Tonic Pain Evoked by Pulsating Heat: Temporal Summation Mechanisms and Perceptual Qualities

Abstract

The properties of a newly developed tonic heat pain model (THPM), which makes use of pulsating contact heat, were investigated in 18 young men. The most important feature of this model is that repetitive heat pulses with an intensity of 1 degree C above the individual pain threshold are employed. This approach was used to tailor the tonic pain stimulation to the individual pain sensitivity. In the first of two experiments, the effects of pulse frequencies ranging from 5 to 30 pulses per minute (ppm) on ratings of pain intensity and pain unpleasantness (visual analogue scales) were examined. At all frequencies, both ratings increased steadily over the 5-min test period. Frequencies of 15 ppm or more appeared to enhance pain intensity throughout the test period compared to the lower frequencies, but did not appear to alter pain unpleasantness. This suggests that only pain intensity is influenced by slow temporal summation and that a sort of frequency threshold exists for this kind of summation. In the second experiment, the THPM was compared to a well-established form of tonic pain stimulation, the cold-pressor test (CPT); visual analogue scales were again used, and in addition the McGill Pain Questionnaire was employed. The CPT appeared to produce stronger tonic pain than the THPM. However, as is typical with tonic pain, both tonic pain models induced relatively higher values on the affective pain dimension than on the sensory pain dimension. The time course of pain was dynamic in the CPT, with an increase followed by a plateau phase, at least in those subjects who could tolerate the CPT for more than 60 sec. In contrast, as in the first experiment, the pain ratings in the THPM were characterized by a slow and steady increase over time. Moreover, there was absolutely no indication of a dichotomy between "pain-sensitive" and "pain-tolerant" individuals in the THPM, although such a dichotomy was evident in the CPT. This implies that the distinction between pain-sensitive and pain-tolerant individuals can be made only with the CPT, and that this distinction represents individual differences in peripheral vascular reactions to cold rather than in pain perception. In conclusion, the THPM appears to produce a stable and predictable temporal pattern of tonic pain with a predominant affective component, and to be suitable for application in the majority of individuals without causing undue discomfort.

Investigating the affective component of pain: No startle modulation by tonic heat pain in startle responsive individuals

“…We decided to use a tonic stimulation paradigm because experimental tonic pain is believed to resemble clinical pain more closely than phasic pain and to trigger sizeable affective responses (Chen and Treede, 1985;Price and Harkins, 1987;Rainville et al, 1992;Lautenbacher et al, 1995). Surprisingly, we detected no potentiation of the startle reflex under painful in comparison to non-painful heat stimulation, although unpleasantness ratings for painful heat were rather high.…”

Region-specific encoding of sensory and affective components of pain in the human brain: A positron emission tomography correlation analysis

“…The Pearson's correlation coefficients between pain threshold and VAS pain intensity (r ϭ 0.13; p ϭ 0.34) and pain threshold and VAS pain unpleasantness (r ϭ Ϫ0.32; p ϭ 0.24) were insignificant in the present and former studies. 25,36 The correlation between pain intensity and unpleasantness over all four presentations of the noxious thermal stimuli was r ϭ Ϫ0.06 ( p ϭ 0.39). Two ϫ four multivariate analyses of variance for pain intensity [F(1,11) ϭ 116.23, p Ͻ 0.001] and pain unpleasantness [F(1,6) ϭ 104.70, p Ͻ 0.001] showed significant differences in the ratings between heat and pain stimulation (Fig 1).…”

Evidence for Tonic Activation of NK-1 Receptors during the Second Phase of the Formalin Test in the Rat

“…The present data support a role of continuous activation of NK-1 receptors in maintenance of tonic pain. Thus, we suggest that the hyperexcitability that characterizes tonic pain (Lautenbacher et al, 1995;Rossi and Decchi, 1997;Bakke et al, 1998) may be at least partly caused by continuous activation of NK-1 receptors (Svensson et al, 1998).…”