Pain perception temporarily exaggerates abrupt thermal stimulus changes revealing a mechanism for nociceptive temporal contrast enhancement (TCE). Although the mechanism is unknown, a non-linear model with perceptual feedback accurately simulates the phenomenon. Here we test if a mechanism in the central nervous system underlies thermal TCE. Our model successfully predicted an optimal stimulus, incorporating a transient temperature offset (step-up/step-down), with maximal TCE, resulting in psychophysically verified large decrements in pain response ("offset-analgesia"; mean analgesia: 85%, n = 20 subjects). Next, this stimulus was delivered using two thermodes, one delivering the longer duration baseline temperature pulse and the other superimposing a short higher temperature pulse. The two stimuli were applied simultaneously either near or far on the same arm, or on opposite arms. Spatial separation across multiple peripheral receptive fields ensures the composite stimulus timecourse is first reconstituted in the central nervous system. Following ipsilateral stimulus cessation on the high temperature thermode, but before cessation of the low temperature stimulus properties of TCE were observed both for individual subjects and in group-mean responses. This demonstrates a central integration mechanism is sufficient to evoke painful thermal TCE, an essential step in transforming transient afferent nociceptive signals into a stable pain perception.
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