pregnancy,
with disease suppression prepartum and exacerbation
postpartum. However, the precise mechanisms involved have
not been fully understood. Here we have reviewed recent information
on the possible role of fetal microchimerism in autoimmune
thyroid disease, focusing on the immunological
consequences of intrathyroidal fetal cells and their contribution
to postpartum exacerbations.
Unfortunately, the article is just slightly too large to post here. I would however be happy to email a copy to anyone who wants it: just send me your email address in a pm and it will be on its way.
Bottom line, I believe it's a mistake to try and draw line between RSD/CRPS and other immunologically based conditions, where a great deal of evidence suggests that we're all in the same soup.
Mike