Vascular Issues
 

Hi, I was wondering if anyone has taken any meds. that helped for their circulation. Hugs, Roz

HI just wanted to post back to you
 

Sorry I have not heard of any thing which will help wiht the vasco constriction except HBOT. Good luck,

Hi Their,

Thanks so much for your reply. I was hoping HBOT would work for me. But it didn't. I ended up with bruises all over me. The Doc insisted I had a blood clot in my lungs, because he said he only saw a reaction like that one time before and that's what they had I guess. But my spiral CT showed otherwise.

I am post OR 9 months from having my subclavicle artery released, and I had surgery on the Brachial Plexus nerves. The best thing I could do is walk, but I get very light headed and dizzy. If anyone has any ideas I would appreciate it.

Hugs, Roz

Hi Again,
I also want to add I have a DX of TOS/RSD. After watching both boards for sometime their seems to be a connection in at least 10% of the TOS DX.

I have also had 2 severe infections this last year. One of them is trying to get rid of cellulitis of my right eye. Which just happens to be also on my eye right RSD arm. I was given 3 antibiotics to take at one time. Their is a serious circulation issue going on with me. Because why else would I have these infections.

A couple Docs have been even concerned with gangrene in my case.

I have had to be on so many antibiotics thru this whole nightmare. The pain is just a SX that something is very, very wrong. Hugs, Roz

Hey Roz

I used to take nifedipine to increase the circulation in my arms and legs. It's ok actually. I came off it because I have bp/ pulse stuff.

might be worth a look?

how's your BP?

Rxxxxxxxxxxxxxx

Hi,
Could I be dealing with cell death, because of the circulation issues? I have had The blood pressure meds. they didn't help me, I tried several. My blood pressure ended up bottoming out. Hugs, Roz

Hi Roz,

As you already know, I'm an advocate for HBO in treating RSD. In fact, I believe it is the only available therapy that offers any hope for ending the ravages of RSD, yet I never talk about it here. I guess it's time I started.

I haven't begun until now because I have focused on showing why is actually an ischemia-reperfusion injury (IRI), a disease that wasn't even discovered until 1964 and thus wasn't in the running when Weir Mitchell attributed this to a nerve injury a century earlier.

I won't try to explain IRI here, limiting myself to pointing out that the IRI process ends with the plugging of millions of microvascular systems (MVS), the arterioles, capillaries and venules that deliver arterial blood to the cells and return used blood to the veins.

Blood can't pass through a plugged MVS: Used blood must empty into veins in order for fresh arterial blood to enter the MVS. Block one end of the tunnel and the other is blocked too.

Because our cells get everything they need in order to function properly from arterial blood delivered by the capillaries, IRI explains every sign and symptom of RSD, from abnormal pain (oxygen deprived sensory nerves); to cyanosis (visible proof of IRI: cyanosis is only seen when blood is not flowing through capillaries); to patchy osteoporosis (bones need calcium, which is delivered by the capillaries); to inhibited hair and nail growth. IRI explains it all.

Plugged MVS' can't be unplugged. They don't make Roto-rooters tiny enough to ream them out. Even if they could, we have millions of plugged MVS and cleaning all of them this way would take years.

HBO doesn't fix plugged MVS', it replaces them. It stimulates production of what is called vascular endothelial growth factor (VEGF), and VEGF is necessary to stimulate production of veins, arteries and MVS. Ever since it was discovered that HBO stimulates VEGF, people have been trying to find a way to make it stop.

Increased stimulation of production of VEGF can be harmful for those who don't need it, but not for those who do. Interestingly, some physicians have been fond of calling HBO 'a cure in search of a disease', so its nice to know we can help it find its way home. HBO is the most effective way known to "grow" new MVS.

So what went wrong when you tried HBO?

Right now, most HBO chamber operators use the "one size fits all" model of treatment. If it works for the "bends"; for severe carbon monoxide poisoning, and sometimes works for RSD, why change? And why change when there is no research showing a different percentage of oxygen at a different pressure might help more RSD patients?

Well, common sense has to fit into the equation somewhere, but there are a lot of areas in medicine where common sense is considered unscientific. Better to wait for proof than try something different just because it seems to make sense. RSD and HBO seem particularly affected by these "values". We get a "double-whammy": neither group of experts has any sense.

Common sense tells us that if we need enough VEGF to stimulate the production of millions (or even more) MVS, it will probably take some time; but the "one size fits all" model of HBO demands as few sessions as possible (usually 30 to 40). If you don't want VEGF in the first place, fewer sessions even makes sense.

VEGF is just the start of the process: our bodies need time to assemble the materials to create these new MVS; they don't come pre-built, so it takes time to build all of them. This means that most of our cells aren't going to see reperfusion (restoration of normal blood flow) for a while, so they will need to be resupplied with oxygen at least if we are to prevent further damage during reconstruction.

Using emergency protocols that "push" as much oxygen into the body in as short a time as possible is the right way to treat the "bends" or carbon monoxide poisoning, where people die quickly if not treated dramatically, but it doesn't appear to make much sense when it comes to rebuilding several million (and sometimes several hundred million) MVS.

I'm only guessing, but my guess is that you got 100% oxygen (O2) at 2.5 atmospheres (ATA). That is generally considered to be safe; especially when less could mean the patient's death.

My guess is based on the fact that another RSD patient went to Canada and received 100% O2 at 1.5 ATA, and improved dramatically, but several months later began to relapse. This time she went to Texas, got 100% at 2.5 ATA and during the "therapy" would call to tell me she was getting worse every day.

I told her to get the Hell out of there. Shoot her way out if necessary; that she didn't really have to shoot anyone, just a couple of light fixtures is enough to scare all but the bravest; but get out now. She didn't. She's now saving money for another trip to Canada.

In Texas, they told her that she must be having a reaction to Lyme's disease. They told you it must be pulmonary embolism. I suggest it was too much O2 at too high an ATA.

One size fits all doesn't fit every RSD patient. In fact, some have gone into HBO, gotten better, then catastrophically relapsed within a few days; some even ending up worse than before.

(I have read many reports of casastrophic relapses, and while there isn't space here to present the reasons, I can report that I know of no one who had begun taking the antioxidant grape seed extract prior to HBO who later reported this.

(In my next post about symptom migration: what causes it and how to prevent it [hint: buy grape seed extract], I will discuss the role of oxygen free radicals (OFRs) in both processes. And lest someone labels me a health food fanatic, I don't have enough money to buy vitamins. I urge everyone to take GSE because it works).

Here is another problem: The research necessary to find an optimal dosage of HBO for RSD/IRI will never be done. There is no way to license HBO, which means no one can have a monopoly on using it and make billions of dollars. If you can't make billions selling it, why spend millions researching it? It aint gonna happen.

What will happen is that those of us who advocate for HBO will finally find the backbone to talk about what we believe - and why - despite the fact that the experts only have to point out that they're experts and we're not. Hell, we aren't even scientists; just people who care enough to spend years researching something no one else is interested in unless they can make a buck from it.

Over time, as more RSD people hear from people who have successfully undergone HBO, more RSD people will try it. Some will get better and some will be like you and my other friend. I figure that in 15 to 20 years, people will have sorted out in their minds the O2 and ATA dosage they feel will best serve them.

Of course during this 15 to 20 years, most RSD people will wait for an answer from the experts; and suffer from the symptoms of this disease all that time.

You see, in RSD the experts have been 100% wrong for 100% of the time. They are still telling us that this is a neurological disorder, despite that fact that at least some of them know about IRI (one even wrote an article about it), and know that this makes more sense.

In the next few days I will publish a post showing why RSD can't be the result of a nerve injury; I expect two or three polite comments while no one pays any attention to what it says. It's going to be an interesting (albeit frustrating) next 15 to 20 years.

What I wrote here offers a hint as to why I haven't finished writing my article for publication: I'm not a scientist and I have no research upon which my conclusions will be based. I expect that if it is published, I'm gonna get beat up pretty bad in the responses. That's ok, they can kill me, but the law says they can't eat me.

I will not be writing to the experts: my target audience are those conciencious HBO chamber operators who want their patient's to leave better than they came in. The ones who will be willing to try less O2 at lower ATA if it makes sense to them.

My only real hope for the immediate future is that some work comp insurance co will learn enough about HBO to investigate it. Right now they are fighting us with everything they have; because they know we aren't going to get better. If just one major company figures out how to treat us (and thus stop having to pay us), the future could change overnight.

Isn't HBO expensive? It is when we have to pay for it. People who work for insurance companies are very good bean counters, though; profits are everything lives mean nothing: so if their computers tell them that one spinal cord stimulator will pay for, say 100 HBO sessions (more than anyone ever gets today); and if their actuarials tell them that people who get HBO get better while people who get the SCS still get worse. we may see the day when they force RSD patients to undergo HBO.

When/if that day comes, I won't be surprised if they go with what works, rather than wait for experts to do research that will never be done...Vic

Hi Roz,

I just wanted to say how sorry I am to hear you're back in the wars; apart from taking the usual anti-oxidants (which I know you take anyway) I don't know what to suggest.... perhaps Vic's reply may encourage you to try HBOT again? How did these infections start, just spontaneously or was there a precipitating cause?

This doesn't really apply to you - but just thought I'd mention it: last year I had 2 powerful courses of 2 kinds of antibiotics, augmentin and something else(?) - to rid me of the helicobacter pylori bacteria causing stomach ulcer. I never take antibiotics unless it's essential, but in that case it was, and it worked. Hadn't taken any antibiotics, apart from topicals, for several years before that. To my surprise, they cleared up a host of minor complaints I hardly realised I had till they were gone, and this winter I've had no sinus/chest infection - usually the hallmark of my winters. I've always been a bit "anti the antis' if you see what I mean, but I think now I just needed a good strong "cleanout".

Many thanks, Vic, that was wonderfully clear, as always. Maybe you should post this in a separate post as well, I don't want to bust into Roz's thread, but I'd like the opportunity to ask you a few things that arose from my reading of your post, but are not really relevant here...

Hope you can find something to knock this on the head, Roz,
all the best :)

Dear Vicc,

I went to a private clinic. Before I went into the chamber my husband told the operator just go down some feet, I can't recall what the exact words he used to him. But I believe he stated no more than 15 feet.

But for at least the first 15 min. I was doing very well. Able to read even. About 25 min. into the session I felt very shortness of breath. My husband believes they took me to 30 feet. Because it took the operator a bit of time before I could get out of their.

About 24 hours after the session I had bruises everywhere. The Doc who owns the clinic said I had to get a Spiral CT and stated he thought I had a pulmonary embolism. But the CT was neg- for a blood clot. The Doc who owns the clinic gave me a full refund without even asking for one.

I went to my reg. Internal Med Doc. who put the oxygen close pin on my finger, when I was sitting down. My husband told the Doc to walk with me with the oxygen clothes pin. My oxygen levels went way below the norm. In fact the Doc thought it had come off my finger, until he looked down and saw the placement was still their.

So I was reffered to a Pulmonary Doc. who insisted I go thru complete testing. The test showed my oxygen levels down to 77. cont...

Ok here I go again, the Pulmonary MD who I saw told me that if I was dropped to 30 feet it would of been 30x harder for be to breath.

At around this time my husband called another clinic, talked with the owner for at least an hour on the phone. Their conclusion was I did not have enough oxygen.

So I am in 100% percent agreement this is not a one size fits all approach.:rolleyes:

Vicc, do you know what kind of license these operators need to have to regulate the chambers? I hope it's not none.

I have stated before I would't mind at all giving it another go. But certainly with someone that knows what the hell they are doing.
Hugs, Roz

Hi Roz,

I suppose I should look up the relationship between depth in feet and atmospheric pressure, but I can be a rigid old coot; 15 feet is not a scientific way to measure air pressure. It is a throwback to the days when HBO was used almost exclusively to treat divers who suffered the "bends" after rising to the sea surface too fast. I guess they understood depth, but couldn't get their minds around air pressure. I don't know what 15 feet means.

You don't seem to be having much luck in finding doctors: one tells you that he "guesses" the bruises were the result of a pulmonary embolism (was he guessing the embolism was acute or long-healed?). Either way, I think you should have been hospitalized for this severe reaction.

Another doc sees that your O2 level is "way below norm" and refers you to a pulmonary specialist, who tells you your O2 is 77%. In my not so humble opinion, the only explanation for the way you were maltreated is that you don't have medical insurance, or your insurance sucks.

I would have thought that widespread bruising would be enough to see you admitted to the hospital for testing, but there may be relatively benign explanations for that.

77% oxygen is an emergency. Hard to breathe? Hell, as I understand it, O2 that low makes it hard to live. My memory isn't as reliable as it used to be, but I remember when my daughter couldn't take in enough air.

I followed the ambulance to KU Med Center and by the time I got into the ER it seemed like everyone there was gathered around her bed. She was already on oxygen and I heard the words "hyperbaric oxygen" from someone in that group.

I think her O2 was in the high 70 to low 80 percent, and it was clear to me that they weren't sure she was going to live. When they took her to a room, I wondered if I would see her again. I don't know how people can get through stuff like that without God. (I could be wrong about the numbers, it's been many years and lots of oxycodone ago).

Since you're still alive, I won't bother to Google it, but as I recall, below 95% oxygen is not good. Perhaps one of the nurses here could help on that one.

You will be horrified to learn that in most states a person can be making french-fries one day and an HBO "technician" the next. Maybe LisaShea will add her experiences to your horror story.

Anyone contemplating HBO can only be assured of competent staff by making sure the chamber is certified by the Undersea and Hyperbaric Medicine Society.

The manufacture, sales and even advertising of hyperbaric chambers is closely monitored by the FDA. which (like much of the medical profession) suspects HBO is some sort of voodoo medicine. They don't seem to care about what happens to patient's, however, and I suspect that they don't mind a few dying each year; it reassures them that they're right: there is something amiss about HBO.

There are people in the business who are only in it for the money, so buyer beware...Vic

Vicc, I have a few questions for you, if you don't mind...

You state that HBOT "is the only available therapy that offers any hope for ending the ravages of RSD" and I guess I am just wondering, if that is the case, don't you still have RSD? Have you personally had HBOT? Or are you saying it works the best out of all the RSD treatments? In your opinion, are all other therapies useless? There are studies out there for instance, that have proven physical therapy alone has "cured" adolescents with RSD. No medication. Just physical therapy. I guess that is why I am a big advocate of the PT. I am going, it has helped me, and I plan on doing that to recover. I am not against medications (just using that study as an example), and I am using them along with PT.

I am VERY interested in your post about why RSD can't be the result of a nerve injury.

Why do you say, "You see, in RSD the experts have been 100% wrong for 100% of the time. They are still telling us that this is a neurological disorder, despite that fact that at least some of them know about IRI (one even wrote an article about it), and know that this makes more sense." ? How have the experts been 100% wrong 100% of the time? Can you give examples? :confused: What is RSD? What type of disorder, if not neurological? Why isn't it part neurological? The RSDSA states that it is part neurological/ part immune system malfunction (do you think that it could possibly be both???). (http://www.rsds.org/pdf/Recog_Undrstd_TreatRSD_530.pdf)

"CRPS/RSD occurs when part of the nervous
system and the immune system malfunction
as they respond to tissue damage from trauma,
such as an injury or a medical procedure.
The nerves misfire, sending constant pain signals
to the brain. There are two types of CRPS:
Type I (RSD) and Type II (Causalgia), which has
definite nerve damage."



About the GSE- how do you prove that it does stop symptom migration? How can you? My RSD has spread... and spread. Would you really tell me that if I had taken the GSE, it would have stayed only in my one upper extremity, and I would not be dealing with what I am today?

I have read many of your posts. I can get along with your theory of IRI/ RSD. I have RSD in both upper extremities and both lower extremities. I slammed my finger in the car door, and that started my RSD. Your theory seems logical, and maybe you have the right knowledge and answers. I would like to ask you many more questions, if you would be willing. :) Thanks.

Hi Vicc,
I should of used the term pressure instead of feet. I think my husband corrected me at the time as well.

This was around 3 years ago. Maybe when I was in HBO I had a lung infection Vicc I can't remember. I certainly had no blood clot in my lung. Nor have ever had one to my knowledge.

I found out a few weeks later after the fact if your oxygen goes down to 84 or below they are supposed to hospitalize you. I was just DX as well with RSD at the time after being told for 2 years I had a torn rotator cuff with a pinched nerve down my right arm. So I wasn't even sure of the SX of RSD then either. I was bedridden at the time. In very rough shape. In fact I was bedridden for about a year. Between the 2 to 3 year mark.

Thru out most of RSD which I just passed the 5 year mark. I have had to deal with a HMO. In order for a PPO to pick me up they want 2,200 a month. But it still would be a narrow range of the MD's I would be allowed to see.

I have been a cash patient at times even with HMO insurance. My husband makes good money or I would be up the creek without a paddle.

I was offered Ozone therapy before out of the States. But I don't know much about that.

Hugs, Roz

Hi IHH,

I try to mention my history in occasional posts because your first question would be mine. So here goes, and this is the short version.

I was first disabled in 1979, when an ortho surgeon botched two laminectomies; first by puncturing the dura (the outer of three layers of the spinal cord cover) then not plugging the leak properly. A week later I began leaking cerebro-spinal fluid into the tissue of my lower back. He went back in, couldn't find the leak and so grafted a patch of muscle to the dura much like one would patch an old inner tube.

Its kinda tight in that area, and his graft has been pressing against the spinal cord and causing moderate to severe pain for 26 years. The diagnosis was scar tissue/recurrent disk at L5 and L5 radiculopathy on the left.

After ten years of trying to restore my strength and endurance, I finally realized that I was never going to build a bridge or drive a truck again; so I went to college and became a social worker. I could only walk about 200 feet using a cane, so voc rehab bought me a power wheelchair for work.

Then my job description changed so that it would no longer require a licensed social worker; I would do much the same work and get the same pay, but I wouldn't be a SW, nor would the state provide continuing ed for my license.

I took a job as SW at a state psych hospital, where five months later a large and violent patient grabbed a smaller patient by the wrist and began running full-tilt toward me.

The big patient dodged around me, pulling the smaller one into me...and kept running while still holding her wrist. The top half of my body twisted a bit more than 90 degrees while my butt stayed firmly planted in the chair.

The net result was diagnoses of bilateral epidural fibrosis (scar tissue) at S1, compressing both S1 nerve roots (severe pain); bilateral S1 radiculopathy; bilateral leg pain, and arachnoiditis (scar tissue on the arachnoid, the middle layer of the spinal cord cover), and finally - months later - RSD of the left foot.

A work comp whore wrote that I had faked the 1979 disability and was faking the 1995 injury. The MRIs, ct-scan and EMG confirmed the diagnoses. After five years of Hell, and no treatment for any of my injuries (except a couple of nerve blocks for the RSD) the law judge ruled I was too disabled to attend hearings. WC settled at 99% disability.

The bottom line is that since my 1995 injuries I have not been able to tolerate the pain that would go along with trying to access HBO (it takes the pain three days to subside to normal after a trip to my doc's office).

Next; I can't be sure which studies you refer to, but I would guess they are what is called case studies: individual reports about a specific patient. Case studies are not research, they can't be replicated by following the protocols of the original doc (because there were none), and are generally considered only somewhat more reliable than anecdotal reports.

One would think, however, that with so many RSD patients undergoing physical therapy, if it were effective we would at least see dozens, if not hundreds of case studies reporting cures.

PT is about the only way for patients to maintain any range of motion (ROM), which is critical if we are to keep our joints functioning. If RSD is an IRI, however, PT involving more than minimal weight bearing can be harmful: muscle cells "break down" during exercise and are restored to an even stronger state during rest, but only if they receive adequate oxygen and nutrients. IRI means, by definition, that they aren't.

I am currently working on a long-delayed reply to a post in which I describe exactly why RSD cannot be the result of a nerve injury. In it, I may or may not point out that CRPS-I is different from CRPS-II precisely because there is no nerve injury in the former. There is no nerve injury leading to the latter, either: just a convenient nearby nerve injury that can be blamed.

100% wrong 100% of the time: When RSD was first discovered, it was attributed to nerve damage caused by high velocity impacts such as shrapnel or gunshots. It was thought that these types of wounds injured nerves some distance from the actual site. We know now that that even the most insignificant trauma can lead to RSD. High velocity impacts are not the cause of what was called causalgia at the time.

In 1916, a French Army surgeon during World War I saw his first RSD patient, and noted that every place the soldier said was painful was also purple. He had seen cyanosis in a patient who suffered from "a rare sympathetic disorder" who reported severe pain in cyanotic tissue.

He began investigating RSD; examining patients, and noted that most, but not all, showed cyanosis in the areas they reported pain. This was before anyone realized that minor injuries could lead to RSD, but it fit the causalgia picture.

Most sensory nerves of the peripheral nervous system (PNS) are close to the skin surface, while those of the sympathetic nervous system (SNS) are found deeper inside the tissue, where they are more protected from injury.

LeRiche argued that causalgia was the result of damaged sympathetic nerves. These nerves control arterial blood flow by dilating and contracting the smooth muscle that surrounds arteries, so damaged symp nerves were abnormally constricting blood flow through the arteries. This not only explained cyanosis, but every other sign and symptom of RSD; except one, symptom migration (or spread).

In the early 1940s. a test was developed that could measure arterial blood flow. This test would prove LeRiche was right; but it didnt.

Researchers found that arterial blood flow in RSD affected limbs was equal to, and sometimes greater than that in contralateral (opposite) unaffected limbs and the limbs of control subjects. Abnormal vasoconstriction caused by damaged sympathetic nerves is not the cause of RSD.

LeRiche publicly abandoned his hypothesis: Few others followed suit. This disorder was renamed reflex sympathetic dystrophy about two years after it was proved that it isn't RSD. For the next 60 years, there has been nearly unanimous agreement that RSD is caused by damaged sympathetic nerves, despite this proof.

In 1995, a consensus of the International Association for the Study of Pain (IASP) agreed that this isn't RSD, and should be renamed CRPS. They devoutly believe CRPS is the result of a nerve injury, they just can't figure out which nervous system is involved. No one at IASP seems to have noticed the contradiction between belief in a nerve injury and their definition of CRPS-I as having no nerve injury.

There is now a campaign to attribute RSD/CRPS to a spinal cord issue called central sensitization. I will discuss that in my delayed post, so there is no point in going over that now.

High velocity impact: Wrong. Sympathetic nervous system: Wrong. Central sensitization: nonsense, as I will show this week. 100% wrong 100% of the time.

RSDSA has long clung to the SNS view of this disease. The quote you make is their attempt to keep the nerve damage idea alive. They obviously know what IRI is, and are just as obviously distorting the facts to prove a false claim.

The nerves are getting chemical pain messages from oxygen and nutrient deprived cells, which they pass on to the brain. They are also sending pain messages to the brain because they aren't getting enough O2 or nutrients. They can only communicate with the brain by sending pain messages.

One could, I suppose, argue that pain messages from pain sensory cells are abnormal, but they are a response to an abnormal condition (oxygen deprivation), so they aren't abnormally firing after all. Just telling the brain: Houston, we have a problem

Where does the immune system fit in? IRI begins with the immune response to trauma; a response that goes out of control instead of ending after no threat is discovered.

The entire IRI process has been documented by dozens of researchers under strict, scientific protocols. This mishmash from RSDSA is not the result of research. It comes purely from the imaginations of the authors.

BTW, absence of proof is not proof of absence. (I'm not sure exactly what that means, but it sounds neat). I'm guessing it means that just because you can't prove something (like nerve damage in RSD), it doesn't mean you have proved there isn't nerve damage.

Experts in RSD are fond of saying things like that because there is no published research linking nerve damage to RSD; nor is there any neurological test that can demonstrate abnormal nerve activity in RSD. No evidence of nerve damage in RSD but almost 100% agreement that it exists. 100% wrong 100% of the time.

I can't prove that GSE prevents symptom migration. I can, and have, offered my experience in previous posts at BT, all of which are gone now.

Basically, after studying the research into IRI, it seemed more likely to me that this is an IRI than a nerve injury. One of the things I learned during my review of the research was that IRI from surgeries could be prevented simply by applying vitamin E (an antioxidant) to the wound site.

My RSD had already migrated to my right foot by the time I learned this and decided to begin taking GSE, a more powerful antioxidant. Since I began taking GSE in early 1998, I have not experienced any symptom migration.

I stopped taking GSE twice: once deliberately, deciding to rely on the topical antioxidant DMSO instead; one I was so (literally) distraught over personal issues that I forgot to take any for several days.

Both times, within days of stopping, I began to experience the mild sunburn pain of inflammation over 100% of both arms and both legs. After resuming GSE, these symptoms completely subsided.

I can't prove that these signs of inflammation would have led to RSD, but I know that the disease begins with the red warm skin of inflammation, then develops into the cold, blue to purplish color of cyanosis. That was enough to convince me, and I hope it will be enough to convince others.

Some members have told me they began taking GSE after reading my posts. None have reported any symptom migration. That may change now that I've mentioned it. We will have to see.

Finally, I not only welcome questions, I have been known to beg for them. I don't get many. In fact, it is often true that my name as the last to reply to a thread is the kiss of death to that thread. No more replies; it simply falls off the page.

I have been discouraged by this more than once; feeling that no one is really interested. I bounce back, though. People may not read what I write, but I continue writing about RSD.

There are times I wish some evidence would arise that would prove me completely wrong. Then I could stop working on an article I have never been able limit to under 2500 words and start watching Days of Our Lives (is that still on?).

This post is probably more than 2500 words, and doubtless there are many who long for the days when I was too weak to write anything close to that number...Vic

it is very interesting.

Vicc have you considered the portable HBOT chambers?
I know that there are some in the US. Then that would remove the travelling.

I can't belive most HBOT techs in the US aren't trained - where I used to go in the UK was very particular about a) who went and b) had very high levels of training...... I am glad I went but it didn't do anything magic for my RSD despite about 40 or 50 dives over a couple of months. However, it did heal my skin up (which is now re-infected)... so it definetly did something.

Thanks

Rxxx

Vicc,
The HBOT was hell for me. It made the RSD worse on top of my oxygen levels being a problem. Roz

RSD newbie here...can I ask what GSE is?

oops!

I usually use the word, followed by the abbreviation, but this time I didn't.

GSE is grape seed extract, an antioxidant. There are others, most prominantly pycnogonel, but I prefer grape seed to pine bark, besides, both do the same thing but GSE is cheaper and more widely available...Vic

Thanks so much Vicc.

I also sent you a PM with some questions did you see it?

Yeah, I did, and I'm sorry I haven't replied yet, but I will.

I think my entire life can be described as trying to catch up, but the difference between then and now is that I used to think I could.

I promise I will reply...Vic

No worries whatsoever. Take your time.

I just wanted to make sure you got it. :)

You have so much knowledge and I am so appreciative just to read your posts.

Here's a happy V-day hug :hug: Thanks for your help

To Vicc... some more questions for you...
 

Hi, Vicc. I appreciate your reply... I have not forgotten to respond, I have just about no energy, but I do have many comments and questions regarding your post.

First, I am going to try the GSE. Anything is worth a try. Though everyone IS different. That seems to be the case with different RSD treatments, as I am about to say again... I think you have to be careful when saying that it prevents migration of symptoms. That is something you really cannot prove. Yes, you believe it did in your case. But everything is so unsure about RSD. For instance, some people's RSD spreads, and others it doesn't. Some people have sucessful treatment with nerve blocks. Others don't. I think that you never can be sure. RSD plays by no certain set of rules.

Could you please give me the link to the article written by one of the RSD "experts" on IRI? I would really like to read up on that.

The study regarding children/ adolescents with RSD who were treated with physical therapy can be found here:

http://www.rsds.org/2/library/articl...ive/index.html
under: Author: Sherry DD, Wallace CA, Kelley C, Kidder M, and Sapp Lyn.
Title: Short-and Long-term Outcomes of Children with Complex Regional Pain Syndrome Type I Treated with Exercise Therapy.

(check out the other articles they have there, too)

I know that this is children being treated with PT, and not adults, but I still think that it is proof that RSD can indeed be TREATED with physical therapy. In fact, in this specific study of 103 children, they did not use any medications. So, there is proof that physical therapy alone CAN be used for RSD patients. In fact, opposite to what you are saying, weight bearing is the most important thing to do!

If you state that you believe HBOT to be the "only available therapy that offers any hope for ending the ravages of RSD", I do have another question... I have a friend who had RSD 12 years ago. He went to PT for a year, and 9 months into it received nerve blocks. All his symptoms and pain dissapeared through them both (along with medications) and he is symptom and pain free to this day. How do you suppose that people do recover, when they do not receive HBOT? Right here I am suggesting that I think your theory cannot be 100% correct. Because everyone is different. With RSD there is not one thing to do. Different treatments help different people.

Since you don't believe RSD involves the sympathetic nervous system, what causes the sweating, and even blood pressure changes that people with RSD experience? Is that not something that the SNS is doing?

More about the HBOT: it is not always sucessful, huh? Do you think it has better results than any other treatment? It certainly isn't 100%.

I do have other questions for you, but don't have the time or energy right now. I wish I knew 100% that you had it all correctly, but I see flaws with some of the things you are stating. And, I am seriously questioning your statements. Thanks for your time. :Thanx:

I am glad you want questions... but I hope you don't regret that. :D

Hi again, IHH,

Well, you do have a number of questions; comments too, but that's ok. I would like to answer them in detail, but that would take more words than anyone would want to read at a single sitting.

First, I didn't say that GSE prevents symptom migration; I said I can't prove GSE prevents symptom migration, then offered a brief summary of my experiences. In posts at B/T, I wrote in some detail about research into ischemia-reperfusion injury (IRI) that supports the use of GSE to delay onset of symptom migration, and I may write a post here on the same topic. Meanwhile, I would be remiss if I didn't tell others what works for me.

I don't agree that RSD is so different in each individual as to make it impossible to find an effective therapy that works for most: there will always be variables that prevent any therapy, for any disease, from being 100% successful, but that is no reason to stop trying.

You speak of successful outcomes from blocks, but I know of no research confirming this. The consensus today is that blocks provide temporary relief and in the vast majority of cases eventually have no effect whatsoever.

I couldn't find anything in my previous posts about an RSD expert writing about IRI, but I have mentioned it in the past; as an example of someone who knows about IRI and ignores its connection with RSD. His article on IRI is pretty complex, contains a lot of medspeak and says nothing about RSD. I will send it if you want, but it doesn't have anything you're looking for.

Re: The Sherry Study.

Physical therapy has been a component of RSD treatment since Dr Weir Mitchell told his first patient to "walk off the pain". In the 144 years since, there has been only one published article reporting "successful" treatment of RSD patients through PT: this one.

As I said before, if PT were effective, it would have been announced, confirmed and reconfirmed long ago. I won't speculate about the conclusions you cite here, I'll just wait for someone else to confirm them in another article.

As to weight bearing, I am not the only one to say it is harmful; that is the consensus of nearly everything I have read about RSD and PT. I hope you will stop any weight bearing exercises before the pain makes you stop.

When I say that HBOT is the only available therapy that offers any hope for RSD patients, I speak from the perspective of RSD as an IRI; a physical disease process.

The body reacts to physical damage; tries to repair and heal it. Sometimes it works, but most of the time it doesn't. There will be instances of spontaneous remission from RSD, but the rest of us will need to rely upon medical intervention.

The body's response to IRI is to increase production of vascular endothelial growth factor (VEGF), which is the first step in creating new microvascular systems (MVS). But the body doesn't create enough VEGF to do the job.

HBOT is effective in treating RSD because it stimulates production of much larger amounts of VEGF. Interestingly, this is considered an adverse event during HBOT, and many writers consider it sufficient reason to oppose HBO in any but the most extreme emergencies.

I have read skeptics who refer to HBO as a cure in search of a disease. It is the ultimate irony that the very adverse event they warn against is the mechanism of action against the disease HBO has been searching for.

"Different treatments help different people". Nothing helps anyone. The latest rage is ketamine therapy, but as you probably read in another thread, it falls far short of the mark. We will need to wait to see how long the "successful" remissions last.

I don't say the SNS isn't involved in RSD; like everything else in an affected limb it can function abnormally, but that is the result - not the cause - of RSD.

No, HBOT is not always successful. One reason is that few people even resort to it until it is the last, desperate attempt to do something before ending your life. The RSD is usually far along by then. But that isn't why HBO fails too often.

HBO chambers advertise for RSD patients; if it hasn't helped one of their clients already, they know it has helped people, and most are in the business to help fight disease. The problem is that they don't have any idea how it helps, so they usually use 100% oxygen at 2-1/2 atmospheres (ATA); pretty much the industry standard.

2-1/2 ATA works well for emergency situations such as the "bends" and carbon monoxide poisoning, and for late stage diabetic issues such as unhealed wounds, infections and gangrene, but I think it is way too much for RSD.

One reason for this is that HBO is reported to contain as high as 15% oxygen free radicals (OFRs), and these thingies do all the cell damage in IRI. Reports of patients who enjoy dramatic improvement in the first few sessions, then catastrophically relapse a few days after HBO, certainly suggest that secondary damage from this massive influx of OFRs may be the problem.

I have strongly urged people to take GSE during and after HBO, and no one that I know of who has taken an oral antioxidant has reported that sort of relapse.

The main reason I believe HBO should be delivered at less oxygen and a much lower ATA is the evident mechanism of action: stimulation of production of VEGF.

Someone with full body RSD has lost millions of MVS, and these can't be rebuilt overnight. It will take a lot of VEGF, then a lot of time to build new MVS and allow them to mature. Current HBO practices don't take this into account; which makes sense, because the operators don't know that RSD is IRI.

I haven't described the role of OFRs in RSD/IRI, much less how MVS are destroyed, but if you want to learn more you can go to Medscape or PubMed and look up IRI and start reading research abstracts; or you can wait until I take another swing at describing the IRI process: from initial physical trauma through the destruction of MVS.

I think HBO is the only therapy that addresses the problem in RSD, and it is certainly the safest and most cost effective way to treat this disease...Vic

I just wanted to say that I have had success with the blocks and I have several friends here that have. One of my friends is a nurse at the hospital and she has RSD in her right foot and she told me that when she sees it starts coming out she goes to get a block. She has worked at the hospital for at least 15 years and has had the RSD for as long.

I had 3 blocks to help put the RSD into remission and it worked for me. The surgeries I had brought it back out and then I started asking for blocks with the surgeries and the Drs. did them with no argument. I do believe that the blocks work for many people. Maybe not all but many.

As far as PT. I spent over 3 years in PT. It didn't heal me but it helped to get me moving better then I was. I went twice a week for over 3 years to deal with my back which I was bed ridden at the time and they got me walking, then I went for the TOS and got somewhat better but had to have the surgery anyway. Then I went for the RSD and Fibro and I saw a world of difference as far as movement was concerned.

I worry about people saying that the blocks don't work, I believe that they are one of the best ways to help the RSD if they do work for the person getting them. They do sometimes become useless to certain people with RSD but I think people should let the Drs. try them if they offer them to a person.

Ada

Vicc,
Here is where you wrote about the RSD expert writing about IRI... I'd love the article... could you PM it to me? Thanks.

Vicc, I started a thread for you with questions about HBOT, because I do have more questions...

Here's the link:
http://neurotalk.psychcentral.com/sh...ad.php?t=13809


Thanks for being patient with me and answering all my questions, and responding to my comments. :)

I do understand why HBOT is the only treatment if you say RSD is an IRI. Thanks for explaining.

Hope to hear from you more soon.

Hi, nurse here who will confirm that 77% oxygen sats would require intubation in most cases. If this did not occur and Roz was not treated as a medical emergency then I suggest she may have been misinformed regarding how low her sats were.
I have also had 90 "dives" of HBOT as a part of my wound (infected with MRSA) healing treament. It is paid for by my workcover providers.
It has not appeared to be too useful for may pain but certainly has helped my wound.
I feel I must share with you that in the months I have been "diving" and sharing a tank with 6 other people there has never been anyone who has had an adverse reaction to the HBOT.:)

Thanks Vicc, you answered my question of what is the right amount in terms of frequency of visits. I can only do 60 minutes at a time 90 makes me clautrophobic and edgy.

I was doing HBOT after my TOS surgery. Then I stopped doing HBOT and the RSD symptoms are rearing up

I am close to HBOT therapy and am thinking anout starting it again. I am going to print this off and talk to HBOT doc about it and trying your protocol.

I will let you know what he says.

:hug: to you Vicc. God Bless

Since my views on HBO seem to have attracted interest, it seems best to me to bump this thread in order to allow those who want to comment about them to read what I actually wrote.

I've said several times that my goal is to get people interested in learning about ischemia-reperfusion injury (IRI). I'm not so arrogant as to believe that anyone will rush right out and sign up for HBO because I tell them to, but I do hope that by discussing a mechanism of action for HBO, someone will take the time and effort necessary to learn whether IRI might make sense.

In RSD, it really does boil down to which view makes more sense: Those who believe this is the result of a nerve injury and that the success rate of ketamine therapy seems attractive will choose it. Those who take the time to learn for themselves whether IRI is a better explanation for our signs and symptoms will look to HBO.

The best way to make an informed decision is to gather information. I can't provide enough information about IRI to convince anyone; I can only hope to give people a reason to learn about it for themselves...Vic

Vicc,
I never had any signs of RSD until my hip replacement. That is when my siatic nerve damage happened. I have had a hip problem since birth and always had pain. The Docs said I have RSD type 2 because of the nerve damage. Can you tell me what could have caused the RSD if it wasn't the nerve damage? I appreciate all the work that you do on this site. You give us alot to think about.

Sue K

Hi Sue,

I just woke from a nap and read your post. Your question brought a thought in my mind that completely overwhelmed me. I want to do some specific research before I answer.

I promise I will answer this question, but first I have to "hit the books"...Vic

Hi Sue,

I have reluctantly reached the conclusion that I'm no longer comfortable posting here at NT, so I am now just another lurker. I promised a reply to your question before deciding I wouldn't post any more, so here it is:

My answer iis the same one I gave to Joan on post # 21 on the Facts you may not know about RSD thread. If you have other questions, please PM me and I will try to answer them...Vic

I wanted to show that Vic has done his research. Im not sure if he has all 7 documents anymore, but I still have them.

I will email them to ya bro if you dont have them anymore.

I hate to think that someone that has put so much time and effort into something would be silenced. I know I havent spent this much time in any research, but do believe this is worth listening to as much as anyone elses research. This is article #6 out of 7 articles.

Some real good stuff here vic! :winky:

Because they play the most important role the non-specific immune response, I limited my discussion on that topic to OFRs and PMNLs, but other variables are also involved, including antigens such as HLA-DQs.

In a study of 52 CRPS patients, Kemler found “significantly increased” frequency of these antigens when compared with a control group. He stated; “This association provides an indication for an organic basis of RSD”. The SNS view of this disease denies any organic source.

Mast cells are white blood cells, and they too play a role in the immune response; their presence is fairly easy to detect. Huygen compared mast cell levels between affected and unaffected limbs of 20 CRPS patients and not only found increased numbers in affected limbs, but the numbers were correlated with reported pain levels [2].

Using 5-phase bone scintography, Leitha found positive correlations between five signs of inflammation (including PMNLs) among CRPS patients. The author concluded: “…increased micro vascular permeability and bone metabolism…and blood cell counts are suggestive of a sub acute inflammatory process, even in patients with no overt signs of inflammation” [3].

Damage to microvascular systems is associated with the immune inflammatory response. In study using 24 CRPS patients and 25 healthy controls, Schurmann tested arterial, venous and MVS changes.

In the unaffected limbs of CRPS patients and healthy controls, there were no differences.

All measures were significantly higher among CRPS patients, and Schurman noted that the high CFC contributes to edema formation. He reports that his findings are in agreement with the hypothesis of an inflammatory origin of CRPS. [4]

Van der Laan, the most prolific researcher into the role of OFRs and IRI in CRPS, injected specific OFRs into the left hind limbs of rats and after killing them, compared them with the right hind limbs of infused rats and both hind limbs of healthy rats.

He noted that the OFRs mediated the immune response, as shown by increased PMNLs in the interstitium (IS); and edema; vascular, and; skeletal muscle damage in the OFR infused left hind limbs.

There were no changes in the contralateral limbs or in the limbs of the control animals. [5].

Bailey, et al, tested the hypothesis that acute mountain sickness among hikers at high altitude, was caused by OFR damage and hypoxia of skeletal muscle. Blood samples were collected from hikers at various intervals during the ascent. Results showed increasing OFR mediated vascular damage of the blood- brain barrier and also systemic tissue damage. [6]

In another rat study, van der Laan again infused the left hind limbs of test rats while infusing saline in the left hind limb of controls; The test animals showed increased temperature and redness of the paw, impaired function and increased pain reactivity in the OFR infused limbs, with no change in controls or contralateral limbs. Once again, muscle damage in OFR infused hind limbs was visible. [7]

In perhaps his most significant research into microvascular damage in CRPS, van der Laan, et al, examined the above the knee amputated limbs of eight CRPS patients. Nerves, muscle and MVS were examined by light and electron microscopy.

This research showed histopathological findings of muscle similar to that found in muscle in patients with diabetes, atrophic muscle fiber and severely thickened basal membrane layers of the capillaries (MVS destruction).

Efferent (away from the brain) nerve fibers showed no changes, while C afferent (toward the brain) fibers showed abnormalities in four patients [8].

Further evidence of OFR involvement is explicit in five studies showing improvement in early stage CRPS with the application of the anti-inflammatory/antioxidant DMSO [9], [10], [11], [12], [13].

Tissue hypoxia (frequently evidenced by cyanotic skin color) is [should be] the most critical sign of CRPS, despite the profound silence from those who cling to the view that this disease is caused by some lesion involving sympathetic nerves.

Sudarim reports; “Atrophy has been considered to be the most common manifestation of the disease [CRPS]. We catalogued the abnormal skin conditions in RSD by means of chart review.

“Vascular problems were the most common, followed by inflammatory diseases, infections and atrophic diseases. Atrophic disease accounts for a minority of skin problems seen in RSD” [14].

In an important study involving perfusion and the sympathetic nervous system, Goldstein, et al, tested 30 patients with single limb CRPS, comparing and contrasting the CRPS affected limb with the other, unaffected side. 14 of these patients had undergone sympathectomies with later resurgence of pain.

Using PET scanning after administration of specific ammonia to assess local perfusion, (blood flow) this team found that patients with chronic CRPS have decreased perfusion of the affected limb.

Fleurodopamine was used to assess sympathetic innervation, and no difference was found between affected and unaffected limbs. Norepinephrine, a hormone and neurotransmitter released by sympathetic nerves - and its metabolites - were symmetrical in both limbs.

This team, made up of researchers from the National Institute of Neurological Disorders and Stroke (NINDS), concluded: “These findings suggest augmented vasoconstriction, intact sympathetic nerve terminal innervation, possibly impaired sympathetic neurotransmission, and pain usually independent of sympathetic neurocirculatory outflows” [15].

In investigating tissue pH, Heerschap, et al, compared CRPS affected lower leg muscles of 11 patients with unaffected contralateral limbs and found “A significant increase was observed for the average pH of the muscles of the affected side…”

The team concluded that: “The impairment of high energy phosphate metabolism, as deduced by the NMR (nuclear magnetic resonance spectroscopy) date, may be caused by cellular hypoxia or diminished oxygen utilization, which would agree with previous findings that oxygen extraction is reduced in extremities affected by reflex sympathetic dystrophy” [16].

All of this combines to provide powerful evidence of OFR involvement and severely diminished blood flow in CRPS.

The next article will discuss research that supports the SNS view of this disease.


Copies of past and future articles are/will be available.
Just email me at rsd_hbot@hotmail.com

vicc,
Please don't stop posting. Like I said before, I appreciate all that you do. RSD is so confusing to me. All that you do here is amazing to me. I hope my question didn't upset you. I asked because you always have good information and it helps when I go to the Docs. They don't tell me much so now I have the information to ask them the questions. Thank You.


Sue K