That was so nice, thank you.
I just wanted to bring to your attention that without changing the body of my post, I dropped the starred note at the end, which read as follows:
* And if anyone wants to seriously assert that chronic CRPS has nothing to do with the sympathetic nervous system, then how is one to explain edema? A condition which, according to everything I've read, is caused be the failure of the sypathetic nervous sytem to maintin the tone of the peripherical vascular system, on account of which "neurogenic vasodialation" sets in, the vessels become flaccid, and the first thing that happens is that water leaks out of the blood, causing edema, followed ultimately by the loss of some of the hemoglobin itself, causing explained brusing, especially in the most "dependant" parts of the body, i.e., the feet and ankles.
And the reason I did so was not because I believe it's wrong, but because there is an alternative theory of CRPS which Prof. Anne Louise Oaklander of Harvard has been advancing for the last couple of years, that gets us to the basically the same result as does the classic model based upon a dsyfunctional of the sympathetic nervous system. Instead, she suggests that all the the symptoms of CRPS are triggered by the small fiber neuropathy she discovered. See, Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy)
, Oaklander AL, Rissmiller JG, Gelman LB, Zheng L, Chang Y, Gott R, Pain
, 2006;120:235-243, free full text at http://www.rsds.org/2/library/articl..._pain_2006.pdf and RSD/CRPS: the end of the beginning
, Oaklander AL, Pain
, 2008 Oct 15;139(2):239-40. Epub 2008 Sep 13, free full text at http://www.rsds.org/2/library/articl..._editorial.pdf
Dr. Oaklander's has recently restated her views in somewhat greater detail in Is reflex sympathetic dystrophy/complex regional pain syndrome type I a small-fiber neuropathy?
Oaklander AL, Fields HL, Ann Neurol.
2009 Mar 18;65(6):629-638. I have a copy of it, but it's too big to post here. If anyone wants to see it drop me a PM with your email address, and I'll send it out.
Dr. Oaklander's view that small fiber neuropathy can explain all of the symptoms of CRPS were initially questioned in an editorial in the same issue of Pain
in which her study appeared. Is CRPS I a neuropathic pain syndrome?
Jänig W, Baron R, Pain
2006 Feb;120(3):227-9, free full text at http://www.rsds.org/2/library/articl...ology%2006.pdf
And for what it's worth, I personally have a problem with Dr. Oaklander's approach, because in her most recent article, she sets forth on all of the symptoms of CRPS her theory can explain, but fails to mention a big one that it may not: the brains of chronic CRPS patients show anatomical changes from the norm that are different for those seen in people with either chronic low back pain or fibromyalgia. See, The Brain in Chronic CRPS Pain: Abnormal Gray-White Matter Interactions in Emotional and Autonomic Regions
, Geha PY, Baliki MN, Harden RN, Bauer WR, Parrish TB, Apkarian AV, Neuron, 2008;60:570-581, 574- 575, free full text at http://www.rsds.org/2/library/articl...aliki_etal.pdf
Which is to say, how can observed changes in the anatomical structures of the brain simply be an adaptive response to pain (as the small fiber theory holds) if patients with different pain conditions have completely different structural changes to their brains? (And not just as to matters of degree.)
But for purposes of this thread and the questions you raised, it doesn't matter if Dr. Oaklander is right or wrong. In either event, it appears to be the same neuropeptides that would be doing the dirty work:
Neurogenic edema, another facet of CRPS, can be caused by inappropriate release of peptides contained in somatic polymodal C-fibers, including those that innervate cutaneous venules. Denervated venules lose endothelial adhesion markers, permitting plasma leakage. [Oaklander and Fields, 2009 at 633.]
And one of the authorities that is cited for this proposition is Neuropeptides, neurogenic inflammation and complex regional pain syndrome (CRPS)
, Birklein F, Schmelz M, Neurosci Lett.
2008 Jun 6;437(3):199-202, for which the abstract and link to the full text were provided in my response last night to your initial posting. Oddly enough, Oaklander and Field don't mention that Birklein and Schmeltz posited an entirely different mechanism for the role of neuropeptides in CRPS:
Primary afferent nociceptors [peripheral receptors for pain] release a variety of neuropeptides . . . .
* * *
Cytokines also increase the neuropeptide content of primary afferent neurons. Activation of sensitized primary afferents then causes an increased release of neuropeptides into the affected body region. Chronic release of neuropeptides might be responsible for the above mentioned CRPS symptoms [basically everything, including edema]. [pp. 199, 201.]
So with that, the circle may be complete.
Good luck with all of this, not that you'll need it, you being the ultimate trooper and all.