Hi Liz,

It's so very good to see you back and posting in your usual perceptive and witty style
Absolutely, to both points! And, of course, the Odone's research for ALD (the Lorenzo's Oil couple).

Hope you're bearing up OK after the winter, how's that cane these days?
all the best

artist,

wow...thx for the 'perceptive and witty'....in general, i'm doing so-so....good days and bad days....but as long as there r good days, i can manage....and the cane is now a 'sometimes' thing...i was a good girl and did my phys therapy, and my reward is to be able to walk unassisted now and then.

haven't been posting much as i've been up to my ears in helping my daughter prepare for the triplets b'day party.....they wanted a harry potter party, and we got a bit carried away making decorations...but it's been lots of fun and the boys love the stuff....jose has been our party consultant, since she's a huge harry potter fan and made us a list of food mentioned in the books, and found the right colors for us to use for the different 'houses'.

the potter party was the inspiration for my question a while back about treacle tart....i did try making it......the boys loved it, as did my son-in-law, but i'm not too impressed (i probably don't have genuine treacle).

the party is next weekend, so maybe after i "graduate from hogwarts", i'll be here more...i have been keeping up, just not posting much.

liz

Greetings. I hadn't seen Vic's post until Sunday afternoon and had no particular inclination to enter into another round with him.

But, having been "called out" I do have one question for him. In his post, Vic says - in part - that:

It is impossible, Dr Schwartzman, to see thousands of RSDS/CRPS patients and not notice that most of them present with cyanosis; but you never mention the word.

I am frankly confused by the comment, where the disease is commonly known as Reflex Sympathetic Dystrophy and "dystrophy" is in turn defined by the [U.K. – based] “On-Line Medical Dictionary" as "any disorder arising from defective or faulty nutrition, especially the muscular dystrophies." As I understand it, these "nutritive losses can ecompass everything form a loss of oxygen to nerve signals.

Put it another way, if, by definition, we're talking about a loss of "nutrition," I don't see the issue in whether the term "cyanosis" ("a bluish discolouration, applied especially to such discolouration of skin and mucous membranes due to excessive concentration of reduced haemoglobin [sic] in the blood) is used or not, so long as the more general concept of dystrophic changes is firmly in mind. See, RSDSA, Complex Regional Pain Syndrome: Treatment Guidelines, "Introduction and Diagnostic Criteria" pp. 10-11 referencing "trophic changes" as those of the "hair, nail, skin."

The ground that’s being covered is essentially the same, and to say that it’s an area that Dr. Schwartzman has never addressed is just wrong. By example, see, “Pathophysiology of Complex Regional Pain Syndrome,” Robert J. Schwartzman, et al, Expert Review Neurotherapeutics, 2006 May 6(5):669-81,* at 674-75:

Autonomic nervous system and CRPS pain

. . . Several studies have provided . . . potential mechanism for the coupling of sympathetic and sensory systems. Nociceptor and mechanosensitive afferent fibers express adrenorecptors that my be activated following nerve injury. A significant increase in the number of [alpha]-1 adrenoreceptors has been reported in the hyperalgesic skin of CRPS I patients. In addition to sympathetic coupling in the periphery, CNS adrenergic neurons process and modify pain transmission as part of the diffuse noxious inhibitory control (DNIC) system. The recent ischemia-reperfusion model presented by Coderre and collegues is comparible with many of the signs of autonomic dysfunction and pain noted in CRPS I. Prolonged hind-limb ischemia in the art followed by reperfusion causes:

- A hyperemic and warm extremity in 4 g that evolves into a dry and shiny extremity within 4 h;
- Pinprick hyperalgesia, cold and warm mechanical allodynia that lasts up to 4 weeks;
- Contraleteral damage.

The ischemia may sensitize and activate deep tissue noceptors of muscle joints and bones which, to date, has not been explained and, as noted above, is very important in CRPS.

* * *

Autonomic dysregulation & edema

The autonomic nervous system is involved in other aspects of CRPS besides pain, since the diagnosis of CRPS requires that there must be, or at least have been at one time, evidence of edema, change in skin blood flow or abnormal sudomotor activity in the region of pain.

Skin blood flow abnormalities are often obvious clinically as increased redness, livedo reticularis or dusky cyantic- appearing skin. The use laser Doppler fluxmettry has enabled the quantification of skin blood flow, which is largely influenced by sympathetic innervention of the arterioles that control blood to skin capillaries. Unfortumately, an indicator of deep sympathetic control of blood flow to muscle and bone is not available.

An early study using laser Doppler fluxmetry, found that the normal reduction of skin blood flow following activation of the sympathetics by a Valsalva maneuver or cold pressor stimplation was not present in patients with CRPS, and the normal sympathetically mediated spontaneous wavelike fluctuations, known as vasomotion, were also reduced or absent in these patients. A more recent study confirms this observation by demonstrating that vasoconstriction induced by inspiratory gasp, cold immersion or mental stress was reduced in early CRPS. This sympathetic dysfunction may be transient. Evidence of reduced vasoconstriction response in very early CRPS returning to normal has been reported in a longitudinal study. The return of normal vasoconstrictor activity has also been demonstrated to coincide with recovery from acute CRPS I.

* * *

Edema is often a major component of CRPD which may be caused be sever potential mechanisms:

- Increased capillary filtration capacity, a measure of microvascular permeability, has been reported in the affected limbs of CRPS I patients;
- Increased sympathetic stimulation of the lymphatics that is under sympathetic control;
- Neurogenic inflammation.

Sensory fibers contain and release a variety of vasoactive substances from their afferent ending. Subcutaneous perfusion of one such peptide, SP, as well as transcutaneous antidromic stimulation of sensory fibers, has been demonstrated to evoke protein. extravasation. This report has been reported to be active in the affected limbs of CRPS patients. [Emphasis added; citations omitted.]

See, also, “Reflex sympathetic dystrophy,” Schwartzman RJ and Popescu A, Curr Rheumatol Rep. 2002 Apr;4(2):165-9, where the abstract reads as follows:

Reflex sympathetic dystrophy (RSD) is composed of five major features: pain, swelling, autonomic dysregulation, movement disorders, and atrophy and dystrophy. RSD is caused by an injury to a specific nerve or the C- and A-delta fibers that innervate the involved tissue. It is a progressive illness that spreads with time and may encompass the entire body. There is no psychological disposition to the problem, but all patients are severely depressed because of the constant pain, lack of sleep, and complete disruption of their lifestyle. The continuing pain is usually secondary to the process of central sensitization. The autonomic dysregulation has a major central nervous system component. Atrophy and dystrophy are partly due to loss of nutritive blood supply to the affected tissues. The movement disorder is partly due to deficiency of GABAergic mechanisms; the tremor is an exaggeration of the normal physiologic tremor. Treatment consists of decreasing the afferent pain, maintaining barrage from the underlying defect, and blocking the sympathetic component of the process. New developments include the use of neurotrophic factors to reverse the phenotypic changes that occur in the dorsal horn and the use of pharmacologic agents to block the activity-dependent NMDA channels that appear to be instrumental in maintaining central sensitization. [Emphasis added.]

Please forgive me for going on, but the point is a simple as it is fundamental. Unless I am missing something, it would appears that “cyanosis” is but a subset of the general problem of dystrophic changes, upon which much has been written through the years.

Or to recall the words of the Bard, a rose by any other name . . . .

Mike

* I will be happy to email anyone a full-text copy of the article who wants it, just send me a pm with an email address. Unfortunately, the other article cited does not appear to be available in any electronic format.

Oh, goody, Mike. I knew you wouldn't let me down.

There is a more succinct definition of cyanosis in the OMD, it reads: a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood. I like to stick to the KISS (keep it simple, stupid) model, but I know that lawyers pay the bills by confusing and obfuscating things.

The thing is, those "experts" back in the 1940s didn't want people to talk about blue to purplish skin, so they used the word "dystrophy". As I pointed out in my first reply to Bronco's thread Upset, if they used the word "cyanosis" people might ask what causes it, and they were fresh out of neurological explanations, what with the evidence showing no sympathetic vasoconstriction in the disease.

It was more convenient (expedient) to pretend the word simply ceased to exist than try to claim sympathetic dysfunction at the very moment when sympathetic dysfunction had been demonstrated to be not a factor in RSD. I can understand that: lots of people prefer pretending to facing reality

You might like to put it another way, but I'm not going to: we are not talking about a loss of nutrition, we are talking about blue to purplish skin. Blue to purplish skin means the cells aren't getting enough oxygen, and oxygen is only delivered by the arteries, which science had just proved were not being affected by sympathetic vasoconstriction. The experts back then, and doc S and you today, didn't want to talk about blue to purple skin.

The ground that's being covered is not essentially the same. Doc S and the other experts want to define the ground in terms of dystrophy, for a very good reason (and one I may have mentioned before): They have no neurological explanation for cyanosis.

And I'll be damned! Doc S actually did come close to using the C word, but in typical doc S fashion he distorts reality. The clear implication in the phrase "cyanotic-like" is that it may look like cyanosis, but it isn/t. That's just doc S, up to his usual manipulative tricks again.

In fact, the entire article appears to be nothing more that his manipulative tricks. He's either talking out of both sides of his mouth or out of both faces. The next time you two chat, you might ask him is this is the result of a sympathetic dysfunction; which his double-talk here seems to indicate, or if he still stands by his previous statements that RSD pain is caused by a peripheral nerve injury which is later assumed by the spinal cord during spinal sensitization.

You'll have to watch his lips (both sets) carefully, to see whether they are saying the same thing.

I haven't seen Coderre's presentation of this as an ischemia reperfusion injury, but I'll bet its lotsa fun to read: He is after all, the same guy who authored that silly article about ketamine therapy. (Yup, I'm baiting you again. I wasn't real happy when you tossed that in your final post during our last contratemps. You weren't obligated to honor my request that you limit your reply to topics we had already discussed, but you knew I had already said I wasn't going to make another post: that really was a cheap shot, and I'm looking forward to round two).

As to your concluding statement: The point is neither simple nor fundamental when you, doc S and the rest of the RSD "experts" want to hide cyanosis inside a box labelled "dystrophic changes".

You are correct that much has been written about "dystrophic changes" through the years. That's because these liars (doc S included) use that phrase to avoid using the C word. A rose by any other name would smell the same, but "dystrophic changes" isn't a rose; it's a splivet: ten pounds of horse **** in a five pound bag.

In both of my posts on Dana's (Bronco's) thread Upset, I asked people in our forum family to imagine how different things would be if cyanosis were listed among the signs and symptoms of this disease. I now point out how different things are because it isn't:

Instead of an agreed upon sign that leaves no doubt that an objectively identifiable disease process is going on, proof beyond contradiction that RSD is real, we live in a world where lawyers for insurance companies can argue that there is no objective evidence for this disease.

Instead of an agreed upon sign that doctors could immediatly identify and thus confirm that the pain the patient reports is indeed real, we are treated like junkies when we have to go to an ER because even our own doctors won't believe us.

I could go on, but I believe I've made my point. Doc S is a liar. He lied agan when he used the phrase "cyanotic-like". I don't know why he lies. It could be the money he makes off of ketamine; it might be that he simply doesn't have the guts to admit he was wrong all these years; or he may just be a pathological liar. Whatever his motives, he is, as I've said before, not just a liar but a damned liar...Vic

Jose, Liz, Pat, everyone; I finished my reply to Jose's post, and its a biggie: 1900 words. I was too tired to go back and edit it, and too tired to reply to other posts here, but obviously not to tired to do another thousand or so words here.

Don't be mad at me. Yeah, I'm irresponsible, but playing with Mike is so much fun

Hey Jose,

What a joy to see your post! I was instantly flooded with memories of that chat room at BT; feeling like I’m sitting around with friends at the favorite watering hole and Jose comes through the door; people calling out “Hi Jose” and “Jose’s here, we can start the party”. So many conversations about so many things, some serious, some nonsensical. We really had something good happening there.

Auntie Josie, please tell us another Bubba story. Just one more, huh? Huh? I promise we’ll go to bed right after…pleeeaaaasse.

If I had any fears that my words would burn bridges, they’re gone now. Jose’s back. And Liz came out of semiretirement to add her two cents; and Kate’s here too. I never went to high school reunion, but I have to wonder whether that would be any better than seeing so many of my good friends all posting here at the Forum on the same day.

Before I start talking about some of the things you and others have written here, I should tell everyone that I stopped taking Paxil about a week ago. I see smiles and nods of understanding; quitting the happy pills can mean major changes…so why quit?

Those of you who were here when I wrote my first post at NeuroTalk know that I was resigned to the fact that I was gonna die real soon, and that I had already decided that I would choose the time and manner of my death. I was starving myself to death; dropping from 220 pounds to an eventual low of 126 pounds, and stuffing my face wasn’t helping.

If I kept losing weight I would reach the point when I was too weak to live at home and end up in a nursing home. We know that nursing home food is not going to help anyone gain weight. I knew I wasn’t going to starve to death while enduring the indignities that go with living in one of those places, I would wait as long as I could, then I would tuck a .22 pistol under my chin.

Paxil played a significant role in making that scenario not happen, so why would I stop taking it a week ago? Paxil does other things besides help people not pull triggers: It makes the penis useless as a toy, it also makes you not care that its useless. But that was no big deal for me: my back and nerve injuries made “fun” a distant memory and I’m too homely to find anyone who wants to play with me anyway.

But Paxil also puts out the fire in the soul. I wasn’t writing about RSD anymore; I would try, but what I did write sucked. I spent ten years researching and writing about this damn disease and now, when I think I’ve finally found a way to put the words together in a way that won’t make people feel they just took too big a bite of ice cream, I’m asking “Whets the point?”

To me, the choice was between what had been making me miserable and what was making me miserable now. I’ll just have to see what happens next; I know I won’t let myself start looking at my pills and asking “Why not now?” I used to do that a lot; several times a day. I’ve gained weight, so if I see I’m not eating as much I may have to start popping the Paxil again. Maybe I’ll figure out a way to cycle back and forth so I can get something done. Right now, outside of a tendency to feel a bit sorrier for me, I’m doing ok.

I have already finished one article for the website, and I don’t think it’s a coincidence that I suddenly made three posts here after weeks of silence. And the posts on this and other threads, plus the fact that the word cyanosis appears more on page one than in the entire body of literature on written about RSD since 1950, and several “attaboys”, seem to make my decision to quit the right one.

Jose, you’re right about putting everything in one place rather than in replies to others posts. Pat (Artist) said the same thing weeks ago, and that was part of my new plan. But I can be a tad impulsive and those recent posts prove it. I guess stopping Paxil relit all the fires; I know that when I read Dana’s (Bronco’s) post I got really ******. Reading what Frogga said about it being too bad pain doesn’t turn you green was the trigger. It didn’t seem off-topic to me that pain may not turn us green, but cyanosis does turn us some interesting shades of purple. So I said it.

And I said some other things too. I thought I might get people started talking about cyanosis, but for a while it looked like I was wrong. That’s when I wrote the second post. Now people are talking about it, and as you’ve probably already guessed, that makes me feel like my words are finally accomplishing something.

And yeah Jose, I was deliberately calling Mike out. I have faith in Mike; he’s a scrapper and is intensely loyal to doc S. He could still post an interesting reply…or two…or three. So I’m prolly not gonna back away from this in the interest of peace in our time.

And you’re right about the need for long articles. If I’m ever going to convince anyone that there is a way out of this RSD ****, and there is, I’m gonna have to write a lot of words. A whole bunch of words. But this time I’m not going to over-explain until people’s eyes glaze over. I hope it works.

But before I can get anyone interested in ischemia reperfusion injury (IRI), I have to prove that it is simply impossible for any nerve injury, no matter how severe, to mediate the signs and symptoms of RSD. I just finished that article.

That’s just the beginning: ischemia reperfusion injury (IRI) is a very complex process; so complex that doctors didn’t even begin to figure it out until 1963. It begins with the immune system’s response to trauma, and I’m working on that one now. The next one will explain how this immune response goes wrong and turns into IRI.

Oxygen free radicals (OFRs) play a central role in the immune response, and it will take an entire article to explain that. Then I’ll talk about the science supporting my hypothesis that OFRs cause symptom migration and that antioxidants like grape seed extract (GSE) and DMSO can at least delay the onset of this awful complication. It will be the first article on symptom migration that doesn’t rely on things like:

Well, if this happens and then that happens, maybe the other happens, that could explain why symptoms appear in new parts of the body. I’ll write about what scientists know happens, and how putting known facts (not speculation) together really does explain it. For some really dumb speculation about how symptom migration might happen, if God has a sense of humor like Jeffrey Dahmers. email me a request for Maleki’s mostly pointless discussion of the topic. (Just click on my link at the bottom of the page and type “Maleki” in the subject line).

I hope I can fit everything about microvascular systems (MVS’) into one article, because I can’t leave that out. It is a well established fact that IRI plugs MVS, and that leads to cyanosis and tissue hypoxia. And pain and trophic changes and patchy osteoporosis and lower skin temperature.

After I write all that, I have to explain how hyperbaric oxygen (HBO) fixes exactly what IRI breaks, but only if you provide HBO at a much lower level and pressure than the industry does right now. And you can’t rush the job because HBO has to work with the body to replace millions, even billions of plugged MVS. The body can’t do that overnight. Like IRI itself, fixing the damage doesn’t happen overnight.

All of this is going to take a lot of words, and it’s going to take dedication and commitment on the part of those who want to learn. It won’t be an easy task for the reader; it took me four years of intensive study, several hours every day, before I felt I had a really good basic understanding of what is really going on.

This stuff can’t be scattered over dozens of posts, or even dozens of threads; they all fall off page one and eventually fade into oblivion. It will take a dedicated website. Good thing Allen knows how to build them.

Most people will not be willing to take the time and make the effort to learn all of this. I don’t understand why they won’t: This disease is kicking our asses, it is destroying our lives and our families. I would have thought that people would do anything to learn how to stop it, but I haven’t seen much evidence of that so far.

Hell, I’ve been writing about how to delay symptom migration for years. Others have written posts saying they haven’t had any “new” RSD since they started following my advice, and I still cry when I read new posts saying ‘it is happening to me.’ It only costs about $10.00 a month, and I spend more than that on root beer.

I do take comfort in the reasonable belief that the lies about RSD can’t survive much more than another ten years: some physicians are already talking about the possibility that RSD is IRI, and their number can only grow. Those who are still alive in 10-15 years will finally be able to get the treatment they should have begun getting tomorrow; it’s a damn shame that they will choose to suffer all that time.

Oh, and I should have dropped that part about burning bridges: If you had read the first couple of drafts, you’d have probably agreed that someone needed to take my matches away from me; but I eventually calmed down and wrote the posts all of you read. ATTABOY VIC!!! I told you you didn’t have to waste all that money on those stupid anger management classes.

Anyway, I felt kinda shot down when people didn’t respond to my words the way I hoped they would, but I got over it. Getting a bunch of attaboys from people I have loved for so many years helped a lot. And I’m a lot like a terrier: you can beat the crap out of me, but as soon as I start feeling better I’ll be right back in there, biting the Hell out of your toes.

Don’t ever feel bad about your long posts. If someone pressed me hard enough, I might be able to come up with one of your posts that could possibly not have been worth the time it took to read it. Perhaps. Most of em help more people than the one you’re talking to.

(I still remember a post from someone who loves me, a true friend. And friends aren’t people who accept you for who you are all the time; real friends tell you when they think you’re screwing up.

(Do you remember what you said when I wrote about going back to Chiapas? I do. You pretty much demanded to know what was going on in my pointy little head. You said I must be crazy to think about driving 1900 miles when I collapse in pain after just 200. You asked what I would do once I got there – if I got there. How would I find a place to live? How would I shop? Stuff like that.

(I didn’t think about that stuff. I felt so totally emasculated that all I wanted to do was go back to the place where I had proved to myself that I was a man. To the moment that I knew I was willing to die to protect my friends).

Well, old pal, I’m still here, still alive and still writing. I like to think I probably would have recovered my sanity before I drove past the point of no return, but…

Anyway, thank you for that. Thank you for the Bubba stories, thank you for this wonderful attaboy and thank you for being you…Vic

Oh, by the way, my plan to edit the Hell out of my articles is off to a roaring start. Before editing, this was about 1900 words: Now it’s 2200.

I still have things to say to my other dear friends who rushed to support me. I’m just kinda tired right now. Jeez, 1900, erm 2200 words. No wonder I’m tired. Meanwhile, I just found a toy I haven’t played with in years…

Err . . . "art" should have been "rat." (That's what happens when the block and copy feature is disabled in a .pdf file: you're stuck with my typing.)

Quote-
[This stuff can’t be scattered over dozens of posts, or even dozens of threads; they all fall off page one and eventually fade into oblivion. It will take a dedicated website. Good thing Allen knows how to build them.]

Vicc-
You can always start a dedicated thread here by adding your informational posts to the same thread each time.

Even though the thread might drop off the page in time- it will be easily search able and easy to find in the future with a link to it in the useful sticky thread.

Hey Mike, that's what some of us ratists think too, now and then
all the best!

oh, well done.......made me laugh out loud!

my day is made!

liz

Dear Vic -

It is good to hear you sounding so well. (At least when you stay away from personal attacks, which brings out a definatively darker side.) I have to say that it sounds as though you're doing something right.

And for what it's worth, I haven't been in touch with Dr. Schwartzman in a couple of years. When I had a small (non-transmural) MI - which I personally attribute to inflammatory cytokines known to be produced by RSD, among them Interleukin 6 - I was no longer a candidate to participate in his research studies, and hence there was no point in flying across the county just to see his smiling face.

No, most of what I get today is from my docs in LA, specifically the part about dystrophic changes being a function of more than just loss of oxygen. There is at least in the classical model, a loss of some nerve signal that, in and of itself, contributes to a shrinking of muscle mass.

Now I know that you feel that you have shot down every article that has tried to show some damage to nerve cells in CRPS I. That said, I think it would serve you well to carefully re-read to full text of Dr. Oaklander's article, "Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy), Pain 2006; 120:235-243, a copy of which is attached. Put it another way, I know that you feel that you've previously taken care of her thesis down in a couple of sentences, but you might want to look at the article a little more carefully, where it not only survived peer review prior to publication, but has been widely hailed since it came out. Or if you just want to develop your point in further exchange with me, that's fine too.

Having said this, never say I didn't give you anything. Please find attached "Tissue hypoxia in complex regional pain syndrome," M. Koban at al, Pain 104 (2003) 149–157. I'm pretty sure you're already familiar with it, but here it is in any case.

I guess what I'm trying to say is that I don't take issue with the fact that tissue hypoxia is terribly important here, and I've felt that way since I started experiencing debilitating leg cramps, all in the absence of any blue-ish skin. I just think it's not the only answer, not when there really is evidence of nerve damage associated with CRPS I, and not when I had a non-transmural MI with no known risk factors, but one that could be explained by an immunological model. And you are well on record as having extolled the anti-inflammatory properties of grape seed oil. So why not at least take the plunge and start checking out some of the immunological literature? (The water's fine.)

Just to see if it's of any interest, check out "Mast cells are involved in inflammatory reactions during Complex Regional Pain Syndrome type 1," Frank J.P.M. Huygen et al, Immunology Letters 91 (2004) 147–154, a copy of which is also attached.

Be well.

Mike

Attached Files

	Evidence of focal small-fiber axonal degeneration in complex regional pain sybdrme-I.pdf (168.4 KB, 992 views)
	Tissue hypoxia in complex regional pain syndrome.pdf (205.1 KB, 1116 views)
	Mast cells are involved in inflammatory reactions during CRPS-1.pdf (96.8 KB, 1372 views)