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.