ACUTE PAIN MECHANISMS
Section snippets
Nociceptors
Receptors transduce energy of a specific modality into generator and then action potentials. Nociceptors, frequently called “free nerve endings,” are unencapsulated nerve endings that are activated in response to stimuli that threaten or actually produce tissue damage. Some respond exclusively to one modality, such as chemical or noxious heat; others are sensitive to several varieties of noxious stimulation (i.e., polymodal nociceptors). Virtually all nociceptors are innervated by a
Nociceptive-Specific Cells
Lamina I and, to a lesser degree, deeper laminae (particularly V and X) contain many nociceptive-specific cells that respond selectively to high-threshold, potentially tissue-damaging stimuli (Table 2). Although some are modality specific, others respond to both thermal and mechanical stimuli applied to their receptive fields, as well as to noxious chemical stimuli. Many also fire in response to decreases in pH and during reperfusion after temporary ischemia. Regardless of modality specificity,
SPINAL MODULATION OF NOCICEPTIVE TRANSMISSION
Clearly, a relationship exists between afferent fiber input and spinal cord output to the brain leading to pain perception; however, even in the processing of acute nociceptive input, this relationship is not immutable, and the output is dependent on far more than mere hard-wiring. Behavioral relevance of the signal, attention, movement, and previous experience are all factors. As the pain state progresses toward chronic, the system becomes even more complex. Plasticity of the input–output
SUMMARY
The systems activated by tissue-injuring stimuli are complex. The nociceptive primary afferents have little spontaneous activity under normal conditions; however, after tissue injury, they display longlasting, ongoing activity. This results, in part, because the injury elicits the release of active factors that sensitize or excite the peripheral nerve terminal. A threshold that is lowered to the extent that body temperature and the pressure of edema are adequate stimuli results in spontaneous
ACKNOWLEDGMENT
We would like to express appreciation to Carmen Doom for editorial assistance.
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Address reprint requests to Linda S. Sorkin, PhD, Department of Anesthesiology, University of California, San Diego, School of Medicine, 9500 Gilman Drive #0818, La Jolla, CA 92093–0818
This work was supported by grant no. NS3560 from the National Institutes of Health.