I BELIEVE THAT IT WOULD SERVE US ALL WELL TO CONSIDER AN INFECTION CONNECTION IN RSD, BE IT LYMES OR ANOTHER BACTERIAL OR VIRAL COMPONENT. FINDING RESEARCH ABOUT RSD IS EXTREMELY LIMITING, BUT IF WE ARE WILLING TO EXPAND OUR THINKING TO INCLUDE SIMILAR ILLNESSES (FIBRIMYALGIA, CHRONIC FATIGUE, AND LYMES TO NAME A FEW), THE COMMONALITIES ARE SIGNIFICANT AND MAY JUST PROVIDE MUCH NEEDED INSIGHT INTO THIS TRAGIC SUFFERING.

I EXTRACTED THE FOLLOWING FROM A DOCUMENT. IF YOU WOULD LIKE TO READ IT IN ITS ENTIRITY, YOU CAN GOOGLE:

THE MARSHALL PROTOCOL FOR TREATING CHRONIC FATIGUE SYNDROME AND FIBROMYALGIA: HOPEFUL RESULTS EMERGING

I AM NOT PROMOTING THIS PROTOCOL BUT AM ENCOURAGED TO LEARN THAT CHRONIC PAIN RELIEF IS BEING REALIZED WITH ANTIBIOTIC TREATMENTS. ALSO, IF YOU TAKE THE TIME TO GOOGLE LYMES MISDIAGNOSED, YOU WILL DISCOVER MUCH TO CONSIDER.

I PRAY THAT THE MANY BRILLIANT MINDS WHO VISIT THIS FORUM WILL PULL TOGETHER AND INVESTIGATE THIS CONSIDERATION.

JEANNE

to read more please follow this link
http://www.prohealth.com/library/sho...784&t=CFIDS_FM

What I am trying to understand on this is:

IF RSD is caused by an infection then does this throw injuries out the window and therefore anyone fighting for WC or trying to sue a Dr. for surgery gone worng goes out the window too?

I'm not saying what you are saying isn't right but it sure would hurt a lot of lawsuits the way it sounds if it turns out this way.

Ada

if I may throw something into the mix as a parent and wife of guys with chronic illness....

sometimes illness can manifest with symptoms very similar to another illness, but not both have necessarily the same cause nor even be the same disease/disorder. I know of many examples where patients were misdx because their symptoms "fit" a particular illness. However when further tested it was found their illness was caused by a different agent, and yes, in some cases infection (eg strep, mycoplasma, lyme and other microbial agents)

We have a young girl we know whohas been ill since very young. She was first dx with epilepsy and then Multiple Sclerosis....but it turns out she has Lyme disease as well as untreated strep (something known as PANDAS)
Once correct treatment starts, (although in some cases much damage done by prior wrong/no treatment) yet improvement begins

I know very little about RSD...except to deeply sympathize with the pain that you all suffer

but could it not be possible that there is more than one cause for the symptoms that manifest in CRPS? and the possibility that some may be misdx.
For those that have a clear "trigger" point of an injury, surgery, blood draw etc it seems something related to that set the disease in motion.

Similarly the damage caused by untreated infection can cause a malfunction.

so all I am saying is it doesnt have to be *only* one or the other cause because it isnt always necessarily the same illness that manifests with similar symptoms

Dear Jeanne,

Thanks so much for taking the time to research this article, it really gives everyone of us something to think about. We need solutions to our RSD DX.. This article could very well help people.

Much Love, Roz

Dear Ada,

Some peoples lives are really at stack here. Much Love, Roz

I just saw this thread in the index...

As luck would have it, this article in a very recent Science News discusses mitochondrial damage as a source of chronic illness.

http://www.sciencenews.org/view/feat...ndria_Gone_Bad
This makes more sense to me because what is coming out of the new research is that ANTIBIOTICS and other drugs (like statins), can damage mitochondria. The autism community has some interesting new studies showing vaccines may do this and antibiotic treatment for ear infections or other things that happen to little kids, often precede the appearance of autism.
The mitochondria in our cells are basically similar and actually derived FROM bacteria. So agents that KILL bacteria, may kill our mitochondria too.

example:
http://www.autism.com/medical/resear...ntibiotics.htm

There already is a supplement made by Dr. Bruce Ames who studies mito deterioration as a cause of aging:
Juvenon
http://www.bruceames.org/

I think it is more likely that RSD is closer to mito damage than is to sarcoidosis. The treatment the Marshall Protocol uses is a angiotensin receptor antagonist like Benicar (also used to lower blood pressure). This protocol also requires very low intake of Vit D...and that alarms me since Vit D is showing anticancer, and antidepressant and many other positive effects for people. I have seen many fibro patients on this and another forum improve when Vit D levels were normalized from very low. This implies to me that using the Marshall Protocol for fibro would not be a good idea. This protocol remains very controversial among doctors still.

Please read the mito article at the beginning of this post, and look at the diagram included. It makes it easier to visualize how this chemistry works.

Dear Mrs. D,

Thanks so much for your knowledge. But don't you think a serious pathogen in the body can effect cell to cell signaling? Much Love, Roz

Yes, Roz. The cell to cell signals are mediated by Cytokines.
These are short range hormonelike substances.

Thromboxane initiates platelet actions during trauma.
Leukotrienes initiate the release of histamine from mast cells and signal the immune system to fight invaders.

There are families of these substances. PGE1s, PGE2s, PGE3s, etc. All with certain functions. The Series One type are for homeostatis, and the Series 2 type are mostly for inflammation
and response to trauma and stress, the Threes, are mixed.
There a just an amazing array of others.

The body favors PGE1s on a daily basis IF and only IF certain nutrients are available to make them. This is Omega-3 territory, alpha linolenic acid, from nuts and seeds..like flax.
The Omega-6 fats come from plants also, and favor making the PGE2s. When the diet is too low in Omega-3, then we don't do well...we get stuck in the inflammatory side and that causes inflammation, blood clots, allergies etc. So a balance is needed.

So far using DRUGS on this system has brought some failures.
Cox-2 inhibitors which block PGE2 inflammation and arthritis pain, fail and Vioxx actually killed people because one of the PGE2 cytokines is a vasodilating agent..the body uses in trauma (swelling), but also keeps our coronary heart arteries open. Singulair which blocks leukotrienes and reduces allergy, and asthma, will also fail to signal when bacteria get out of control in the lungs, and the result may be pneumonia and death. NSAIDs like ibuprofen work in the short term for swelling for pain, but if taken for over 6 wks in a row, they actually block healing PGE2s that we need for tissue repair.
(they are good and bad both).

In the end, it is balance we need. Our bodies will balance if we provide them with the proper nutrients. So far drugs for these systems have not worked very well.

Bacteria stimulate the release of many cytokines so our bodies will survive. Leukotrienes to motivate white cells, and PGE2s for swelling (increasing blood flow) of the area.

Dear Mrs. D,

I hope your day is so full of love because you are truly a blessings to soo many of us.
I just want to thank you from the bottom of my heart, for making the time to help us.

Much Love, Roz

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.