STUDIES OF HEAT PAIN SENSATION IN MAN - PERCEPTION THRESHOLDS, RATE OF STIMULUS RISE AND REACTION-TIME

Afferent impulse frequency, one of the determinants of subjective magnitude of sensation, varies with the rate of rise of stimulus intensity: the faster the increase in stimulus energy, the higher the frequency of firing for a given amount of energy. This predicts that the steeper the stimulus ramp the lower will be the threshold for perception. While such inverse relation holds for myelinated fibre mediated cold sensation and mechanical pressure sensation, the opposite has been reported for unmyelinated fibre mediated heat pain and cold pain sensations. These paradoxical results intuitively suggest possible reaction time artefact. Indeed, a fixed time interval that includes conduction of the impulses to the brain, central processing and efferent conduction, intervenes between sufficient peripheral stimulus and the voluntary signal in reaction to subjective experience. As stimulus temperature continues to rise along this time, an artefactually high threshold reading results: the steeper the temperature rise, the larger will be the artefact, particularly for submodalities with longer reaction time. The present study compared heat pain threshold, obtained through a method that involves reaction time participation, with heat pain thresholds obtained bypassing reaction time. It was found in 16 volunteers that: (a) Heat pain thresholds decreased as the rate of temperature rise increased when reaction time was not a factor (P < 0.001). (b) Heat pain thresholds determined through the method involving reaction time participation were significantly higher than those obtained bypassing reaction time (P <0.01). Such difference increased with increasing rates of temperature rise, (c) Peripheral conduction velocity calculated from average reaction time was found to be approximately 0.6 m/sec. This indicates that at the rates of temperature rise utilized for the present study, heat pain thresholds reflect activity in unmyelinated C nociceptors rather than in small myelinated Aδ nociceptors. © 1990.