(Originally posted on another thread by InHisHands)

Hello, Vicc

I appreciate your replies to my various questions. I have a few regarding HBOT, if you wouldn't mind answering them.

I may have an opportunity to access HBOT, at an alternative medicine Doctor's office. My younger brother has autism, and so my family has worked with this Dr. before. If he feels comfortable treating someone with HBOT that has RSD, then I might give it a go.

I understand now a lot better why you feel HBOT is the only treatment for RSD if you are looking at it from an IRI standpoint.

In order to completely heal I understand that you need more than a few treatments. But, approx. how many? And how often? Is it a long term thing (months and months of treatment) or 4 weeks will do the job?

You speak of setting the HBOT chambers at certain depths... how do you tell a Dr. (who knows or at least thinks he knows what he is doing) not to set it at certain depths or to set it at a certain depths?

Since you claim it has been successful in others with RSD, how many others do you know who have had it and are doing better from it? Can you put me in contact with any? Are any here on this board?

Thanks again... I am willing to try just about anything about now... and HBOT sounds hopeful.


Hi again, IHH,

I’m sorry for the long delay in responding to your questions, it’s been a really difficult week but I’m recovering and at least able to type again.

I hope what you read here will be of some use to you, but I don’t think anyone will find it persuasive until you understand more about ischemia reperfusion injury, so I plan to devote most of my time and energy into a series of posts describing what it is and how it explains the signs and symptoms of RSD. I hope that after reading some of them, what I say here will be more useful in making informed decisions about treatment.

As I said earlier, IRI destroys microvascular systems (MVS), the arterioles, capillaries and venules that deliver arterial blood to all of our cells and returned “used” blood to the veins. It doesn’t destroy every MVS; if it did the result would be death by gangrene in a very short time as none of our cell would receive either of those essentials, but it randomly destroys enough to seriously affect cell functioning throughout the affected area(s).

Those areas with the most widespread damage show the most serious symptoms, which explains why some of us experience more pain than others and some of the rarer symptoms (such as hyperhydrosis), can be severe in some and absent in others. The fact that almost all of us are extremely hypersensitive to cold is one of the most significant signs that this is an IRI, and I will explain why in one of the first few posts in my campaign to show why the medical world is wrong.

Now, in response to your questions: the apparent mechanism of action of HBO is stimulation of vascular endothelial growth factor VEGF. This is why it is approved for the treatment of IRI, making it one of a very short list of disorders the FDA and the Dept of Health and Human Services (HHS) will allow hospitals to treat with HBO.

There is no research describing the long term effects of stimulation of VEGF by HBO, but there is enough science to warrant some basic assumptions, among them: The body may not have the ability to create unlimited supplies of VEGF on demand despite intense stimulation, and that artificial stimulation of VEGF could result in an adaptive response to the increased stimulation (the body may not respond to normal stimulation after prolonged artificial stimulation)

It is also likely that the creation of new MVS is limited by the body’s ability to marshal the necessary materials where they are needed and that it is reasonable to view new MVS as similar to new plant growth; that it takes time to mature and become fully functional.

These assumptions are based partly on what is known about the healing process in general, but are also upon the fact that little is known about the long-term effects of HBO in people who have undergone the therapy. We could expect that if the results were overwhelmingly successful the news would have gotten around by now. Some of the successful ones would have taken time out of their restored lives to tell others about their continuing remission.

.Since RSD/IRI, means that millions, or even more that a billion, MVS have been plugged and functionally destroyed, the assumptions I cite mean it will take time to create enough VEGF to begin the process of replacing all of them; time to marshal the necessary material, and; time for the new MVS to fully establish themselves.

This is why I believe that the delivery of 100% oxygen (O2) at 2.5 atmospheres (ATA) for 20 to 30 daily sessions – not an industry standard, but pretty typical for most free standing chambers - may actually be harmful to RSD/IRI patients in the long run: even the most intense stimulation of VEGF would be useless if the body simply can’t produce enough in just 30 days. If the body adapts to require increased stimulation in order to respond, this would mean less VEGF during the time directly following the end of HBOT.

There is an added problem with treating RSD/IRI using HBO: Oxygen free radicals (OFRs).

(OFRs are oxygen molecules that are missing one or more electrons. This makes them highly unstable and the only way to restore stability is to steal the needed electrons from a nearby molecule; turning that molecule into a free radical (FR) that must in turn steal electrons from another molecule.

(This chain reaction of thefts is what damages cells, and it can only be ended by a FR coming into contact with an antioxidant, which can surrender electrons without becoming a FR itself, or by two FRs coming into contact, which results in one being restored and the other becoming an entirely different molecule.

(OFRs always initiate these chain reactions. They are the weapon the immune system uses to destroy cells and pathogens during the non-specific immune response (NSIR) to pathogens and cell debris. In high concentrations, OFRs produce so many chain reactions the target is literally ripped apart. Our cells are attacked by OFRs as many as hundreds of times per day, but the cells are able to repair themselves when this happens. A significant increase of OFRs could destroy newly created MVS’ before they are fully established).

Most of the research into OFRs during HBO reports that as much as 15% of the O2 delivered in this way is or becomes OFRs. This has been recently disputed and is the source of some controversy among HBO researchers, but even if the percentage turns out to be much lower, I believe that the increase in OFRs is directly responsible for reports from many RSD/IRI patients who suffered catastrophic relapses after reporting initial improvement during HBO

This alone is sufficient to demand that the maximum ATA for us be no more than 1.5. I would point out, however, that those people who have undergone HBO after talking to me have taken the antioxidant grape seed extract (GSE) and none have suffered a catastrophic relapse. A sample of five is too tiny to mean anything, but the precaution of taking antioxidants before, during and after HBO seems wise to me.

I don’t think we will ever know the best therapeutic application of HBO for RSD/IRI, I certainly don’t know today. Based on the assumptions I’ve make, however, I can say what I would demand if I were able to access it.

I would begin at 100% O2 at 1.5 ATA for five days, then 50% at 1.5 ATA twice weekly for at least seven weeks (20 sessions) and would be prepared to continue even longer if significant symptoms remained, and to repeat HBOT if I began to show evidence of relapse at any time in the future.

It might be that RSD/IRI requires an even more conservative approach, but if the assumptions I’ve made do apply, a lower O2 percentage at a lower ATA should result in longer periods of remission.

Why would anyone want to consider such a time-consuming and expensive process if relapse is possible or even probable?

The short answer is that if RSD is IRI, the only route to recovery is replacement of those lost microvascular systems, and HBO is the only available treatment that specifically addresses this problem.

Also, compared with other procedures, HBO is relatively inexpensive: prices fluctuate wildly even in areas where several chambers are available, but it can still be obtained for about $350.00 per session. 20 sessions would cost $7,000.00 plus incidental costs of less than $500.00.

When you contrast this with the cost of other procedures, most of which reported significant initial successes that could not be replicated by later clinicians or researchers, 40 sessions for about $15,000.00 is not really that expensive.

This is only true, of course, if RSD really is IRI. You will be better able to judge this for yourself after reading just a few posts in my planned series…Vic

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.

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!

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