Yet another clinical peculiarity of segmental pain is the reduction in power of muscle contraction that it may cause (known as reflex paralysis, or algesic weakness). The term “antalgia” is often used to describe this effort to avoid pain with movement, especially antalgic gait that arises from lumbar disc or other spinal or hip problems.
One of the most perplexing issues in the study of pain is the manner in which chronic pain syndromes arise. Several theories have been offered, none of which satisfactorily accounts for all the clinically observed phenomena. One hypothesis proposes that in an injured nerve, the unmyelinated sprouts of A-d and C fibers become capable of spontaneous ectopic excitation and afterdischarge and are susceptible to ephaptic activation. A second proposal derives from the observation that these injured nerves are also sensitive to locally applied or intravenously administered catecholamines because of an overabundance of adrenergic receptors on the regenerating fibers. These mechanisms are thought to be the basis of causalgia (persistent burning and aching pain in the territory of a partially injured nerve and beyond) and its associated reflex sympathetic dystrophy; either would explain the relief afforded in these conditions by sympathetic block. This subject is discussed in greater detail in relation to peripheral nerve injuries (see “Peripheral Nerve Pain” and Chap. 43).
A third proposed mechanism is through central sensory structures, for example, sensory neurons in the dorsal horns of the spinal cord or thalamus, if chronically bombarded with pain impulses, may become autonomously overactive (being maintained in this state perhaps by excitatory amino acids) and may remain so even after the peripheral pathways have been interrupted. Peripheral nerve lesions have been shown to induce enduring derangements of central (spinal cord) processing (Fruhstorfer and Lindblom). For example, avulsion of nerves or nerve roots may cause chronic pain even in analgesic zones (anesthesia dolorosa or “deafferentation pain”). In experimentally deafferented animals, neurons of lamina V begin to discharge irregularly in the absence of stimulation. Later the abnormal discharge subsides in the spinal cord but can still be recorded in the thalamus. Consequently, painful states such as causalgia, spinal cord pain, and phantom pain are not abolished simply by cutting spinal nerves or spinal tracts.
It is likely that structural or physiologic changes in the spinal cord, of the type alluded to above, are able to produce persistent stimulation of pain pathways. Indo and colleagues review the molecular changes in the spinal cord that may give rise to persistence of pain after the cessation of an injurious episode. It is an open question whether the early treatment of pain may prevent the cascade of biochemical events that allows for both spread and persistence of pain in conditions such as causalgia, but it has been the experience of most clinical pain experts that preemptive treatment of certain painful conditions (e.g., herpes zoster) may reduce the risk of a chronic pain syndrome. None of these phenomena adequately explain the genesis of chronic pain in the absence of an ongoing painful stimulus.
Pain has several other singular attributes. It does not appear to be subject to negative adaptation—that is, pain may persist as long as the stimulus is operative—whereas other somatic stimuli, if applied continuously, soon cease to be perceived. Furthermore, prolonged stimulation of pain receptors sensitizes them, so that they become responsive to even low grades of stimulation, even to touch (allodynia).
The Emotional Reaction to Pain