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Broken Blood Vessels
Hi
I'm in a flare since my dental work and have a couple of broken blood vessels that happened for no reason. Does this happen to you since you got RSD? Pam |
Are you taking 500mg of vitamin C each day? I did this for 50 days after my root canal to help control RSD flaring and to aid healing. I read it somewhere on the Internet. Not sure if it made a difference, but it may be worth a try. I get broken blood vessels all the time. I think the vit-C really helped me, but that is just my system.
Also, the tooth that had the root canal hurt like crazy (really sore and hurt to touch with a toothbrush) for a good three months so don't get discouraged if you have pain and soreness for a while. Mine has really just now started to calm down this past month. Did you take something for pain so you weren't hurting a lot after the surgery? I didn't take anything more than my usual. |
It's funny, I've noticed the same thing for years and having even had the bruises photographed (always at the same spot near the site if the initial injury) but none of the doctors I mentioned this to had any idea what was going on.
On the Vitamin C question, I went to Ask the Dietitian (Joanne Larsen MS RD LD) http://www.dietitian.com/vitaminc.html and got the following: Q: I have a question regarding bruising. I am a very active person, but I bruise a lot easier than I've noticed on other people. Also, when I do bruise, bruises stay for quite a while. I have started taking my multivitamin at the recommended dosage, but I am wondering if I am lacking a certain vitamin or mineral that I should take additionally. I always try to have a very healthy diet. Is there a solution? It is almost embarassing to have bare legs and arms.And this from a site called NaturalNews.com http://www.naturalnews.com/021924.html How to Tone Your Blood Vessels and Reduce Your Risk of Heart DiseaseThe link to hemorrhages and CRPS may be anyone's guess, although it may relate to endothelial dysfunction, where CRPS is known to trigger an increase in certain inflamatory cytokines that are directly tied to heart disease. That said, theory of long standing would support the notion that a release of blood would be read by the sympathetic nervous systrem as trauma, which would trigger production of adrenaline or related substances - whether in the adrenals or specialized nerve cells -that would then cause the immediate constriction of small blood vessels, and this in turn could easily trigger a flair. In fact, I've been specifically warned by one of my doctors to be extremely careful in attempting to trim the dystrophic(?) calluses that have surrounded my RSD effected feet, lest a cut send "the wrong message" to the powers that be. Looked at another way, it's a close analagy to how stress tirgger flairs, of albeit shorter duration, by the production of adrenaline. And once that starts flowing through the system . . . . Mike |
Bumping up
My last post had an incomprehensible concluding paragraph, :o which has now been corrected. And to which I would humbly beg the reader's attention.
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Thanks
Wow,
I really appreciate all the information. I've printed it and plan to read it several times. My comprehension isn't what it was before RSD. Again, thanks so much, Pam |
Check out these abstracts on endothelial dysfunction and CRPS
Exaggerated Vasoconstriction in Complex Regional Pain Syndrome-1 Is Associated with Impaired Resistance Artery Endothelial Function and Local Vascular Reflexes, Dayan L, Salman S, Norman D, Vatine JJ, Calif E, Jacob G. Journal of Rheumatoly 2008 May 1.
From the J. Recanati Autonomic Dysfunction Center, Orthopedic Department B, Rambam Medical Center and Faculty of Medicine, Technion-IIT, Haifa; and Outpatient and Research Division, Reuth Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. OBJECTIVE: Local regulatory mechanisms and microvascular function play a major role in the pathogenesis of hemodynamic and trophic changes in patients with complex regional pain syndrome-1 (CRPS). Venoarteriolar and venoarteriolar-myogenic reflexes (VAR, VMR, respectively) as well as endothelial-dependent vasodilatation are important contributors to local vasoregulation. We examined whether VAR and VMR as well as resistance artery endothelial function are damaged in affected limbs of patients with CRPS. METHODS: We measured reactive hyperemic response as an index of resistance artery endothelial function, VAR and VMR in extremity soft-tissue vasculature in patients with CRPS. RESULTS: Baseline blood flow values were not different between CRPS affected and unaffected upper and lower limbs. Resistance artery endothelial function indices, i.e., values of maximal flow after ischemia and the area under the flow-time curve (AUC), were significantly higher in the unaffected versus CRPS-affected upper limbs (19 +/- 3 vs 16 +/- 3 ml*min(-1)*dl(-1) and 373 +/- 71 vs 319 +/- 70 units, for maximal flow AUC, respectively) and lower limbs (9 +/- 2 vs 6 +/- 1.5 ml*min(-1)*dl(-1) and 160 +/- 51 vs 130 +/- 42 units, for maximal flow and AUC, respectively). Flow indices reflecting VAR were lower in the lower, but not upper CRPS-affected limbs compared with unaffected contralaterals (2 +/- 0.24 vs 1.55 +/- 0.3 ml*min(-1)*dl(-1); p = 0.027). Microvascular myogenic reflex-VMR indices, however, were not different in the upper or in the lower CRPS-affected limbs compared with their unaffected contralaterals. CONCLUSION: Impaired balance exists in CRPS-affected limbs between vascular regulation systems responsible for vasoconstriction and vasodilation. http://www.ncbi.nlm.nih.gov/pubmed/18464300 __________________________________________________ __________________________________________________ _______________ Continuous intra-arterial application of substance P induces signs and symptoms of experimental complex regional pain syndrome (CRPS) such as edema, inflammation and mechanical pain but no thermal pain, Gradl G, Finke B, Schattner S, Gierer P, Mittlmeier T, Vollmar B, Neuroscience 2007 Sep 7;148(3):757-65. Epub 2007 Aug 8. Institute for Experimental Surgery, University of Rostock, Schillingallee 69a, 18055 Rostock, Germany. Substance P is involved in nociception in both the peripheral nervous system and the CNS and has been documented to play a crucial role in the complex regional pain syndrome (CRPS). So far, however, most experimental animal models are restricted to the effect of neurokinin-1 receptor blockers to inhibit substance P and do not directly evaluate its action. Thus, this study was conducted to test the hypothesis that local application of substance P causes signs and symptoms of CRPS. For this purpose rats received a continuous infusion of either substance P or saline over 24 h delivered by a mini-osmotic pump connected to an intrafemoral catheter. Animals were analyzed at either day 1 (n=6, each group) or day 4 (n=5, each group) after start of infusion. Substance P application caused a significant and long-lasting decrease in paw withdrawal thresholds upon mechanical stimulation, while animals did not present with thermal allodynia at days 1 and 4 after onset of infusion. In addition, severe s.c. edema was observed in all animals receiving substance P. In vivo fluorescence microscopy of the extensor digitorum longus muscle of the affected hind paw revealed enhanced leukocyte-endothelial cell interaction with a significant rise in the number of leukocytes both rolling along and firmly adhering to the wall of postcapillary venules, while saline-exposed animals were free of this local inflammatory response. Muscle cell apoptosis, as assessed by in vivo bisbenzimide staining, terminal deoxynucleotidyl transferase nick end labeling analysis and caspase 3-cleavage, could not be observed in either of the animals. In summary, the present study indicates that substance P is responsible for neurogenic inflammation, including local cell response, edema formation and mechanical pain, while it seems not to contribute to the generation of thermal allodynia. http://www.sciencedirect.com/science...56267685a9ecbb |
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