Reflex Sympathetic Dystrophy (RSD and CRPS) Reflex Sympathetic Dystrophy (Complex Regional Pain Syndromes Type I) and Causalgia (Complex Regional Pain Syndromes Type II)(RSD and CRPS)


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Old 02-13-2007, 03:33 AM #11
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Hey Mike,

Please take this as the joke it's intended to be....no! maybe if his treatment had been successful you would be, but as it wasn't....you remain completely unmonstered (I now have a picture of Dr. S in a crypt surrounded by giant crackling electric coils ).
all the best!
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Old 02-13-2007, 08:34 AM #12
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Wow - I didnt post the article to start the war of the words....Just thought that the information was interesting and hope for some of us. At least SOMEONE is doing something.

Honestly - I dont think the "coma" is way off track....I personally know someone who had RSD who ended up very sick (from another sickness) - they had to put them into an induced coma like state to keep them from hurting themselves (severe infection raging in their body) and after they came out of it slowly progressed in the right direction and their RSD went into a remission of a sort. The RSD was not gone - as with the girl in the video but more managable....We never gave it much thought as to why that could have been before seeing that video but now it makes a little sense...

Maybe there is something to this........
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Old 02-13-2007, 12:47 PM #13
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To Everyone,

I 100% believe that DR. S heart is totally right. He is in his 70's the last thing he needs is money. He has money. He is devoted. He wants his patients out of wheel chairs and off of drugs. Which the Ketamine has done in several cases.

He has several patients coming into his office with this horrid RSD pain. RSD is a very rough DX.

Ketamine is not as bad as going under general. My husband has spoken to quite a few Anesthesialogists. Which I have considered Ketamine and might end up doing it myself.

I want to get the point across that DR. S is not the only one that believes in Ketamine treatment.

25,000 thousand is nothing to be having to be checked on and continually monitored for 5 days if not more. Do you or anyone else have a clue what it costs to monitored and be hospitalized.

Anesthesialogists, make big bucks anyway let alone for them to have to check on a patient for 5 days if not more. 25,000 is peanuts to them, IT REALLY IS. They can make that in surgery in a day and a half. Hugs, Roz

Last edited by buckwheat; 02-13-2007 at 02:31 PM.
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Old 02-13-2007, 01:03 PM #14
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To Vicc,

Let's recall Duke. Who is a surgeon and put his 12 year old thru Ketamine. Only to give her some of her life back.

Today she is happy and riding her horse. Do you recall the photo on Brain Talk 1. Hugs, Roz
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Old 02-13-2007, 04:56 PM #15
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I don't think anyone disputes that ketamine is important and often effective in treating chronic pain (treating, not curing). But there is a big difference between subanesthetic "ketamine treatment", and anesthetic "ketamine coma treatment". This article from Neurology Today may help forum members to see the difference - it's long, very readable and seems to me to be unbiased .

It's middle of my night here, just woke up (with hiccups!), now off back to bed.
all the best!

http://www.rsdfoundation.org/en/NeurologyToday.html

Neurology Today:
Volume 6(3) 7 February 2006 pp 1,17-19 TWO APPROACHES TO KETAMINE MOVE FORWARD FOR COMPLEX REGIONAL PAIN
Hurley, Dan

Two approaches to using ketamine to treat the complex regional pain syndrome (CRPS) - one employing anesthetic doses, the other subanesthetic - both show promise despite the risks associated with prolonged administration of the drug, researchers say.

Neither technique has yet been validated in a randomized, or even an open prospective trial; indeed, the more extreme of the two approaches, using ketamine to induce a coma, has not been published in a peer-reviewed journal. What's more, the senior researchers involved in the two approaches are unwilling to vouch support for the others' techniques.

Yet both research teams have ardent supporters; both are reporting dramatic progress in treating the otherwise intractable condition; both believe their technique works by disrupting central sensitization of pain transmission neurons, which they see as key to the disorder; and both have followed fascinating paths to investigate new uses for an old drug.

This drug has a bad reputation, far in excess of truth, because of how it was initially used, where terrible hallucinations and emergence reactions were associated with it, said Rodney E. Willoughby, Jr., MD, Associate Professor of Pediatrics at the Medical College of Wisconsin in Milwaukee. I can attest to how leery people are of this drug, even for an infection that is otherwise one hundred percent fatal.

INDUCED COMA FOR RABIES

Dr. Willoughby gained international attention last year after he treated a 15-year-old girl who had unwittingly contracted rabies from the bite of an infected bat and had not been vaccinated. With no other known treatment, he and colleagues quickly opted to induce a coma with ketamine because the drug had shown neuroprotective and anti-viral effects against rabies in animal studies, and because much of the destructive effects of the infection are due to disordered brain function, rather than pathophysiologic destruction. The girl became the first known survivor of rabies without receiving a vaccine (N Eng J Med 2005;352:2508-2514).

In his view, Dr. Willoughby said in an interview, The ability of anesthesiologists and other experts to use this drug safely with good outcome cannot be disputed.

What is disputed, however, is the extent to which the two ketamine regimens being tested for the pain syndrome will prove most effective with the least side effects.

CRPS (type 1 was formerly known as reflex sympathetic dystrophy, or RSD) is a chronic pain condition, which typically occurs out of proportion to the severity of local traumatic injury, and worsens rather than improves with time. The pain usually affects one limb with dramatic changes in color and temperature of the skin, intense burning sensation, skin sensitivity, sweating and swelling.

The coma-induction regimen grew out of work by German researchers who had previously used ketamine to treat phantom-limb pain syndrome, said Robert J. Schwartzman, MD, Chairman of Neurology at Drexel University School of Medicine in Philadelphia. He has co-authored two meeting abstracts on the approach and championed it in the lay press.

One of the German doctors had a relative with RSD that was not responding to [any other] treatment so he tried the [ketamine-induced coma] treatment and it worked, Dr. Schwartzman said.

(Dr. Willoughby said he understood that the German team's discovery was in fact a chance finding involving a patient with pre-existing CRPS who suffered severe trauma in a car accident. They had to induce a coma to protect the brain, Dr. Willoughby said. When they brought the patient out of the coma, the chronic pain was gone. It had nothing to do with theory. It was an incidental observation.)

In any case, once the German team became confident enough in the new approach to begin talking about it informally at international meetings, Dr. Schwartzman began referring patients who had tried and failed every other treatment.

KETAMINE TREATMENT REGIMEN

To date, he said, 30 patients have been treated by the German physicians, led by Ralph-Thomas Kiefer, MD, and Peter Rohr, MD, of Eberhard-Karls University in the city of Tuebingen. Treatment is initiated by bolus injections of ketamine (0.5 mg/kg) and midazolam (2.5-5 mg) until deep sedation is reached. Therapy is maintained with infusions of ketamine (3-7 mg/kg/h) and midazolam (0.15-0.3 mg/kg/h) over five days. On the fifth day infusions are slowly tapered.

So far, nine of the 30 patients have experienced complete and permanent remission from their previously intransigent symptoms, Dr. Schwartzman said. Of the remaining 21 patients, all of whom had at least a partial remission, seven were entirely pain-free for six to seven months, after which the pain slowly returned, he said. Ten of the patients are now being treated by Dr. Schwartzman with subanesthetic doses of ketamine in an attempt to boost the initial effect.

Side effects, Dr. Schwartzman said, have been minimal. Patients do experience hallucinations, he said. We try to prevent this by giving the patient midazolam and clonidine when they are in a coma. Some patients have experienced weight loss, abnormal appetite, and abnormal sweating for up to a month. There have been no severe complications. Pneumonia developed in five of the 30 patients, and kidney infections in six, but all responded to treatment. Detailed psychological tests performed in 15 of the 30 patients before and after treatment have shown no change of mental function, he added.

A paper he has co-authored with the German researchers on their results has been rejected by one journal and submitted to another, Dr. Schwartzman said. We're going to have a hell of a time getting it published, he said. The journal editors want a double-blind controlled series. You can't do that with coma.

FIRST US STUDY APPROVED

Although he has not yet employed the procedure himself, Dr. Schwartzman will be collaborating on the first US study of the technique, which has just been approved by the institutional review board at Tampa General Hospital in Florida. The study will be led by Anthony F. Kirkpatrick, MD, Assistant Professor of Internal Medicine and Director of the Pain Management Center at the University of South Florida in Tampa.

I see between 200 and 300 new patients with RSD each year, Dr. Kirkpatrick said. I probably see more than anybody else in the world now. I've referred so many patients for the treatment in Germany that it reached a point where I had to prove it to myself, using our standards of scientific proof.

The study will involve up to 10 patients with advanced disease that affects multiple limbs, and is progressing despite other treatments. Three patients will initially be treated with ketamine-induced coma, after which a safety monitoring board will review the results.

If the safety factors look acceptable, said Dr. Kirkpatrick, we'll do seven more. The cost to each patient will be $25,000, slightly less than the estimated $30,000 in total costs for patients traveling to Germany, he said.

CASE REPORTS: SUBANESTHETIC APPROACH

As for the alternative subanesthetic approach to using ketamine for CRPS, the first peer-reviewed report of a single case study was written by Ronald E. Harbut, MD, PhD, June 2002 in Pain Medicine (3:147-155) with a remarkable editor's introduction: This report of a single case study is presented in unusual detail because of the exceptional promise of the technique described, and the importance of further study.

The treatment was built on the pioneering work of Graeme E. Correll, MBBS, a Fellow of the Australian and New Zealand College of Anaesthetists [sic]. Having begun his career as an anesthesiologist in remote jungle villages of Papua-New Guinea, where medical resources were scarce, Dr. Correll relied on low-dose intravenous ketamine as an analgesic, and became well versed in carefully titrating it to avoid the hallucinations typically associated with higher doses. Upon moving to the more developed community of Mackay, Australia, he found the low-dose ketamine to be useful for patients with chronic pain that had been unresponsive to other treatments.

Eventually, Dr. Correll's work came to the attention of Dr. Harbut while he was working in Mackay on an assignment as a visiting anesthesiologist from the United States. After returning to the US, Dr. Harbut developed a treatment protocol in 2002 while at the Mayo Clinic in Scottsdale, AZ. He is now Director of the Neuropathic Pain Treatment Center and Assistant Professor in Anesthesiology and Pain Medicine at the Milton S. Hershey Medical Center in Pennsylvania. Following Dr. Correll's method, Dr. Harbut treated a 44-year-old woman with a nine-year history of intolerable CRPS that left her all but home-bound and using a cane. Treatment began with 10 mg/hr of ketamine, increased by 10 mg/hr every two hours to a maximum of 30 mg/hr, and was maintained for six days, by which time the patient's pain had completely disappeared and she had tapered off her sustained-release oxycodone by 50 percent, which was completely discontinued at one month.

A second report, co-authored by Dr. Correll, Dr. Harbut, and others, followed 15 months later in Pain Medicine (2004;5:263-275) describing the case notes of 33 patients previously treated by Dr. Correll and colleagues in Australia. They initially achieved complete pain relief in 25 (76 percent) of the patients, partial relief in six (18 percent), and no relief in two (6 percent) patients. The relief lasted at least three months in 54 percent of the patients, and at least six months in 31 percent. Twelve of the patients received a second round of the ketamine after the initial treatment, and all 12 experienced complete relief of their CRPS pain initially, including four who remained pain free for over three years.

Dr. Harbut likened ketamine therapy to the healing of a broken bone. If someone breaks a bone and you simply put the two pieces back rogether, they won't immediately heal. However, if you add a splint and hold the bones juxtaposed and steady for a period of time, and take away the splint later, the bone is healed. I think that the ketamine treatment does something similar; it lends support and allows the abnormally sensitized nerve cells to heal themselves, so that when you finally take away the ketamine, the pain is reduced or gone.

This second report stood out with the addition of a black-box warning at the end, which noted that recent animal studies had found dose-dependent neurotoxic reactions in the cingulate or retrosplenial cortices of adult rats given the drugs phencyclidine and MK-801 which, like ketamine, are NMDA (N-methyl-D-aspartate) antagonists. Treatment with the drugs for 24 to 96 hours resulted in irreversible neuronal degeneration and death in the retrosplenial cortex and other certain regions of the adult rat brain, the warning noted. But this effect, as well as the previously known psychomimetic and cardiostimulatory side effects of NMDA antagonists, appeared preventable with alpha-2-adrenergic agonists, such as clonidine, guanabenz, or dexmedetomidine. As a result, the authors recommended that suitable neuroprotective agents be included whenever ketamine infusion therapy is undertaken for the purpose of treating CRPS.

Clonidine has become the agent of choice for preventing the potential complications of ketamine, according to Dr. Harbut. Drs. Harbut and Schwartzman agree on the need to treat CRPS by disrupting central sensitization through the blockade of NMDA receptors.

The original injury to a peripheral nerve causes central sensitization of pain transmission neurons, said Dr. Schwartzman. The bottom line is that the body's pain cells become hyper-activated.

But they part ways on how to use ketamine. Subanesthetic doses help but do not cure patients, Dr. Schwartzman said. Only the anesthetic doses have cured patients. We have done subanesthetic doses in 100 patients without a cure.

Dr. Harbut would not comment on the use of ketamine to induce coma, but said of his subanesthetic approach, I believe this area of work is going to become and stay extremely exciting for years to come, because of the relief it has and will bring to care for intractable CRPS. The difference between a cure versus remission is how long the relief lasts after treatment.

Clearly, not all patients with CRPS treated with subanesthetic ketamine respond with meaningful or lasting relief. On the other hand, some patients do respond well. The longest remission we have seen thus far has been about three years.

Perhaps surprisingly, Dr. Willoughby, who successfully used ketamine to induce a coma in the rabies case, expressed reservations about Dr. Schwartzman's approach. While complete remission in nine out of 30 patients would be a slam dunk if confirmed, he said, the published results with the subanesthetic approach look almost as impressive. The question then is why you have to push it that far, he said.

But two neuro-intensivists said they thought that ketamine-induced coma sounded like a reasonable approach worth further testing.

It could seem crazy to a neurologist who is not used to practicing in a critical care environment, who is not used to using ketamine as adjunctive pain medicine, said Claude Hemphill, MD, Associate Professor of Neurology at the University of California-San Francisco, and Director of Neuro-critical care at San Francisco General Hospital. In the neuro-intensive care unit (NICU), he said, Treating pain with large doses of sedative agents is an everyday thing. They might even end up on the ventilator for a week as they're deeply sedated to coma or near coma. So I don't think it's a priori unethical to put someone in a coma just because they're in severe pain and not critically ill. If they have disabling pain, that's fair to consider.

Neuro-intensivist Stephan A. Mayer, MD, Associate Professor of Clinical Neurology and Neurosurgery at Columbia University School of Medicine and Director of the medical center's NICU, supports the underlying theory of using a pain holiday to achieve long-term remission.

The more pain you're in, the more pain you're in, said Dr. Mayer. The pain-sensitive structures in your brain become irritated and hyper-sensitized. It becomes this vicious cycle. What Schwartzman may be doing is breaking a vicious self-propagating cycle of pain, through analgesic sedation. If in fact it really works, it's of interest because it provides insight into the very nature of chronic pain.

He drew a parallel between the experimental method for treating CRPS and an established treatment for status epilepticus. These are seizures that repeatedly hammer the brain and don't stop, Dr. Mayer said. You get stuck in this self-propagating nightmare. What we find in neuro-intensive care is the only thing that will work is a definitive seizure holiday. We put the patient under anesthetic-level sedation for a day or two days, or sometimes a week.

What no one disputes is the need for an effective remedy for CRPS. These patients get morphine, dorsal column stimulators - none of it works, said Dr. Schwartzman. As a result, I've got a three-year waiting list. That's bizarre. There are thousands and thousands of these patients.

Ultimately, we all want to find a way to improve the quality of life of those who suffer with intractable and intolerable CRPS, Dr. Harbut said. Although the early findings are optimistic, more work is needed to further establish the safety and efficacy of this novel approach.

ARTICLE IN BRIEF
Two teams of investigators are reporting dramatic progress in treating chronic regional pain syndrome - one group with anesthetic doses of ketamine, the other with subanesthetic doses of the agent.

REFERENCE
Willoughby RE, Tieves KS, Rupprecht CE, et al. Survival after treatment of rabies with induction of coma. N Eng J Med 2005;352:2508-2514.

Correll GE, Maleki J, Harbut RE, et al. Subanesthetic ketamine infusion therapy: A retrospective analysis of a novel therapeutic approach to complex regional pain syndrome. Pain Medicine 2004;5:263-275.

Harbut RE, Correll GE, Successful treatment of a nine-year case of complex regional pain syndrome type-I (reflex sympathetic dystrophy) with intravenous ketamine-infusion therapy in a warfarin-anticoagulated adult female patient. Pain Medicine 2002;3:147-155.

IMPORTANT NOTE: The author, Dan Hurley, acknowledges that the following inaccuracies were inadvertently included in the report: 1. Pneumonia developed in 8 of 30 subjects, not in 5 of 30 as stated. 2. Tampa General Hospital is requiring a down payment of $27,000, not $25,000. This hospital charge does not include consultation services. However, physicians in critical care and in the clinical laboratory have agreed not to charge research subjects for their services. 3. The article states that Tampa General Hospital has approved the study. However, the article does not mention that approval by the IRB for the University of South Florida is still pending.

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Old 02-15-2007, 07:42 AM #16
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Mike:

When I first read your two posts in reply to my comments about doc S, I thought they were pretty silly: Everyone knows you're talking about what I wrote, so why all this extra stuff like “some”, “a view out there”, “folks”, “others piling on” and “a bunch of town folk”?

(OK, artist did try to defuse things by talking about amiable disagreements, and she did describe her horror upon learning about Kit’s experience, but she certainly isn’t one of the “others” you talk about. Or is she? There's not a lot of "others" to choose from. Your call).

Anyway, I couldn’t understand why you just didn’t directly reply to my words; then I understood. You’re a lawyer, and when lawyers don’t have facts they resort to tricks. Lawyers use words to distort reality; to pee on our legs and make us believe it’s raining.

Making me into the leader of some sort of conspiracy against doc S shifts the focus from his unethical behavior and onto this witch hunt gimmick. Lest the metaphor be lost on readers, you provide us these visual cues:

Frankly, and at the risk of alienating some, I am at times left with the imagery of a bunch of town folk, storming the castle with torches and pitchforks.

Mike, we both know that all those town folk are just me. That’s me with the pitchforks; that’s me over there with the torches. But talking about a bunch of Vic’s doing all this doesn’t serve your purposes. A witch hunt needs more people.

It’s the same with: …then others are coming along and piling on him [doc S] like he's the Anti-Christ. Describing me as piling on like he’s the Anti-Christ, doesn’t quite create the picture you want people to see. You need imaginary “others” doing the piling on.

Well, Mike, the truth is that it’s just me, and this witch hunt thing is just plain nonsense.

I know that some feel otherwise, and that's their right, but this forum should NOT be understood to be a place that supports a unitary view that Dr. Schwartzman is a snake oil salesman.

I agree that it wouldn’t make sense to begin with; “I know that Vic feels otherwise…” This is hardly the image of the unitary view you claim to be protecting us from, but should you but make your point by using distortions? Is there a point without your distortions?

And why not trust the truth and just use my words? I didn’t say doc S is a snake oil salesman; I said he is a ketamine huckster. Or is truth so irrelevant that it isn't necessary even when it is useful?

I see I’m “folks” again when you write: I just believe folks are making a mistake in ascribing to [Schwartzmann] all of the sins, real or imaginary of the medical community.

Mike, all the “imaginary” is on your end. I said that he is unscientific in ascribing RSD to central sensitization; and I gave good, solid reasons for saying it. I also said that he wrote an article that (in my view) was unethical as he used the word “permanent” to describe remissions he knew would soon become relapses.

Your “paraphrasing” of my words crossed the line into fabrication and distortion:

And for that matter, who among us hasn't labored in an occupation for a good number of years where our professional views haven't changed over time? Yet what's going on here is that stuff is being pulled out against a man, as though every position he took over God knows how many years is being held against him as though it was yesterday,

That’s lawyer talk for “I can’t argue the facts here, so let’s pretend we’re talking about something completely different”. What amazes me is that you would make this ridiculous claim on the same thread as my actual words.

In your first post you say:

Finally, I know that there is a view out there that hold that “I’ll stick with stuff I can understand.”

Now I may be a little thin-skinned at this point, but since all the other “folks”, “others”, etc, were clearly me, when you say “there is a view out there” you’re probably talking about me again.

I’m not sure how even a lawyer could accuse me of holding the view that “I’ll stick with stuff I can understand.” People who dedicate four years of their life to studying anything are not the kind to stick with what they understand: they want to understand more. This crap is more in the nature of a personal attack; hiding behind “a view out there” notwithstanding.

No one likes having their words misquoted or distorted in a way that tries to make them appear deceitful or foolish. None of us can avoid feeling personally attacked when this happens; I certainly did. But I have known you long enough to believe these posts aren’t the real Mike.

Maybe you were so angry about me talking about someone you think of as a friend that you just slipped into your “lawyer mode” without thinking of how it would affect me. I don’t believe you will look back on these posts with a lot of pride.

I wish I could just leave these posts unanswered, allowing them to fall from page 1 and into eventual oblivion, but two things make this impossible for me: pride (which we know goeth before the fall), and the fact that I believe my credibility is important if I am to persuade others that their hope for recovery from this disease lies in making the effort to learn what RSD really is. I can’t allow assaults on my credibility to go unanswered.

I hope we can find a way to restore amiable disagreement, but it won’t come at the price of my silence on anything I strongly believe. I will try to refrain from talking about doc S in personal terms, but he’s fair game when it comes to his writing.

I would like to see this end now, but after 42 years of marriage I’ve become resigned to never having the last word. If you choose to add anything further, I hope it will be limited to a reply to my assertion of unethical conduct. (I think we can agree to quietly disagree over my personal opinion of doc S)…Vic






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Old 02-15-2007, 11:31 AM #17
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Dear Vicc,
Both Mike and myself care very deeply aboout Kit. WE REALLY DO.

I beg of you to please stop this. We are blessed to have Mike here.

He is beyond a asset. Roz

Last edited by buckwheat; 02-15-2007 at 07:05 PM. Reason: Put in the right grammer from crap to this.
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Old 02-15-2007, 12:38 PM #18
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All can say is that I have been on ketamine for the last 14 months. It has NOT cured me... it has not MAGICALLY made me better. BUT...... it has given me some quality of life back - which I personally think is good.

I am tried EVERY medication out there - I have taken methdone, fentanyl, pethidine, morphine, oxycodone (I know it's similar to morphine - but slightly different too), calcium channel blocks, sleeping tablets, anti epileptics, anti depressants, muscle relaxants, blood pressure meds (to allow more blood to my extremeities), botox, epidurals, sympathetic blocks, had a sympathectomy...

Ketamine has been the most successful pain killer I have had. MY pain never drops below a nine - but I can now move around, I can get out of bed, I am not crying all day and all night. The last 14 months have seen me go from someone that didn't go out or do anything but cry and work to someone that can now eat, attend university full time, and have a social life. To be honest, I don't CARE how it works....as long as it does.

I really don't feel that we should be arguing between us - I know we are always going to have individual thoughts on RSD and how it should be treated, I just feel that we should all remeber we are fighting for the same thing - a treatment that WORKS, doctors that UNDERSTAND US, and the under lyng physiology that leads to the development of RSD. There are so few of us already, we can't dilute what we are aiming for by fighting between ourselves...

To steal a very corny phrase "It's all for one and one for all".. Also, all of us are ratty (and I mean ALL OF US) from too much pain, no sleep and just total eughiness... we are all going to take things personally - I know I do - I have been reminded by several people on this forum that when people go on about wheelchair use they are not dissing people who have to use them... it's something i have a very thin skin on

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Old 02-15-2007, 11:32 PM #19
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At the risk of prolonging this encounter, I just want to respond to the one narrow point upon which Vic has invited my comment, and that is his assertion of Dr. Schwartzman's "unethical" conduct in promoting remedies which he knew or should have known were not as effective as he claimed.

Vic starts with reference to an unspecified article in which Dr. Schwartzman suggested that surgical sympathectomies gave "permanent" remission (which it is asserted was artificially defined as two years) of symptoms. I have tried to find this assertion, but going through a number of articles by Dr. Schwartzman that are posted on the RSDSA Medical Articles Archive page [http://www.rsds.org/2/library/articl...ve/index.html], it's not there. Now, obviously Dr. Schwartzman has written a lot more than these articles, but if you look at them, none of them are truly leading the clarion call for sympathectomies in the absence of the then available medical data, as has been suggested. Check these out:

1. "Reflex Sympathetic Dystrophy, A Review," Schwartzman RJ, McLellan TL., Archives of Neurology 1987; 44: 555-561

2. "The movement disorder of reflex sympathetic dystrophy," Schwartzman RJ, Kerrigan J., Neurology 1990; 40: 57-61.

3. "Reflex Sympathetic Dystrophy, Occurrence of Inflammatory Skin Lesions in Patients With Stages II and III Disease," Webster GF, Schwartzman RJ, Jacoby, RA, Knobler RL, Uitto JJ, Archives of Dermatology 1991; 127: 1541-1544 and

4. "New Treatments for Reflex Sympathetic Dystrophy," Schwartzman RJ, The New England Journal of Medicine 2000: 654-655.

Yes, if you go back to his 1987 article with McClellan, "Reflex Sympathetic Dystrophy," he says, at page 558 that, "[f]or patients with severe or long-standing disease, sympathectomy should be performed early if there is any response to a paravertebral ganglion block." And in his 1990 piece with Kerrigan, "The movement disorder of reflex sympathetic dystrophy," there is the following at page 60, "[s]ympathectomy in an extremity that has been successfully blocked gives the best long term result." But these writings cannot be taken wholly out of context.

Indeed, I think I have found the article Vic may have had in mind. See, "Long-term outcome following sympathectomy for complex regional pain syndrome type 1 (RSD)," Schwartzman RJ, Liu JE, Smullens SN, Hyslop T, Tahmoush AJ, J Neurol Sci. 1997 Sep 10; 150(2): 149-52 (retrospective study of 29 patients with CRPS1 (RSD) who were initially examined between 1983 and 1993, and had either transthoracic (lower third of stellate ganglia to T3) or lumbar (L2-L4) sympathectomy; patients were followed from 24 to 108 months after surgery; patients with unsuccessful surgical outcomes had significantly longer duration of symptoms before surgery (median, 36 months) than those with successful outcomes (median, 16 months); all seven patients (100%) who had sympathectomy within 12 months of injury, nine of 13 patients (69.2%) who had sympathectomy within 24 months of injury, and only four of nine patients (44.4%) who had sympathectomy after 24 months of injury obtained permanent (greater than 24 months) symptom relief; patient age, sex, occupation, site of injury, type of injury, presence of trophic changes, and duration of follow-up were not significantly related (P>0.05) to surgical outcome).

But once again, that article has to be seen against the backdrop of the time in which it was written. See, e.g., "Sympathectomy for reflex sympathetic dystrophy: factors affecting outcome," AbuRahma AF, Robinson PA, Powell M, Bastug D, Boland JP, Annals Vasc. Surg. 1994 Jul; 8(4): 372-9 (study included 12-year experience with chemical sympathetic blocks and surgical sympathectomies for causalgic pain of reflex sympathetic dystrophy (RSD) with emphasis on factors affecting clinical outcome; medical records of patients undergoing sympathectomies for causalgic pain were analyzed; patients were classified according to Drucker et al. as stage I, II, or III; results of chemical and surgical sympathectomies were analyzed using both univariate and multivariate methods; 21 patients had lumbar and seven had cervicodorsal sympathectomies for RSD; mean duration between initial injury and chemical sympathetic block was 10 months with a mean of 11.4 months to surgical sympathectomy; patients with stage II presentations were significantly more likely to have satisfactory early (92%) and late (79%) outcomes than stage III patients; patients with an excellent response to chemical sympathetic block were more likely to have satisfactory early and late surgical outcomes; multivariate analyses demonstrated that the most important independent factor in determining early and late satisfactory outcomes of sympathectomy was the time between injury and sympathectomy).

But by the time you get to his 2000 editorial in The New England Journal of Medicine, any reference in his writings to sympathectomies appears to have ended. Yet in much of the rest of the medical world, they were still the rage. Indeed, here's a discussion I downloaded today from the site maintained by the UCLA Dept. of Neurosurgery, in which they have the following (and quaint) discussion of the treatment of "causalgia":
How is causalgia diagnosed?

The initial step in diagnosis is a thorough history and physical examination. Physical examination is difficult to perform secondary to pain. The diagnostic procedure of choice is proof of complete or partial relief with a sympathetic block.

How is causalgia treated?

Medical therapy is usually ineffective.

Sympathetic block: 18-25% of patients have satisfactory long-lasting relief after a series of sympathetic blocks. Temporary regional blockade can be achieved by local anesthetic (e.g. lidocaine) injection of the stellate ganglion, the lumbar ganglia, or the celiac plexus. These procedures lead to sympathetic denervation of the head, neck and upper extremity, the lower extremity, and the abdominal region, respectively.

Surgical sympathectomy: Relieves pain in >90% of patients. Techniques used include anterior thoracic, thoracic endoscopy, percutaneous radiofrequency and supraclavicular. Sympathectomy has been reported to provide complete relief in over 80% and significant relief in 95% of patients with causalgia. Similar results have been obtained with reflex sympathetic dystrophy. The risk of significant complication is approximately 5%. These include a pneumothorax, intercostal neuralgia, spinal cord injury, and Horner's syndrome.
[http://neurosurgery.ucla.edu/Diagnos...PainDis_1.html]
Vic's next assertion is that Dr. Schwartzman is on record as telling patients that ketamine works virtually 100% of the time. I was his patient and he certainly never told me that. In fact, in the CNN story, it says that ketamine works in approximately 50% of the cases. Who really takes issue with that? See, also, "Tackling depression with ketamine," NewScientist.com 20 January 2007 [free text available at http://www.lca-uk.org/lcaforum/viewt...7005e9e459b17]
Schwartzman's methods are not for the faint-hearted. He gives RSD sufferers doses of ketamine high enough to put them in a coma for five days, accompanied by anti-anxiety medications to reduce the nightmare of the k-hole. But for many, the results are worth it. In 14 cases out of 41, according to Schwartzman, patients were completely cured. "We haven't cured the original injury," he says, "but we have cured the RSD or kept it in remission. The RSD pain is gone."

"No one ever cured it before," he adds. "In 40 years, I have never seen anything like it. These are people who were disabled and in horrible pain. Most were completely incapacitated. They go back to work, back to school, and are doing everything they used to do. Most are on no medications at all. I have taken morphine pumps out of people. You turn off the pain and reset the whole system."

“In 40 years, I have never seen anything like it."
Vic also suggests, with respect to the principle study on the use of ketamine, to which I had previously made reference - "Subanesthetic Ketamine Infusion Therapy: A Retrospective Analysis of a Novel Therapeutic Approach to Complex Regional Pain Syndrome," Correll GE, Maleki J, Gracely EJ, Muir JJ and Harbut RE, Pain Medicine 2004; 5:263-275 (in patients who underwent a second course of ketamine infusion, results indicated that 58% of the patients had relief for at least 1 year and that almost a third of the patients remained pain free beyond 3 years) - as follows:
. . . I read the study Mike wrote about, and I noticed that patients who had RSD less than six months had the really long periods of remission. Amazingly long.

Those patients who had been diagnosed more than three years previous showed more ambiguous results: mainly because someone forgot to do follow-ups on them
.
This assertion is simply not borne out by a close reading of the study. (Also available on the RSDSA Medical Articles Archive page.) If you look at Table 1 on pp. 266-67 of the study, of the 8 out of 33 subjects for which there was an incomplete follow up, only 2 of those 8 had a CRPS history of greater than 8 months! What the study said, at pp. 270-271, is as follows:
In five patients the condition was fairly acute and of less than 1 month in duration. Nevertheless, it did appear to the physicians evaluating these patients that they indeed had early CRPS, as opposed to acute posttraumatic nociceptive pain. The patients were offered this alternative treatment and they recovered. We recognize that, in those five, patients the CRPS symptoms might have improved spontaneously.

It is impressive to note that the treatment has the potential of eliminating even the pain of those patients who have been suffering from the condition for several years, and not just more recently developed cases. In the case of Patient 25, CRPS was present for more than 20 years until it was completely suppressed with the ketamine infusion. This also points out the dynamic nature of the pain processing system and its long-lasting responsiveness to what appears to be neuromodulation therapy.
Finally, it should be borne in mind that the man has by no means reached the limit of his endurance with his work on ketamine, but remains in the forefront of work looking at the immunological aspects of this disease. See, e.g., "Changes in Cerebrospinal Fluid Levels of Pro-inflammatory Cytokines in CRPS," Alexander GM, van Rijn MA, van Hilten JJ, Perreault MJ, Schwartzman RJ, Pain 2005;116: 213-219, also available on the RSDSA Medical Articles Archive page.

I know I've covered a lot of ground and I appreciate the reader's patience. I've just tried, as best I could, to disabuse anyone of a notion that a guy who has probably done more - over the course of his long career - for the good of RSD patients than any other living individual is somehow a fraud and a huckster. And with that, I am done.

Mike

Last edited by fmichael; 02-16-2007 at 03:56 PM.
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Old 02-16-2007, 01:08 PM #20
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To Everyone,

Surgical Sympathectomies are done by Thoracic Vascular surgeons. They go to school for several years. I was offered a Sympathectomy last year. I had surgery on the nerves instead.

No Neurogists in the States as far as I have ever heard took a knife to the patient. Hugs, Roz
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