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