Pain is determined by the neurologic properties of receptor organs, neurons, and their interconnections. These may become supersensitive or hyperreactive following denervation (Cannon's Law). A common cause of denervation in the peripheral nervous system is neuropathy or radiculopathy as a sequel to spondylosis. Spondylosis in its early stage may be ldquo;asymptomaticrdquo; or painless and hence unsuspected, because small-di ameter pain fibers may not initially be involved despite the attenuation of the other component fibers of the nerve. The term ldquo;prespondylosisrdquo; is introduced here to describe this presently unrecognized phase of insidious attrition to the other functions of the nerve, especially the trophic aspect. It is postulated that many diverse pain syndromes of apparently unrelated causation may be attributed to abnormal noxious input into the central nervous system from supersensitive receptor organs (nociceptors) and hyperreactive control systems at internuncial pools. Furthermore, trauma to a healthy nerve is usually painless or only briefly painful, unless there is preexisting neuropathy. Some pain syndromes in muscle (eg, trigger points and myofascial pain syndromes) and nerve (eg, causalgia and diabetic neuropathy) that may be related to denervation are discussed.
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