Articles: hyperalgesia.
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Pain to light touching of the skin is a hallmark sign of causalgia. The purpose of this study was to determine whether myelinated or unmyelinated afferent fibers signal this hyperalgesia. Sensory testing was performed in 17 patients with long-standing hyperalgesia after nerve injury. ⋯ The mean latency for detection of pain in the hyperalgesic region was 414 +/- 18 msec, compared to 458 +/- 16 msec for the detection of touch to the same stimuli applied to the opposite normal foot. These 3 lines of evidence indicate that myelinated primary afferents, perhaps A beta fibers, signal the hyperalgesic pain in causalgia. These fibers may be sensitized A beta nociceptors or low-threshold mechanoreceptors.
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A method to measure cutaneous hyperalgesia to thermal stimulation in unrestrained animals is described. The testing paradigm uses an automated detection of the behavioral end-point; repeated testing does not contribute to the development of the observed hyperalgesia. ⋯ Both the thermal method and the Randall-Selitto mechanical method detected dose-related hyperalgesia and its blockade by either morphine or indomethacin. However, the thermal method showed greater bioassay sensitivity and allowed for the measurement of other behavioral parameters in addition to the nociceptive threshold.
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This study analyzed neuronal encoding and response thresholds to thermal stimuli at the ventro-basal (V. B.) thalamus level during a hyperalgesic inflammation induced by intra-plantar injection of carrageenin in the rat. The threshold and the encoding capacity of the cells were studied during two phases of the inflammatory process, namely the "acute" phase (the first two hours following the injection), and "sub-acute" phase 24 h after). ⋯ By contrast to the acute phase, the two groups of neurones exhibited only a weak ability to encode the stimulus intensity especially when the stimulus was applied to the inflamed paw. Both peripheral and central mechanisms are likely to be involved in the modifications of response threshold and encoding capacity at the VB thalamus level seen in these conditions of hyperalgesic inflammation. The differential time course of the responses to a liminal or to a supra-liminal temperature during the inflammation, are discussed in reference to some of the mismatches occurring in clinical situations of hyperalgesia.
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Comparative Study
Time-intensity profiles of cutaneous pain in normal and hyperalgesic skin: a comparison with C-fiber nociceptor activities in monkey and human.
Contributions of evoked discharge in nociceptors with C-fibers to the temporal profiles of magnitude judgments of pain by humans were determined for heat stimulations of the skin before and after the development of hyperalgesia (increased sensitivity to pain) produced by a mild heat injury. Human subjects continuously rated the magnitude of pain evoked by short-duration heat stimuli of 39-51 degrees C delivered to the hairy skin of the arm or leg (calf or foot) before and after the development of hyperalgesia produced by a conditioning stimulus (CS) of either 50 degrees C for 100 s or 48 degrees C for 360 s. During heat stimulations of the leg in humans, magnitude judgments of pain were obtained simultaneously with recordings of evoked discharges in single C-fiber mechanoheat (CMH) nociceptive afferent fibers. ⋯ Despite minor discrepancies, there were similarities in the changes in these histograms for monkey and human CMHs following heat sensitization after the CS. It was concluded that CMHs in monkeys and humans have similar response magnitudes and temporal profiles of response to heat. The major differences in the temporal profiles of CMH responses and human pain ratings were the latencies at which CMH responses and pain ratings began, reached maximum, and ended.(ABSTRACT TRUNCATED AT 400 WORDS)