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Pain: Physiological Mechanisms

In the late 1960s, John F. Hahn, a sensory gener-alist in the tradition of Henri Piéron and Frank Geldard, taught that pain is not only a sensation in search of a stimulus, but in search of a receptor as well. In the years since those discussions, understanding of the mapping of stimulus on receptor to sensation has not changed much. There is no question that pain is a dramatic and attention-grabbing event when it occurs—when skin temperature is too high or too low, when we taste or touch chemicals, such as capsaicin (from chilies) or when we stub our toe—and then again a few seconds later, but perceived differently—duller and less sharp. But one could argue that the most interesting aspect of pain is when it doesn't occur and yet seems like it should. Phenomena such as phantom limb pain, the wounded soldier who continues to fight unaware of an injury, or the “anesthetic” effect of clenched fists in response to stubbing a toe underscore the fact that pain is a separate, complex sensory-perceptual experience. These also illustrate that the experience of pain is strongly subject to nonsensory (“top-down”) central influences, like affective state and peripheral modulating influences. Perhaps more than any other sensory modality, it can't easily be explained by stimuli activating a pain receptor and being transmitted to the brain, challenging straightforward physiological analyses. But physiological mechanisms must underlie at least the initial triggering of the experience. This entry begins by placing the search for physiological mechanisms in historical context and then describes the results of contemporary research on physiological mechanisms.

Pain is Different from Other Tactile Sensations

The perception of pain is different from other sensory experiences, and the physiology of “pain receptors” has been similarly difficult to define. At least tactually, pain is not just “very intense touch.” Historically, there had been a debate whether painful stimuli were just examples of very intense energy of some type (heat, pressure, etc.), reported by our touch receptors responding to these extremes on a continuum from normal and innocuous to painful, injurious, and noxious. The alternative view has been that there were specific receptors, called nociceptors, for the stimulus extremes. Observations described in the following text relating certain fiber types to stimuli described as “painful” support the latter notion. The brain, which reports the presence of pain or inhibits our appreciation of this illusive experience, can be explored surgically without resulting in pain, as Wilder Penfield was able to demonstrate in his explorations of cortical function during procedures when the patient was awake, because there are no pain receptors in the brain itself. Possessing only free nerve endings, somehow the cornea of the eye is able to distinctly report touch, temperature, and pain. (Bruce MacIver and Darrell Tanelian do point out that there is a distinction in the way in which the nerves branch out in the cornea, but there is no other apparent specialization in the endings.) So pain involves both affective (central) and sensory (peripheral) components. Other entries discuss some of the cognitive determinants of pain, its measurement, and current theories involving central nervous system pathways and interactions among them. This entry discusses the physiological bases of pain, particularly in the responses of specific peripheral receptor systems, called nociceptors.

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