Endogenous pain modulation: The impact of a noise stressor on capsaicin-induced primary and secondary hyperalgesia

Abstract

In searching for new human pain models that more closely resemble clinical pain states, the capsaicin pain model has emerged as a viable model for both inflammatory and neuropathic pain states. A principal benefit of the capsaicin model is that it allows study of two different pain processes, primary and secondary hyperalgesia. Studies using the human capsaicin model have concentrated on deciphering the neural mechanisms of hyperalgesia, however little has been done to examine the impact of stress on the model. The present study examined the impact of a noise stressor on capsaicin-induced primary and secondary hyperalgesia. An 0.6% capsaicin solution was topically applied to the forearms of healthy undergraduates and then a series of post-capsaicin pain tests were given. Subjects were then randomly assigned into a noise stress (105 dB bursts of white noise) or neutral condition. This was followed by an additional series of pain tests. Heart rate and self-reported affect were used as manipulation checks for fear induction. Primary hyperalgesia was tested by measuring thermal pain to the capsaicin-injured site. Secondary hyperalgesia was tested using a firm von Frey hair on the volar forearm in the area surrounding the capsaicin-injured site. Manipulation checks indicated that negative affect and arousal were induced. The stressful event produced an expansion of the area of secondary hyperalgesia in males while contracting the area of secondary hyperalgesia in females. In primary hyperalgesia, a ceiling effect emerged due to a possible cross-sensitization between capsaicin and the thermal stimulation. However, the noise stressor did impact thermal pain on the control arm, which is similar to previous studies examining the impact of noise stress on thermal pain (Rhudy & Meagher, 2001). In searching for new human pain models that more closely resemble clinical pain states, the capsaicin pain model has emerged as a viable model for both inflammatory and neuropathic pain states. A principal benefit of the capsaicin model is that it allows study of two different pain processes, primary and secondary hyperalgesia. Studies using the human capsaicin model have concentrated on deciphering the neural mechanisms of hyperalgesia, however little has been done to examine the impact of stress on the model. The present study examined the impact of a noise stressor on capsaicin-induced primary and secondary hyperalgesia. An 0.6% capsaicin solution was topically applied to the forearms of healthy undergraduates and then a series of post-capsaicin pain tests were given. Subjects were then randomly assigned into a noise stress (105 dB bursts of white noise) or neutral condition. This was followed by an additional series of pain tests. Heart rate and self-reported affect were used as manipulation checks for fear induction. Primary hyperalgesia was tested by measuring thermal pain to the capsaicin-injured site. Secondary hyperalgesia was tested using a firm von Frey hair on the volar forearm in the area surrounding the capsaicin-injured site. Manipulation checks indicated that negative affect and arousal were induced. The stressful event produced an expansion of the area of secondary hyperalgesia in males while contracting the area of secondary hyperalgesia in females. In primary hyperalgesia, a ceiling effect emerged due to a possible cross-sensitization between capsaicin and the thermal stimulation. However, the noise stressor did impact thermal pain on the control arm, which is similar to previous studies examining the impact of noise stress on thermal pain (Rhudy & Meagher, 2001).