Human pain responsivity was defined as the subject's behavioral pain endurance time (PET) to the 1 +/- 0.3 degrees C cold-pressor test, a naturalistic and clinical analogue tonic pain model. Over the past 2 years, we have consistently observed a behavioral dichotomy of pain responsivity in each of our 6 studies (all at P less than 0.000001 effect level), totaling 205 subjects. Overall, the pain-tolerant (PT) subjects could endure the whole 5 min (note that 3 min was the ceiling criterion in the last study) of cold-pressor test, while the pain-sensitive (PS) subjects could merely tolerate the test for an overall mean of 60 sec, 20% of PET in the PT group. No overlapping of distribution was observed between these 2 populations. Further, we observed that the percentage of subjects in each of these 2 groups varied substantially across studies. The mean pain perception (Visual Analogue Scale) of tonic pain ranged from 60-70 for both aversiveness and intensity scales. The characteristics of this tonic pain, assessed by the McGill Pain Questionnaire (MPQ), showed similar patterns across each study with a high degree of consistency. Although ratings of pain aversiveness did not differ in the PT vs. PS subjects, ratings of pain intensity did differ, with the PT subject reporting less pain. It was found that state anxiety correlated with MPQ scores for PS, but not PT, subjects. Additionally, psychological tests (Tellegen Absorbance Scale, Kleinknecht Fear, Spielberger Trait-Anxiety) were positively correlated with certain MPQ measures for PS, but not PT subjects. Multivariate regression analyses indicated, in the PS but not the PT group, that 36% of variance in pain score (MPQ-T) could be predicted by the psychological trait factors. The general level of fear contributed singularly as the major predictor variable in the pain-sensitive individuals. We consider this tonic pain model indeed offers a succinct empirical paradigm to study human pain responsivity in general. The psychological/physiological etiology of such drastic human pain responsivity requires intense systematic investigations. This report discusses the results in: (a) individual differences in pain responsivity, (b) characterization of the cold-pressor test as a model for tonic pain, (c) contrast between PS and PT groups of pain perception and state anxiety, and (d) psychological determinants of measures for cognitive, perceptual and affective domains. Discussion was also focused on the experimental tonic pain model and its generality for clinical pain, as well as the basic model of the cold-pressor test for human tonic pain responsivity.

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Individual differences in human pain responsivity were characterized by the 1 degree C cold-pressor test. Behaviorally, a pain-tolerant group (PT = 29 Ss) tolerated the entire 3-min test (means = 180 +/- 0 sec), while a pain-sensitive group (PS = 13 Ss) averaged only 50.31 +/- 20.81 sec of the cold-pressor test (t = 16.75, P less than 0.0001), replicating our earlier studies. Physiologically, the PT group exhibited no mean differences from the PS group in cortical power densities at the baseline stage. Under the noxious stress of the cold-pressor test, both groups exhibited markedly heightened delta and beta cortical power densities. However, the PS subjects showed significantly higher delta power, but not beta power, than the PT subjects. We conclude that heightened delta activity may reflect the stress component of human pain responsivity, and that beta activity reflects the vigilance scanning of pain processes.

Electrical potentials evoked by 5 intensities of painful dental stimulation were recorded at the scalp. During testing, volunteers indicated subjective painfulness by verbal pain ratings and visual analogue scales. Evoked potentials (EPs) to each intensity, observed between 50 and 400 msec, were characterized by 4 waveform components. The peak-to-peak amplitudes, but not the peak latencies, of all 4 EP components systematically increased with increased stimulation. The amplitudes of the two earlier components correlated with stimulus intensity when the effect of subjective painfulness was controlled, but this was not the case for the later components. In contrast, the amplitudes of the two later components were associated with subjective painfulness but not with stimulus intensity. A strong linear relationship was observed between subjective painfulness and peak-to-peak amplitude for the EP component observed between 175 and 260 msec. The data suggest that the earlier EP components may reflect sensory transmission processes while the later components indicate brain activity when pain is perceived.