While following up on a post for another thread -RSD/antiinflamatory diet - I was commenting on a recent article, the abstract of which noted only a single pro-inflammatory cytokine being associated with chronic cases of CRPS, namely calcitonin gene-related peptide (CGRP), but when I ran a Wikipedia search on CGRP, it noted, among other things, that:

It is the most potent peptide vasodilator and can function in the transmission of pain [fn. 2: Brain SD, Williams TJ, Tippins JR, Morris HR, MacIntyre I (1985), "Calcitonin gene-related peptide is a potent vasodilator," Nature 313 (5997): 54–6] [fn. 3: McCulloch, J., et al. (1986), "Calcitonin gene-related peptide: Functional role in cerebrovascular regulation," Proc Natl Acad Sci USA 83: 5731–5735, abstract at http://www.pnas.org/content/83/15/5731] . . . . CGRP receptors are found throughout the body suggesting that the protein may modulate a variety of physiological functions in all major systems (eg, respiratory, endocrine , gastrointestinal, immune, and cardiovascular). Increased levels of CGRP have been reported in migraine and Temporomandibular joint disorder patients as well as a variety of other diseases such as cardiac failure, hypertension, and sepsis.

Regulation of the calcitonin gene related peptide (CGRP) gene is in part controlled by the expression of the mitogen-activated protein kinases (MAPK) signaling pathway, cytokines such as TNFα and iNOS. 5HT1 agonists such as sumatriptan increase intracellular calcium which cause decreases in CGRP promoter activity. Botulinum toxin type A is able to prevent stimulated release of CGRP through the cleavage of SNAP-25 protein [fn. 15: Durham, P., R. Cady, and R. Cady (2004), "Regulation of calcitonin gene-related peptide secretion from trigeminal nerve cells by botulinum toxin type A: implications for migraine therapy," Headache 44 (1): 35–42, abstract at http://www3.interscience.wiley.com/j...RY=1&SRETRY=0]. Receptor antagonists such as telcagepant, which is in phase III from Merck Pharmaceuticals, also has promise in limiting the effects of CGRP [fn. 16: Tepper, S.J. and M.J. Stillman (2008), "Clinical and preclinical rationale for CGRP-receptor antagonists in the treatment of migraine," Headache 48 (8): 1259–68, abstract at http://www3.interscience.wiley.com/j...4225/abstract] [Citations partially omitted; emphasis added.]

http://en.wikipedia.org/wiki/Calcito...elated_peptide

And here's the abstract of the article I was initially looking at:

Systemic inflammatory mediators in post-traumatic complex regional pain syndrome (CRPS I) - longitudinal investigations and differences to control groups, Schinkel C, Scherens A, Köller M, Roellecke G, Muhr G, Maier C., Eur J Med Res. 2009 Mar 17; 14(3):130-5.

Berufsgenossenschaftliche Kliniken Bergmannsheil, Department of Surgery, Ruhr University, Bochum, Germany. christian.schinkel@ruhr-uni-bochum.de

OBJECTIVES: The Complex Regional Pain Syndrome I (CRPS I) is a disease that might affect an extremity after trauma or operation. The pathogenesis remains yet unclear. It has clinical signs of severe local inflammation as a result of an exaggerated inflammatory response but neurogenic dysregulation also contributes to it. Some studies investigated the role inflammatory mediators and cytokines; however, few longitudinal studies exist and control groups except healthy controls were not investigated yet. METHODS: To get further insights into the role of systemic inflammatory mediators in CRPS I, we investigated a variety of pro-, anti-, or neuro-inflammatory mediators such as C-Reactive Protein (CRP), White Blood Cell Count (WBC), Interleukins 4, 6, 8, 10, 11, 12 (p70), Interferon gamma, Tumor-Necrosis-Factor alpha (TNF-a) and its soluble Receptors I/II, soluble Selectins (E,L,P), Substance-P (SP), and Calcitonin Gene-Related Peptide (CGRP) at different time points in venous blood from patients with acute (AC) and chronic (CC) CRPS I, patients with forearm fractures (FR), with neuralgia (NE), and from healthy volunteers (C). RESULTS: No significant changes for serum parameters investigated in CRPS compared to control groups were found except for CC/C (CGRP p = 0.007), FR/C (CGRP p = 0.048) and AC/CC (IL-12 p = 0.02; TNFRI/II p = 0.01; SP p = 0.049). High interindividual variations were observed. No intra- or interindividual correlation of parameters with clinical course (e.g. chronification) or outcome was detectable. CONCLUSION: Although clinically appearing as inflammation in acute stages, local rather than systemic inflammatory responses seem to be relevant in CRPS. Variable results from different studies might be explained by unpredictable intermittent release of mediators from local inflammatory processes into the blood combined with high interindividual variabilities. A clinically relevant difference to various control groups was not notable in this pilot study. Determination of systemic inflammatory parameters is not yet helpful in diagnostic and follow-up of CRPS I.

PMID: 19380284 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez

Now this may cast Botox in a potentially different light, where CGRP appears, at least according to this one study, to be about the only thing approaching a pro-inflamatory cytokine that folks with chronic CRPS have in statisically greater amounts than the general population.

What do you think?

Mike