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Member
Join Date: Dec 2006
Posts: 808
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To Vicc... some more questions for you...
Quote:
Originally Posted by Vicc
Hi IHH,
I try to mention my history in occasional posts because your first question would be mine. So here goes, and this is the short version.
I was first disabled in 1979, when an ortho surgeon botched two laminectomies; first by puncturing the dura (the outer of three layers of the spinal cord cover) then not plugging the leak properly. A week later I began leaking cerebro-spinal fluid into the tissue of my lower back. He went back in, couldn't find the leak and so grafted a patch of muscle to the dura much like one would patch an old inner tube.
Its kinda tight in that area, and his graft has been pressing against the spinal cord and causing moderate to severe pain for 26 years. The diagnosis was scar tissue/recurrent disk at L5 and L5 radiculopathy on the left.
After ten years of trying to restore my strength and endurance, I finally realized that I was never going to build a bridge or drive a truck again; so I went to college and became a social worker. I could only walk about 200 feet using a cane, so voc rehab bought me a power wheelchair for work.
Then my job description changed so that it would no longer require a licensed social worker; I would do much the same work and get the same pay, but I wouldn't be a SW, nor would the state provide continuing ed for my license.
I took a job as SW at a state psych hospital, where five months later a large and violent patient grabbed a smaller patient by the wrist and began running full-tilt toward me.
The big patient dodged around me, pulling the smaller one into me...and kept running while still holding her wrist. The top half of my body twisted a bit more than 90 degrees while my butt stayed firmly planted in the chair.
The net result was diagnoses of bilateral epidural fibrosis (scar tissue) at S1, compressing both S1 nerve roots (severe pain); bilateral S1 radiculopathy; bilateral leg pain, and arachnoiditis (scar tissue on the arachnoid, the middle layer of the spinal cord cover), and finally - months later - RSD of the left foot.
A work comp whore wrote that I had faked the 1979 disability and was faking the 1995 injury. The MRIs, ct-scan and EMG confirmed the diagnoses. After five years of Hell, and no treatment for any of my injuries (except a couple of nerve blocks for the RSD) the law judge ruled I was too disabled to attend hearings. WC settled at 99% disability.
The bottom line is that since my 1995 injuries I have not been able to tolerate the pain that would go along with trying to access HBO (it takes the pain three days to subside to normal after a trip to my doc's office).
Next; I can't be sure which studies you refer to, but I would guess they are what is called case studies: individual reports about a specific patient. Case studies are not research, they can't be replicated by following the protocols of the original doc (because there were none), and are generally considered only somewhat more reliable than anecdotal reports.
One would think, however, that with so many RSD patients undergoing physical therapy, if it were effective we would at least see dozens, if not hundreds of case studies reporting cures.
PT is about the only way for patients to maintain any range of motion (ROM), which is critical if we are to keep our joints functioning. If RSD is an IRI, however, PT involving more than minimal weight bearing can be harmful: muscle cells "break down" during exercise and are restored to an even stronger state during rest, but only if they receive adequate oxygen and nutrients. IRI means, by definition, that they aren't.
I am currently working on a long-delayed reply to a post in which I describe exactly why RSD cannot be the result of a nerve injury. In it, I may or may not point out that CRPS-I is different from CRPS-II precisely because there is no nerve injury in the former. There is no nerve injury leading to the latter, either: just a convenient nearby nerve injury that can be blamed.
100% wrong 100% of the time: When RSD was first discovered, it was attributed to nerve damage caused by high velocity impacts such as shrapnel or gunshots. It was thought that these types of wounds injured nerves some distance from the actual site. We know now that that even the most insignificant trauma can lead to RSD. High velocity impacts are not the cause of what was called causalgia at the time.
In 1916, a French Army surgeon during World War I saw his first RSD patient, and noted that every place the soldier said was painful was also purple. He had seen cyanosis in a patient who suffered from "a rare sympathetic disorder" who reported severe pain in cyanotic tissue.
He began investigating RSD; examining patients, and noted that most, but not all, showed cyanosis in the areas they reported pain. This was before anyone realized that minor injuries could lead to RSD, but it fit the causalgia picture.
Most sensory nerves of the peripheral nervous system (PNS) are close to the skin surface, while those of the sympathetic nervous system (SNS) are found deeper inside the tissue, where they are more protected from injury.
LeRiche argued that causalgia was the result of damaged sympathetic nerves. These nerves control arterial blood flow by dilating and contracting the smooth muscle that surrounds arteries, so damaged symp nerves were abnormally constricting blood flow through the arteries. This not only explained cyanosis, but every other sign and symptom of RSD; except one, symptom migration (or spread).
In the early 1940s. a test was developed that could measure arterial blood flow. This test would prove LeRiche was right; but it didnt.
Researchers found that arterial blood flow in RSD affected limbs was equal to, and sometimes greater than that in contralateral (opposite) unaffected limbs and the limbs of control subjects. Abnormal vasoconstriction caused by damaged sympathetic nerves is not the cause of RSD.
LeRiche publicly abandoned his hypothesis: Few others followed suit. This disorder was renamed reflex sympathetic dystrophy about two years after it was proved that it isn't RSD. For the next 60 years, there has been nearly unanimous agreement that RSD is caused by damaged sympathetic nerves, despite this proof.
In 1995, a consensus of the International Association for the Study of Pain (IASP) agreed that this isn't RSD, and should be renamed CRPS. They devoutly believe CRPS is the result of a nerve injury, they just can't figure out which nervous system is involved. No one at IASP seems to have noticed the contradiction between belief in a nerve injury and their definition of CRPS-I as having no nerve injury.
There is now a campaign to attribute RSD/CRPS to a spinal cord issue called central sensitization. I will discuss that in my delayed post, so there is no point in going over that now.
High velocity impact: Wrong. Sympathetic nervous system: Wrong. Central sensitization: nonsense, as I will show this week. 100% wrong 100% of the time.
RSDSA has long clung to the SNS view of this disease. The quote you make is their attempt to keep the nerve damage idea alive. They obviously know what IRI is, and are just as obviously distorting the facts to prove a false claim.
The nerves are getting chemical pain messages from oxygen and nutrient deprived cells, which they pass on to the brain. They are also sending pain messages to the brain because they aren't getting enough O2 or nutrients. They can only communicate with the brain by sending pain messages.
One could, I suppose, argue that pain messages from pain sensory cells are abnormal, but they are a response to an abnormal condition (oxygen deprivation), so they aren't abnormally firing after all. Just telling the brain: Houston, we have a problem
Where does the immune system fit in? IRI begins with the immune response to trauma; a response that goes out of control instead of ending after no threat is discovered.
The entire IRI process has been documented by dozens of researchers under strict, scientific protocols. This mishmash from RSDSA is not the result of research. It comes purely from the imaginations of the authors.
BTW, absence of proof is not proof of absence. (I'm not sure exactly what that means, but it sounds neat). I'm guessing it means that just because you can't prove something (like nerve damage in RSD), it doesn't mean you have proved there isn't nerve damage.
Experts in RSD are fond of saying things like that because there is no published research linking nerve damage to RSD; nor is there any neurological test that can demonstrate abnormal nerve activity in RSD. No evidence of nerve damage in RSD but almost 100% agreement that it exists. 100% wrong 100% of the time.
I can't prove that GSE prevents symptom migration. I can, and have, offered my experience in previous posts at BT, all of which are gone now.
Basically, after studying the research into IRI, it seemed more likely to me that this is an IRI than a nerve injury. One of the things I learned during my review of the research was that IRI from surgeries could be prevented simply by applying vitamin E (an antioxidant) to the wound site.
My RSD had already migrated to my right foot by the time I learned this and decided to begin taking GSE, a more powerful antioxidant. Since I began taking GSE in early 1998, I have not experienced any symptom migration.
I stopped taking GSE twice: once deliberately, deciding to rely on the topical antioxidant DMSO instead; one I was so (literally) distraught over personal issues that I forgot to take any for several days.
Both times, within days of stopping, I began to experience the mild sunburn pain of inflammation over 100% of both arms and both legs. After resuming GSE, these symptoms completely subsided.
I can't prove that these signs of inflammation would have led to RSD, but I know that the disease begins with the red warm skin of inflammation, then develops into the cold, blue to purplish color of cyanosis. That was enough to convince me, and I hope it will be enough to convince others.
Some members have told me they began taking GSE after reading my posts. None have reported any symptom migration. That may change now that I've mentioned it. We will have to see.
Finally, I not only welcome questions, I have been known to beg for them. I don't get many. In fact, it is often true that my name as the last to reply to a thread is the kiss of death to that thread. No more replies; it simply falls off the page.
I have been discouraged by this more than once; feeling that no one is really interested. I bounce back, though. People may not read what I write, but I continue writing about RSD.
There are times I wish some evidence would arise that would prove me completely wrong. Then I could stop working on an article I have never been able limit to under 2500 words and start watching Days of Our Lives (is that still on?).
This post is probably more than 2500 words, and doubtless there are many who long for the days when I was too weak to write anything close to that number...Vic
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Hi, Vicc. I appreciate your reply... I have not forgotten to respond, I have just about no energy, but I do have many comments and questions regarding your post.
First, I am going to try the GSE. Anything is worth a try. Though everyone IS different. That seems to be the case with different RSD treatments, as I am about to say again... I think you have to be careful when saying that it prevents migration of symptoms. That is something you really cannot prove. Yes, you believe it did in your case. But everything is so unsure about RSD. For instance, some people's RSD spreads, and others it doesn't. Some people have sucessful treatment with nerve blocks. Others don't. I think that you never can be sure. RSD plays by no certain set of rules.
Could you please give me the link to the article written by one of the RSD "experts" on IRI? I would really like to read up on that.
The study regarding children/ adolescents with RSD who were treated with physical therapy can be found here:
http://www.rsds.org/2/library/articl...ive/index.html
under: Author: Sherry DD, Wallace CA, Kelley C, Kidder M, and Sapp Lyn.
Title: Short-and Long-term Outcomes of Children with Complex Regional Pain Syndrome Type I Treated with Exercise Therapy.
(check out the other articles they have there, too)
I know that this is children being treated with PT, and not adults, but I still think that it is proof that RSD can indeed be TREATED with physical therapy. In fact, in this specific study of 103 children, they did not use any medications. So, there is proof that physical therapy alone CAN be used for RSD patients. In fact, opposite to what you are saying, weight bearing is the most important thing to do!
If you state that you believe HBOT to be the "only available therapy that offers any hope for ending the ravages of RSD", I do have another question... I have a friend who had RSD 12 years ago. He went to PT for a year, and 9 months into it received nerve blocks. All his symptoms and pain dissapeared through them both (along with medications) and he is symptom and pain free to this day. How do you suppose that people do recover, when they do not receive HBOT? Right here I am suggesting that I think your theory cannot be 100% correct. Because everyone is different. With RSD there is not one thing to do. Different treatments help different people.
Since you don't believe RSD involves the sympathetic nervous system, what causes the sweating, and even blood pressure changes that people with RSD experience? Is that not something that the SNS is doing?
More about the HBOT: it is not always sucessful, huh? Do you think it has better results than any other treatment? It certainly isn't 100%.
I do have other questions for you, but don't have the time or energy right now. I wish I knew 100% that you had it all correctly, but I see flaws with some of the things you are stating. And, I am seriously questioning your statements. Thanks for your time. 
I am glad you want questions... but I hope you don't regret that. 
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