Hello everyone,
I ran across a couple articles about the spread of CRPS through the blood stream by vasoactive chemicals released into the blood stream.
www.suite101.com/article.cfm/pns/17374/1
www.suite101.com/article.cfm/pns/17374/2
It implies that vasoactive agents occur as result of kallikreins, or by injury thus producing endothelin which is responsible for vasodialation and constriction. Vasoconstriction causes hypoxia of affected tissue the first noticable sign of RSD.

Well my RSD spread body wide from the onset of burning in my limb within one week. This happened about six weeks after my surgery. I had petchia on my lower limb about 2 weeks after surgery. Doctors think I am quacked because I have told them the CRPS is everywhere. I have burning and cold water sensations inn my veins. I had an accute incident of broncioles dialation, I have pulse rate increase and blood pressure fluctuations. My chest gets tight often.

Long story short. My Dr wanted me to do another stress test, a "chemical stress test". The thought of injecting anything into my blood stream again scared me. Then the thought hit me. I had a "chemical stress test" the day before my surgery and a vasoactive agent is what is used in the test. I started looking at the common drugs used in chemical stress test and low and behold, some affect the sympathetic nervous system. These articles imply there may be a cure with the correct drugs if indeed the spread came through a chemical compound through the blood stream.

My question I would like to ask everyone is how many people here with body wide RSD or rapid spreading have had a chemical nuclear stress test done before the spread occured?

I hope I am on to something and already am talking to DR next week about this.

This makes me wonder about vasoactive drugs like blood pressure meds. So simple.

I cannot explain such a rapid spread of CRPS unless by something like through chemicals in the blood stream.

Looking forward to hearing from you. Maybe someone has already gone down this road before me, let me know.

Thanks,
Jerie

Dear Jerie -

There is a ton of literature about the role of inflammatory cytokines - immune signalling cells - in the advent of RSD/CRPS. For a brief article, easily accessible to the general reader, check out this piece on the RSDSA site, "Curing Chronic Pain—Hope on the horizon?," Linda Watkins, PhD http://www.rsds.org/Research_Article...icpain_05.html For perhaps the best scientific article on the subject, see, Birklein F, Schmelz M, Neuropeptides, neurogenic inflammation and complex regional pain syndrome (CRPS), Neurosci Letters 2008;437:199-202. http://www.rsds.org/pdfsall/Birklein_Schmelz.pdf

There is also literature suggesting that patients who are already under chronic stress at the time of injury have a significantly higher chance of getting RSD/CRPS. (I'll fill in that citation as soon as I can.) The presumed relationship is that chronic stress produces inflammatory cytokines - hence its relationship with heart attacks - and that with a higher cytokine load at the time of injury, one is much more likely to have the neuro-autoimmune reaction that is now known to trigger RSD/CRPS, which in turns induces the production of a whole new batch of pro-inflammatory cytokines, etc.

What this leads me to, sadly, is whether by giving you a chemical stress test the day before surgery, your doctors may have raised your cytokine levels, leading to where you are today. So, without knowing more about how this test worked - in detail and particularity - under no circumstances would I repeat the test without talking to a serious CRPS specialist first. In fact, it sounds time to find a new doctor on general principles.

And your question on blood pressure drugs is prescient. While endothelial responses are complicated and difficult to explain. For an EXCELLENT article on the subject, check out Regulation of peripheral blood flow in Complex Regional Pain Syndrome: clinical implication for symptomatic relief and pain management, George Groeneweg, Frank JPM Huygen, Terence J Coderre and Freek J Zijlstra, BMC Musculoskeletal Disorders 2009, 10:116 http://www.biomedcentral.com/content...474-10-116.pdf

That said, currently available blood pressure medicines (such as calcium channel blockers) do so by simply relaxing vasal tone throughout the body. Which sounds wonderful, until you realize that CRPS can become in short order a disease of profound autonomic dysregulation, leading to neurogenic-vasoconstriction in one part of the body, while giving you edema secondary to vasodilation in another part, at the same time! I in fact had the chance to live this movie when my cardiologist gave me Norvasc - a calcium channel blocker - because it appeared that I was having episodes of cardiac vasospasms, only to have to return a week later with legs that he would later tell me looked like I had elephantiasis! We brought the edema down in about 6 weeks with a lot of Lasix (taken with a prescription potassium supplement, than you) but that's not a long term solution where for each liter of "interstitial fluid" diuretics remove, they take 2 liters of blood out of your system. Not a good recipe for long term kidney health, according to a nephrologist with whom I consulted when it became clear that I couldn't urinate unless I had had a diuretic within the preceding 6 hours.

And of course, autonomic-dysregulation well could explain some of your other issues. See, e.g., Complex regional pain syndrome with associated chest wall dystonia: a case report, Irwin DJ, Schwartzman RJ, J Brachial Plex Peripher Nerve Inj. 2011 Sep 26;6:6 http://www.jbppni.com/content/pdf/1749-7221-6-6.pdf AND Atypical chest pain: evidence of intercostobrachial nerve sensitization in Complex Regional Pain Syndrome, Rasmussen JW, Grothusen JR, Rosso AL, Schwartzman RJ, Pain Physician 2009 Sep-Oct;12(5):E329-34 http://www.painphysicianjournal.com/...;E329-E334.pdf

See also, Syncope in Complex Regional Pain Syndrome, Smith JA, Karalis DG, Rosso AL et al, Clinical Cardiology, 34:4, April 2011 http://onlinelibrary.wiley.com/doi/1.../clc.20879/pdf

But back to cytokines, there is one avenue of research, at least for patients whose illness is still immune-modulated (fka "sympathetically maintained") that hasn't bee looked at serious, at least in this country, even though the one published case study I am aware of was written by, among other people, Frank Birklein, MD, a young Dutch scholar who is currently doing some of the most important work going in looking at the immunological aspects of CRPS. Worth a look in any event: Successful intravenous regional block with low-dose tumor necrosis factor-alpha antibody infliximab for treatment of complex regional pain syndrome 1, Bernateck M, Rolke R, Birklein F, Treede RD, Fink M, Karst M, Anesth Analg. 2007 Oct;105(4):1148-51 http://www.anesthesia-analgesia.org/.../1148.full.pdf

I hope this is useful.

Mike

Jerie -

I realized that post my hadn't commented on the role of "kallikreins" mentioned in the online article you cited by Les Abrams, whose professional qualifications are not stated. As an initial matter, I learned that kallikreins are defined as "a hypotensive protease that liberates kinins from blood plasma proteins and is used therapeutically for vasodilation." I then ran a PubMed search for "vasoconstriction kallikreins," this was the topped ranked article in English, for which only an abstract is readily available:

Mechanisms of disease: the tissue kallikrein-kinin system in hypertension and vascular remodeling, Madeddu P, Emanueli C, El-Dahr S, Nat Clin Pract Nephrol. 2007 Apr;3(4):208-21.

Abstract
The pathogenesis of arterial hypertension often involves a rise in systemic vascular resistance (vasoconstriction and vascular remodeling) and impairment of salt excretion in the kidney (inappropriate salt retention despite elevated blood pressure). Experimental and clinical evidence implicate an imbalance between endogenous vasoconstrictor and vasodilator systems in the development and maintenance of hypertension. Kinins (bradykinin and lys-bradykinin) are endogenous vasodilators and natriuretic peptides known best for their ability to antagonize angiotensin-induced vasoconstriction and sodium retention. In humans, angiotensin-converting enzyme inhibitors, a potent class of antihypertensive agents, lower blood pressure at least partially by favoring enhanced kinin accumulation in plasma and target tissues. The beneficial actions of kinins in renal and cardiovascular disease are largely mediated by nitric oxide and prostaglandins, and extend beyond their recognized role in lowering blood pressure to include cardioprotection and nephroprotection. This article is a review of exciting, recently generated genetic, biochemical and clinical data from studies that have examined the importance of the tissue kallikrein-kinin system in protection from hypertension, vascular remodeling and renal fibrosis. Development of novel therapeutic approaches to bolster kinin activity in the vascular wall and in specific compartments in the kidney might be a highly effective strategy for the treatment of hypertension and its complications, including cardiac hypertrophy and renal failure.

PMID: 17389890 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/17389890

Then we have this, AT(2) receptor-dependent vasodilation is mediated by activation of vascular kinin generation under flow conditions, Katada J, Majima M, Br J Pharmacol. 2002 Jun;136(4):484-91. FULL TEXT @ http://onlinelibrary.wiley.com/doi/1...jp.0704731/pdf

Abstract
Physiological roles of angiotensin II type 2 receptor (AT(2)) are not well defined. This study was designed to investigate the mechanisms of AT(2)-dependent vascular relaxation by studying vasodilation in pressurized and perfused rat mesenteric arterial segments. Perfusion of angiotensin II in the presence of AT(1) antagonist elicited vascular relaxation, which was completely dependent on AT(2) receptors on endothelium. FR173657 (>1 microM), a bradykinin (BK) B(2)-specific antagonist, significantly suppressed AT(2)-dependent vasodilation (maximum inhibition: 68.5% at 10 microM). Kininogen-deficient Brown Norway Katholiek rats showed a significant reduction in AT(2)-mediated vasodilatory response compared with normal wild-type Brown Norway rats. Indomethacin (>1 microM), aprotinin (10 microM) and soybean trypsin inhibitor (10 microM) also reduced AT(2)-dependent vasodilation. Our results demonstrated that stimulation of AT(2) receptors caused a significant vasodilation through local production of BK in resistant arteries of rat mesentery in a flow-dependent manner. Such vasodilation counterbalances AT(1)-dependent vasoconstriction to regulate the vascular tone.

Comment in Br J Pharmacol. 2002 Jun;136(4):481-3.

PMID:12055126 [PubMed - indexed for MEDLINE] PMCID: PMC1573373

http://www.ncbi.nlm.nih.gov/pubmed/12055126

And finally, we have, The role of the renal kallikrein-kinin system in diabetic nephropathy, Riad A, Zhuo JL, Schultheiss HP, Tschöpe C, Curr Opin Nephrol Hypertens. 2007 Jan;16(1):22-6. FULL TEXT @ http://www.ncbi.nlm.nih.gov/pmc/arti...nihms43252.pdf

Abstract
PURPOSE OF REVIEW: Diabetic nephropathy is one of the most common complications in diabetes mellitus. Multiple pathogenic mechanisms are now believed to contribute to this disease, including inflammatory cytokines, autacoids and oxidative stress. Numerous studies have shown that the kallikrein-kinin system may be involved in these mechanisms. This review focuses on recent research advance on the potential role of the kallikrein-kinin system in the development of diabetic nephropathy, and its clinical relevance.

RECENT FINDINGS: A collection of recent studies has shown that angiotensin-converting enzyme inhibitors, which inhibit angiotensin II formation and degradation of bradykinin, and vasopeptidase inhibitors attenuated the development of diabetic nephropathy in experimental animals and clinical settings. The role of the kallikrein-kinin system in diabetes is further supported by findings that diabetic nephropathy is worsened in diabetic mice lacking bradykinin B2 receptors. Although long-acting bradykinin B2 receptor agonists have been shown to have renal protective effects, their therapeutic benefits have not been well studied.

SUMMARY: Current experimental investigations demonstrated that pharmacological intervention of the kallikrein-kinin system improved renal conditions in diabetes mellitus. These findings suggest that the kallikrein-kinin system may be a therapeutic target in preventing and treating diabetic nephropathy.

PMID: 17143067 [PubMed - indexed for MEDLINE] PMCID: PMC2276846

http://www.ncbi.nlm.nih.gov/pubmed/17143067

And in particular, please see the following paragraph form the PubMedCentral (author's manuscript) version of the last article:

Interactions between inhibition of the renin–angiotensin system and activation of the renal kallikrein–kinin system

The investigation of the therapeutic actions of angiotensin-converting enzyme inhibitors (ACEI) and angiotensin type 1 (AT1) receptor antagonists revealed complex interactions between the RAS and KKS. Such interactions are supported by the following findings. ACE efficiently degrades kinins or bradykinin. Angiotensin fragments such as ANG-(1–7) exert kinin-like effects. KLK probably serves as a prorenin-activating enzyme. Several studies have demonstrated experimentally that the protective effects of ACEI are at least partly mediated by a direct potentiation of kinin receptor response to bradykinin stimulation. We previously showed that kinins are partly involved in the antiproteinuric action of ACEI in experimental diabetic nephropathy. Furthermore, studies on AT1 antagonists, which do not directly influence kinin degradation, and studies on angiotensin-receptor transgenic mice, have revealed additional interactions between the RAS and the KKS. There is mounting evidence to suggest that an autocrine cascade including kinins, nitric oxide, prostaglandins, and cyclic GMP is involved in at least some of the angiotensin type 2 receptor effects. In addition, Siragy et al. showed that Ang II tonically stimulates renal kinin peptide production due to AT2 receptor stimulation. Although the mechanisms have not been well understood, the interaction of the KKS and RAS is further supported by our findings, showing that the renal expression of ACE in transgenic rats expressing the human KLK1 gene is reduced, whereas it is increased in kidneys of kininogen-deficient rats (Fig. 1). The clinical relevance of the newly elucidated mechanisms of ACE inhibitor inducing a cross-talk between ACE and B2 receptors, the role of ANG-(1–7)-dependent bradykinin-accumulation and the importance of AT2 receptor-dependent KKS stimulation during AT1 antagonism still remain to be determined, however. [Citation omitted.]

http://www.ncbi.nlm.nih.gov/pmc/arti...nihms43252.pdf

As I read it, what we have can be boiled down this. There are different forms of vasoconstiction. The most common, that which is in particular associated with diabetes, may be subject to the kallikrein–kinin system. On the other hand, what we are dealing with in RSD/CRPS is something altogether different, neurogenic-vasoconstiction, which is not mediated by the endothelial cells that line the blood vessels, but rather by the autonomic nerves that "enervate" (are profused through the tissue) of all but the smallest of blood vessels, i.e., the capillaries, thereby regulating the "tone" of the vessel, in other words, allowing it to expand or contract as necessary. In support - and in plain English - allow me to submit the following extended excerpt from the (non-copyrighted) Wikipedia article on Blushing:

Blood vessels

The skin contains a network of small blood vessels that have tiny muscles inside the walls. These muscles are under the control of the sympathetic nervous system. Blood flow to the skin provides nutrition to the skin and regulates body heat. Usually, the muscles are partly contracted (squeezed). If the muscles contract more than normal, for example in cold weather, the blood vessels also contract so that less blood passes through them, and also reduces the loss of body heat. If the blood flow is restricted, the skin becomes pale and white. When the muscles are completely relaxed, for example in warm weather, the blood vessels dilate (widen). This allows more blood to pass through the skin, and resulting in the body radiating more heat, and making the skin appear red.

The circulatory system of the skin contains three major types of blood vessels:

(1) Arteries, capillaries, and veins that serve mainly nutrition needs.
(2) The subcutaneous venous plexus that plays a major role in the conduction of heat, and contains a major fraction of the cutaneous blood volume.
(3) Arteriovenous anastomoses which can be found in areas of the body especially exposed to maximal cooling like the hands, feet, nose, lips and ears. These areas are called apical structures and are richly innervated. The anastomoses connect cutaneous arterioles and venules directly, playing an important role in the reduction of blood flow in a cold environment

Regulation of blood flow in the skin

Blood flow in the cutaneous resistance vessels and the subcutaneous venous plexus are both neurally and locally regulated. However, there are some important differences. One is, that cutaneous resistance vessels exhibit a basal tone independently of innervation in reaction to passive stretch induced by blood pressure. This intrinsic basal tone is normally absent in cutaneous capacitance vessels.

Along with this basal tone, all resistance vessels in the skin receive a tonic outflow from sympathetic vasoconstrictor fibers. This tonic outflow is inversely associated with body temperature. Vasodilation therefore occurs passively in resistance vessels the (alpha-adrenergic) vasoconstrictor tone decreases. Furthermore, an active neurogenic vasodilation must be assumed in the human skin. However, it is not clear if this vasodilation is mediated by specific vasodilator nerve fibers or if neuro-humoral effects are involved that are associated with the sympathetic cholinergic activation of sweat glands. Although some experiments lead to the conclusion that sympathetic outflow is involved in facial vasodilation 40 years of research have not clarified the mechanism behind active vasodilation.

Cutaneous veins also are richly innervated with sympathetic vasoconstrictor fibers. The effect of activation of the outflow of these fibers is reduced by local cooling. In addition, cutaneous veins are temporarily reactive to various other stimuli. Each of the following can cause remarkably intense venoconstriction without obvious value to the organism: emotional stimuli (e.g. startle, apprehension, discomfort), hyperventilation, deep inspiration, and the Valsalva maneuver.

In resistance vessels, increased pressure mainly increases flow per time unit. In the cutaneous venous plexus with its generally slow flow rate, pressure mainly influences volume. Because of its enormous volume variability and its large potential capacity the venous plexus is believed to determine skin color. Since pronounced blushing is also characterized by a deep reddening of the skin, vasodilation of the venous plexus is probably the physical mechanism underlying it. Emotional blushing is only visible or apparent in a specific area called the blush region. The area is restricted to the face, ears, neck, and in some rare cases the upper body. Two main hypotheses to explain this regional restriction have been proposed. One is that vasodilation takes place throughout the entire skin of the body but is only visible in the blush region due to special anatomical structure of that region. The second is that a specific form of vasodilation takes place exclusively in the blush region. It is likely, that a combination of these two factors accounts for blushing. [Citations omitted]

http://en.wikipedia.org/wiki/Blushing

I apologize for the length of this post, but in the interest of clarity, I thought it important to make the distinction as clearly as possible.

Mike

Hi Jerie,

You have certainly had a very rough time of it. Please avoid a repeat of this procedure. If your doctor pressures you maybe it is time to seek another opinion. Additionally, if your doctors don't believe that CRPS spreads you must keep looking.

If I might add another caution please be very careful with internet sources that you select for guidance in your journey. The material posted by Les Abrams is questionable. Mr. Abrams describes himself as a "researcher" when in fact his professional experience has nothing to do with clinical research. A little hunting revealed that he has some sort of background in computers and prepares blog like material on everything from "plant intelligence" to "consumer issues." He uses no citations to validate his assertions.

I only mention this because I have seen other forum members recommend Abrams and it is potentially quite risky. Really do your homework. It is far safer to search Clinical Trials.Gov or Pub Med as Mike quite proficiently and routinely does.

Have you exhausted less invasive treatments? Do you have a treatment team open to trying more cutting edge treatments. Although many pain management doctors are knowledgeable in CRPS, many are the one way docs. You are the nail and they are the hammer.

You sound like you are already a great self-advocate! Better days are ahead for you!

Hi,
I have not even gotten of the ground yet .I have no doctor and no treatment plan. I want to do the aggressive attempt to close the sympathetic gate because I had surgery in May this year and I already have CRPS body wide and internal. I also am a recovering alcoholic. I did not survive addiction to live on medication the rest of my life. I am only 51 and I would like to have a little quality of life. I spent most of my life before sobriety in misery. I would like to have some emotional and physical "normal life time" during the rest of my stay on earth. I am still trying to talk a VA anesthesiologist at the pain clinic into helping me. Maybe I should just go inpatient to their Florida hospital that does nothing but pain. The VA doctor said she had RSD experience but I am still not convinced yet. When I came to the visit she wanted to address fibromyalgia and I had called 2 times before my appointment to make sure she knew something about RSD and to affirm I was not coming to discuss fibro, but CRPS. I have been repeatedly under treated and it spread so fast before they even got on board with RSD. If I hadn't taken pictures of my leg when I was having edema and color changes they still would be blowing me off. I probably need more help than she can give me. But I don't want to have to reinvent the wheel every time I see a new doctor. I want to start treatment now. I believe nerve blocks are the best thing to do for my organs considering the issues are wide spread sympathetic burning and cold water sensations in my veins and skin. I only have one kidney. Thanks for the heads up on the researcher. I now need to try to decipher all these articles into laymans terms I can understand. I kind of got the impression that the vasodialation and constriction may not even be related to those particular chemicals noted in Abrims articles in CRPS.
Jerie

Hi Mike,
Thank you so much for all the information. It is pretty much over my head so I will have to take a while and try to digest what all this means. I just started down this path when I saw the blood spread theory because it made sense to me in my case. Like I said I just had a "small still voice moment" when worrying about doing another chemical stress test. One of my first trails was concerning vasodialation as I had bronchioles dilation and flushing up my neck one day and I went and got a toradol shot because my body was freaking out. I started looking at arterioles dilatation due to SNS activity. I do wonder about substance P as I do have fibromyalgia too. Your experience with elephantiasis type symptoms leaves one to be careful what treatment you do and what you let doctors do to you.
I appreciate the information. I have to see the anesthesiologist at the pain clinic weds and I need to have an intelligent conversation about the approach I want to take and why. I was thinking a clonidine patch might benefit me because it settles sympathetic activity down, but who knows what blood pressure meds will do to me. I thought alpha and/or beta blockers might help too. Now I am not so sure if I want to go down that trail or not.
Right now I have low sodium and high potassium levels. I have high ferritin levels and low blood iron. My calcium level is on the low side and proteins are low too which is weird because I am a meat and dairy heavy diet carnivore. I also eat salt like crazy. It's like I am not absorbing nutrients and they are dumping in the tissues and bones or out of my body. I didn't have protein in my urine though. Nothing but my ferritin level is really that abnormal, the rest is just outside normal ranges. I'm not a scientist, chemist or doctor. I am educating myself as fast as I can because everything I have read indicates prognosis is poor for the kind of symptoms I have. I need to get the SNS turned off asap. I tried antihistamines to see if I got any relief and I didn't.
If you have a short story explination I'll take it too.
Thanks,
jerie

Jerie -

Really quick. It just occurs to me that if the "nuclear/chemical stress test" was simply an [insert name of isotope] blood perfusion study - typically of the heart - where addenosine is used to stimulate cardiac activity, I wouldn't worry about it, I have had them done repeated since getting CRPS and the worst thong I got was an apparently false negative: followed by a small heart attack a few months later.

But then I don't understand why a doctor would be wanting to re-administer it within such relatively short period of time. Which would suggest that you may have had another test entirely???

And as far as the other symptoms you describe, I am equally at a loss. Running a search for "ferritin weight loss night sweats" in PubMed gives me four articles, each pertaining different diagnoses, although there appears to be a slight tipping of the scales in favor of rheumatological disorders. Right now, I think the most important thing you can do is to be worked up by a good internist. Not sure whether the VA is up to this or not.

But when you before you see your pain specialist next Wednesday, you might want to go onto PubMed at http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed and run the search I suggested or just click on http://www.ncbi.nlm.nih.gov/pubmed?t...night%20sweats which includes the search terms. Then click on the boxes by each journal reference and hit "Send to" in the upper right portion of the screen. That will produce a small drop-down screen, on which you should click "Email." Doing so lengthens the drop-down screen and gives you more fields. Under format, scroll down to "Abstract" and then beside it check the box "MeSH and Other Data," then enter your email address and under "Additional text," type in "PubMed search results for 'ferritin weight loss night sweats,'" so that the email will be nicely labeled. Then click on the "E-mail" button, which should present a screen with a green check mark at the upper left and the notation “E-mail sent to [email account address].”

Then check your email for something from “Sent by NCBI,” open it and you should have a nice page with each of the four abstracts, which you can print out and bring to your appointment. If you have a spam filter in place, check the “Suspect Email” box, or whatever it might be called in your email program.

And should your doctor ask you just what type of an internist you had in mind, it couldn’t hurt to start with a rheumatologist. The worst they will do is draw a lot of blood and send it off for analysis.

Short of getting you the promised authority on a suggested link between chronic stress at the time of "injury" and CRPS - which I will get you - that's much of what I know. Again, I'm just like you, my formal training in the biological sciences doesn't extend beyond a couple of classes I took in college to satisfy the general degree requirements, on my way to getting a BE in Econ and then a law degree. If I have any advantage it's that 20 years of practicing law made me fairly comfortable with online data bases, skills that transferred with surprising ease into the public medical data search tools ballerina mentioned earlier.

Good luck!

Mike

Hi Mike,
I think I may have a couple issues going on and one may be arthritic. I am changing my diet to see if I can get my body to use iron instead of dump it into my bones and tissue. I think Iron overload is a real probability from my animal product diet. It may not even be related to RSD. I did find an interesting article on substance P and neurogentic inflamation in arsenic-induced vascular dysfunction. I had high arsenic in a hair sample done at a naturalpathic doctor along with very high uranium levels. A cross over of issues may need to be addressed. I am getting a radon test for my home and will do a metal toxicity chealation and see what happens next. Thanks for all you help. I appreciate it.
I had another disturbing health event this week. I had severe head pain in the back of my head along with severve cold sensations in my left eye and surrounding area. I almost went to the ER. The next day I had double vision in my right eye so bad stop signs were even difficult to read. Hope RSD isn't in my brain. This stuff is weird, very weird.

http://www.ncbi.nlm.nih.gov/pubmed?t...%20dysfunction

Dear Jerie -

Thanks for linking me to Involvement of substance P and neurogenic inflammation in arsenic-induced early vascular dysfunction, Chen SC, Tsai MH, Wang HJ, Yu HS, Chang LW, Toxicol Sci. 2007 Jan;95(1):82-8 Epub 2006 Oct 20 http://toxsci.oxfordjournals.org/con.../1/82.full.pdf That said, you don't offer a guess as to how you might have been exposed to arsenic.

Then too, uranium and radon, while both radioactive, are two entirely separate elements with distinct chemical properties. To be candid, my suspicion is that your naturalpathic doctor may be selling you a bill of goods. There should however be an easy way to check this out, where either diagnosis would cause major alarm among public health officials. I can't imagine that it would be too much of a problem to arrange for free and independent testing through your county health department. PLEASE do so before giving any more money to this "doctor."

You then say:

Hope RSD isn't in my brain. This stuff is weird, very weird.

Please don't take this the wrong way, but after a few years, CRPS/RSD is literally "all in your head." It is in fact maintained by the brain.

The two most prominent articles are 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 http://www.rsds.org/pdfsall/Geha_Baliki_etal.pdf and Abnormal thalamocortical activity in patients with Complex Regional Pain Syndrome (CRPS) type I, Walton KD, Dubois M, Llinás RR, Pain 2010 Jul;150(1):41-51, Epub 2010 Mar 24 http://www.rsds.org/pdfsall/Walton_Pain_2010.pdf

However, both articles are exceedingly technical. Your best bet may be the "Commentary" that was published to the study by Walton, Dubois and Llinás, Thalamocortical dysrhythmia and chronic pain, Jones EG, Pain 2010 Jul;150(1):4-5. Epub 2010 Apr 14 http://www.rsds.org/pdfsall/JonesEG_Pain_2010.pdf

Hey, at least we have a disease that's interesting. That must count for something. Right?

Mike

Hi Mike,
The natropathic dr said they test for naturally occuring uranium and radon is a by product of natrally occuring uranium. He told me to get a radon test done in my house. I would not be at all surprised what is in our water supply in my town. We have TCE contamination and an active plume here, which I lived in the active area for 5 years and didn't even know it. No one drinks the water here. I use to get rashes after showering when I lived at my old house. Arsenic in the water wuld be the first place I looked, or my husband is over me, lol. He suggested a chelation for metals in my report but never pressured me for anything or to buy anything. I did think I needed to retest. It did seem as high as my uranium levels were the health department should have been notified. I'll ask them tommorrow about it.
I personally think CRPS is all in the spine and the brain is it's victim. The chicken or the egg? Who knows, it is complex for sure. I bet when they fiugre it out it will be something simple to turn if off. It seems like many factors set it up, but does it really? Maybe we just haven't figured out the common denominator yet.