Those of you who remember the discussion we had on the old BT will recall that we went into this topic in some depth:

Pain. 2009 Apr 15. [Epub ahead of print]

Autoantibodies in complex regional pain syndrome bind to a differentiation-dependent neuronal surface autoantigen.

Kohr D, Tschernatsch M, Schmitz K, Singh P, Kaps M, Schäfer KH, Diener M, Mathies J, Matz O, Kummer W, Maihöfner C, Fritz T, Birklein F, Blaes F.
Dept. of Neurology, Justus-Liebig-University, Am Steg 14, 35392 Giessen, Germany.

Complex regional pain syndrome, which is characterised by pain and trophic disturbances, develops frequently after peripheral limb trauma. There is an increasing evidence of an involvement of the immune system in CRPS, and recently we showed that CRPS patients have autoantibodies against nervous system structures [6]. Therefore we tested the sera of CRPS patients, neuropathy patients and healthy volunteers for surface-binding autoantibodies to primary cultures of autonomic neurons and differentiated neuroblastoma cell lines using flow cytometry. Thirteen of 30 CRPS patients, but none of 30 healthy controls and only one of the 20 neuropathy sera had specific surface binding to autonomic neurons (p<0.001). The majority of the sera reacted with both sympathetic and myenteric plexus neurons. Interestingly, 6/30 CRPS sera showed binding to undifferentiated SH-SY5Y neuroblastoma cells. However, differentiation of SH-SY5Y into a cholinergic phenotype induced a surface antigen, which is recognised by 60% of CRPS sera (18/30), but not by controls (p<0.001). Our data show that about 30-40% of CRPS patients have surface-binding autoantibodies against an inducible autonomic nervous system autoantigen. These data support an autoimmune hypothesis in CRPS patients. Further studies must elucidate origin and function of these autoantibodies in CRPS.

PMID: 19375222 [PubMed - as supplied by publisher] [Emphasis added.]

And please note the presence of Drs. Maihöfner, Birklein and Blaes, who are among the most prominent CRPS researchers in the world right now. I'll try to get a full text version of the article.

Mike

All Autoimmune Disorders have two factors in common

"1. A hereditary predisposition thought to be a combination of certain (as yet mostly unknown) genes.
2. An environmental trigger or triggers. Again many are unknown. It often occurs after recovery from infection. Some bacteria produce toxic products that cause T cells to bind to macrophages - perhaps this is how T cells learn to recognize the body's own tissues, which they now attack. (Autoimmune disorders are caused when cytotoxic T cells and normal antibodies attack an individual's own body cells).

In addition, Autoimmune Disorders can be difficult to diagnose. Symptoms may vary from person to person. Remission (where no outward signs of the disorder are present) is common, sometimes for many years.

It is also not unusual for a person with an undiagnosed Autoimmune Disorder to be told they are malingering, a hypochondriac, etc.
A few have even been sent for Psychiatric treatment."

For more information:

http://www.autoimmunity.co.uk/
http://www.autoimmunity.co.uk/information/common.php

For an article that appeared a couple of years ago by some of the same authors in the study referred to above, and which is is probably the article referred to in Footnote 6 in the cited abstract, check out "Autoimmunity in Complex Regional Pain Syndrome," Blaes F, Tschernatsch M, Braeu ME, et al, Ann NY Acad Sci. 2007; 1107: 168-173, free full text at http://www.rsds.org/2/library/articl...tsch_Braeu.pdf The abstract for that article follows:

ABSTRACT: Complex regional pain syndrome (CRPS) is an etiologically
unclear syndrome with the main symptoms being pain, trophic and autonomic
disturbances, and functional impairment that develops after limb
trauma or operation and is located at the distal site of the affected limb.
Because autoantibodies against nervous system structures have been
described in these patients, an autoimmune etiology of CRPS is discussed.
These autoantibodies bind to the surface of peripheral autonomic neurons.
Using a competitive binding assay, it can be shown that at least some
of the CRPS sera bind to the same neuronal epitope. Autoimmune etiology
of CRPS is a new pathophysiological concept and may have severe
impact on the treatment of this often chronic disease.

Apparently, the new article takes this a step futher, which may be one reason it's been published in Pain, the most prominent medical journal in the field.

And for an article on the use of anti-TNF[alpha] drugs in CRPS patients, check out "Successful Intravenous Regional Block with Low-Dose Tumor Necrosis Factor-[Alpha] Antibody Infliximab for Treatment of Complex Regional Pain Syndrome 1," Bernateck M, Rolke R, Birklein F, Treede RD, Fink M, Karst M, Int Anesth Res Soc. 2007;105(4):1148-1151, free full text at http://www.rsds.org/2/library/articl...teck_Rolke.pdf And here's the abstract:

Cytokines, particularly tumor necrosis factor-[alpha], may play an important role in the mediation of mechanical hyperalgesia and autonomic signs in complex regional pain syndrome 1. We performed an IV regional block with low-dose administration of the tumor necrosis factor[alpha] antibody, infliximab, in a patient with typical clinical signs of complex regional pain syndrome 1 (moderate pain, edema, hyperhidrosis, elevated skin temperature compared with the contralateral side). A significant improvement of clinical variables was observed 24 h after infliximab treatment. Almost complete remission was reached within 8 wk, but sensory signs improved only after 6 mo. No adverse events were observed.
(Anesth Analg 2007;105:1148 –51)

BTW infliximab is the black labeled drug I referred to in my posting under the Paula Abdul thread: http://neurotalk.psychcentral.com/thread85284-2.html

Hi Mike,

Remember this one?


Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

http://physrev.physiology.org/cgi/content/full/82/4/981

Peripheral nerves are the origin of almost all forms of neuropathic pain. This section is divided into two major subsections. Section IIA provides an overview of peripheral nerve anatomy and immunology, by addressing issues of 1) anatomy and immune surveillance, as well as nerve damage caused by 2) antibodies, 3) complement, 4) T lymphocytes, and 5) trauma. The purpose is to provide the background for the clinically relevant discussion that follows. Section IIB focuses on painful neuropathies that involve nerve trauma and/or inflammation. Within this, three clinical neuropathic pain syndromes are examined: 1) complex regional pain syndromes associated with peripheral nerve trauma and/or inflammation, 2) autoimmune neuropathies, and 3) vasculitic neuropathies. For each, an examination of the clinical findings is first discussed followed by a summary of data from relevant animal models. The argument to be developed is that immune attack of peripheral nerves, or even simply immune activation near peripheral nerves, is sufficient to create increases in peripheral nerve hyperexcitability and/or damage so as to be considered a significant contributor to the neuropathic pain observed.

Roz -

That was for a good while the lone voice in the wilderness, at least as far as we knew. Txs.

xxx
Mike

ps Although I'll admit I didn't understand a lot of it at the time.

Dear Mike,

In school, cell biology was not my thing, but I excelled in Art.

It was this article that led me to study about proinflammatory cytokines and T Cells.

The T cell's not balancing right is really a fright to me.

Which led me to my immune system not being protected, so I wondered what got in their in my case. In other words why am I so weak, and my immune system at ground level.

So I starting asking questions to MD's if it was possiable if something invaded my immune system and could effect the nerves as well.

cont..

As far as understanding goes, they make alot of these medical journals very difficult to comprehend, they certainly do not use the KISS method.

You know how I feel about THINGS entering the BBB in my case, in my opinon they require treatment. But 99.9% of MD's will not even have a clue.

Like for instance, cell to cell signaling plays a huge role as well. If you do some resarch on that one, it's like the article's are in French.

Much Love, Roz

PS. Help me with spelling bud.

I am a firm believer that the immune system plays a role in RSD. I personally believe that my immune system was taxed before my surgery for a number of reasons, and therefore my immune system wasn't able to deal with surgery effectively. This may seem like a stretch, but I've been looking at the similarities with Autism (although obviously the symptomology is different, both are neurological). There are a lot of people with autism that have an improvement in symptoms after doing things to clean up their immune systems detoxing, changing diet getting rid of yeast, gluten, casien, cleaning up their gut--getting rid of bad bacteria and introducing the "good" and even getting rid of parasites, going organic so it's one less thing for the immune system to deal with (processing pesticides), taking different supplements. If this can help with a neurological problem like autism (which was thought to be "incurable," than why not RSD, if it really is related to an immune problem? I actually did try quite a bit of this, as I was reading "Mother Warriors" as I was going through HBOT. I'm not sure how much it played a role in my improvement compared to everything else I've tried, but I AM better now. I haven't stuck with the diet, though, after I began to feel better.

Hi Miller,

I love your spirit and atitude.

Much Love, Roz xoxo

Hey Mate,

I have been doing a little research on the Parvo. I won't hold the Mayo this time.

http://www.ncbi.nlm.nih.gov/pubmed/7861814