Hi Again Vicc,
I know on the HBOT it is not FDA approved. Which not being FDA approved doens't mean a whole lot with me. I know a bit about how lobbiest can work, I wil leave it at that.

But I realy think Respiratory therapists need to be controlling the HBOT. But since it is not FDA approved no hospital or any R/T that I am aware of will do the treatment? Do you know of any R/T that is regulating the chambers? Because I would give it ago and book a flight right away.

Big Huge Hugs, Roz

Please checkout Buckwheat's thread entitled Scientific Presentations at http://neurotalk.psychcentral.com/sh...2485#post52485 as well as my post therein, regarding this absolutely amazing article from last Tuesday's Boston Globe that someone here was kind enough to share with me a couple of days ago, "Imaging could furnish proof of chronic pain Emotional, legal boost for patients," December 19, 2006, which includes an interview with Dr. Anne Louise Oaklander - an author cited earlier in the thread for a piece published earlier this year - and gives insight into how she has already built on that work, translating it into an honest to God treatment option:

http://www.boston.com/yourlife/healt...c_pain/?page=2

Mike

Hi Roz,

First, if/when my view that RSD is an ischemia-reperfusion injury (IRI) is eventually vindicated, the FDA problem, and Medicares threat to stop paying for Medicare patients at any hospital that uses HBO to treat anything but the disorders included in the FDA protocol, will come to an abrupt end: IRI is one of the eight (I think) disorders will allow hospitals to use HBO to treat.

I can understand your linking HBO with respiratory therapists, in a way, it is a breathing therapy. HBO, however is used to suffuse the entire body with more oxygen than our red blood cells can possibly deliver; the blood plasma carries oxygen too.

By increasing the air pressure to a higher atmospheric level than that of air at sea level, HBO somehow delivers this plasma oxygen to parts of the body that the blood in our circulatory system can't reach (in IRI, our microvascular systems (MVS) are plugged; blood can't pass through the venule of the MVS into the vein so no fresh arterial blood can't enter the MVS).

Since the problem isn't a respiratory disorder, I don't think any of the skills an R/T develops over time would be of any value.

Another problem with trying to use R.Ts is that the HBO chamber is a machine, one that constantly requires inspection and maintainence in order to insure it functions properly; especially that it delivers the desired oxygen leve at the proper atmospheric level.

LisaM's horrible experience with HBO is the result of the failure of the FDA, or even the Consumer Product Safety Commission, to establish any training or other qualifications for the people who operate HBO chambers. The FDA has very strict regulations involving the manufacture and even the advertising of HBO chambers, but doesn't appear to give a damn whether a chamber owner hires someone who has only worked at a car wash to operate one.

During the few times I have mentioned HBO, I have urged anyone considering trying this therapy to be sure that the chamber is accredited by the Undersea and Hyperbaric Medical Society (UHMS). They set very high standards for accreditation.

The problem today is that no one at the UHMS understands the nature of RSD or by what mechanism HBO affects this disease. This is why I intend to submit my article to their journal.

Also, without understanding the nature and course of RSD, there is no way to determine the amount of oxygen and the pressure it is delivered in order to achieve the best possible outcome.

The standard today appears to be 100% oxygen at 2-1/2 atmospheres (2-1/2 times the air pressure at sea level); I believe that this is too much O2 at too high an atmosphere. I hope to address this problem in my reply to Sydney's thread on HBOT, and intend to discuss it in some detail in the article I plan to submit for publication.


Mike, fair's fair, I've hijacked other peoples threads to talk in detail about what I've learned about RSD, so I'm in no position to complain about your introducing your agenda here.

I do have a question, though; I don't have time to read the link you just posted and still finish a promised reply on another thread, so can you please tell me what ",,,honest to God" treatment option Dr Oaklander offers?

I am still working on (and nearly finished) my reply to your earlier post, and have some remarks about what Oaklanders research really proves -- and it isn't that a nerve injury causes RSD -- hang in there, my friend and adversary...Vic

Vicc -

The relevant portion of the Boston Globe article is as follows:

At Mass. General, for example, Dr. Anne Louise Oaklander is already measuring "the objective correlates of pain" by counting the numbers of pain-sensing nerve endings in tiny skin samples from patients with unexplained pain. Paradoxically, patients with previously unexplained pain tend to have fewer such endings.

Such skin biopsies allow researchers to diagnose "small fiber neuropathies," the nerve damage that is sometimes a side effect of diabetes and other diseases. The nerve endings are so tiny that they have been largely invisible, Oaklander said, but skin biopsies are "opening a window into the pain system, allowing us to see when it is damaged."

Oaklander's work recently helped a college athlete who suddenly began experiencing an unbearable burning sensation in his palms and on the soles of his feet, according to a paper slated for publication in the February issue of the journal Anesthesia & Analgesia.

Greg Palladino, a lacrosse goalie at Southern New Hampshire University, was on a team trip to Bermuda last year when he began suffering a pain that only submersion in ice would alleviate. It was as though broken glass were running through his veins, he told his doctors.

He returned home and was treated repeatedly at area hospitals for weeks. Despite extensive tests, the doctors were baffled, said Palladino's father, Steven. Medicine failed to help, and he lost 55 pounds in weeks.

When Oaklander was called in, she did a skin biopsy that showed conclusively that Palladino's "erythromelalgia" -- his red, burning appendages -- stemmed from severe damage to small nerve fibers that apparently came on because of an auto immune reaction. For some reason, his body had started attacking its own nerve cells.

The biopsy gave doctors the confidence to put Palladino on enormous doses of steroids to stop the auto immune attack, and he has almost completely recovered, his father said. [Emphasis added]

I hope this is helpful. And seriously, I wasn't attempting to hijack your thread, it was just when you came on more than a little strong against Dr. Schwartzman and said catagorically that there was no evidence linking RSD to peripheral nerve changes that I felt that I had to come in.

Mike

Hey, my friend,

I posted a reply to another thread where I talked about misunderstandings over a few words...in my reply here I did my best Al Gore imitation; ruining a punchline. You apparently misunderstood some of my words too.

I did not say there is no evidence linking nerve damage to RSD; it is obvious this disease damages nerves as well as bone, tissue and vascular systems. What I said was that there is no evidence linking traumatic nerve damage to the etiology (cause) of RSD.

Now, whatever Palladino went through doesn't sound at all like RSD. It sounds terrible, but not RSD.

When a began taking the antioxidant grape seed extract (GSE), I wasn't taking enough, and about once a months I would begin to feel the sunburn pain of cutaneous inflammation and to see redness at the inside of my left wrist. I would apply DMSO (another antioxidant) topically to the area and after a couple of days the stinging and redness would subside.

During this period, my neuro let me experiment taking a prepackaged oral steroid series when I began experiencing inflammation in my wrist. It had absolutely no effect. I began to be fearful of the inflammation spreading and returned to applying DMSO.

I did continue through the end of the oral steroid regimin, as I was all too aware of the complications that can arise if one suddenly stops taking steroids. The adrenal glands can be damaged simply by taking steroids, as well as by not properly ending the regimin, but I know Oaklander knows more about this than me, and she used them appropriately with Palladino.

This is not to say that I don't believe steroids might have a role in RSD. Two months after the injuries that led to my RSD, among other things, I had a series of epidural steroid injections in the hope that they might relieve inflammation at my spine and reduce the pain there; it didn't, but it was worth a try.

Anyway, I haven't mentioned this in a long time, but I still suspect that this series of injections, and another series five months after my injuries, might have influenced the course of my RSD.

I still wonder whether steroids during the acute (inflammatory) stage might be helpful. I know from reading the literature that they are of no value in treating the chronic (ischemic) stage of this disease.

Sorry, my friend and others who might think from reading about Palladino that steroids might be the answer; they aren't...Vic

Dear Vicc -

From what I understand, we're talking about truly massive levels of steroids here. And from what I've been advised by my rheumatologist, they've known for a while that a number of people with conditions presenting like RSD respond well to such dosages, it's just that they can't be maintained over time. As such, the idea is in finding anti-inflammatories that can be taken on a long term basis.

So I guess that, when I referred to this as "an honest to God treatment option," I could have oversold it, although the language of the story suggests otherwise.

That said, it was my assumption on reading the Boston Globe piece that the sort of "small fiber neuropathies" referenced in there was the same anomoly Dr. Oaklander found in CRPS-1 patients in the study that's posted on the RSDSA webpage. See, "Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy)," Oaklander AL et al., Pain, 2006;120: 235-243 (showing a significant deduction epidermal neurite densities among CRPS-1 patients).

If anyone knows otherwise, please chime in.

Mike

Vic,
Once again you totally amaze me. You don't know how much I appreciate all that you do for all of us that suffer from this horrible disease, and while you are dealing with so much crap yourself you still find time to try and work on this for all of your fellow RSD'ers. You do truly amaze me. Thank you so much for everything you do, and as always your theory really makes a lot of sense.

Please keep up the good work. I know there are times you just have to take a break for yourself and I know that but just don't ever give up doing what you do. I know I need you.

Love ya,
Janet

Hi Vicc,
Hang in their with me. I have to have Hanukkah and Santa. Hugs, Roz

INTRODUCTION: In order to understand and appreciate the quality of my reply to Mike's previous post, it really is necessary to compare the two side-by-side or one above the other.

This is easily done by opening this thread twice, one screen for Mike's post and the other to see my reply. You can use the "restore" option and reshape the windows into two columns or one over the other.

I always try to make point by point replies, so the reader will find them in the same sequence as that in the post to which I'm replying. You won't have to look up and down either post to find the points that correspond to one another.

Hi Mike,

First, when I began working on this reply it was going to be another (typical Vic) 1,000 or so word essay. A recent insight into the serious flaws in my approach to writing about this disease (see 4-1/2 years of being wrong), altered my thinking about the need to overexplain, and I hope this will be much shorter.

I don't think I'm being hasty in my conclusion that Dr S is a fraud; we have discussed him in posts at the other forum and back then I had serious reservations about his views on this disease, but I didn't conclude that he is a fraud (in this case a deceiver who manipulates facts and research to fit into his own agenda; part of which involves garnering excessive profits from a very questionable procedure; ketamine infusions). You are the lawyer, if my analysis of his behavior and apparent motives are correct, would he be a fraud? More on Dr S later.

Yes, I do prefer abstracts over articles for many reasons; not the least of which is money. I could never afford to build up my small library of the literature on RSD, ischemia-reperfusion injury, or even the immune response to trauma if I had to pay for all those individual articles.

In addition, the damn things are nearly impossible for me to read and gain a comprehensive understanding of what is being said, too much statistical information and too many new words in "med-speak" that I would have to look up, only to learn that they are procedure specific rather than helpful in understanding the topic under discussion.

I would never post an article or link to one because I feel my several years of reading research and then learning to translate med-speak into people talk, qualifies me as the closest thing to an expert on RSD in the lay community. If I can't understand everything the article says, I am not going to pass it on to others who are even less able to understand them. If this makes me seem arrogant, so be it.

The RSDSA website does offer a limited number of research articles, but RSDSA is run by people who, the last time I looked, still believed in the SNS model. Dr Kirkpatrick, Medical Chair of RSDSA wrote a relatively recent article expounding on the benefits of the surgical sympathectomy. The man is a disosaur and RSDSA reflects his anachronistic thinking.

While many of the articles offered by RSDSA are reflective of that organization's continuing SNS agenda, doc S is also on the board, and is a powerhouse in the RSD community, so many of the remaining articles reflect his agenda. Both of these views are wrong, so I consider RSDSA a source of inaccurate and often deceptive purported research that obfuscates rather than edifies.

Speaking of inaccurate, and especially deceptive research, the article Subanesthetic Ketamine Infusion Therapy is a perfect seg-way; the first thing I noticed when I went to RSDSA to read the article is that one of the coauthors, Maleki, is a doc S co-conspirator; he authored another article that included doc S as a coauthor. That put my b**l-s**t detector into maximun overdrive. I do believe in guilt by association. If you lay down with dogs, you rise up with fleas.

The figures you cite from this study are impressive; at least until you look at them more carefully:

16 of the 33 subjects had a history of RSD of less than one year. We all know that earlier interventions offer more optimal outcomes. When half of the subjects come from this group, one can only conclude that subjects were screened to select patients with the best chance of a good outcome (no matter what procedure is being studied).

There is enough information in the literature to conclude that many patients in the acute stage of this disease spontaneously recover. The body is designed to fix itself and it sometimes does this even with RSD,

Only two of the subjects who reported having RSD longer than 24 months were followed up for more than 24 months. This represents another deceptive practice; screening subjects out from follow-up protocols. The thinking behind this is that if we don't ask them we won't have to report what we believe will be a greater number of unsuccessful outcomes.

Finally (about this article), “…every suggestion of a mechanism of action is tied to ketamine’s role as [an] NMDA receptor antagonist...” is not mere overstatement, it too is outright deceptive.

The arguments against this conclusion are too complex and involve too much med-speak to try to discuss here, but the bottom line is that the benefits from an NMDA receptor antagonist do not and cannot solve the problem of RSD, Yes they are useful; so are GABAergic agonists (stimulants) like gabapentin and gabatril (and others in this category), but the need to supplement one or inhibit the other are part of treating the symptoms of RSD, not of addressing its cause or of the process that leads to a use for these medications.

RSD begins with a physical trauma to an extremity and its signs and symptoms progress (actually retrogress) from that. Suppressing excitatory neurotransmitters or activating inhibiting ones can provide symptom relief, but they act on specific synapses in the spinal cord; they do nothing that can cure the actual disease.

Also, our neurological systems are plastic, meaning that if one route of transmission to or from the brain is blocked, new connections through other neurons will eventually be created. If the message is constantly being sent, it will find a way to reach its destination.

Your reply to my assertion that there is absolutely no research linking nerve damage to the signs and symptoms of RSD (CRPS-I or CRPS-II), cites the Oaklander and Albrecht studies, but neither of them make that link.

Oaklander found destruction of C-fiber nociceptors (pain sensory nerve endings), but did not suggest a cause for this destruction. My arguement that RSD is the result of blockage of arterial blood flow to a large number of cells in RSD affected areas offers a scientific explanation for such nerve destruction; 25% of our C-fibers are not getting adequate oxygen or nutrients, so they die.

Albrecht, et. al., report neuropathic dysfunction in the peripheral and sympathetic nervous systems. Evidence of this is not evidence that it is caused by a peripheral nerve injury, and contradicts the idea that RSD is maintained by central sensitization; which no one claims can mediate physical alteration of nerves in the body.

They report a loss of vascular endothelial [cell] integrity, then go on to claim this must be the result of neuropathic changes. Nonsense! Please refer to my first post in reply to Sydney's thread asking about HBOT. In it, I go into some detail describing a scientific fact; that the immune response to trauma always results in a temporary loss of endothelial cell integrity, and in ishcemia-reperfusion injury, the material needed to restore this cell integrity simply cannot reach the damaged cells. Without repair, this loss of integrity becomes permanent.

Now, at last, doc S, the RSD guru: In my long and checkered history I have had the opportunity to meet and talk to some really talented con-men; from "carnies" who make a few bucks to one person in particular who defrauded people of millions. The really good ones always come across as caring and compassionate; concerned for improving the quality of life of their victims. Your description of doc S does not automatically exclude him from being a fraud.

In the past, doc S has used the word "permanent" to describe remission of RSD following sympathectomies; long after everyone in medicine knowledgeable about RSD knew that these operations were anything but permanent.

In an editorial, Explaining RSD in the journal Pain, he described "research" involving a single subject who purportedly suffered from RSD, as "...an elegant study", Balderdash! This "elegant study involved a young man diagnosed with RSD only two weeks after the injury that caused the purported RSD.

This "research" discovered that at only two weeks post injury, the central nervous system was already involved. I believe you posted the link to this "elegant study" at the other forum, but I don't think you understood the implacations or the flaws within at the time.

I had read the abstract much earlier, and my b**l-s**t detector went from standby mode to warp drive in an instant. It wasn't science, it was (and is) a "splivet"; ten pound of horse manure in a five pound sack.

Further evidence that this is a hackneyed study is the fact that the subject being studied soon fully recovered, without any discussion of any intervention that might have led to his recovery. A study that finds lots of new facts about RSD from a subject who probably never had this disease is anything but elegant; but it furthered doc S' agenda, trying to link RSD to central sensitization, so the old fraud used it.

I knew doc S was willing to play fast and loose with words a long time ago, but I didn't conclude that he is a fraud, pure and simple, until he wrote, without any evidence at all, that both CRPS-I and CRPS-II are the result of a peripheral nerve injury.

My conclusion was confirmed when he went on to try to link RSD to central sensitization (CS) when he knew that nothing learned in research into CS had any connection to RSD pain, and that CS does not explain, cannot explain, and in fact excluded any patient who showed any objective signs of an active injury or disease process.

Osteoporosis; loss of 25% of C-nociceptive fibers; abnormal hydrosis (sweating); hair loss and inhibited nail growth; symptom migration; loss of endothelial cell integrity and; cyanosis are all objective signs of an active disease process. Any one of these signs would be sufficient to exclude a subject from research into CS. Those investigating CS were looking at pain that appears to have no cause.

CS, however, sells ketamine, and not coincidentally, doc S sells ketamine. He is nothing less than a deliberate fraud out to make money from patients in severe pain. He cares not a whit that they may have taken a 2nd mortgage on their home, hoping they will be the exception. That doc S says it's possible that ketamine may provide years of remission. He sells ketamine at an outrageous price and that is the only thing he cares about.

Yes, my friend (and adversary), this sanctimonious old fraud will continue to publish "research". I take comfort in the word "old" in my previous sentence. He is old. Hopefully so old that he will die soon.

I don't wish death on people who simply annoy me; I celebrate that Saddam Hussein has been sentenced to death and look forward to his execution. Using him, and doc S as examples of my criterion for wanting to see certain people taken off the planet because it will be a better place without them; I'm sure others can accurately guess about others I prefer not to see continue to waste oxygen.

Perhaps, when he dies, the big lie about RSD will die with him, but I don't plan to sit idly by waiting for doc S to "exit, stage left". I will continue to advocate for the science supporting IRI as the only rational explanation for this disease.

I hope my small contribution will help advance the date when this explanation finally becomes the last diagnosis for causalgia/RSDS/CRPS and long term remission from, if not outright cure of this awful disease becomes a reality for everyone who must now suffer with it.

If that day comes before doc S dies, I won't have any reason to continue keeping him on my "better dead" list. If it happens this way, he will no longer be the single greatest barrier to effective treatment of RSD; he will simply become irrelevant...Vic

P.S. This thing ended up to be yet another long Vic post. Such posts will happen in the future; I can try to edit out the stuff you don't absolutely need to know, but sometimes my judgement of what you need to know will require lots of words.

In this instance, I had to answer Mikes citations of several journal articles, and I think I did that pretty well. I could not do it by offering one paragraph refutations, however. In order to show the reader why Mike's citations did not fulfill the promise of proving the unprovable, I tried to use as few words as I possibly could. Sometimes as few words as possible still require a lot of words.

Dear Vicc -

Along with Roz I have to plead the holiday excuse of responding in any detail to you post, specifically, your very thoughtful treatment of the Oaklander and Albrecht studies. I will respond later to them in more detail.

But a couple of preliminary points first. I consider the biggest thieves in this business to be the makers of implantable stimulators and/or pumps and the doctors who reflexively implant them. I saw one of them a few years ago, to say that I got an "entrepreneurial" vibe from him and his accept no medical insurance private single-purpose hospital in Beverly Hills would be an understatement. (And while I have wondered from time to time about the "relationship" between said docs and the implantable medical device manufacturers, I have nothing other than a general sense with which to support my speculations.) On the other hand, and for what it's worth, I know from personal experience that Dr. Schwartzman is a man in his seventies who will if necessary schedule a hospitalization such that he has to come in for a discharge interview on the weekends. I worked as a business bankruptcy lawyer for 20 years, largely cleaning up after massive frauds, and while I too know that these guys can be charming, I doubt very much that they regularly come into the hospital to see their patients on the weekend. (You would be surprized how many people I've known who've spent time in the joint.) Dr. Schwartzman treated me at my bedside, for goodness sakes. I too can read human nature, especially when it's up close and personal.

As noted above, I've seen guys who fit the entrepreneurial profile and in my experience, Dr. Schwartzman doesn't. He and his hospital regularly accept medical insurance payments at reduced rates, "entrepreneurial" doctors don't. Secondly, when I was registering for the trip to Germany I was given detailed instructions as to how payment to the hospital there was made. To suggest without any evidence that Dr. Schwartzman was/is receiving kickbacks from these hospitalizations is, in my opinion, not only outrageous but actionable.

Vicc, with all sincerity, I believe that your hostility towards Dr. Schwartzman is misplaced. We all agree that neurological based treatments such as sympathetic nerve blocks make a great deal of difference if given early in the course of the disease. Studies I have posted on the old board also showed gray matter atrophy in pain and specifically CRPS-1 patients, an atrophy that NMDA receptor antagonists such as Namenda may block: which is why I'm on it. I know that none of this proves a "unitary" CNS/SNS based mechanism, but it's not inconsistent with it either. Nor do I believer that Dr. Schwartzman is irrevocably linked to that model, where some of his recent work is specifically focussed upon the immunological components of this disease.

Finally, I want to be really clear on one point: I don't reject that there is a vascular component to CRPS-1. If you are aware of peer-reviewed published research that isn't making it to the RSDSA page, you should take it up with their executive director, Jim Broatch. His email address is as follows: jwbroatch@aol.com On the other hand, if your point is that no effective work can be done so long as one man or group of men lives, then I don't know what to say.

May this holiday season bring you peace and an alleviation of suffering.

Mike

p.s. One follow up comment regarding the Subanesthetic Ketamine Infusion Therapy article. You note that:

Only two of the subjects who reported having RSD longer than 24 months were followed up for more than 24 months. This represents another deceptive practice; screening subjects out from follow-up protocols. The thinking behind this is that if we don't ask them we won't have to report what we believe will be a greater number of unsuccessful outcomes.

I think you may have missed the point of the study: at some point they had to cut off their research and publish. Thus, the fact that some patients were "followed" for more than 24 months where others were not, seem to me to be more likely than not just a function of when the respective patients were treated during the course of the study.