• J A Markenson.
• Cornell University Medical School, New York, New York, USA.
• Am. J. Med. 1996 Jul 31; 101 (1A): 6S-18S.

AbstractChronic pain differs from acute pain in that it serves no useful function, causes suffering, limits activities of daily living, and increases costs of healthcare payments, disability, and litigation fees. Pain perception begins with activation of peripheral nociceptors and conduction through myelinated A delta and unmyelinated C fibers to the dorsal root ganglion. From here, signals travel via the spinothalamic tract to the thalamus and the somatosensory cortex. Modulation of sensory input (i.e., pain) occurs at many levels. Nociceptors are also neuroeffectors, and transmission can be modulated by their cell bodies, which secrete inflammatory mediators, neuropeptides, or other pain-producing substances. Descending pathways from the hypothalamus, which has opioid-sensitive receptors and is stimulated by arousal and emotional stress, can transmit signals to the dorsal horn that modulate ascending nociceptive transmissions. Modulation to alter the perception of pain also can occur at higher centers (e.g., frontal cortex, midbrain, medulla) by opioids, anti-inflammatory agents, as well as antagonists and agonists of neurotransmitters. This article will review our current knowledge of the mechanisms involved in (1) the transduction of tissue injury or disease signals (nociception and nociceptive receptors); (2) the transmission of signals rostrally to the thalamus and higher nervous system centers (involving perception of the quality, location, and intensity of noxious signals); and (3) the modulation of ascending sensory messages at all levels (periphery, spinal cord, and higher centers).

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