Relationships Between Skin Temperature and Temporal Summation of Heat and Cold Pain

Abstract

. Relationships between skin temperature and temporal summation of heat and cold pain. J Neurophysiol 90: 100 -109, 2003; 10.1152/jn.01066.2002. Temporal summation of heat pain during repetitive stimulation is dependent on C nociceptor activation of central N-methyl-D-aspartate (NMDA) receptor mechanisms. Moderate temporal summation is produced by sequential triangular ramps of stimulation that control skin temperature between heat pulses but do not elicit distinct first and second pain sensations. Dramatic summation of second pain is produced by repeated contact of the skin with a preheated thermode, but skin temperature between taps is not controlled by this procedure. Therefore relationships between recordings of skin temperature and psychophysical ratings of heat pain were evaluated during series of repeated skin contacts. Surface and subcutaneous recordings of skin temperatures revealed efficient thermoregulatory compensation for heat stimulation at interstimulus intervals (ISIs) ranging from 2 to 8 s. Temporal summation of heat pain was strongly influenced by the ISIs and cannot be explained by small increases in skin temperature between taps or by heat storage throughout a stimulus series. Repetitive brief contact with a precooled thermode was utilized to evaluate whether temporal summation of cold pain occurs, and if so, whether it is influenced by skin temperature. Surface and subcutaneous recordings of skin temperature revealed a sluggish thermoregulatory compensation for repetitive cold stimulation. In contrast to heat stimulation, skin temperature did not recover between cold stimuli throughout ISIs of 3-8 s. Psychophysically, repetitive cold stimulation produced an aching pain sensation that progressed gradually and radiated beyond the site of stimulation. The magnitude of aching pain was well related to skin temperature and thus appeared to be established primarily by peripheral factors. I N T R O D U C T I O NTemporal summation of pain occurs reliably when pulses of heat or electrical stimulation are delivered repetitively at rates as slow as one pulse in 3 s. Enhanced discharge of nocireceptive central neurons ("windup") can be observed under these conditions (Mendell 1966;Tommerdahl et al. 1998). Temporal summation for psychophysical and neural responses to heat is dependent on activation of unmyelinated (C) nociceptors and is dependent in part on activation of central N-methyl-D-aspartate (NMDA) receptors (Dickenson 1990;Graven-Nielsen et al. 2000;Price et al. 1994). Most investigations of heat pain summation have utilized triangular ramps from a Peltier device in constant contact with the skin. This method has the advantage of returning the skin to a baseline temperature between each ramping heat stimulus. However, because of limitations on the ramp speeds of Peltier thermodes (especially during down ramps), distinct first and second pain sensations that are attributable respectively to activation of myelinated (A-delta) and C nociceptors are not produced. Possibly because of inhibitory influe...

Gender differences in postoperative pain after laparoscopic cholecystectomy

“…Body temperature is known to rise when strong pain is felt [9], and this supports the rise in VAS score observed in the current study. Postoperative pain, a stressor in both humans and animals, has been previously reported to alter several molecular/ biochemical stress markers including adrenocorticotropic hormone (ACTH) [1], corticosteroids [11], ornithine decarboxylase [14], and core body temperature [2].…”

Variable Threshold of Trigeminal Cold-Thermosensitive Neurons Is Determined by a Balance between TRPM8 and Kv1 Potassium Channels

“…This population appears to be functionally distinct from conventional C-type polymodal nociceptor neurons that exhibit broad spikes and lack inward rectification (Scroggs et al, 1994;Fang et al, 2005). The high-threshold cold receptors we describe probably underlie the common sensation of unpleasant cold discomfort (Mauderli et al, 2003), accompanying, for example, sudden body immersion in cold water or exposure to very cold air. Polymodal nociceptors that appear to respond only to overtly injurious cold, and that elicit sensations of burning cold pain, may require more prolonged and/or deeper cooling for activation and require further study (Wahren et al, 1989;Simone and Kajander, 1997).…”

“…Figure 1C shows the distribution of threshold temperatures in a large population of CS trigeminal neurons (n ϭ 393) during temperature ramps down to 19°C. Because of pronounced thermal gradients across the skin, this range of temperatures (from 35 to 19°C) in culture covers those values to which intracutaneous sensory nerve endings of humans are subjected in vivo, even during maintained surface exposure to noxious cold temperatures (Morin and Bushnell, 1998;Mauderli et al, 2003). We considered low-threshold CS neurons (LT-CS) those with a threshold temperature Ͼ26.5°C.…”

Diversity in the Neural Circuitry of Cold Sensing Revealed by Genetic Axonal Labeling of Transient Receptor Potential Melastatin 8 Neurons

“…This number is even greater considering that fewer TRPM8 ϩ DRG neurons were NF200 positive. Additionally, as sensory afferents expressing TRPV1 and CGRP are considered to be largely nociceptors, coexpression of these markers with Trpm8 GFP demonstrates that a portion of TRPM8 neurons are putative nociceptors and that activation of neurons coexpressing TRPV1 may account for the sensation of burning pain that occurs at cold extremes (Yarnitsky and Ochoa, 1990;Davis, 1998;Mauderli et al, 2003). Interestingly, Trpm8 GFP was observed in neurons that label with either marker exclusively, or with both CGRP and TRPV1, further demonstrating diversity of channel expression, in this case in nociceptors (supplemental Fig.…”