Dear Vicc -
You will pardon me if I say that I think you are being a little hasty in knocking Dr. Schwartzman as a man who represents all in your view that is wrong with the treatment of RSD by the medical establishment in this country. I can tell you that I was his patient for a number of months in 2004. I ultimately wasn't enrolled into either the high-dose ketamine study in Germany or a low-dose ketamine study he was running at his hospital in Philadelphia, due to a couple of disqualifying physical conditions, but I can tell you that he was about as compassionate and caring a doctor as I think I've ever met, and I've known a few. (Forgive me old friend, but this discussion seems very familiar, we may have gone through it once before on BT1.)
I know you prefer abstracts to articles, but thanks to the assistance of the RSDSA Medical Articles Archive at
http://www.rsds.org/2/library/articl...ive/index.html there are now a lot of important studies that we can all have free full-text access to, studies that go directly to a number of issues you've raised.
First of all, on ketamine, I think the most impressive study I've seen is "Subanesthetic Ketamine Infusion Therapy: A Retrospective Analysis of a Novel Therapeutic Approach to Complex Regional Pain Syndrome,"Correll GE, Maleki J, Gracely EJ, Muir JJ and Harbut RE,
Pain Medicine, 2004; 5:263-275 (following the first course of therapy, 54% of 33 individuals remained pain free for ≥3 months and 31% remained pain free for ≥6 months, after the second infusion, 58% of 12 patients experienced relief for ≥1 year, while almost 33% remained pain free for >3 years). I don't know about you, but I find those numbers to be impressive. Especially where every suggestion of a mechanism of action is tied to ketamine's role as an N-methyl-D-aspartate (NMDA) receptor antagonist. But granted, it doesn't cure everyone.
Moving on there is the assertion that no evidence has been put for identifying CRPS-1 with any actual nerve injury, I refer you to two articles that appeared earlier this year in the journal
Pain. The first article was "Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy)," Oaklander AL et al.,
Pain, 2006;120: 235-243 (showing a significant deduction epidermal neurite densities among CRPS-1 patients). For a short article/press release written in plain English on the significance of this study, please go to the following link to EurekAlert! dated January 30, 2006:
http://www.eurekalert.org/pub_releas...-sfn013006.php
The next was "Pathologic alterations of cutaneous innervation and vasculature in affected limbs from patients with complex regional pain syndrome," Albrecht PH, Hines S, Eisenberg E, et al.,
Pain, 2006;120: 244-266 ("in CRPS affected skin, several neuropathologic alterations were detected, including: (1) the presence of numerous abnormal thin caliber NF-positive/MBP-negative axons innervating hair follicles, (2) a decrease in epidermal, sweat gland, and vascular innervation, (3) a loss of CGRP expression on remaining innervation to vasculature and sweat glands, (4) an inappropriate expression of NPY on innervation to superficial arterioles and sweat glands and (5) a loss of vascular endothelial integrity and extraordinary vascular hypertrophy; the results are evidence of widespread cutaneous neuropathologic changes").
Finally, in the interest of open academic debate, an editorial by two German researchers who have long been critical of any unitary theory based upon peripheral nerve disorders was also printed by in the same issue of the journal. "Is CRPS I a neuropathic pain syndrome?," Janig W and Baron R,
Pain, 2006;120:227-229.
All of these articles can be accessed through the RSDSA page with the free Adobe Acrobat Reader program, and while I leave everyone to their own judgment, my reading of the Janig and Baron piece was that their criticisim of Oaklander's paper was particularly weak. Using what looks like an old litigator's trick, they direct most of their fire first at Albrecht's study [read: the straw man] not saying all that much about Oakander's article, one which I understand met a lot of excitement on it's publication, as showing the strongest link to-date between CRPS-1 and actual changes in peripheral nerve physiology.
And as far as Dr. Schwartzman is concerned, he's still out there publishing away. I put this up on another thread this evening, but it bears mention here as well: "Changes in immune and glial markers in the CSF of patients with Complex Regional Pain Syndrome," Guillermo M. Alexander, Marielle J. Perreault, Erin R. Reichenberger, Robert J. Schwartzman, Brain, Behavior, and Immunity xxx (2006) xxx–xxx [Epub November 28, 2006], abstract:
Complex Regional Pain Syndrome is a severe chronic pain condition characterized by sensory, autonomic, motor and dystrophic signs and symptoms. The pain in CRPS is continuous, it worsens over time, and it is usually disproportionate to the severity and duration of the inciting event. This study compares cerebrospinal fluid (CSF) levels of pro- and anti-inflammatory cytokines, chemokines and several biochemical factors (glial fibrillary acidic protein (GFAP), the nitric oxide metabolites (nitrate plus nitrite), the excitatory amino acid neurotransmitter glutamate, calcium, total protein and glucose) in patients afflicted with CRPS to levels found in patients suffering with other non-painful or painful conditions. The aim of the study is to determine the degree of involvement of glial cells and immune system mediators in the pathophysiology of CRPS. There was no elevation or reduction of a CSF marker that was specific for CRPS patients. However, there were several patterns of markers that could be helpful in both elucidating the mechanisms involved in the disease process and supporting the diagnosis of CRPS. The most common pattern was found in 50% (11 out of 22) of the CRPS patients and consisted of; elevated IL-6, low levels of IL-4 or IL-10, increased GFAP or MCP1 and increases in at least two of the following markers NO metabolites, calcium or glutamate. The results from this and other similar studies may aid in elucidating the mechanisms involved in the pathophysiology of CRPS. A better understanding of these mechanisms may lead to novel treatments for this very severe, life-altering illness.
As noted in the other thread, I will be happy to email a full copy of this article to anyone who want it, just send me your email address via a pm. (Personal, non-commercial use only, please.)
Lastly, I know that sometimes I come across as a trained monkey who's pretty good at stringing disparate materials together, whether or not I actually understand them. And there may be some truth to that, where that's a good part of that on a lot of the preliminarly stages of most legal research projects. Nevertheless, these articles are out there, they're free and I think it behooves us to make the most of them. In the meantime, maybe antioxidants will prove to be the Holy Grail. I'm not ruling anything out.
Be well,
Mike