When we visit a doctor (except, of course, one who works for the insurance empire), we assume he/she combines science with other learned skills and experience in order to figure out whether we have a medical problem; if so, what; and find a way to treat it if treatment or an effective therapy is possible. We believe that of the doctors who treat us for our RSD.

The truth is, however, that our doctors can’t use science to understand RSD, because there is absolutely no research showing what causes this disease, how it spreads or how it progresses. There is no science telling anyone that this is a neurological disorder. Without research identifying something about the nature of a disease, speculative conclusions about it can result in attempting to tread a problem that doesn’t exist while ignoring the one that does.

Doctors talk to us as if nerve injury in RSD is a proven fact, but when we stop to think about it, we know this isn’t true: The reason there are two diagnoses: CRPS-I, where no nerve injury can be identified, and: CRPS-II, where the RSD is attributed to a nearby nerve injury, is that there is no evidence that CRPS-I is caused by a nerve injury. CRPS-I patients make up the vast majority of RSD people.

(CRPS-II is equally hampered in that no one is able to describe how a nerve injury can develop into all the signs and symptoms of this disease, which can involve dysfunctions of every one of our nervous systems. It doesn’t leave a trace of evidence, hopping from one nervous system to another without any sign of any nerve damage in its wake. Science demands evidence, and no one has yet provided any evidence that it is even possible for nerve damage to produce the signs and symptoms of CRPS-II, much less that it really does).

The fact is that doctors aren’t dumb, they know that it is unlikely that two disorders with two different etiologies would develop identical signs and symptoms; that it is much more likely that both disorders have the same cause and course. They tell us that the causes may be different, but they have chosen to assume they aren’t; that CRPS-I is also a neurological disorder even though they have no evidence that it is.

Most doctors who treat RSD patients have never investigated this disease; they are too busy treating patients to devote the time necessary for this sort of independent research into a disease that only affects a small percentage of their patients. Researching every disorder they treat would be like trying to reinvent a wheel for every use. Physicians read what the experts have written and assume the experts are right; unfortunately, history is filled with examples of experts who were wrong, and there is no reason to believe it can’t happen today.

The reason Mitchell assumed causalgia resulted from severe nerve injuries is simple: he couldn’t think of any other conceivable explanation. Physicians who followed him couldn’t find any other conceivable explanation either, and through the passage of time Mitchell’s assumption somehow became incontrovertible fact. Facts are based on evidence, however, and there is simply no evidence that Mitchell was right.

You may be thinking; “Of course there’s evidence, everyone wouldn’t agree that it starts with a nerve injury if they weren’t sure of that fact”.
There is one way to prove I’m wrong, you can read everything written about this disease in the medical literature, find documented research and post it here.

The problem is that this takes time, a lot of time. I researched RSD for two years and didn’t get close to reading even half of it. I stopped when I realized I had gone back far enough that I was reading “facts” that had later been disproved. It is much easier to confirm what I say by simply by reviewing the history of causalgia/RSD/CRPS:

RSD was first discovered during the Civil War (1863). Dr Weir Mitchell was a neurologist, but we need to keep in mind that not much was known about neurology 140 years ago. He thought it involved peripheral nerve injuries severely traumatized by high velocity impacts from gunshots and shrapnel. Either the speed of the projectile or the widespread damage it caused resulted in an unending and widening painful response by an increasing number of nerves of the peripheral nervous system (PNS). Mitchell called the disease “causalgia”.

The next major discovery came in the midst of another war: World War I. French Army surgeon Rene LeRiche noted that the painful areas of wounded soldier’s skin was cyanotic. He knew that a sympathetic nervous system (SNS) dysfunction also caused cyanosis, so he hypothesized that this disease might be the result of damage to sympathetic, not peripheral nerves.

He proposed severing sympathetic nerves entering the affected area to relieve symptoms, tried it, and it seemed to work; patients got dramatically better almost overnight. Later, other physicians more knowledgeable about the SNS explained exactly what happened in RSD: During this era everyone had RSD; not RSD-I or RSD-II.

Accoring to experts back then, the high velocity impact damaged sympathetic nerves, deeper within the tissue, without actually coming into contact with them. The SNS controls blood flow by dilating and contracting the arteries, and in this disorder it was abnormally contracting them, reducing blood flow into the affected area.

REFLEX: an involuntary response. SYMPATHETIC: self explanatory. DYSTROPHY: a word pertaining to nutrition. (e.g. cells are not getting nutrition from arterial blood.

RSD: an involuntary and abnormal SNS response (to trauma) that lowers arterial blood flow to tissue resulting in diminished delivery of oxygen and nutrients to tissue. Causalgia suddenly had a new name, a new explanation and a cure.

Well, it wasn’t a cure; for most patients the pain returned in about two years. This was easily explained, the severed nerves had regrown and reconnected; but second sympathectomies, both above and below the original surgery, failed to again reduce the pain. By all logic, they should have, since the nerves were again severed. The operation didn’t cure the patient.

Another problem appeared: sympathectomy patients had reduced SNS control of arteries in previously unaffected areas below the site of the RSD, blood would pool in the feet of patients who had undergone sympathectomies for RSD of the thigh, knee or calf. Obviously not all of the severed nerves had “regrown” and reconnected, perhaps none had.

This new explanation fell apart in the 1950s when researchers discovered that arterial blood flow into RSD affected tissue is not diminished, that it in fact is equal to, or even greater than, arterial blood flow into unaffected contralateral limbs and is generally the same as in non-RSD affected controls. Damage to sympathetic nerves is not causing abnormal vasoconstriction.

LeRiche had had enough; he publicly abandoned his hypothesis as untenable. Other doctors were unwilling to give up on the SNS. From the 1950s to the early 2000’s they confidently told patients that the SNS is the problem, despite the fact that they knew better.

Younger physicians probably read the SNS explanations that are still being written today, and may have never learned about the research showing that abnormal SNS vasoconstriction is not the problem. Only two or three researchers have recently replicated those earlier studies, achieving the same results, and you have to carefully read everything written about RSD if you are going to stumble on these studies. You won’t find them cited at the RSDSA website.

So, doctors continued merrily doing sympathectomies (and raking in money), but the popularity of this operation eventually waned as newer surgeons learned that they provided only temporary relief and caused impaired circulation below the surgical site. Today, only a few surgeons recommend sympathectomies, and then only in the most severe, intractable cases.

We can count ourselves fortunate, if the sympathectomy had only begun being introduced in 1990, most doctors today would be telling us to have one done. Our predecessors paid the price for their doctor’s mistakes. When I joined the other forum about 9 or so years ago, there were still a couple of members who had undergone that operation and, of course, still had RSD.

It took the experts 50 years after proof that the SNS doesn’t cause RSD before they finally stopped talking about it (some of them still do). Today, it is CRPS, and Schwartzmann (the RSD guru, who once wrote about permanent recoveries from sympathectomies), now tells us that indeed, CRPS is the result of a peripheral nerve injury; not just CRPS-II but CRPS-I also.

Dr S (and others of this opinion), offers absolutely no evidence showing any peripheral nerve damage in CRPS-I, but then no one has ever shown that those nerve injuries found in patients diagnosed with CRPS-II are linked to the signs and symptoms of this disease), but he is THE EXPERT today, so people assume he must know what he’s talking about.

Doc S doesn’t stop with a peripheral nerve injury, however. He tells us that the transmission of pain messages to the brain is later taken over by nerves in the spinal cord. He bases his conclusion on research into what physicians now call central sensitization or autonomous pain. Pain that continues long after an injury has healed. In this he is making a scientifically untenable link between chronic pain and RSD pain.

It is untenable because nearly all of the research into autonomous pain has involved patients with chronic lower back pain that doesn’t have an evident medical explanation. Patients with chronic low back pain who showed any evidence of any real or even possible injuries were excluded from these studies. Researchers wanted to learn why people feel pain when no cause for the pain can be found.

Aside from pain, which is described as subjective, there are objective signs of RSD: Lowered skin temperature; osteoporosis; decreased hair and nail growth, and, even though Dr S avoids using the word; cyanosis. These are objective signs of a disease that also causes pain, and are reason enough to exclude RSD patients from this research.

This leads to a third reason Doc S’ is scientifically untenable: RSD pain has never been part of any research into autonomous pain. You can’t simply lift a body of research into one thing and try to apply it to something entirely different, simply because you want to. You need to provide evidence that the research can be linked to the disorder you are trying to link, something S hasn’t bothered to do.

There is yet a fourth reason this research can’t be applied to RSD: This disease actually involves three kind of pain: burning sensation of the skin; allodynia, and; painful hypersensitivity to cold. It is nothing like the unexplained chronic low back pain that was studied.

There is a simple reason why I’ve chosen to focus on discrediting Schwartzmann’s claims: they are being quickly integrated into “theories” about RSD and they are wrong. Dr S has chosen to lead the peripheral nerve injury and central sensitization parade. He is THE EXPERT and he’s leading a parade in the wrong direction.

(I also think he’s a fraud who is doing everything he can to divert others from paying attention to the admittedly still very small amount of research pointing toward a non-neurological cause for RSD while busily lining his pockets with enormous profits from a relatively inexpensive procedure: outpatient ketamine infusions, but that’s just my opinion).

Therapies for treating RSD don’t work. Hope that ketamine would provide the panacea is not being fulfilled; the one member from the other forum who went to Germany for the “coma technique” returned without any recovery and with complications resulting from poor screening for other medical disorders.

Outcomes from outpatient ketamine infusions reported by forum members range from months of relief to none at all. Repeat infusions are being done despite the absence of any research into the safety of multiple doses of the drug, which is licensed as a surgical anesthetic and only a small percentage of the population can be expected to have as many as three surgeries in a year.

A TV commercial for a big cancer center tells people that we have to take responsibility for our recovery. RSD is destroying your life; the FDA will (hopefully) never approve the German coma method, and; outpatient infusions offer temporary relief for some, but there is no data on how many times this procedure will be effective.

Some of you know that I have written countless posts at the other forum about another disorder that is too remarkably similar to RSD to overlook, even though the medical profession has overlooked it for years. The disorder I describe wasn’t discovered until 100 years after RSD, so no conceivable explanation was even possible for a century after Mitchell discovered it.

Now there is an identifiable injury that, I believe, makes more sense than nerve damage that no one can find, or when nerve damage is nearby, no one can link directly to RSD. I can’t prove it, because the research necessary to link it to RSD hasn’t been done, but I think anyone who takes the time and effort to study will agree it is a more likely explanation than nerve injury.

I don’t think my words are going to persuade anyone to reject the neurological view of this disease. I see my role, and my goal, as finding a way to get others interested enough in what I say to decide to learn for themselves whether the disorder I describe (called ischemia-reperfusion injury [IRI]) is the most likely explanation for RSD. I try to do this by:

Describing how the IRI process begins, using words more people can understand. This involves teaching how the immune system responds to cell debris from physical trauma, how this immune response usually ends and what happens when it doesn’t end as it should.

Describing what has been shown to occur during the IRI process that leads to the destruction of hundreds of thousands and even millions of microvascular systems (the arterioles, capillaries and venules that deliver arterial blood to the cells and return “used” blood to the veins), making it impossible for arterial blood to reach the cells served by these systems.

Describing how this blockage of arterial blood flow to the cells affects soft tissue; bone, nerves and the body’s natural healing.

Since this involves teaching the reader facts you need to understand about how the immune and microvascular systems function, necessary before you can begin to understand how they malfunction, it involves lots of words. These processes are complex and the reader can’t learn them by simply skimming what I write. It may take several readings to understand each step.

It is easy to think of me as just Vic, another forum member, and not as someone who has carefully researched every word I write. I can’t do anything about that except keep writing and hope other members will decide that my dedication to this education process reflects my conviction that RSD is an ischemia-reperfusion injury, and that “my doc isn’t really helping me, the experts haven’t come up with any real solutions, I have time on my hands, so why not look further?”

In order to confirm that the facts I present are really facts, I will list citations as if there were a bibliography. When I actually posted biblios and offered copies of abstracts to anyone requesting them, no one ever asked for even one.

This time, anyone who wants to read the actual research abstracts need only press the link to my email address (on my signature line), type in the title of the post and the citation numbers you want to read, and I will reply with the abstracts included as attachments.

Please keep in mind that I’m still very weak and that I’m working on the article I plan to submit for publication. I don’t have the time or energy to reply to multiple requests for abstracts. If you wish to read that much research, and it aint easy; there will be lots of words you won’t understand, you will be better served by researching ischemia-reperfusion injury on your own.

As long as God chooses to keep me on this planet and allows me enough strength to continue writing about RSD, that is exactly what I will do. Maybe not as often as in the past, but as often as I can…Vic