What’s coming up… so much is happening in the understanding of RSD… what could that mean for us as patients.
February 8, 2012 at 10:41pm
There has been a lot information about Reflex Sympathetic Dystrophy Syndrome (RSD)/Complex Regional Pain Syndrome (CRPS)/ Causalgia (and the other 20+ names this disease has gone through in the last 150 years). Until 2007, we didn’t know the biomechanical makeup of the condition and therefore it was classified as a syndrome. A syndrome is the association of several clinically recognizable features, signs (observed by someone other than the patient), symptoms (reported by the patient), phenomena or characteristics that often occur together, so that the presence of one or more features alerts the healthcare provider to the possible presence of the others. As all things in the medical field, it is taking time to get the new information out to the healthcare professionals on the front line, but organizations such as American Academy of Pain Management, American Academy of Pain Medicine are forging the way in healthcare provider’s education.
According to Dr. Prager, the International Study of Pain Association is currently working on an update of the classification of RSD and anticipate having that information available on our website by mid-March. He is currently the Chair of the Pain and the Sympathetic Nervous system (PSNS) Complex Regional Pain Syndrome Group of the International Association for the Study of Pain (IASP).
Now that we know that RSD is a disease not a syndrome there has been a bit of buzz about a name change. Neuro Inflammatory Disease is the name being reported to the Power of Pain Foundation by multiple researchers and scientists in the RSD community. We have been talking about this name change since September, 2009 and it only makes since that the more we learn, the more accurate in naming the disease, diagnosing the disease, and treatment options that are more specific, will make leaps and bounds. I actually stopped the printing of my second book, on RSD entittled ReMission Possible, due to the new information that came out right as we were going to press. I wanted to be sure to include it before printing. A great article in Pain Practicinar interviews Dr Cooper (who’s daughter has RSD and he is a board member of rsdsa) talks a lot about the advancements that are being made in this area as well. http://www.rsds.org/pdfsall/conference%20speakers%202011%20pdfs/Pain%20Practitioner.pdf
We now know that when you have RSD you have glial activation or Neuro Inflammation in your spine and brain. Glial cells, sometimes called neuroglia or simply glia, are non-neuronal cells that maintain homeostasis, form myelin, and provide support and protection for neurons in the brain, and for neurons in other parts of the nervous system such as in the autonomic nervous system.[1] In the human brain, there is roughly one glia for every neuron with a ratio of about two neurons for every glia in the cerebral gray matter.[2]
Neuroscience currently identifies four main functions of glial cells: to surround neurons and hold them in place, to supply nutrients and oxygen to neurons, to insulate one neuron from another, and to destroy pathogens and remove dead neurons. For over a century, it was believed that they did not play any role in neurotransmission. That idea is now discredited;[3] they do modulate neurotransmission, although the mechanisms are not yet well understood.[3][4][5]
Studies done by Dr. Linda Watkins demonstrate the glia activation that occurs in RSD patients. http://www.rsds.org/pdfsall/watkins.pdf. Dr. Bonati from Australia, was the first doctor I have heard of to bring to light the F-MRI being used in RSD patients and can be used as a way to determine if a patient has RSD. I am not sure if he is the first doctor to discover it, but he has been instrumental in it. Dr. Joshua Prager says F-MRI’s are widely available instruments and increasing applied technology, no radiation is involved, better spatial and temporal resolution than PET or SPECT scans, Anatomic and functional imaging performed at same setting, and F-MRI’s are a practical and unique tool for assessing neurological disorders. More from Dr. Prager can be found at http://www.rsds.org/pdfsall/CRPS%20%20for%20RSDSA_Prager.pdf. Another study w/ published results on F-MRI reveals distinct CNS processing during symptomatic and recovered complex regional pain syndrome in children done by David Borsook, MD, PhD, P.A.I.N. Group, McLean Hospital, can be found at http://www.rsds.org/pdfsall/Lebel_Becerra_Wallin.pdf.
There is also talk of RSD being an autoimmune condition after a recent paper was published by Pain® printed by IASP published this past April, 2011. According to this article, researchers have found that some CRPS patients had functionally active autoantibodies against the muscarinic 2 receptor(M2R) and the beta2 adrenergic receptor (b2AR). Intriguingly, their initial investigations did not target the nervous system, but eventually they returned to it. Here their objective was to identify the autoantigens to the antibodies and to assess the functional activity of the antibodies. Theoretically, the agonistic M2R antibodies found in the CRPS patients should thus be protective and should counteract the pathological process in CRPS. Of course, the effect of M2R antibodies may be different in in vitro and in vivo settings. For this reason, any conclusions drawn must be considered tentative. In particular, before treatment is directed at the autoantibodies, more information as to their function, i.e. whether they are pathogenic or potentially protective,, should be collected. I have posted the full article at https://www.facebook.com/note.php?note_id=10150348483394860. This is exciting news and we again, have been told by reliable sources that since this paper was published, that more advancements have been made and that they are projecting that a blood test be available in the United States for RSD by the end of 2012.
As we all know, it takes time to get any changes to our medical diagnosis, treatment option coverage and education of healthcare professionals and patients. Please keep looking for more and more info on these issues because it will be developing over the coming years. Health journals and publications are slow to put out new information as well, but as the next few years go by we can only hope that what is being reported to us is accurate and will come to light, giving even more hope to everyone affected by RSD/CRPS or whatever else it is being called.
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Jessen, Kristjan R. & Mirsky, Rhona Glial cells in the enteric nervous system contain glial fibrillary acidic protein Nature 286, 736 – 737 (14 August 1980); doi:10.1038/286736a0
a b c Azevedo FA, Carvalho LR, Grinberg LT, Farfel JM, Ferretti RE, Leite RE, Jacob Filho W, Lent R, Herculano-Houzel S. (2009). Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. J Comp Neurol. 513(5):532-41. PubMed
a b Swaminathan, Nikhil (Jan-Feb 2011). “Glia—the other brain cells”. Discover.
Gourine AV, Kasymov V, Marina N, et al. (2010-07-15). “Astrocytes control breathing through pH-dependent release of ATP”. Science 329 (5991): 571–575. doi:10.1126/science.1190721. PMID 20647426
Wolosker H, Dumin E, Balan L, Foltyn VN (2008-06-28). “Amino acids in the brain: d-serine in neurotransmission and neurodegeneration”. FEBS Journal 275 (14): 3514–3526. doi:10.1111/j.1742-4658.2008.06515.x. PMID 18564180
