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In Remembrance
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Join Date: Nov 2006
Location: SE Kansas.
Posts: 374
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In Remembrance
Join Date: Nov 2006
Location: SE Kansas.
Posts: 374
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Hi Debby,
"Cold" RSD describes the 2nd stage of the disease, when skin temperature usually lowers and painful hypersensitivity to cold begins; it includes the painful burning and the allodynia too.
There is research showing endothelial impairment and destruction in RSD; what this means is that capillary walls, which are made up only of endothelial cells, have been damaged and destroyed. It isn't endothelial cell damage that causes the pain of RSD, however, it is that a huge number of microvascular systems (MVS) [the arterioles, capillaries and venules that make up what most of us refer to as capillaries], are no longer functioning.
Arterial blood is no longer reaching the cells through these MVS', and since all of our cells receive all of their oxygen and nutrients through arterial blood, those cells that depended upon the now destroyed MVS' first become hypoxic (oxygen deprived), then dystrophic (nutritionally deprived).
This disease was called RSD to explain the dystrophy, but when researchers proved the sympathetic nervous system (SNS) was not abnormally blocking blood flow, the originator of this hypothesis, Rene LeRiche, abandoned it. The rest of the medical profession has taken about 60 years to catch up with him. They spent many of those years pretending that cyanosis (that blue to purplish skin color) doesn't really exist; and destroying patient's circulatory systems by severing their sympathetic nerves (sympathectomies).
Many physicians have stopped pretending that SNS damage causes RSD and now pretend it is peripheral nerve damage (PND), but since PND cannot explain cyanosis, they still don't mention that word.
When we see this skin discoloration, what we actually see are capillaries close to the skin that are filled with hypoxic arterial blood. This blood is trapped in the MVS where its oxygen is leeched out, and there it sits, unable to pass back into a vein and be replaced by fresh arterial blood. MVS' below the skin are also cyanotic, but we can't see them.
The reason for "cold" RSD is that our soft tissue cells generate all of the heat in our bodies; when enough MVS' are destroyed, these cells can't get the oxygen and nutrients they need in order to function. It is by combining these two things that cells generate heat and meet their energy needs.
Not all of the MVS in an area are destroyed: If they had been, cells would begin to die and tissue become necrotic (gangrene), killing us in rather short order.
Our nerve cells need oxygen and nutrients too, and when they don't get enough, they become dysfunctional; pain sensory nerves send pain signals, while other sensory nerves (touch, etc), react to a breeze as if it were sandpaper on a sunburn. Other complex nerve dysfunctions are also taking place, but all of this seeming nerve damage is the result of hypoxia and dystrophy.
Hair and nails need oxygen and nutrients; when they don't get enough, nail growth slows and hair loss can occur. Bones also need arterial blood in order to replace calcium; without it, spotty osteoporosis results, with some parts of the bone still getting adequate arterial blood while others don't.
The only neurological explanation for inadequate arterial blood is SNS dysfunction, which isn't taking place; that's why they finally stopped calling it RSD and now call it CRPS.
These other signs, however, prove that this is more than a complex pain disorder: We may notice the pain most, but nerves; bone; muscle; MVS; and other cells are being destroyed too.
This is what endothelial dysfunction in CRPS really means, and if sodium nitropusside (vasodilation) had any lasting therapeutic effect, the cure to this disease might be at hand; but I suspect that widespread infusion affecting both damaged and undamaged MVS would pose life-threatening risks and even if effective would only be temporary,
As to your hot feet: the redness is usually a sign of continuing inflammation (the first stage of the disease). I don't know why this would continue, but there are many things I don't understand about this disease.
What I do understand, however, is that there is a disorder called ischemia-reperfusion injury that seems identical to RSD; the problem today is that IRI in internal organs was identified nearly 50 years ago, but only relatively recently in skeletal muscle. I strongly suspect that if the word "cyanosis" hadn't virtually vanished from the lexicon of RSD, more physicians knowledgeable about IRI might suddenly become intensely interested in this disease.
Eventually this secret will get out, however, and when that happens this neurological house of cards will collapse and effective therapies for RSD will finally begin. Meanwhile, I try to keep writing posts while I pray that I will eventually be able to finish my journal article. Even that will only help a few people, but a few more than are being helped now...Vic
Last edited by Vicc; 12-04-2006 at 12:53 PM.
Reason: making minor word changes
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