Hi Everyone,

Mike posted both of these articles from the RSD site. I was DX with Severe Nerve, Subclavilce and Vein involvement. But why do some get the RSD/TOS DX. Their has to be a root for all this.


This is perhaps the single most important article I've seen thus far.

It does nothing less than give strong evidence of a link between the mechanism of pro-inflammatory cytokines (including IL6) with vasodilation in patients with chronic CRPS-1. Or as set forth in the abstract, "the aim of [the] study was to determine the involvement of vasoactive substances endothelin-1 (ET-1) and nitric oxide (NO) during early chronic CRPS1."

From the "discussion" portion of the article:

In a previous study we observed that treatment with anti-TNF-α initiates recovery during the inflammatory stage of CRPS1. The effect of this intervention on the release of ET-1 and NOx is still unclear. Assuming a diminished blood flow, inhibition of the NO synthase is not advisable; on the contrary, NO donors should be supplemented. Besides the smooth muscle constrictive effects of ET-1, hyperalgesia and pain could also be the result of ET receptor stimulation. Therefore, specific ETA receptor antagonists (such as atrasentan) could provide remission. In pulmonary arterial hypertension, after treatment with the ET receptor antagonist bosentan, the suppression of NO synthesis was abolished and reversed to normal values of controls.

During the acute stage of CRPS1 large amounts of NO will be formed through activation of the inducible NO synthetase (iNOS). In that stage, the blood distribution has been increased which causes an increase of local skin temperature. In the endothelial cell [from the endothelium, "the layer of epithelial cells that lines the cavities of the heart and of the blood and lymph vessels and the serous cavities of the body, originating from the mesoderm"] NO will be formed from L-arginine through eNOS activation. Formation of NO could also occur after receptor stimulated activation of constitutive NOS (cNOS) or activation of neuronal NOS (nNOS) in nerve endings. In all cases this will result in increased vasodilation. TNF-α counteracts the activation of eNOS, whereas induction of iNOS in smooth muscle cells will be stimulated to generate NO. In the trophic phase of CRPS1 there will be a decline in the contribution of inflammatory mediators. Consequently, in combination with disuse of the extremity, less NO could be generated, resulting in diminished basal relaxation and retarded blood distribution, after which signs of the 'cold dystrophy' will become apparent.
[Citations omitted.]
Check it out. "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 , et al, BMC Musculoskelet Disord., (2006) 7: 91. 2006 November 30

http://www.pubmedcentral.nih.gov/art...medid=17137491