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Vicc · 08-15-2007, 09:29 AM

Allodynia is a condition in which ordinarily nonpainful stimuli evoke pain ~ Online Medical Dictionary (OMD).

It is what makes the touch of silk feel like electrified sandpaper on a sunburn and that forces you jerk your hand away when a baby tries to grasp your finger. It’s pain that shouldn’t hurt and it’s the result of damage to the sensory nerves that aren’t supposed to tell the brain about pain.

Our sensory nerves are divided into two types: A-fibers (Afs); which tell the brain about the things we touch or that touch us, and C-fibers (Cfs), aka nociceptors, that have special receptors that react to chemicals released by damaged cells and transmit pain messages to the brain.

It seems logical that Cfs would be responsible for allodynia, but they aren’t: This pain is directly traceable to damage to Afs; because they have a second function, one that it performs at synapses (gaps between two nerve cells) inside the spinal cord.

Nerve signals are sent across this gap by neurotransmitters (NTs): a group of substances that are released on excitation from the axon terminal of a presynaptic [transmitting] neuron (OMD). The electrical message from the first nerve is translated into a chemical one (an NT), which crosses the gap, connects with a receptor on a dendrite of a postsynaptic [receiving] neuron, where it is retranslated back into an electrical message and carried on to the brain.

At the synapse, Afs stimulate the release of NTs called GABAs which carry no message; their job is to fill up the receptors of the receiving nerve so that “real” messages have no place to land. According to the OMD: …This helps control the nerve cells from firing too fast, which would overload the system.

Here is why we need GABAs: If you ever hit your thumb with a hammer you probably remember it as one of the more painful events in your life. Thousands of crushed cells released pain NTs that flooded the receptors of Cfs, which promptly sent the message that this really hurts like Hell. If Afs hadn’t released GABAs you would probably have passed out from the pain.

In RSD, Afs are damaged and don’t stimulate the release of GABAs: this is why just bumping against something hard produces a pain as intense as hitting your thumb.

Afs are larger and faster than Cfs, which means that their messages reach the synapse first, releasing GABAs into the synapse before the pain signals from Cfs arrive, and turning down the volume before those messages are sent on to the brain.

Evidence that Afs are not releasing GABAs at the synapses is found in how well GABAergics (synthetic GABAs), such as gabapentin (Gabatril); pregabalin (Lyrica); and; lamotrigine (Lamictal), control allodynia in RSD.

Allodynia is clear evidence that Afs suffered some sort of damage in RSD, and we’re told that nerve damage causes RSD, so why don’t the “experts” talk about Af damage? Well, they can’t find any damaged Afs, and don’t know how to explain invisible nerve damage.

(You may have noticed they talk about nerve damage (a lot), but never get around to telling us which nerves are damaged. That’s because all of our nerve damage is invisible).

Even if Af nerve damage could be found, it would only explain allodynia; it would not explain other kinds of pain or any of the other signs and symptoms of this disease, such as patchy osteoporosis; hyperhydrosis; inhibited hair and nail growth, or; muscle weakness and atrophy.

Nerve damage doesn’t explain cyanosis either, but cyanosis can explain Af nerve damage, and here’s a simple experiment (that RSD people should never attempt on themselves), that shows how:

Wrap a blood pressure cuff around a subject’s arm, inflate it to above systolic, then wait 20 minutes. During this period you will watch the arm become bluish, then purplish, this is cyanosis: After 20 minutes have passed, and the arm is nice and purple, touch an ice cube to anyplace on the arm or hand and ask what he/she felt. The subject will always report intense, burning pain: Allodynia.

When the cuff is inflated to above systolic is causes ischemia: (localized tissue anemia due to obstruction of the inflow of arterial blood). This is because the inflated cuff won’t allow arterial blood to enter the arm (obstruction). Ischemia causes hypoxia (a deficiency of oxygen reaching the tissues of the body), because oxygen is only delivered to the cells in arterial blood.

Cyanosis is visible proof that our cells aren’t getting enough oxygen, and can’t function properly. But they don’t fail instantly: The mitochondria combine oxygen and nutrients to make energy packets called ATP, which allows them to continue functioning for a little while or during an emergency, but not our nerve cells. They have no ATP reserves, so they begin to malfunction quickly when they can’t get oxygen.

The likelihood that ischemia is causing your allodynia increases exponentially when you have visible cyanosis: That means that the first thing your doctor (and RSD “experts”) should do is try to find out what is causing the cyanosis; NOT pretend that it isn’t even there.

They pretend it isn’t there because they can’t find a neurological explanation for it, and they don’t want people looking for a cause. If you did that, you might run across “ischemia”, and that leads to questions they don’t want anyone to ask, like: Does ischemia explain any of the other symptoms of RSD?

It does, and following posts will describe exactly how it causes each on of them. Once you have read them, you will have read the only explanation of RSD that doesn’t rely on: “Trust me; I have a rectal thermometer in my pocket, so I’m smarter than you”.

It is my prayer that if you don’t understand everything I’ve written here, you’ll ask questions. Knowing that ischemia causes our symptoms will lead you to find therapies to treat it; therapies that will lead to happier and much more productive lives. Those therapies are available today.

Again, if you don’t fully understand everything I’ve said, please ask. If I left out the one thing that could convince you that ischemia causes RSD, I failed…Vic