The Wall/ McHenry database has been bombarded with Central Pain subjects who report muscle pain with CP. Now, electromyography confirms this. The wave changes were there all along, but are just now being recognized.
In the September European Journal of Applied Physiology, Kallenberg, et al take a closer look at myography in chronic pain. We are not familiar with electromyography being used to evaluate Central Pain and it would not likely be of help unless the clinicans were familiar with Kallenberg’s approach. Given the prevalence of hyperpathia to sharpness in CP, it does not appear likely many could endure electromyography, which involves insering needles into muscles.
However, with the very large number of CP patients having muscle pain, such as burning, tightening, cramps, pulling, drawing, teearing etc. the electromyographic findings are interesting. CP muscle pain comes in at least two varieties, pain with movement (a burning with muscle loading or kinesthetic dysesthesia) and pain at rest (isometric dysesthesia, which involves cramping, pulling, tightening etc).
Pain intensity is a function of the frequency of the action potential The action potential is a sudden change (spike) in voltage difference (called a “potential”) between the outside and inside of the nerve cell. This jolt repeats itself all the way up the axon until a synapse is reached. Inhibition of pain is the job of the brain and the thalamus, which send a message down to the synapse to quiet the activity.
This inhibition by the brain is disabled in nerve injury pain by what is called “anion reversal”. Anion reversal refers to the relative inability of injured neurons to produce the protein, KCC2, which carries the anion, choride (Cl~) to the neuronal membrane. The result of this is that the anion step is reversed, turn the anion step into an excitatory one. This is like a light swtich which is turned upside down, or when the faucet is set backward. The brain makes the expected move, but it backfires.
Anions are ions with a negative charge. By contrast, positively charged ions EXCITE the neuron. Depending on the chemistry present at the synapse, the action potential frequency may diminish, increase, or disappear. Normal pain typically causes only AMPA release on the far side of the synapse, but with sufficient excitation, NMDA is released on the far side of the synapse and in conjunction with certain fatty acids related to prostaglandin, initiates CGRP activity and firing in the VR-1 calcium channels. (See the article by J.Coull, and The Smoking Gun, elsewhere at this site, using search, if necesaary).
Since pain is FREQUENCY modulated, it is not surprising that the frequency of the action potentials would be increased in chronic pain. What is surprising is that this increase appears in MUSCLES. Carl Saab, who has written elsewhere at this site, was the first to show activity on fMRI in parts of the brain coordinating muscle movement. Now, Kallenberg has also shown actual increases in frequency of the action potentials going to muscles. He concludes that the central nervous system has much greater input to the muscles in chronic pain than in normals.
Also astonishing was Kallenberg’s ability to see a difference in shape of the action potential on an oscilloscope in chronic pain. This is no small credit to him since this change in electromyograms has not been picked up before. In fact, the superficially negative findings on electromyography were sometimes used to challenge CP patients who had muscle pain.
Kallenberg is to be congratulated for pushing this knowledge to the forefront.