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


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Old 08-15-2007, 09:27 AM #1
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Default 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
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Old 08-15-2007, 09:29 AM #2
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Allodynia is a condition in which ordinarily nonpainful stimuli evoke pain ~ Online Medical Dictionary (OMD).

It is what makes the touch of silk feel like electrified sandpaper on a sunburn and that forces you jerk your hand away when a baby tries to grasp your finger. It’s pain that shouldn’t hurt and it’s the result of damage to the sensory nerves that aren’t supposed to tell the brain about pain.

Our sensory nerves are divided into two types: A-fibers (Afs); which tell the brain about the things we touch or that touch us, and C-fibers (Cfs), aka nociceptors, that have special receptors that react to chemicals released by damaged cells and transmit pain messages to the brain.

It seems logical that Cfs would be responsible for allodynia, but they aren’t: This pain is directly traceable to damage to Afs; because they have a second function, one that it performs at synapses (gaps between two nerve cells) inside the spinal cord.

Nerve signals are sent across this gap by neurotransmitters (NTs): a group of substances that are released on excitation from the axonterminal of a presynaptic [transmitting] neuron (OMD). The electrical message from the first nerve is translated into a chemical one (an NT), which crosses the gap, connects with a receptor on a dendrite of a postsynaptic [receiving] neuron, where it is retranslated back into an electrical message and carried on to the brain.

At the synapse, Afs stimulate the release of NTs called GABAs which carry no message; their job is to fill up the receptors of the receiving nerve so that “real” messages have no place to land. According to the OMD: …This helps control the nerve cells from firing too fast, which would overload the system.

Here is why we need GABAs: If you ever hit your thumb with a hammer you probably remember it as one of the more painful events in your life. Thousands of crushed cells released pain NTs that flooded the receptors of Cfs, which promptly sent the message that this really hurts like Hell. If Afs hadn’t released GABAs you would probably have passed out from the pain.

In RSD, Afs are damaged and don’t stimulate the release of GABAs: this is why just bumping against something hard produces a pain as intense as hitting your thumb.

Afs are larger and faster than Cfs, which means that their messages reach the synapse first, releasing GABAs into the synapse before the pain signals from Cfs arrive, and turning down the volume before those messages are sent on to the brain.

Evidence that Afs are not releasing GABAs at the synapses is found in how well GABAergics (synthetic GABAs), such as gabapentin (Gabatril); pregabalin (Lyrica); and; lamotrigine (Lamictal), control allodynia in RSD.

Allodynia is clear evidence that Afs suffered some sort of damage in RSD, and we’re told that nerve damage causes RSD, so why don’t the “experts” talk about Af damage? Well, they can’t find any damaged Afs, and don’t know how to explain invisible nerve damage.

(You may have noticed they talk about nerve damage (a lot), but never get around to telling us which nerves are damaged. That’s because all of our nerve damage is invisible).

Even if Af nerve damage could be found, it would only explain allodynia; it would not explain other kinds of pain or any of the other signs and symptoms of this disease, such as patchy osteoporosis; hyperhydrosis; inhibited hair and nail growth, or; muscle weakness and atrophy.

Nerve damage doesn’t explain cyanosis either, but cyanosis can explain Af nerve damage, and here’s a simple experiment (that RSD people should never attempt on themselves), that shows how:

Wrap a blood pressure cuff around a subject’s arm, inflate it to above systolic, then wait 20 minutes. During this period you will watch the arm become bluish, then purplish, this is cyanosis: After 20 minutes have passed, and the arm is nice and purple, touch an ice cube to anyplace on the arm or hand and ask what he/she felt. The subject will always report intense, burning pain: Allodynia.

When the cuff is inflated to above systolic is causes ischemia: (localized tissue anemia due to obstruction of the inflow of arterial blood). This is because the inflated cuff won’t allow arterial blood to enter the arm (obstruction). Ischemia causes hypoxia (a deficiency of oxygen reaching the tissues of the body), because oxygen is only delivered to the cells in arterial blood.

Cyanosis is visible proof that our cells aren’t getting enough oxygen, and can’t function properly. But they don’t fail instantly: The mitochondria combine oxygen and nutrients to make energy packets called ATP, which allows them to continue functioning for a little while or during an emergency, but not our nerve cells. They have no ATP reserves, so they begin to malfunction quickly when they can’t get oxygen.

The likelihood that ischemia is causing your allodynia increases exponentially when you have visible cyanosis: That means that the first thing your doctor (and RSD “experts”) should do is try to find out what is causing the cyanosis; NOT pretend that it isn’t even there.

They pretend it isn’t there because they can’t find a neurological explanation for it, and they don’t want people looking for a cause. If you did that, you might run across “ischemia”, and that leads to questions they don’t want anyone to ask, like: Does ischemia explain any of the other symptoms of RSD?

It does, and following posts will describe exactly how it causes each on of them. Once you have read them, you will have read the only explanation of RSD that doesn’t rely on: “Trust me; I have a rectal thermometer in my pocket, so I’m smarter than you”.

It is my prayer that if you don’t understand everything I’ve written here, you’ll ask questions. Knowing that ischemia causes our symptoms will lead you to find therapies to treat it; therapies that will lead to happier and much more productive lives. Those therapies are available today.

Again, if you don’t fully understand everything I’ve said, please ask. If I left out the one thing that could convince you that ischemia causes RSD, I failed…Vic
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Old 08-15-2007, 04:23 PM #3
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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


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Old 08-15-2007, 04:39 PM #4
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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. 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?

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
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Old 08-16-2007, 09:33 AM #5
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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
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Old 08-16-2007, 04:52 PM #6
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Default 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
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Old 08-16-2007, 05:00 PM #7
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Wink 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
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Old 08-16-2007, 09:38 PM #8
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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.
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Old 08-16-2007, 09:43 PM #9
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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
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Old 08-16-2007, 09:52 PM #10
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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
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