Originally Posted by fmichael

I'm sorry to be getting in late on this one, but the Marshall Protocol has been around these boards for a very long time, and I have yet to see any published studies (controlled or not) on it's efficacy. So I am inclined to think of it as hocum.

And as to mitochondrial damage, yes we know it causes ulcers. There are an incredible number of studes going on right now. PubMed lists 11,293, but when you add Complex Regional Pain or CRPS to the search, you get a big fat O. I do not want to offend anyone, but it is my considered view, for what it's worth, is that you guys are going off half cocked on this one, without support in the peer reviewed literature. Search PubMed, and then if you indeed find something, get the article and then we can have a more informed discussion.

Now, to answer Ada's question, it's my understanding that the researchers who are looking at infections as having a relationships wuth CRPS/RSD are doing so only as a predisposing factor, a setting of the stage if you'll have it. In legal terms, the subsequent injury becomes the "proximate cause" of the CRPS. See, Vosburg v. Putney, 80 Wis. 523, 50 N.W. 403 (Wisc. 1891) (stating the now well-settled proposition that the tortfeasor must take his victim as he finds him; that is, the mere fact that the plaintiff is more susceptible to injury does not mitigate the tortfeasor's liability). http://en.wikipedia.org/wiki/Vosburg_v._Putney

To then going on to Jeanne's inquiry, it's my personal and relatively uniformed view that how infections potentially predispose us to CRPS will in the end have little role in actual treatment, where many but not all of these links show historic antibodies but no trace of active infections: IgG v. IgM. My sense is that, at least in the chronic stage, CRPS while showing up in the small-fiber axonal nerve degeneration in the extremities* is maintained in the brain, and while the brain does itself produce a cascade of cytokines, it's not in response to a specific infectious agent. Rather, part of the basic process of neurimmunology. But what drives chronic or "cold" cases of CRPS are disturbance in the basic structures of the brain itself. ** And that's what any truly effective therapies must address.

Mike

* “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

** See, e.g., “The brain in chronic CRPS pain: abnormal gray-white matter interactions in emotional and autonomic regions," Geha PY et al., Neuron, 2008 Nov 26;60(4): 570-81 at 575:

Regional gray matter density comparison indicated atrophy within a single cluster for the whole group of CRPS. The same brain region or portions of the same cluster exhibited atrophy even after subdividing the group by age or by laterality of CRPS pain. Hence, the atrophy spanning AI [anterior insula], VMPFC [right ventromedial prefrontal cortex], and NAc [nucleus accumbens] seems a robust result in CRPS and is right hemisphere dominant. Moreover, this atrophy was related to the two fundamental clinical characteristics of CRPS, duration and intensity, which impacted the density of this cluster above and beyond normal aging. When the cluster was subdivided into separate anatomical regions, the right AI correlated with duration of CRPS pain. The insula is the brain structure most often observed activated in acute pain tasks (Apkarian et al., 2005). In CRPS patients, bilateral AI activity correlates with ratings of touch-induced pain (allodynia) and pin-prick hyperalgesia (Maihofner et al., 2005, 2006). Moreover, recent human brain imaging studies, consistent with the older literature regarding the role of the insula as a viscerosensory cortex (Craig, 2002; Saper, 2002), highlight the role of the right AI in the representation of autonomic and visceral responses (Critchley, 2005). Patients with pure autonomic failure due to peripheral disruption of autonomic responses exhibit reduced right AI activity (Critchley et al., 2001) and atrophy in right AI (Critchley et al., 2003a). In healthy subjects, neural activity in right AI predicts subjects’ accuracy in heartbeat detection, while local gray matter volume, at coordinates closely approximating the center of the cluster we observed atrophied in our CRPS patients, correlates with subjective ratings of visceral awareness (Critchley et al., 2004). Furthermore, by comparing brain activity and autonomic responses in a fear conditioning task between healthy subjects and pure autonomic failure patients, Critchley and colleagues conclude that the right AI is involved in emotional representations, ‘‘wherein ‘feelings’ are the integration of both the mapping of internal arousal and conscious awareness of emotional stimuli’’ (Critchley et al., 2002). Given that CRPS patients are presumed to be in a constant negative emotional state and exhibit multiple signs of abnormal autonomic function, atrophy of right AI in CRPS corroborates the above studies and suggests that central anatomical abnormalities may explain fundamental symptoms of CRPS.

PMID: 19038215 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/sites/entrez
I will be happy to email a copy of the full text article to anyone who wants it. (Personal, non-commercial use only please.) Just drop me a PM with your email address. Thanks.