Sympathetic Pain Versus RSD
There are many kinds of nerve fibers. Two that are easy to understand are the motor fibers, which let us move, and the sensory fibers that let us feel. Another important group of fibers that is harder to understand includes the sympathetic nerves. These nerves arise from ganglia, which are collections of the fibers located outside of the spinal cord.
The ganglia function independently (automatically) from the rest of the nervous system.
The sympathetic nerves send branches to many places, including internal organs, coverings of the spinal cord (dura), intervertebral disks, muscles, tendons, ligamentous structures, and blood vessels. The job of the sympathetic nerve is to tell the brain and spinal cord when something goes wrong with any of the tissues that it innervates.
The injury may be major or minor in severity. When you sprain an ankle, first you feel a sharp electric pain, and then you feel a burning pain. The sharp pain comes from the fast pain fiber, and the second burning pain comes from the sympathetic nerve fiber. Usually, over time, this burning pain will stop. This type of sympathetic pain is entirely normal.
Sometimes the burning will not stop. When this happens, people often have a hard time describing where their pain begins or ends, but usually can tell you that the cold or shifts in the weather makes it worse. They may have noticed that since becoming hurt, the painful part always feels cold. As it becomes more severe, their skin can become sweaty, and they won’t want to move the painful part (stage 1). When it is more severe still, they do not want anyone (or anything) to touch them where they hurt.
Unfortunately, most health care providers are not familiar with the proper diagnosis and treatment of sympathetic pain. However, when they hear this kind of complaint, they should at least begin to think about it. If they do, often a diagnosis of Reflex Sympathetic Dystrophy (RSD) is made.
In true RSD, there is a decrease in the local blood flow of the injured part. If allowed to persist, then the cold, sweaty and swollen skin of stage 1 progressively gets worse until there is loss of range of motion or even loss of muscle mass (stage 2). In even more severe cases, the bones may thin as well (stage 3).
In RSD, the sympathetic nerve is felt to be overacting. Liken it to a car engine that is dieseling: the ignition is off, yet the engine is still on. In this case the sympathetic nerve stays on, even when the injury itself is old and no longer represents a new injury.
In the past, diagnostic studies were not that helpful for this disorder, so most doctors who knew anything about it at all felt that performing a sympathetic ganglion block could prove a diagnosis of RSD. This block is supposed to stop the ganglion from dieseling, and therefore decreased pain and increased blood flow should occur once the block is done.
If the desired response did not occur, then the patient was frequently said to have psychological factors affecting their perception of pain (this was also the case if no one thought of the diagnosis to begin with). This approach, by in large, has been a failure. Many people still complained of pain, and often were felt to have obvious physical signs of injury, even though they did not respond to blockade. Others had few or no signs of injury, but persisted with their complaints in a consistently reliable manner over time.
Fortunately, There is now awareness that not all sympathetic pain represents RSD. There is also greater understanding of how to use diagnostic studies to categorize what type of sympathetic pain exists. The two tests that are used to objectify the presence of sympathetic pain syndromes are bone scans and thermography.
The bone scan is felt to be more specific, but the thermogram is far more sensitive. In order for a bone scan to be positive, there must be up to 30% bone loss. If the three-phase study is used, then there must be vasoconstriction (decreased blood flow) of large enough magnitude to allow it to be seen on x-ray.
The thermogram shows skin temperature changes, but it does not tell you the source of those changes. While skin temperature is felt to be under the control of the sympathetic nerve fibers, the study only tells you if it is present or not; there is no specificity as to the underlying generator (or injury site) causing the change. Further, up to one-third shows increased, not decreased blood flow.
Clearly, waiting for a positive bone scan is far too late to treat patients with this disorder, and the characteristics of the thermogram require explanation in order to provide greater utility. With the classification of different types of sympathetic pain, the objective findings as well as the clinical presentation and response to treatment are now readily identifiable.