Hi All!
I am new to this site and have a questions. A little bit of background. I was diagnosed with RSD almost 3 years ago of my right foot and lower leg. I had a neurospinal stimulator implanted this winter and it has been a life saver. Before the stimulator I was using ms contin, oxycodone, and fentanyl patches to get through every day. I am now down to 3 or 4 5 mg Norco.

So to my question. We found out last week that I am 8 weeks pregnant(not planned). I met with a high risk perinatal doc. He said that staying on the norco was fine and I would have to wean off it the last month. The RSD has gotten much worse. Has anyone had any experience with pregnancy and RSD. I have cut back on my activity(hunter/jumper horse rider). I just need a little help with what to expect and what I can do to maintain the pregnancy and the deal with the increasing symptoms.

Thanks in Advance!
Becky

Dear Becky -

Congradulations! It sounds as though you are getting top medical care. And in contrast to what you've experienced over the last 8 weeks, a lot of women appear go into remission during pregnancy, but I'm not sure exactly at what point that kicks in. (And for what it's worth, your pre-pregnancy level of activity sounds pretty good for an RSD patient; and I wouldn't be surprised if cutting back on equestrian stuff wasn't asked of most pregnant women in the first place.)

This is a topic that been the subject of a number of good threads here over the years. Here are five of them, beginning with the oldest start date:

1. Pregnancy and RSD - 10/03/06 http://neurotalk.psychcentral.com/showthread.php?t=2612

2. pregnant with rsd - 04/15/08 http://neurotalk.psychcentral.com/sh...ad.php?t=43620

3. 9 weeks Pregnant Again!! - 02/22/09 http://neurotalk.psychcentral.com/sh...ad.php?t=78574

4. CRPS and autoimmunity - 04/25/09 http://neurotalk.psychcentral.com/sh...ad.php?t=85435

- and -

5. New to the board and have never done a message board before - 09/20/09 http://neurotalk.psychcentral.com/sh...d.php?t=103142

The reason I included CRPS and autoimmunity is because it goes to the apparent mechanism of remission, which is (1) there is strong evidence, especially in the first 3 years of RSDS/CRPS that there is a neuro-aotoimmune component, and (2) a number of autoimmunue diseases have been shown to go into remission during pregnancy, where the whole purpose of immune systems is to distinguish "self" from "other" and take out the "other" - something that obviously goes very wrong in autoimmune conditions - but that is really besides the point. The key thing is that during pregnancy, the woman's body can't go around trying to neutralize the "other" she is carrying, and as a result, some immune activity is given a time out for the duration. That it may come back in a big way post-partem is also part and parcel of the same suggested mechanism.

In CRPS and autoimmunity there is a citation to a key article that wasn't then available in free full text:

Autoimmune disease during pregnancy and the microchimerism legacy of pregnancy, Adams Waldorf KM, Nelson JL, Immunol Invest. 2008; 37(5): 631-44.

Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA. adamsk@u.washington.edu

Abstract
Pregnancy has both short-term effects and long-term consequences on the maternal immune system. For women who have an autoimmune disease and subsequently become pregnant, pregnancy can induce amelioration of the mother's disease, such as in rheumatoid arthritis, while exacerbating or having no effect on other autoimmune diseases like systemic lupus erythematosus. That pregnancy also leaves a long-term legacy has recently become apparent by the discovery that bi-directional cell trafficking results in persistence of fetal cells in the mother and of maternal cells in her offspring for decades after birth. The long-term persistence of a small number of cells (or DNA) from a genetically disparate individual is referred to as microchimerism. While microchimerism is common in healthy individuals and is likely to have health benefits, microchimerism has been implicated in some autoimmune diseases such as systemic sclerosis. In this paper, we will first discuss short-term effects of pregnancy on women with autoimmune disease. Pregnancy-associated changes will be reviewed for selected autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus and autoimmune thyroid disease. The pregnancy-induced amelioration of rheumatoid arthritis presents a window of opportunity for insights into both immunological mechanisms of fetal-maternal tolerance and pathogenic mechanisms in autoimmunity. A mechanistic hypothesis for the pregnancy-induced amelioration of rheumatoid arthritis will be described. We will then discuss the legacy of maternal-fetal cell transfer from the perspective of autoimmune diseases. Fetal and maternal microchimerism will be reviewed with a focus on systemic sclerosis (scleroderma), autoimmune thyroid disease, neonatal lupus and type I diabetes mellitus.

PMID: 18716941 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

A free PubMed Central copy of the entire article is now available at http://www.ncbi.nlm.nih.gov/pmc/arti...ihms116398.pdf I recommend it highly. It has also been recently followed by another freely available article co-authored by one of the study's authors:

The hidden maternal-fetal interface: events involving the lymphoid organs in maternal-fetal tolerance, Taglauer ES, Adams Waldorf KM, Petroff MG, Int J Dev Biol. 2010;54(2-3): 421-30, FULL TEXT @ http://www.ijdb.ehu.es/web/paper.php?doi=082800et&a=f

Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS, USA.

Abstract
The genetic disparity between the mother and fetus has long enticed immunologists to search for mechanisms of maternal tolerance to fetal antigens. The study of antigen-specific tolerance in murine and human pregnancy has gained new momentum in recent years through the focus on antigen-presenting cells, uterine lymphatics and fetal antigen-specific maternal T cell responses. In mice, we now know that these responses occur within the secondary lymphoid structures as they can be conveniently tracked through the use of defined, often transgenic fetal antigens and maternal T cell receptors. Although the secondary lymphoid organs are sites of both immunization and tolerization to antigens, the immunological processes that occur in response to fetal antigens during the healthy pregnancy must invariably lead to tolerance. The molecular properties of these maternal-fetal tolerogenic interactions are still being unraveled, and are likely to be greatly influenced by tissue-specific microenvironments and the hormonal milieu of pregnancy. In this article, we discuss the events leading to antigen-specific maternal tolerance, including the trafficking of fetal antigens to secondary lymphoid organs, the properties of the antigen-presenting cells that display them to maternal T lymphocytes, and the nature of the ensuing tolerogenic response. Experimental data generated from human biological specimens as well as murine transgenic models are considered.

PMID: 19876825 [PubMed - indexed for MEDLINE] PMCID: PMC2846427

http://www.ncbi.nlm.nih.gov/pubmed/19876825

I hope these threads are useful.

Mike