Well, the Feb edition is out, and it contains the letter from our member mollymcn, with a reply from Dr. Oaklander. It's a must-read.

Here's the original thread on this forum:
http://neurotalk.psychcentral.com/sh...logy#post66800

Here is the Letters to the Editor link:
http://appneurology.com/showArticle....leId=197007799

There is also a most interesting article regarding Ketamine and its use for treating depression:
http://appneurology.com/showArticle....leId=197002958
Ketamine and NMDA Receptor Antagonists for Depression
February 01, 2007
Walter A. Brown, MD

Happy reading
all the best.

Dr Oaklander states: and I quote:

Every other published study of CRPS has reported a mean age at CRPS onset of about 40. I draw attention to a study by Veldman and colleagues2 of 829 patients with CRPS that was published in the Lancet in 1993. Patients' average age was 42 years, and the most common duration of CRPS was 2 to 6 months (in 242 patients). Only 28% of patients had CRPS lasting longer than 1 year.

NOW - My husband suffered from RSD in his leg from 1995 thorough present - That would be....12 years so far - Although I will state - that the symptoms have decreased dramatically and he is somewhat functional (leg-wise) with a brace and continued at home exercise. ALSO - He developed RSD (in that leg) at the ripe old age of 25.

The age thing is not what really bothers me here - It is the statement that based on 829 patients the Dr states that only 28% had CRPS for more then one year - Really??? Now how many people in this country are affected with this? Let alone the world suffer from CRPS? I believe that one study based on a mear 829 patients is hardly "significant evidence" to support what the dr claims as fact. Just with the people I personally know who are close to me with RSD my husband has had this for 12 years, a friend of my mothers 4+, and another friend of ours over 1 year (occured in her early 30's) - that would be..................oh you guess.........100%????

Maybe were just wierd here in Wisconsin - Or it's the water or something but I believe the dr is not real accurate with the facts and figures here and might want to do a little more research and some more studies before spouting off numbers like that.

Dont get me wrong here - I would LOVE to see REAL numbers like that, but the fact is, is it's just not true.

Oh and good Dr Oaklander if your reading this, I would be pleased if you could find something a little more current. The study you gave reference to, Veldman is from 1993 - Something that is that outdated (14 years) could hardly be called useful

Hi HWRSD,

I read the Veldman article and saved it, but after two computer failures that I thought I had prepared for, I can't find it today. I think I remember it well enought to show how Oaklander misused it.

Veldman has been a "voice in the wilderness" for years, pointing out that Sudek was right when he reported evidence that this disease begins with widespread inflammation. The community of RSD "experts" were still locked into the view that the disease results from some sort of abnormal sympathetic nervous system activity but could not refute Sudek, so they claimed what he found represented a rare variant of RSD and began calling it Sudek's Dystrophy; making it irrelevant to "the real" RSD.

RSD appears to be a significant problem in Holland and a fair amount of the literature comes from that country. It is such a problem that early diagnosis is important there, where red, warm skin and edema are among the primary diagnostic criterion.

Using this criterion, Veldman showed that a large number (approaching 50% as I recall) of RSD patients recovered spontaneously within six months of diagnosis; during the inflammatory stage.

At that time he was clearly unfamiliar with ischemia-repefusion injury (IRI), so he wasn't able to explain how this became what many call "cold RSD"; when skin becomes cyanotic and skin temperature drops significantly. He could only say that 28% of that sample did enter this second stage, and that this stage is usually long-lasting.

Two years after this study was published, a new researcher (van der Laan) had joined his research team and published his first article on the role of oxygen free radicals (OFRs) in acute (inflammatory) RSD. van der Laan is a vascular surgeon and is familiar with IRI.

(It was van der Laan's article that led me to begin researching the literature of OFRs that then led me to IRI, which explains every sign and symptom of this disease).

Anyway, Veldman's article emphasized that RSD begins with inflammation, and the body is better able to deal with inflammation that with the second (ischemic/hypoxic) stage. He has since published research showing that antioxidants (specifically DMSO), improve the chances of remission at the front end (the first few months).

Oaklander does use his numbers, but with the implication that they support her view that spontaneous remission is also common in ischemic/hypoxic RSD, which simply isn't true.

(By the way, the Dutch govt has mandated that antioxidants be made available to RSD patients. It can't mandate that patients use them, of course, and use of antioxidants during the second stage is too late to stop inflammation that is now hypoxia.

(I plan to begin a series of posts on IRI, and one of them will talk about symptom migration. I will talk about the science that supports the hypothesis that antioxidants can delay [if not prevent] the onset of new symptoms in other parts of the body]).

That 28% represents us; those who continued into the second stage, where spontaneous remission is so rare as to be insignificant. Oaklander's deliberate misuse of these numbers to justify her claim that people recover from second stage RSD is a major disservice to us. If we're going to get better, why bother?

Her minimizing of suicide among RSD patients is, I believe, another distortion of the numbers. My pain from nerve injuries is much more severe that the RSD pain, but it is relatively well controlled by opiates. I'm severely limited physically, but I am not tormented by uncontrolled pain. Opiates do nothing for my RSD pain, at least at the dosages I take.

Many who suffer the severe pain of full-body RSD, poorly controlled at best, who see no hope for improvement, are more likely to take their lives in a moment of despair or after deliberately planning it.

In a recent post I found myself suddenly thinking of people I have known during the past nine to ten years; I wondered how many of them had stopped posting because they chose death over living Hell. My recent posts about HBOT are the direct result of that first post.

It was wrong of me to withhold what I knew about HBO simply because I couldn't cite research confirming it. My hope now is that people contemplating suicide will first consider HBO.

Sorry, I went off on another tangent, but I was talking about suicide among RSD people, and I am convinced that many of my friends took that route.

Oaklander cites Smith's findings among nonfatal pain patients, but most pain patients don't have RSD, their pain is usually fairly well controlled, and they still see hope in the future.

Her comments about weakness in all four extremities betray a poor awareness of the fact that those who experience symptom migration suffer identical symptoms in the newly affected limbs. Atrophy is a primary sign of retrogression in RSD, and anyone who has suffered from secondary symptoms will experience weakness in affected limbs in very short order.

Her claim that RSD is often a misdianosed small fiber polyneuropathy is patently false. So far as I know, the only two disorders that present with cyanosis, severe hyper-sensitivity to cold and lower skin temperature are RSD and diabetic neuropathy. Diabetic neuropathy is the result of arterial damage that gradually diminishes blood flow to the point that nerves begin telling the brain that something is seriously wrong: the pain nerves can only send pain messages.

"Accurate diagnosis is the foundation for effective treatment". What effective treatment? Why not tell us what works, Dr Oaklander?...Vic

Hi everyone,

I want to say thank you for the articles on this thread, and for all the other information this forum provides. It is good to read even older articles and compare to newer ones just to see how RSD has progressed as a viable condition and not just a diagnosis because nothing else fits. I had one doctor tell me there is no such thing as RSD!

I have been watching this forum with interest, and as a learning tool. I have had RSD for one year now, most likely resulting from an unsuccessful CTS Release. It has been an awful year while being diagnosed. Why can't doctors agree on anything? One says yes, one says no, one says maybe, and so goes the circle of uncertainty. As of a final diagnosis last week, I have bilateral UE RSD, more severe on my dominant side. I recently hooked up with a great physician who has me on the correct medications and has ordered a specific physical therapy program. W/C did not deny the CTS, but they are fighting the RSD disanosis. Doesn't make a bit of sense to me that they would conclude this as not a consequence of CTS. I am working fulltime and have no intentions of stopping, unless/until I am physically unable to get out of bed.

I hope to be more active here and just wanted to say hi. I had never heard of RSD before. I ignore most people so I don't have to explain, even my family.

Hi WhatsRSD,

Glad you stopped lurking and decided to join us; good for you. Sorry about the diagnosis, though...

Since I was diagnosed with RSI in my dominant right hand (RSD left hand) I've become much more aware of the almost epidemic proportions of this condition and recently have been finding more websites stating that RSD is indeed a risk for patients undergoing RSI surgery. I think this will be a big issue in the future. I shall post more on this topic in a different thread when I can make the time.
Anyway, welcome!..all the best.

Hey there - Glad to see you've posted - Sorry that your here for the reason you are but I believe that knowledge is power and the more we share the more we can learn from each other and someday have the answer to defeat this beast.

Vicc,

What a wonderful response and write up. I greatly appreciated all the detailed information and glad to see I was not the only one reading the inaccururate or mixed up, misconstrued information the "dr" wrote about. It makes me angry when I see someone with these opinions (which is what they are to me), it does nothing to help the real Dr's who care nor the patients and furthermore hurts the patients in the long run and that is definately something we/they dont need.

I look forward to reading more from you and your posts - your information is truly valued. Thanks so much again.

This reply from Dr. Oaklander has brought to the surface something I've been wondering about for a while concerning the current classifications of RSD/CRPS. Bear with me while I explain, and please understand that I'm a medical illiterate.

Oaklander says:
"CRPS begins in association with a trauma to either an arm or leg, and symptoms are worse in the affected limb.

Because CRPS is so poorly understood, incorrect diagnoses are common. It is most commonly confused with a generalized problem—usually a small-fiber polyneuropathy. I would be delighted to speak with Ms McNulty's friend to find out more about her condition. Accurate diagnosis is the foundation for effective treatment."

BTW, yes, Vic, wouldn't it have been useful if she'd told us what an effective treatment might be.

Anyway, she seems to be saying that if things don't fit with her classification then it's not RSD/CRPS.

But she doesn't give us her definition and in this, admittedly necessarily short statement, seems to completely ignore the 2 current classifications of CRPS type 1 and 11 and is talking solely from the perspective of CRPS Type 11 (I think, she's a bit woolly here).

The two classifications at present "...are meant as descriptors of certain chronic pain syndromes. They do not embody any assumptions about pathophysiology. For the most part the clinical phenomena characteristics of CRPS Type I are the same as seen in CRPS Type II. The central difference between Type I and Type II is that, by definition, Type II occurs following a known peripheral nerve injury, whereas Type I occurs in the absence of any known nerve injury."
http://www.guideline.gov/summary/sum...=4215&nbr=3223

Her own research used patients with CRPS Type 1:
"Study finds nerve damage in previously mysterious chronic pain syndrome - Reduction in small-fiber nerves may underlie complex regional pain syndrome-I (reflex sympathetic dystrophy)"
http://www.massgeneral.org/news/rele...oaklander.html
and
http://www.ninds.nih.gov/news_and_ev...ticle_CRPS.htm

So her own research has shown that there is, in fact, nerve injury/damage in CRPS Type 1. So does that mean that there is actually no difference between the two classifications, and that the only difference between the two has been our ability to measure nerve damage?

Back to her reply to the letter, ... "small-fiber polyneuropathy" - her own research has shown that CRPS Type 1 can be identified by a clinical test that shows evidence of small-fiber changes. Polyneuropathy can be defined as "....a neuropathy pattern, whereby the nerve damage initially starts in both feet and may progress to involve the feet, calves, and fingers/hands. Another word for this pattern is a Stocking and Glove Neuropathy.
http://www.stoppain.org/pain_medicin...neuropathy.asp

If you put these two things together they sound exactly like CRPS to me, as the vast majority of us, the sufferers, have experienced it. So I'm wondering just what her definition of RSD/CRPS is, and why she has responded from such a narrow perspective. Or has she, in her own mind, abolished the two classifications and is now treating them both as a single condition?

This quote from the original article is what started me seriously thinking about the current classification of this condition/disease:
"In time, we may recognize half a dozen different kinds of CRPS, not just two," said Ricardo A. Cruciani, MD, PhD, vice chair of the Department of Pain Medicine and Palliative Care at Beth Israel Medical Center in New York City.

I frequently see articles on conditions, like Raynaud's and erythromyalgia for example, that make me think "hang on, but isn't this RSD?": are the medics not seeing the wood for the trees? Is RSD/CRPS just one manifestation of a much wider-reaching underlying physical malfunction?

I have a gut feeling that Cruciani's musing may turn out to be true in general principle.

all the best

Is RSD/CRPS just one manifestation of a much wider-reaching underlying physical malfunction?


Right On, Artist