Facts you may not know about RSD
 

INTRODUCTION:

A few people have suggested that I put my posts on specific aspects of RSD into a single thread so that it will be easier to see how they fit together. I shoulda figured that out. Unlike Hooshmond’s Puzzles, however, which flit from one idea to another like a demented moth, I will try to place them in some rational order.

Those of you who remember my posts at BrainTalk remember long and extremely boring lectures on the immune response to trauma; ischemia-reperfusion injury (IRI) and; oxygen free radicals (OFRs). There is no way to make these subjects exciting, but I think if I had taken more time to show why they are so important, readers would have found a reason to plow through them.

The best reason to learn about those things is the knowledge that they are the best explanation of the cause, course and nature of the disease we share. Why learn what causes ischemia unless you know that ischemia causes RSD?

The first three posts of this series will provide all of the proof anyone needs in order to understand exactly how ischemia is responsible for every sign and symptom of this disease.

The first will talk about allodynia, and will present undisputed facts about how or sensory nerves function and how ischemia causes some of them to malfunction. I think that after reading it, most here will agree that it certainly can cause allodynia.

The next will talk about how ischemia causes the deep, bone chilling cold, and the lowered skin temperature we all suffer. I also hope to talk about it can cause the burning sensations on our skin. The last will help the reader understand how ischemia can cause every other sign and symptom of this disease.

Once you have read exactly how ischemia causes each one of your symptoms, you may be less inclined to rely on vague talk about “nerve damage”; talk that never gets around to telling us which nerves – or even which nervous systems – are damaged. That will prepare you for posts on why our nerves can’t do what the RSD “experts” tell us they do.

Those who have read my posts on hyperbaric oxygen (HBO) in Buckwheat’s thread Vascular Issues, will have to wait a while before I talk about the ischemic damage that HBO repairs, but at least now you can be pretty sure you will eventually find that information here. (Assuming my strength endures and He doesn’t pull me out of the game early, like I keep asking Him to do).

Finally, if I haven’t explained things so that they make sense to you, please ask questions. These are just letters on a page unless you understand them completely. If you find a contradiction, point it out: challenge me, make me prove every detail. If I can’t do that, ischemia may not be the answer to RSD, but if I can, you really need to learn all about this stuff…Vic

what a picture!
 

LOL....a demented moth?????......i agree with u, but the phrasing enchants me!....which is polite-speak for " i'm just laughing like a fool at the image invoked by that phrase!"

thx for the chuckles....always good medicine!

liz

:ROTFLMAO:

Hi Vicc. First, I've read all that you've written over the years and I can't tell you how much I appreciate all the work you've done to break down all the mumbo jumbo to a more managable level. :D I've read lots of mumbo jumbo and technical papers until my brain leaked out, but pushing on has helped explain a great deal as well.

What you say here makes a great deal of sense. I can't think of anything specific to question that you've put down. There was one thing that did pop to mind while reading this. I read somewhere, I'm pretty sure it was one of those mumbo jumbo papers, that after having RSD for as little as 6 months, the nerves, specifically in the affected limb are damaged beyond repair. I believe they mentioned nerve endings as well.

Seeing as we're talking about the same here, is that true? Have you found in your research that the nerves and/or nerve endings become damaged beyond repair? To me, this makes quite a lot of sense actually given the nature of RSD and all that it does to our bodies from the inside and the way it spreads through our body as well. I almost picture in my head, a tiny little army of invaders on the march reeking havoc and leaving destruction behind on our nerves, nerve endings and also cell damage, behind them as they move where they will.

I mention cell damage because it was another thought that has occured to me some time ago. With the reduced/restricted blood flow to the affected limb/limbs, is it bound to also damage or destroy cells or change the function of cells in our bodies?

This has all been floating around in my head for a long time now and since you've done so much, I can only hope that maybe the things I mention here can be either confirmed or denied and why. I have always had an insatiable need to KNOW stuff and like a little kid, ask why? :D

Thank you for taking the time to help us all understand the why of this horrible conditon we live with every day.

Karen

PS. I agree with Liz, that demented moth comment had me laughing hysterically as well and is sooooooooo appropriate!!! LMAO

Hi Vic,
well i must say you have taken me back to my A&P, cellular level, days of nursing school with these postings and i am intrigued. i am going to read up more on ischemia and give it some though as to the connection of my own problems. i also have nerve palsy from the hip surgery that lead to my RSD so i tend to get the signs and symptoms bunched into one ball and am never sure which is coming from what.
i can tell you i have often thought that if my leg was 'positioned wrong' during a 6 hour surgery, which is what they tell me happened, there was probably not just a stretching of the nerve as was told to me, but a lack of proper blood flow during the event.
so you have peaked my interest, and although i tend to accept my RSD as forever, i do hold out that 'something', that is totally not being researched, is the answer to the cure for us all. i say that, because i do not think any doctors have a clue to the disease, and all are just using what they believe is the best way to 'control' the symptoms. i am not interested in control, i am interested in a cure. i research and control my own pain with a doctor i had worked with in the hospital for years, who lets me pick and choose what i want.
so i will be reading along with your postings and look forward to the educational recall you are giving me.
i will also pray that HE does not take you for a long time despite your willness to go, i think you have more work to do, i think we all do ....
joan

joan
 

hello,

I'm wondering what meds you have picked and chosen? I too am a nurse(just and lpn) not RN. I guess i always want to know what is working/not working for everyone else. I've been thinking about asking for trental? Ever tried it?:) just curious, jenny:hug:

Thank you
 

I am looking forward to your posts following this one... You seem well educated and i am intrested in what you have to say... Thank you for taking the time to pick my intrest!

Thanks again vic!

Pain free hugs to all :grouphug: :grouphug:

Reply
 

Gosh GF,

For someone who can’t think of any questions to ask, you sure came up with some great ones.

I have simply stopped paying attention to anything written about RSD unless something on the page gives me a good clue that the paper involved real research, so I would probably have merely glanced at the article you describe and dismissed it as just more speculation.

There is one article that discusses Cf neuron loss in RSD: Oaklander, et. al., [1]*, recently published a study in which they reported that skin biopsies of RSD patients showed a 25% reduction in Cf neurons in the skin of RSD patients.

I didn’t find any mention of Afs, which, being larger should have been easier to see and count. It supports what you read, although six months may have been just speculation. Whatever time it takes, it’s clear that some of our neurons are disappearing.

Oaklander concludes: The major implications of our results are theoretical. They support the concept that CRPS-I is a neurological
condition, and that small-fiber axonal damage is involved in pathogenesis.

I don’t see how this research supports the view that RSD is a neurological condition (but how does neurology explain patchy osteoporosis; diminished hair and nail growth or cyanosis? This is beyond neurological), but the second half certainly appears to be true (and would be explained by ischemia).

(She might be thinking that this is some sort of “ethnic cleansing” and that the survivors (75%), did the others in and then hid their weapons. (You have a vision of a small invading army; mine is of all those surviving neurons standing around trying to look innocent).

It makes sense that hypoxia would destroy small fibers; they have no ATP reserves, after all, and can’t survive forever, but there is good news here: 75% of them are still around.

In a future post I will show how IRI is random; that it doesn’t result in complete ischemia, and perhaps use this article to suggest that the ischemia in skeletal muscle and tissue is not as widespread as has been found in internal organs (which is what most IRI research has been focused).

Oaklander goes on to say: They challenge other views that
CRPS-I arises exclusively in the brain, or is a‘‘pseudoneurological’’
illness cultivated consciously… and I agree with that.

I wonder why she didn’t mention the spinal cord as well as the brain; maybe she thinks Schwartzmann (the major proponent of RSD as a product of central sensitization (in the spinal cord), is a nice old man and just didn’t want to hurt his feelings.

I’m a bit upset with Oaklander (as I am with all RSD “experts”) for not saying anything about evident cyanosis of the tissue of their RSD patients: and there is no way any of them just never noticed.

Anyway, yeah, it looks like we suffer some permanent nerve loss.

On the other hand, while some people report a sense of numbness in affected tissue, I haven’t read anything in the literature or at any forum, that talks about complete loss of pain sensitivity; a cut still hurts and a burn still burns, so I’m not worried about the future in that respect.

I’m worried about the future because everyone seems focused on symptom (pain) relief, not finding the cause or a cure for this disease. Well, I am, but it’s been a lonely battle.

You mention cell damage, which I plan to discuss in a future post. For now, I’ll limit myself to saying that cell damage is evident everyplace you look: muscle atrophy and weakness; tendon contracture; osteoporosis; hair and nail growth are all evidence of cell dysfunction, and those cells aren’t functioning properly because they’re damaged.

The good news about cell damage is that our bodies come with an instruction manual that tells cells what to do in almost any imaginable situation: It contains step-by-step instructions on how to turn oxygen and glucose into ATP, and instructions on how to transfer oxygen and nutrients from one cell to another during a famine (like hypoxia).

I will go into much more detail about this when I write about cell damage, and about how the brain is currently trying to fight tissue hypoxia in RSD. (It isn’t working, but that’s because RSD isn’t a situation the instruction manual is prepared for).

RSD isn’t an army of invaders on the march in the way the Mongol Hordes swept across Europe. It isn’t even like a parachute drop into specific places by the 101st Airborne Division. It is trillions of “enemies in our midst”, waging a constant battle against our bodies. And I’ll leave it at that in the hope that it piques some interest in reading the boring stuff. And it’s on the way.

Joan, I’m glad you have courses in A&P to look back on. I’m counting on nurses here to try like Hell to find flaws in my posts, and to be honest enough to admit if you can’t. I think that if you study IRI like you did A&P, you’ll learn exactly what I learned. Your training will make it much easier for you connect the dots.

You wrote …there was probably not just a stretching of the nerve as was told to me, but a lack of proper blood flow during the event, but look at your skin today; don’t you think that there is a lack of proper blood flow now?

Finally, guys, I liked the “demented moth” line too. And it accurately describes doc H’s writing style. He knows he’s selling nonsense, but by arranging it that way, no one can figure it out. "If you can’t dazzle ‘em with brilliance, baffle ‘em with ********". Thanks for noticing…Vic.


*A [ ] with a number inside means I will email you a copy of the article cited. Just click the “rsd_hbot” link at the bottom of the page and type in the title of the post and the number(s) you want to receive.

Hi Jenny,

Missed you post; sorry. I haven't taken Trental, sorry again...Vic

This is too short, so....

Q: What do they traditionall call the person who graduates last in his/her class at medical school?

A: Doctor.

Vic

hi vic,
my A&P was a long time ago, and i spent my years as a surgical and surgical ICU nurse, so the cellular part was not used much in my day to day nursing.
but as far as, do i think that my leg shows blood flow problems now, absolutely without a doubt. i have constant blood pooling when my legs are down. that is why they swell, and discolor, and hurt like the dickens ... so i am with you on that. i guess the 'theory' of the medical professionals is that the nerves do not tell the vasoconsticting mechanisms to pump the blood back up .... do i buy that? i don't buy anything. and one big problem is, i think many doctors get a theory in their head, and then can't see anything else as even a possibility. and may i add, many doctors are smart, and many are average, and many are not bright at all ... thus, my reason to not buy anything i hear.
so keep writing and i will keep reading! and thanks for keeping my brain going.
joan

You probably learned in high school that our cells combine oxygen (O2) with glucose (Gl), to generate the energy that keeps them alive: No Gl and no O2 = no energy. You probably also learned that our cells also create all of the heat necessary to keep the body at a constant 98.6 degrees. Heat is a by-product of cells transforming matter into energy.

Without any O2 or Gl, the cells would die, if enough cells die, the body temp would begin its drop to the temp of the air around it. There is a mid-range, however, when the cells aren’t getting enough 02 or Gl to function properly, but still survive. But the temperature will drop.

The only explanation I have found for our painful hyper-sensitivity to cold and lowered skin temperatures is that the cells aren’t getting enough O2, or Gl, or both. This is that mid-range I just talked about.

I’ll talk more about exactly why RSD falls into this mid-range in future posts, but my purpose here is to show how ischemic hypoxia: blood flow to cells and organs that is not sufficient to maintain their normal function.* explains these symptoms, while nerve injury does not.

The only way to stop or decrease cell metabolism is by reducing the amount of O2 or Gl reaching it.

We can know we suffer from tissue hypoxia simply by looking at our blue to purplish skin. That is the color defined as cyanosis: a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood.*

Our skin is supposed to be a normal, healthy color; you know: “Skin color”, so why isn’t it? Cyanosis is a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood.*It is visible proof of hypoxia. If our skin is cyanotic, our cells are hypoxic.


When we see cyanosis, we are actually looking at millions of microvascular systems (MVS) filled with oxygen depleted blood, and that blood isn’t moving. Our MVS are part of the circulatory system and blood is supposed to be constantly moving, never stopped. Those MVS are ischemic. A low oxygen state usually due to obstruction of the arterial blood supply or inadequate blood flow leading to hypoxia in the tissue.*

MVS are the arterioles, capillaries, and venules that deliver “fresh” arterial blood to the cells and return “used” blood to the veins. The blue color means that blood is not flowing through the arterioles and into the capillaries that supply everything the cells need. When this happens, our cells do what they are programmed to do to:

They switch from aerobic metabolism to glycolysis; generating energy without using O2, but glycolysis doesn’t generate any heat, and isn’t nearly as efficient as aerobic metabolism. It does provide enough energy for the cells to survive, but not enough for them to function properly.

They also release chemical neurotransmitters (Nts) that tell the brain that they aren’t getting enough 02; and they tell other nearby cells the same thing: Nearby cells may be served by functioning MVS, and if they are, they transfer some O2 and Gl to the needy ones. This helps keep those cells alive, but it also means the donor cells now don’t have enough of either to function properly. Now they aren’t able to generate enough heat to keep the limb warm.

This works pretty well during an emergency, but if crisis lasts very long, all of the cells suffer. In RSD, the crisis lasts too long. Many, if not most of the cells in the affected area are now dysfunctional and the temperature of the affected limb begins to fall.

The temp doesn’t need to drop much before the cells begin releasing Nts telling the brain they’re cold. Our bodies are designed to maintain a constant temp of about 98.6 degrees; a drop of one degree can cause the cells to begin complaining, 96.6 degrees feels bitterly cold, and a core temperature of 95.6 degrees will produce violent shivering.

When the air temp in my room drops to 68 degrees, it gets too cold for my feet: They start screaming that they’re freezing. Other things may be contributing to the cold pain I’m experiencing; my “pain nerves”, C-fibers (Cfs), aren’t getting enough 02 either, and they may be amplifying the cold messages from the cells.

The bottom line is that when cells don’t get enough O2 and Gl, they can’t generate enough heat to warm themselves, much less the tissue around them. They start sending out frantic signals because this is a real crisis.

They send signals telling the brain they aren’t getting enough O2, so the brain tells the sympathetic nerves to increase blood flow, and this aggravates things because one of the things the SNS does to increase blood flow is to stimulate the release of adrenalin. Adrenalin increases the burning pain of RSD.

We know that adrenalin does this because if you inject norepinephrine (artificial adrenalin) just below the site of a recent sympathetic block; the burning pain comes back. That is what sympathetically maintained pain (SMP) is, and it is why blocks work: They are blocking normal sympathetic release of adrenalin, NOT blocking some abnormal SNS activity.

Several things can cause the kind of cyanosis we see in RSD: In late stage diabetes, the disease has damaged small arteries so badly that they can’t carry enough arterial blood to supply the cells; in Raynaud’s Disease, spasming of the arterioles in the MVS prevent arterial blood from getting into the MVS. In both of these disorders, too many cells die and gangrene can develop, making amputations necessary.

RSD patients sometimes end up with an amputated limb, but not because of gangrene: When microcirculation is impaired, wounds can’t heal properly and infections can develop; antibiotics are delivered in arterial blood, so the amount that reaches the site where they’re needed is too little to do the job.

Something else causes the cyanosis in RSD, and after ten years of research the only explanation I’ve found that makes sense is ischemia-reperfusion injury (IRI). It begins with a physical trauma, followed by inflammation and then by ischemia in which some cells still get enough O2 and Gl.

I’ll explain more about IRI in future posts, but before I get to that I need to prove that ischemia can cause every sign and symptom of this disease. I hope that once I’ve done that, you will be more open to the idea that this disease is NOT caused by nerve damage. My next post will talk about those other signs and symptoms…Vic

* Online Medical Dictionary (OMD)

Things I know

My RSD was NOT caused by restricted blood flow, IRI, lack of oxygen to the arm etc etc etc.

My RSD WAS caused by nerve injury.

People who know me know the full story.

People who refuse to accept my account of how I contracted this don't know me at all and sure don't know my history (or maybe just choose to take the parts they want to hear).

In keeping on topic... this will be my only post on the subject.

Ladies, I hope you all have a wonderful day today. Keep up the good work

Hi Farm Wife,

You are no way alone with the aetiology of your RSD. As I have said in a previous post that if RSD can come from a paper cut or a mosquito bite then there is absolutely no restricted blood flow causing it.
Sorry, I don't know your history but you can be sure that there would be no reason why I would question your account of your injury, you sound like a very well educated and I would gather a resourceful women.
Wishing you heaps of luck
Tayla:hug:

Hi Farm Wife,

I try to avoid talking about the personal views of forum members, but I do think it appropriate to point out that in previous posts I have said that diagnoses of CRPS-II have not been discussed in the literature, that some tissue injuries can also injure nerves, and there is nothing in the literature that describes how a nerve injury can cause the signs and symptoms of this disease.

Also, I don't know how one can say: My RSD was NOT caused by restricted blood flow, IRI, lack of oxygen to the arm etc etc etc. Unless tests have excluded IRI or tissue hypoxia. The absence of cyanosis does not exclude either of these, as cyanosis is only visible when the microvascular systems at the skin surface are ischemic.

Many people diagnosed with RSD don't present with cyanosis because the injury involves fractures, ligament injuries, nerve entrapments (which can initiate the immune response to trauma), etc, that don't involve blunt force trauma to the skin.

Finally, while I don't claim to have read all the literature on what might cause painful hypersensitivity to cold, I have look for other explanations for this symptom and couldn't find any that didn't involve diminished cell metabolism due to tissue hypoxia.

I am not arguing with you; I'm simply pointing out that a diagnosis of a nerve injury does not exclude tissue hypoxia. At this stage in my life, I would be relieved to learn that I am wrong about IRI. If that were to happen, I could refocus back to reading history and even possibly write a thesis that could earn a Master's degree in that subject.

Until and unless that happens, however, I feel compelled to explain why RSD is an IRI and that IRI is treatable...Vic

Hi Vic,
First, before I get in trouble, let me state that I enjoy everyone fo your postings and think you do lots and lots of homework. i agree with a lot of what you say and then there are times when i am confused my it. so that being said:
I would like you to explain something to me. i had hip surgery and awoke with nerve damage, unable to control my left foot and numbness here and there from the knee down, then the crmaps started and then the pain and the sweeling and the cyanosis, all within a matter of days. i was of course later diagnosed with RSD. so could you please explain to me, what you think the exact process was?
I ask you this because i can't quite connect the fact that i had a nerve damaged, that caused the nerve palsy, and then the RSD symptoms emerged, and i would like to fit this into your IRI theory and see how i feel about it because i do think you make a good point there.
i will say right out, i do not have a clue what rsd is, or how i got it, or how anyone gets it, or why, or what to do for the pain, or what a cure might be or when ...but i am intersted in your opinion.
thanks, joan

Nerve damage
 

CRPS II is nerve damage, and it sounds like what you have experienced Joan. You might read up on that. That is what I have also, a known nerve damage.

That said, I wonder if anyone has thought about the relationship of the nerves and the vascular system? If you have nerve damage, wouldnt you think it would influence the vascular system?

I mean the nerves control the muscles, and that means all, even the muscles in the vascular system. It could be quite possible that the 2 camps are both "right" here. It seems logical to me that no matter how you got RSD, once you have it there would be complications with anything the nerves had anything to do with.

In my case I got CRPS II from ischemia, which in turn caused nerve damage.
Now there is symptoms of both going on in my body. Kinda like everything is spiraling out of control. Now if we can get blood oxygen flowing in to the damaged areas it would make sense that the nerves could have a chance at healing. Maybe the nerves are not allowing enough oxygen to flow in enough to get any healing, and after a length of time the damage is so far gone nothing is working properly?

I think we should all keep an open mind since even the experts cannot agree completely on the hows or whys of RSD. In my mind the two, nerve damage and vascular go hand in hand, and can both be resultant in RSD no matter which came first.

Tayla,

If you would take the time to learn about the immune response to trauma (IRT), you would know that both paper cuts and mosquito bites are trauma, and the immune response always involves ischemia: blockage of arterial blood flow.

It happens this way: White blood cells respond to the site of the trauma, where they release reactive molecules called oxygen free radicals (OFRs), OFRs are responsible for the inflammation and swelling that are obvious in injuries such as hitting your thumb with a hammer, but even if unnoticed, is present in the IRT to a paper cut.

Swelling compresses the tiny nearby arteries and veins that deliver blood to the capillaries and return "used" blood to the veins. This compression is ischemia.

IRI is a disorder that involves an IRT that doesn't end as it's supposed to; instead, the inflammation and swelling (ischemia) spreads over an increasingly widening area. The second stage of IRI is the blockage of arterial blood flow to the capillaries, which means that the cells no longer receive the O2 and Gl they need in order to function properly.

As I have said before, IRI is a complex series of events which I can't possibly explain in just a few hundred words. In fact, I haven't been able to explain IRI and OFRs in less than several thousand words. I am working on a briefer explanation, which would make it easier to understand, but necessarily means that I won't be able to provide all the information necessary to describe how all of this takes place.

If you are unwilling to accept this necessarily brief discussion of the IRT and IRI, I suggest you should learn for yourself what takes place. With your nursing education and experience, it should take you less time to learn than it took me...Vic

Hi Joan,

I just want you to know I will reply to your questions, but I've been awake all night, and my brain simply refuses to help me out right now. I really do appreciated your questions, because they give me the opportunity to explain a little more about IRI...Vic

Vicc,

Just wondering also how you can get your statement below..

"Also, I don't know how one can say: My RSD was NOT caused by restricted blood flow, IRI, lack of oxygen to the arm etc etc etc unless tests have excluded IRI or tissue hypoxia. The absence of cyanosis does not exclude either of these, as cyanosis is only visible when the microvascular systems at the skin surface are ischemic..."

I had a neuroma removed from my foot. Now a neuroma is a growth on the nerve and i had that removed and just like Joan my symptoms started after the surgery. Cramps, swelling, color changes, skin temp changes, and skin changes and then my foot started to invert. I did not have any thing on my leg during surgery that would cause restricted blood flow or lack of oxygen. My total surgery time was 9 mins. What else would cause RSD expecially since they removed sometihng from the nerve itself and I have nerve damage on 2 toes due to the surgey. (it was expected damage, just a result of the neuroma surgey, i knew that this would happen before the surgery.. just not that RSD was also part of it)

Now I may be repeating my self but cant go back a reread all the other posts, but what test are there to test for IRI??

Amber

I must say that Vicc you have your point of view as I said befor you may be right, who knows but I still have to say that it is just your theory, I do not agree with saying all docs who study this are wrong. Vicc my friend you cannot say that, based on what? your theory that is why more money must be made to study this, and why it is called COMPLEX so many diffrent things happen with RSD/CRPS and why no one test can prove it and diffrent people have a wide range of symptoms, it seems as if one patient has symptoms 1,3,5 patient # 2 has 2,4,6 see it is complex that is why they changed the name.
Again Vicc you should argue this with the medical field first, but do not call the docs who study this all wrong your research material you have did come from the medical field you say are wrong, and are you a doc? please to give some respect to men and women who do study this most with a MD with PHD's in front
I'm not targeting you, or flaming you just disagreeing with you thats all and it is healthy to disagree friend.
I also feel it is wrong to target this site on a another board, I wish you well and please if you can stay here it is good that you are here :)
sorry if I miss spell it is getting very hard to remember as of late and pain is way up,I may have to have another surgery everyone wich in a way I have nothing to lose, this one deals with my TOS and may help a little so I wish you all well.

Hi Joan,

You wrote: First, before I get in trouble, let me state that I enjoy everyone fo your postings and think you do lots and lots of homework. i agree with a lot of what you say and then there are times when i am confused my it. so that being said:

I have become increasingly impatient with two people who have followed me from thread to thread and repeatedly misquoted me, falsely summarized my views and asked questions that I have already answered more than once. In my view they are harrassing me. On the other hand, I consistently ask for questions and for arguments.

Replying to them has sapped my energy and made it appeat that I object to legitimate questions or debate. I don't.

You and Amber ask essentially the same question in different ways: You apparently suffered nerve damage during your surgery, while she suffered nerve damage that led to the surgery and possibly more nerve damage during the procedure; these injuries are in addition to what appears to be classic models of IRI.

I think that neither group of surgeons recognized that both of you suffered a classic ischemia reperfusion injury: Some sort of tourniquet ischemia done in order to prevent blood loss, followed by a widening area of inflammation and then by a new ischemic stage in which the arterial blood is blocked from reaching the capillaries and thus the cells.

The fact that they failed to correctly identify an IRI is easy to understand: The disorder was long believed to only occur after surgeries involving internal organs. In the 1980s, researchers learned that it can happen in skeletal muscle, but very little has been written about this, and the little I was able to find involves transplanted tissue or restoring amputations (cases that involved long periods of ischemia due to being completely disconnected to the circulatory system).

I believe that physicians who understand IRI believe they completely understand how it is caused and haven't shown any interest in looking for other examples of possible IRI. This makes sense.

I think it important to point out than in just 20 years they discovered a completely new disorder, learned how to prevent it and how to effectively treat it. Contrast this with RSD "experts", who can't agree on a cause for this disease; have no idea how to prevent it, and; have no clue as to how to effectively treat it.

It is time that the RSD "experts" to look beyond nerves and nervous systems, which have led nowhere after 140 years, but they won't. They continue focusing completely on some sort of nerve damage thay hope to find someday, and have closed their minds against any other possible cause.

I believe if they were aware of evidence of tissue hypoxia in RSD, specialists in IRI might suspect what I concluded, that RSD is IRI; They don't know about tissue hypoxia in RSD because they are mostly thoracic surgeons who never see an RSD patient, and if they did have occasion to operate on a patient with RSD and looked up this disorder, they wouldn't see a word about cyanosis, which could provide the clue they need. They don't find it because RSD "experts" deliberately refuse to mention this most important sign.

In a previous post, I went out on a limb and said that every instance of RSD following surgery is, by definition, an IRI. I don't regret saying that, and believe it is only a matter of time before this becomes a uniform belief among medical professionals.

I believe that if cyanosis had not been deliberately omitted from the signs and symptoms of this disease, it is possible that someone familiar with IRI would have already figured this out.

Amber, while my reply was directed to Joan in order to keep it focused, it is the same reply I would make to you. I suggest that both of you suffered both nerve damage AND an IRI...Vic

Flippnout.

I must say that Vicc you have your point of view as I said befor you may be right, who knows but I still have to say that it is just your theory, Can we agree that it is my hypothesis and that I have the right to present it and allow readers to decide whether it makes sense?

I do not agree with saying all docs who study this are wrong. Vicc my friend you cannot say that, Yes I can, and I will whenever I believe they are wrong. You may call me "friend", but I think your posts betray a different attitude.

Again Vicc you should argue this with the medical field first, but do not call the docs who study this all wrong your research material you have did come from the medical field you say are wrong,

I argue that RSD is an IRI where I feel my words will accomplish something. I have no more access to publish my views in medical journal articles than you. I do have access to people who suffer from this disease. I do what I can.

and are you a doc? You have asked this before, but I will answer it one last time: No I am not a physician, nor is a medical degree required in order to post opinions at this forum.

please to give some respect to men and women who do study this most with a MD with PHD's in front The M.D. or Ph.D follows the name, it doesn't precede it. I respect honest physicians, but when one of them deliberately omits a primary sign of this disease, he/she is harming us and deserves contempt, not respect.

I also feel it is wrong to target this site on a another board, I have no idea what this means.

I wish you well and please if you can stay here it is good that you are here Ok, if you say so.

This is your third post in which you have said essentially the same things. If you choose to make a fourth, similar reply, I won't bother to answer...Vic

I use Trental & have for over 3 years now. I think my nerve meds worked better after I started it. I take Neurontin & now also Lyrica for the nerve pain, numbness & full feeling that RSD causes in my feet.

To whoever it was who had a neuroma removed from their feet,
Also when they do remove neuroma's in the feet they use a tourniquet. I had two removed in one foot & have left the neuroma/s in my other foot alone. I had the neuromas before I had surgery & they caused RSD to happen in my feet. The removal of the neuroma in my left foot only made RSD MUCH MUCH worse in that foot. Lately tho the right foot hurts worse probably cause that neuroma has grown. It has been 4 years since all this happened to me.

Vicc,
I can't say that I totally understand all that you say, but what I do understand I appreciate knowing. Thanks.

DebbyV

A few respectful questions
 

Hello Vicc;
perhaps I am misunderstanding you but:
I assume that as you are on this site you suffer from RSD/CRPS. You maintain it is an IRI which is treatable - have you received treatment and are you better?
I do hope you are.
If you don't mind, could you please share with us how you resolved your RSD?
What treatments were you given for the IRI that is your RSD?
How efficacious were they?

Have you sought out a practitioner who is able treat your RSD in the way you view so adamently it should be treated?
Again I do so hope you have.
Or
If your pain and RSD is maintained, then I am sorry because this condition ain't no fun to live with. .....
but where does that leave us?
I do hope you have news of a positive personal outcome to report to the rest of us.

Kind regards
Auberon

Hello Auberon,

Thank you for questions that others might have (wrongly) felt might be inapproptiate. They are completely proper to ask of someone who says what I say about this disease and possible treatment.

Yes, I am diagnosed with RSD; a diagnosis either made or confirmed by 11 or 12 physicians of various specialties, but I'm sure everyone here would gladly accept the level of pain I experience from RSD of both feet. I will talk about why I think my pain levels are so low in a moment, but first I need to explain why I have to answer that I have never undergone hyperbaric oxygen (HBO) therapy, which has been shown to be efficacious in the treatment of IRI:

My medical history dates back to a back/spine injury I suffered in 1979, which was severely aggravated by two bungled laminectomies. I came out of them with the diagnosis of arachnoiditis (scar tissue of the middle layer of the tissue that surrounds the spinal cord). It is absolutely untreatable and can leave someone with anything from mild to severe pain. I suffered moderate pain with L/5 radiculopathy of the left leg.

I was unable to work at any of the jobs I had ever done, and spent ten years trying to support a family on the pittance that SSDI gives people. I was fiannly able to return to college (I had done 2 years in the 70s) and major in social work.

I was a psychiatric social worker at a state psych hospital in 1995, when a newly-admitted patient assaulted me. It was totally unexpected and I was in a wheelchair, so I was severely injured before help could arrive.

My diagnoses from that incident included bilateral S1 radiculopathy resulting from narrowing of the foraminal space and nerve root compression from scar tissue, and RSD of the left foot.

The arachnoiditis and L5 and S1 radiculopathy left me with moderate ro severe pain that is well-controlled by opiates UNLESS I do any physical activity, at which the pain becomes severe and opiates don't help much. A trip to my doctor leaves in markedly increased pain for 3 days (I pray I don't come down with diarrea; I know I couldn't tolerate that level of pain). The radicular pain could be at least partially relieved by endoscopic surgery, but spine the few neuros who do that won't touch me: it is barely past the experimental stage and they only want patients they can completely cure).

The primary reason I have not presented for HBO is that the travel, transfers and arrangements within a chamber make it too painful to contemplate. I would, however, figure out some way to get it done if I suffered as badly as so many here.

I believe my RSD pain is so mild because I never had the opportunity to aggravate it. I have been pretty much confined to living in a recliner chair 24/7 since my injury and my condition has worsened over time so that now, the only times I get out of this chair are to use the toilet and be bathed at the kitchen sink, and I must have assistance to transfer.

Immediatly after my 1995 injury, doctors prescribed physical therapy, so I went. I didn't make any friends at that place; refusing to do anything that caused my pain to increase, which, of course, means anything at all. The PTs were unable to persuade me that "no pain, no gain" makes sense in all situations, so my RSD was not aggravated by PT.

Being confined to a recliner chair from the onset meant that my feet were almost constantly elevated. I can't explain why that seemed to be efficacious, but I know that when they are elevated, my skin color is normal, while they turn purple in five minutes in a dependent position. I guess you could say my belief is an intuitive impression.

Additionally, when my condition began to really deteriorate about 4 years ago and I entered the stage at which I am today, my feet have been elevated 24/7/365; After this began, my burning pain and allodynia began to subside, and I no longer take the GABAergic drug Lamicatl. I now take oxycodone only, and that for my back/spine pain; I never noticed any RSD pain relief from it.

The only treatments for RSD I received were two sympathetic blocks. The 1st didn't help and the 2nd only a couple of hours of some relief. When I returned fot the 3rd, a PM doc actually told me that since the first 2 hadn't cured me, there was no point in trying a 3rd. (I'm usually pretty sharp, but I confess it didn't occur to me -- at that moment -- to ask hum why I would want a 3rd if the 2nd had cured me. I deeply regret that lapse).

There you have it: No treatments, no PT (yet full range of motion in my ankles), no activity; but I have gotten slightly better.

My hypothesis that RSD is IRI is based on my study of the literature about this disease, my intimate knowledge of its signs and symptoms, and my extensive research into IRI.

I concluded that since every sign and symptom of RSD can be explained by hypoxia alone and since both both diseases began with physical trauma, followed by a period of spreading inflammation that later becomes hypoxic (usually accompanied by cyanosis), it is more reasonable to assume they are one and the same, than to assume RSD is caused by nerve damage -- damage that the RSD community agrees does not occur in CRPS-I -- and that has never been linked to all of the signs and symptoms of this disease.

I read your most recent post in Abstracts, and pretty much agree with everything you said, but you left the big question unasked and unanswered: What in the Hell can we do about it?

Generations have accepted that this disease is incurable. They lived, suffered and died with RSD. They probably never met anyone who shared this awful disease.

Today, for the first time in the history of the world, we have access to almost everything ever written about medicine. All we need to do is click a mouse. I took advantage of this fact and spent two years studying everything I've discussed in all posts on RSD.

I'm not asking anyone to run out and sign up for HBO based on what I say; I'm trying to give everyone here a reason to do the work necessary to learn all this for themselves. I write that hypoxia alone can cause every sign or symptom that anyone here is experiencing. If it is truly part of RSD, it can be explained by hypoxia.

I hope this persuades someone to look up hypoxia and learn whether the things I say are really true. If fixing hypoxia can fix your RSD, it might be worth taking the time to learn the facts about hypoxia.

Talking about HBO is another reason that might cause someone to take the time to learn about it; if it is possible to find remission through HBO -- and at a lower cost than any other purported therapy that we already know won't work -- it might make sense to look into exactly how it acts upon RSD.

Every road leads to ischemia reperfusion injury. Taking the time to learn does not mean leisurely reading of a few journal articles that don't make a bit of sense to you. The only way to do it is to work hard.

Most people won't even consider it; others will try for a few days; others even further: I am guessing that two or three people will read far enough to confirm that everything I present in my posts is accurate up to this point, so there is no reason to assume I might suddenly start making things up. If this happens, I'm berring that at least one of them will try HBO.

I only hope that if someone does, she/he will come back here and tell everyone else about it; and someone else will decide to try it. I have been disappointed in the past, as I persuaded three people -- who I believed were contemplating suicide within days or hours -- to try HBO first. That their lives were worth risking a couple thousand dollars before they decided to end them.

They got better. One continued to post at BrainTalk for a few months, one wrote a couple of posts, and one talked about his experiences in the BT chat room but wouldn't post on the forum; I hoped that others would pay attention, but they didn't.

But I have nothing better to do than try again. So I'll write posts that just **** some people off: How dare think he's smarter than a doctor?" And I'll hope that someone listens. In the words of Kris Kristofferson: "Cause I don't believe that no one wants to know."

I see I have completely hijacked your post into a new course, but I have a bad habit of doing that. Anyway, I don't think I've ever layed out my goal like that before and I think I want everyone to know what I'm doing; and it took too long to write all that stuff, and I can't just delete it; so I guess your post is officially hijacked. I'll try not to do it again...Vic

VIC,
i thank you for your info. i will read and re-read it so it will sink in. it was a very long surgery, and i am sure preventing blood loss was a huge issue. now, i have one more question for ya! how would one treat iri vs how one treats rsd?? in your humble opinion, of course. fondly, Joan

enough is enough is all I can say peace to you all and pain free day!

Bumped My Question For Vic ....
 

I asked a question and just wanted to make sure you had seen it ... thanks vic. hope you are feeling better. joan

Hi Joan,

As it happens, I just finished my answer to your question; and when I hit "preview" it came out with all of that <font> arrow stuff. Totally unreadable. I suppose it has a purpose, but it would be nice if people talk were the default.

I tried toggling the box at the upper-right corner, but that didn't work. I don't know what to do except post this and hope someone will come up with a helpful answer. I'll just leave that reply up and hope help arrives.

Otherwise, I'm going to have to wait until tomorrow to rewrite my reply...just too damn tired to try again right now. I will post a reply...Vic

no rush vic ... i'm sure i'll still have rsd after you get some rest!! take care.
joan

do you all have PM pop ups enabled in your User CP section?

So if a PM is sent to you it will instantly pop up a small notice of that?

Hi Jo,

I think most of us have pop-up blocker programs in our pcs. Could enabling these pop-ups confuse my computer? It's already confused enough...Vic

You may also need to add in the browser settings "allow pop ups from neurotalk"

I use FireFox browser I just checked my pop up settings.
On the content tab -
In the pop up setting section click the exceptions and add the main forum link {what I used}
here- http://neurotalk.psychcentral.com/
then click Allow button.

I just checked IE and it's quite similar - in the privacy section.

They just dont know why
 

"We're lost in the woods here about the causes of complex regional pain syndrome [CRPS], because the definitive trials could cost millions and the NIH is not funding pain research now," said R. Norman Harden, MD, director of the Center for Pain Studies, Rehabilitation Institute of Chicago.

What to do? The Reflex Sympathetic Dystrophy Syndrome Association estimates that the CRPS affects between 200,000 and 1.2 million Americans. The underlying causes of the syndrome have yet to be defined, and no definitive diagnostic test exists even though CRPS was first described in the late 19th century by the neurologist Silas Weir Mitchell. Mitchell referred to the cluster of symptoms he noticed in some of the Civil War soldiers who were under his care as "causalgia."1 The soldiers persistently complained of severe, burning pain long after their wounds had healed.2 They also experienced swelling, redness, and temperature fluctuations at the injured site, typically a limb.

More than a century later, in 1994, the International Association for the Study of Pain (IASP) gave the syndrome its official name-complex regional pain syndrome-and developed clinical criteria for diagnosis.3 Confusion about CRPS remains, however, and may be part of a larger shortcoming related to overall pain management. "Physicians know very little about pain in general and even less about CRPS," said Anne Louise Oaklander, MD, PhD, associate professor of neurology at Harvard Medical School in Boston.

DIAGNOSTIC CRITERIA
CRPS has 4 diagnostic criteria. The first-which is not necessary for diagnosis-is the presence of trauma or a cause of immobilization. Second is continuing pain, allodynia, or hyperalgesia in which the pain is disproportionate to any known inciting event. Third is evidence of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of pain. Fourth is the exclusion of other conditions that would account for the degree of pain and dysfunction.

The IASP further divides CRPS into CRPS I, in which major nerve damage is not present, and CRPS II, in which major nerve damage is present. CRPS II replaces Mitchell's old term "causalgia," while CRPS I replaces the term "reflex sympathetic dystrophy," which was introduced in 1946 by a Boston physician named James Evans.4

At least one neurologist rejects the IASP criteria, specifically for the diagnosis of CRPS I. "You diagnose CRPS I only when there is no medical explanation for the symptoms," said Jose Ochoa, MD, PhD, professor of neurosurgery and neurology at the Oregon Health and Science University and director of the Neuromuscular Unit at Legacy Good Samaritan Hospital and Medical Center in Portland, Oregon. He said that such a diagnosis of exclusion is illogical. In his view, it means that the clinician simply has failed to diagnose the true cause of pain-whether it be nerve injury, arthritis, phlebitis, hysteria, or malingering.

But most physicians accept the criteria, although it is possible that the definitions could change as clinicians gain a better understanding of the syndrome. "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.

A CLINICAL DIAGNOSIS
Diagnosis of CRPS is clinical, based on the patient's history and examination findings. "This is a disease that really puts a premium on the clinical diagnostic skills of the neurologist because there is no MRI scan or electromyography study that can make this diagnosis," said Oaklander.

Neurologists should look for focal signs of nerve injury, such as weakness, loss of pin sensation, reflex changes, or Tinel signs, explained Oaklander. They can check for mechanical allodynia with a light touch and for temperature allodynia using test tubes of warm and cool water. The clinician should also take note of trophic changes to the skin, nails, and hair and look for signs of autonomic disturbance, such as neurogenic edema or the differences in temperature or color in the patient's limbs.

Thermography or a spot temperature measurement can be used to document vasomotor autonomic disturbances. Changes in perspiration can be assessed by dragging a smooth-handled instrument across the skin of the affected and unaffected side; the instrument will glide more easily over sweaty skin than dry skin.1 The clinician may also note decreased range of motion, weakness, dystonia, tremor and, in some cases, myoclonic activity.1

Bone scans and sympathetic nerve blocks do not aid in diagnosis, but some clinicians will use a 3-phase bone scan to reveal whether CRPS has resulted in osteopenia and use a sympathetic nerve block to determine whether the sympathetic nervous system is involved-which it is in about 20% of cases, according to Cruciani. In addition, Oaklander said that she will occasionally do a somatic nerve block to identify exactly which nerves have been damaged. Radiographs should be used only in cases where an orthopedic problem is suspected to be the cause of the syndrome.

POSSIBLE CAUSES
CRPS is usually triggered by an injury such as a fracture, sprain, crush injury, or penetrating injury. Oaklander pointed out that even something as innocuous as having blood drawn can lead to CRPS, as can undergoing a surgical procedure. "Damage to cutaneous sensory nerves has been shown to be the culprit, but we don't understand why only very rare patients are left with problems after such routine procedures," she said.

What exactly goes wrong in CRPS is poorly understood. It has alternatively been explained as a hypersensitization of the CNS, an inflammatory process, and a disorder of the sympathetic nervous system. According to Cruciani, constant pain signals from the periphery may lead to changes in the posterior horn of the spinal cord, such as an increase in the number of N-methyl-d-aspartic acid (NMDA) receptors that bind glutamate, an increase in the number of certain types of sodium channels, or a change in the expression of the calcitonin gene-related peptide. An increase in proinflammatory cytokines also has been identified. "All of these changes at the molecular level may have a correlate in the excitability of the somatosensory cortex," he said, explaining that plastic changes in this area have been correlated with chronic pain.

One hypothesis is that the pain of CRPS I is caused by undetected nerve injuries. In an effort to identify these injuries, Oaklander undertook a skin biopsy study of 18 adults with CRPS I and 7 osteoarthritic patients with disabling leg pain, swelling, and disuse. "We found anatomical evidence that patients with CRPS I had fewer sensory nerve endings in the epidermis of their painful CRPS-affected area than in nearby control areas," reported Oaklander.5

It is not clear, however, whether these nerve changes are the cause of CRPS I or a consequence. Harden, who also is associate profes-sor in the Department of Physical Medicine and Rehabilitation at Northwestern University Feinberg School of Medicine, Chicago, argued that the changes are probably a consequence: "The most likely explanation is that these people have this intense vasoconstriction from the disease . . . and this causes a dying back of the nerves," he said. Oaklander agreed that cause and effect remain unclear but pointed out that her study found no evidence of nerve losses in the control group with other painful injuries.

SOMATIZATION?
One of the biggest controversies in CRPS is the role of the mind. Some experts maintain that CRPS often has a psychogenic cause, such as depression. "Fifty percent of people with chronic pain are depressed," said Cruciani. It's unclear, however, whether depression is a cause or a consequence of the syndrome. Sociologic considerations also may play a role, especially if the patient has a financial incentive to be disabled.

"I would say that it is a biomedical disease, a psychological disease, and a sociologic disease," said Harden. "It is all of those things in every patient; it's just to be determined in what measure."

By contrast, Robert J. Schwartzman, MD, chair of Neurology at Drexel University College of Medicine in Philadelphia, remarked that "it's never, ever psychiatric. When you have severe pain that totally wrecks your life, you're depressed."

Oaklander took a slightly different approach, pointing out that if the patient's chronic pain can be attributed to a psychogenic cause, the condition is not CRPS. She also cautioned neurologists not to attempt to make psychiatric diagnoses. She pointed out that the country's current disability system discourages patients from recovering. She echoed the idea that there might be economic reasons why patients maintain their disability. However, she said that she did not encounter malingering any more frequently among patients with CRPS than among patients with any other medical condition.

TREATMENT STRATEGIES
Treatment of CRPS usually involves several specialists, all of whom must have expertise in the syndrome. For example, Cruciani, who works at a referral center for patients with CRPS, reports that his team includes neurologists, anesthesiologists, rehabilitation experts, psychiatrists, and a psychologist. "You have to have a team that's knowledgeable about CRPS and how to treat it," said Harden. "If you don't have that kind of team in place, you fail."

Treatment of CRPS is far from straightforward. The FDA has not approved any pharmacologic or interventional treatments. The most common therapies, however, are medication, physical rehabilitation, and nerve blocks. Some patients also undergo spinal cord stimulation, drug pump implantation, or other surgery.

Medication. Many of the drugs used in CRPS are chosen based on their success in treating other types of neuropathic pain disorders, such as diabetic retinopathy and postherpetic neuralgia.6 For example, opioids, the anticonvulsant gabapentin (Neurontin), and tricyclic antidepressants have not been evaluated for treatment of CRPS but are often used because randomized clinical trials have shown them to be effective in treating other neuropathic conditions.

Although opioids are the gold standard for treating acute pain, their use is highly controversial in CRPS.6 "We know that opioids cause hyperalgesia," said Harden. "If you have a drug that causes hyperalgesia and a disease that is characterized by hyperalgesia, how logical is it to use that drug in that disease?" Oaklander agreed that it was theoretically possible for opioids to worsen CRPS, but she said that this should not prevent physicians from prescribing opioids for certain patients who have CRPS. She did, however, caution that the lowest effective dose should be used. Some pain specialists advocate the use of methadone for the management of CRPS, according to Cruciani. Another possibility is an opioid in combination with an NMDA antagonist such as memantine (Namenda).

The best-studied treatment for early CRPS is the bisphosphonate drugs. Placebo-controlled studies have shown improvements in active movement and motor function with intranasal calcitonin,7 intravenous clodronate,8 and intravenous alendronate (Fosamax)9; one placebo-controlled study showed no improvement with intranasal calcitonin.10 Clodronate may be the most effective because it acts on several inflammatory mediators.6 However, Oaklander pointed out that bisphosphonates have not been tested for use in chronic CRPS.

Another common treatment for CRPS is systemic corticosteroids. In a study of 23 patients, 30 mg/d of oral prednisone was significantly more effective than placebo was.11 "We use that strategy to break the cycle of pain when a patient goes into a flare," said Cruciani.

Several studies have looked at topical medications for CRPS. One study found topical dimethyl sulfoxide to be as effective as an oral free radical scavenger.12 Topical lidocaine patch also was effective in an open-label study.13 Experimental medications for CRPS include thalidomide, which has not yet been studied in controlled trials; etanercept (Enbrel); ketanserin; and ketamine. In a highly controversial procedure, Schwartzman sent 31 patients to Germany to be treated with anesthetic doses of ketamine that produce a coma lasting 5 days. Schwartzman reported that 10 of those patients are now cured, including 1 who has been in remission for 9 years. Adverse effects included hallucinations and flashbacks; potential complications include memory loss, pneumonia, blood clots, and stroke. Harden said that most clinicians view the ketamine coma treatment as questionable, but that its true value would remain unknown until randomized controlled trials are performed.

Schwartzman also has developed a 10-day course of intravenous ketamine that is delivered on an outpatient basis. Positive results were achieved in an open-label study.14 He said that he and his team have used the treatment in about 150 outpatients.

Cruciani pointed out that ketamine has been helpful in the treatment of postherpetic neuralgia. He cautioned that the drug has significant adverse effects and that most patients would be unable to tolerate it in doses high enough to control the pain of CRPS.

Physical rehabilitation. Most experts stress the importance of physical rehabilitation, including both physical and occupational therapy. Rehabilitation should be started immediately or as soon as medication has had a chance to relieve the most severe pain.

"The most important thing is physical therapy," said Cruciani. "Not only do physical therapy and exercise improve CRPS in the affected limb, they also prevent it from migrating to other parts of the body." Cruciani refers patients with CRPS of the lower extremities to physical therapists and patients with CRPS of the upper extremities to occupational therapists. The goals of physical rehabilitation include minimizing edema, normalizing sensation, promoting normal positioning, and decreasing muscle guarding.15

Nerve blocks. Nerve blocks for CRPS usually contain local anesthetics-either alone or in combination with clonidine, NSAIDs, corticosteroids, bretylium, or guanethidine.16 There are no universally accepted guidelines for the use of lumbar sympathetic or stellate ganglion nerve blocks, and the quality of published reports is generally poor.16 However, some clinicians do use nerve blocks in select cases, especially if pain is severe enough despite treatment with oral medication to interfere with physical or occupational therapy. If a nerve block is effective in decreasing pain, the clinician may want to consider repeating the treatment. However, there is no convincing evidence to support the use of long-term treatment with nerve blocks.16

"Sympathetic nerve blocks can relax the blood vessels and give temporary relief, but meta-analysis shows that there's no evidence of long-term disease modifying benefits," said Oaklander, who advised that patients receive only a few.

Spinal cord stimulation. Many experts recommend the use of spinal cord stimulators in CRPS, especially for patients who are responsive to sympathetic blocks.17 Research on the stimulators is far from conclusive, however. In the one randomized trial conducted on spinal cord stimulation for CRPS, patients assigned to spinal cord stimulation plus physical therapy had a significant reduction in pain compared with those assigned to physical therapy alone.18 Harden argues that 1 trial is not enough to go on for clinical decision making. "The study suggests that perhaps spinal cord stimulation works a little bit better than physical therapy alone, but it's unclear what the nature of the control treatment was." He said that given the risks and high cost of implanting a surgical device, more studies are needed. "You should not be charging $40,000 for an implanted device like this without more evidence," he said.

Still, many experts find the devices to be beneficial. "We use a lot of spinal cord stimulation," said Cruciani. He said that the treatment works well in the limbs but is less effective for pain in the center of the body. In addition, Oaklander said that she often recommends the stimulators but cautioned that they are expensive, invasive devices that do not help all patients. She conceded that more research is needed to determine how the devices work and which patients are most likely to benefit.

Implanted drug pumps. Implanted drug pumps are even less well studied than spinal cord stimulators, with most research consisting of case reports.19 "The implanted pumps that deliver opioids can be useful for someone with pain that responds best to treatment with an opioid but who develops intolerable adverse effects from taking it as a pill," said Oaklander. "We also consider baclofen pumps for patients with intractable CRPS dystonia that's too widespread to be treated with botulinum toxin [Botox] . . . so there is a very specific and limited number of patients for whom that might be an appropriate treatment." Cruciani, by contrast, said that he has many patients on the pumps in his group practice. He pointed out that in addition to opiates, clonidine, baclofen, and bupivacaine independently or in combination could be administered by pumps. He also has treated several patients with ziconotide (Prialt), a new drug that has been advocated for patients whose pain is resistant to opioid therapy or who develop intolerable adverse effects from opioids.

Surgery. A number of surgical approaches have been attempted in an effort to cure CRPS. "The most effective treatment for painful nerve injury is surgery, when indicated," said Ochoa, such as in the case of surgery to decompress a trapped median nerve, manage a neuroma, or manage a tumor or disk compressing a nerve.

Cruciani agreed that surgery is essential when a clear surgical cause can be found. However, he estimated that only about 10% of CRPS cases can be addressed surgically. "It tends to be the exception more than the rule," he said. Some surgeons have performed sympathectomy in an effort to resolve pain, but results of published reports are not encouraging. In some cases, the procedure may lead to a worsening of pain.16

Here is the link to this information

http://appneurology.com/showArticle....leId=196513289

Hi Allen,
Thanks for this great article that truly shows the variance in opinion between one expert and another----Is it any wonder we are confused?
There are some things that are said that I find rather troubling, such as----
~~~~~~~~~~~~~~~~~~

"SOMATIZATION?
One of the biggest controversies in CRPS is the role of the mind. Some experts maintain that CRPS often has a psychogenic cause, such as depression. "Fifty percent of people with chronic pain are depressed," said Cruciani. It's unclear, however, whether depression is a cause or a consequence of the syndrome. Sociologic considerations also may play a role, especially if the patient has a financial incentive to be disabled.



By contrast, Robert J. Schwartzman, MD, chair of Neurology at Drexel University College of Medicine in Philadelphia, remarked that "it's never, ever psychiatric. When you have severe pain that totally wrecks your life, you're depressed."

Oaklander took a slightly different approach, pointing out that if the patient's chronic pain can be attributed to a psychogenic cause, the condition is not CRPS. She also cautioned neurologists not to attempt to make psychiatric diagnoses. She pointed out that the country's current disability system discourages patients from recovering. She echoed the idea that there might be economic reasons why patients maintain their disability. However, she said that she did not encounter malingering any more frequently among patients with CRPS than among patients with any other medical condition."
~~~~~~~~~~~~~~~~


I know we would be in denial to refuse to believe that there are SOME patients to whom the secondary gain of a chronic illness is a reality but I do not believe for one minute it is more than a miniscule percentage.
For me the suggestion that there may be economic reasons why patients maintain their disability is offensive in the extreme.:mad:
The fact that I have lost my 6 figure salary in return for a $400 a week WC allowance with which we are supposed to raise 6 children makes good economic sense doesn't it:confused:
I would challenge anyone who has gone through what most RSD patients have gone through on their RSD journey to NOT suffer some type of Reactive depression.
Opinons such as these just help to further demoralise us and isolate us from a society, some of whom may just believe this.


I'd also like to comment on this statement by Dr Oaklander


" Oaklander pointed out that bisphosphonates have not been tested for use in chronic CRPS."

Here in Australia we frequently use Pamidronate Infusions in an attempt to relieve the bone pain of RSD.
Is there anyone else who has had these?

Cheers everyone
Tayla:hug:

Hi Joan,

Finally your question: i have one more question for ya! how would one treat iri vs how one treats rsd??

Since I believe RSD is IRI, the simplest answer would be that the most useful treatment for RSD is one that has been shown to be efficadious in IRI; that therapy is hyperbaric oxygen.

There are differences between RSD and IRI, however, and the most significant of these are the fact that IRI is quickly diagnosed and treatment begun early, while many, if not most RSD patients suffer for years without effective treatment.

The damage done over these long years will take much more time to repair.

In Buckwheat's thread Vascular Issues, I offer my rationale for a longer, slower and more temperate use of HBO in treating RSD. My post on that topic isn't complete, and I tried to fill in a few details in the post that died last night, something for which I am now grateful. I think it better to write a post specifically on RSD and HBO, so I won't try to recreate last night's post here.

I hope this answers your question.

Allen, your post is incredible. It is a goldmine of opportunities to show why IRI makes more sense than nerve damage as the cause for this disease. I have a bad habit of going into things full-tilt, but I'm smart enough to know that replying to your post is too big to try all at once.

I'll be breaking your post down into individual parts, and discussing them in individual posts. I figure it will take at least two separate posts, but could take as many as four.

I guess everyone should be prepared to see this thread on page 1 for quite a while...Vic

I'm wondering why in this "is it psychogenic or physical" debate and science /med/bio research that I haven't seen any studies about :

central spinal fluid and its changes from rsd
blood studies post rsd (the entire spectrum... everything about blood studies)

I guess I throw this out there as I am (after more than a decade) really wanting to see something beyond ( big time beyond) the ole psychogenic vs "real" physical cause.

Also, I would like to point out (since I know that some people still mix up "somatic" as a word with "psychosomatic") that the word "somatic" when used in anything re health does NOT refer to in- the- mind -stuff but refers to something that is body caused (i.e. physical) ....

pls anyone reading anything.... make sure you do not mix up somatic with psychosomatic.... they are two entirely different things.....

Hi,
I am not quite sure what you mean in your post but I was discussing Somatisation as mentioned in Allen's post which a psychiatric disorder where people present with symptoms with no identifiable origin.
Cheers Tayla:hug:

Thank You Vic For Your Time And Effort. Hbo, Hmmmm? I Will Have To Look Into That??? I Know Basically What It Is, But I Am Wondering If It Is Covered By Insurance And Also If When You Stop The Treatments,do The S&s Of Rsd, Or Iri If You Will, Return??? I Will Be Reading.
Have You Tried It? I Know Your Back Is A Big Problem For You, And Not Part Of This Whole Monster, But Another One All Together. But I Thought I Would Ask.
I Do Fairly Well With My Rsd, And I Do Have The Nerve Palsy, And Often Wonder What S&s Are From Which. But My Pain Is Controlled Fairly Well With The Neurontin And Tranxene For The Leg Cramps Which Are Starting Up From The Cool Weather Coming In. It Is The Swelling, And The Freezing Cold Feet And Left Hand, That Make Me Crazy! I Would Love The Swelling To Go, If Nothing Else. It Is Better With My Feet Elevated But I Try To Keep Active So The Feet Are Up And Down All Day Long. Which S&s Would The Hbo Help? Oh I Know I Am Driving You Crazy Picking Your Mind! But I See Something In Your Postings That Intrigues Me.
So Rest Up My Friend And Write When You Can.
Fondly, Joan

Hi Tayla...

the word "somatic" when used by itself means "of the body" and nothing more....

"psychosomatic" means the mind is connected to the body.... meaning in layman's terms that the mind put some symptom or illness in the body...

the two words are Not interchangeable.....

http://en.wikipedia.org/wiki/Somatic

Perhaps the above link helps clarify the meaning of the word somatic ...

be well all,
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