Note: This article explains some theories about how RSD works. This is a current working definition based on the best animal research that has been done to date. Nobody can say that this is definitely the way RSD works but it is the best that many researchers know. This is a very technical and difficult article. If you get lost, please read each sections called Remember and you will get a general idea about what is being discussed. 
The information for this article comes from a tape of Dr. Schwartzman's presentation at the RSDS Association of America's first conference in October of 1995; Chapters by Dr. Schwartzman in 1) Vascular Medicine, 1995 2)Handbook of Clinical Neurology: Vol.17(61) Chapter 7 pg.121-136 Spinal Cord Trauma and information I've gotten from previous articles including studies that have been done with RSD patients throughout the years

 The pain of RSD consists of a variety of different pains The most common and consistent pain is a severe burning. This burning is the neuropathic pain that has become the landmark of RSD. The other pains have been described as: stabbing, tearing, crushing, bursting, or throbbing pain felt deep in the affected part.
Many describe the pain as exhausting and causing the patient to feel wretched and miserable. The autonomic nervous system affects our blood vessels, endocrine system, and the functioning of all of the organs in our body. The motor function problems can be divided into two major areas 1) spasms or myclonic jerks and 2) problems with initialing movement (RSD doesn't cause paralysis.)
 

 a.. 1) Fibers from layers 1&2 of the spinal cord cross with fibers from layers 5&6 forming the spinothalamic tract. The crossing of these fibers allows the pain signals to be carried to the brain.
b.. 2) The amount of pain=3D the frequency that the pain projecting neurons fire.
c.. 3) The type of pain that you feel is controlled by the type nerve fibers that are firing. (C-nociceptor Fibers carry burning pain, the A nerve fibers carry the dull aching pains.
 

 a.. 1) Allodynia is pain due to a stimulus that does not usually cause pain. Allodynia takes a stimulus that should not cause pain and changes it to a painful one. A shirt sitting on your arm should not cause pain but for those with allodynia it is very painful.
b.. 2) Hyper-ralgesia occurs when there is too much pain from a stimulus. The pain is magnified. This is different than allodynia in that these are stimulus that normally cause pain but the stimuli causes the C-nociceptor nerve fibers to fire too easily, causing increased pain.
c.. 3) Hyperpatheia is when it is hard to feel a stimulus but once the threshold is passed, the pain reaches a maximum intensity too quickly
The pain is overwhelming and doesn't stop when the stimulus is removed. A repetitive stimulus such as stroking an arm makes hyperpatheia even worse. This is a terrible pain that usually comes in late stage RSD and is generated from the central nervous system.
Most people with RSD have all three types of pain. We need to know how these types of pain work so we can control them. Most of the information that follows has been discovered recently through research that has been conducted on the animal models of RSD. Dr. Bennet of the NIH (National Institute of Health) discovered how to give rats RSD about 6 or 7 years ago. Since then research on RSD and neuropathic pain has taken off and the results of this research, may lead to a cure or control of these overwhelming pain conditions.
When there is an injury, inflammatory substances such as brandykins and prostaglandin are released in the area of the injury. These chemicals are synthesized by activity between the tissues and white blood cells that come to heal the injury. There is a large list of chemicals, such as serotonin, acidosis, hydrogen ions, potassium, etc. which are released in the area of an injury that sensitize c-nociceptor nerve fibers causing their threshold to be lowered. The lowered threshold make these nerve fibers fire more frequently causing more intense pain. The cycle that I just described and is shown in Chart #1 shows the chemical reactions that start the vicious pain cycle that runs RSD. It is this chronicity of pain that causes RSD to develop from a minor injury to an injury with sensitized nerve fibers and permanent changes in the cells of the dorsal root in the spinal cord. Constant noxious peripheral stimulation (from damaged c fibers) in the spinal cord can cause the neurophysical phenomena of sensitization which is when the pain fibers fire too easily. The spinal cord around the sensitized nerve fibers changes. This sensitized area touches areas around it causing the nerve fibers adjacent to the sensitized area to fire more easily thus causing a larger sensitized area and the spread of the pain to new areas of the spinal cord and body. This spread causes "the wind-up" phenomena which occurs when the c nerve fibers are sensitized in the dorsal horn causing them to fire many times for each pain stimuli that is received. The wind-up phenomena is responsible for the constant pain of RSD and explains how hyperpathia happens. This is one of the areas where researchers are trying to interfere with the cells firing.
Damaged nerves in the area of injury and in the peripheral nervous system try to regenerate by growing nerve sprouts. These new sprouts fire too easily and allow too much sodium to enter the nerve sprouts. The excess sodium increases the senativity of these sprouts lowering the threshold which causes multiple nerve firings for each stimulus received. These sensitive nerve sprouts give off alpha adrenonetic receptors which stimulate the sympathetic nerves to fire and carry pain.
This sympathetic stimulation drives RSD in the early stages. The development of the nerve sprouts is wonderful because the body is trying to heal itself but instead the new nerve sprouts actually cause more problems. In a normal state the sympathetic nerves do not carry pain stimulus but the sensitization of these nerves by the alpha adrenonetic receptors and the chemical reactions caused by chronic pain (explained above) cause the up regulation of the sympathetic system and allows it to carry pain stimulus.
 

 Sympathetic blockade will alleviate these motor manifestations. If not treated early, they may become permanent because the motor disorders as well as the pain become independent of the sympathetic nervous system.
1)Dystonia is a term used to describe a neurologic disorder characterized by sustained involuntary muscle contractions and spasms which result in abnormal postures and movements. In the dystonia caused by RSD, you will often find a contracted or hyper extended hand, foot, finger or toe. These contracture remain in sleep. Even the facial muscles have become dystonic in some patients.
What causes the dystonia of RSD? To move any part of the body, you need two muscles that work in opposition to each other. One causes the wrist to bend the other straightens it out. When one muscle get strong and the opposite one weak a contracture or extension will happen. *The sympathetic innervation during the early stages of RSD causes the release of too much norephedrine causing type I or aerobic muscle to get weak.
Type 2 (anaerobic) muscles get hyperactive. This is called the Orbelli effect.
Dystonia can often be treated by injections of Botox, which is a very minute amount of the botulism toxin. It weakens the musle that is too strong by actually causing a lvery localized nerveblock that permanently distroyes some odf the overtight muscle fibers.
2) RSD does not cause paralysis. The nerve impulses that cause movement do get to the limb even though there may be a delay in the order to begin the movement This may become apparent when a person is walking. Each foot moves forward so quickly when the brain sends the proper signal that we move without a thought. If there is a delay between the brain and movement of the leg, a person will fall because the forward movement of the body will continue without a leg to take the weight. I found that I was falling often and didn't know why until a friend was watching me walk when he observed the delay in action and my fall.
3) Increased tone/spasms ocurrs when the sympathetic system is activated and it secrets neuropeptides. The sympathetic nerves innervate the muscles and these chemicals cause the muscle spindles to shorten thus increasing the tone in muscles. Some RSDers have muscle wasting in their affected limb and for some of us the increased tone actually causes the muscle to be bulkier even though it is weak.
AUTOMATIC DYSFUNCTION is evident throughout the course of RSD. Early in the disease the involved limb is usually warm, red and dry but with time it becomes cool, pale, sweaty and cyanotic. Often the discoloration,and mottling of the skin may be seen in the contralateral limb. These symptoms appear to be caused by the peripherial nerve injury, chronic pain and chemical reaction that occur in the injured limb but no one is exactly sure how this happens. Early in the disease vasoconstriction of the blood vessels may be caused by a hyperactive sympathetic system. Vasoconstriction causes a cold limb. When the RSD becomes SI, the vasoconstriction may be caused by the chemical reactions that we discussed earlier, namely an increase of epinephrine. SP still causes blood vessels dilate.

 There have been many studies done that show that there is a central reorganization of the sympathetic nervous system. Normally throughout each day the blood vessels dilate and constrict in a rythemic fashion causing the small vessels to go up and down spontaneously. This helps regulate the temperature of the skin. After this reorganization the rythemic dilation and constriction stop and other things control the dilation and constriction of the blood vessels. The release of epinephrine as mention above is one. I am just guessing about this but it seems t to make sense that once this reorganization occurs, the temperature of the air may even regulate the blood vessel size. Many people that I know who have RSD have told me that the environmental temperature changes the temperature of the affected limb. When the temperature is over 85, my right hand becomes hot and red.
There is a test that will show whether the reorganization has taken place. Put one limb in a bucket of ice. The normal sympathetic system will allow only the limb in the ice to vasoconstrict, the rest of the limbs stay warm. If the sympathetic nervous system has already reorganized, a person with RSD will find that all of his/her limbs constrict. This is because the central mechanisms of the Sympathetic Nervous System have been damaged.
Dr. Schwartzman believes that when the limbs change temperature, what we are actually seeing as a warfare between the neuropeptides such as Substance P which causes vasodilation and the sympathetic system adrenoic receptors which let off epinephrine which causes vaso- dilation. There are time when a person with the ABC syndrome of RSD with cross temperature modulation can have one finger hot and the next cold.
AUTOIMMUNE DISORDERS
The autoimmune response of RSD has not been very well researched but we see the symptoms of a compromised system in the late stages of RSD. Most of this research is happening in Europe. The symptoms that show that the Autoimmune system has been compromised are:
a.. 1) Gardner Diamomd syndrome- This appears as large discolorated areas that look like a raised welt. It is caused by a reaction to your own blood when some of the blood leaks into the tissue
b.. 2) Chronic Infections: too many infections and the ability to fight the infections becomes compromised.
c.. 3) Tissue Necrosis Factor is an autoimmune attack on your own skin. Collagen doesn't work and the skin sloughs off in the areas affected.
d.. 4) Fever of unknown origin is caused by the lymphocytes that go to the hypothalamus (area of the brain that control many of our bodies functions & emotions) and affect the temperature.
Remember: that RSD causes movement disorders, changes in the autonomic nervous system and the autoimmune system in people who suffer from this syndrome. Many of these symptoms seem impossible to physicians who are not familiar with RSD and the odd symptoms may cause many doctors to feel that you are faking it. Research will continue to bring us answers that will convince most physicians that we really do suffer as we say we do. It will just take time. RSD DOES SPREAD: Besides the sensitization and spread of the pain in the spinal cord which we discussed earlier, most of these ideas about how RSD spreads have not been researched. There seems to be an overall sensitization of the sympathetic system so that new injuries can cause the spread of RSD. Injuries as slight as an IV being put into a healthy limb or using crutches which stretches the brachial plexus can cause this spread of RSD.
Dr. Schwartzman believes that the spread of RSD can be prevented by:
a.. 1)Blocking the nociceptor pain.
b.. 2)Actually correcting when possible but definitely blocking the pain source so active physical therapy can be started.
c.. 3) This physical therapy is not just for mobility. What it will do is change the molecular genetics and prevent the firing of the pain nerve fibers from going through other nerve fibers through retrograde transport to carry the pain fibers.

 Dr Schwartzman believes that even many cases of severe RSD can be corrected if the pain can be controlled so that movement and active Physical Therapy can be done.
Remember: So much has been learned about how pain in general and RSD works. This is very promising because the more we know the closer we are to finding a medication to stop the transmission of the pain. The best hope is with the NMDA receptors. The only problem is that the NMDA receptors are needed to think, feel and do all the functions of life and the medication needs to target only the specific NMDA receptor sites that carries pain or it can cause all types of problems such as hallucinations.