Previous research indicates that exposure to shock decreases thermal pain sensitivity in humans. This hypoal
gesia has been attributed to a centrally mediated fear state that activates descendin
g inhibitory pathways. Animal research su
ggests that distraction alters the activation of these hypoal
gesic systems. To determine whether the pain memory alters the activation of hypoal
gesic systems in humans, the present study examined whether a post-shock distractor attenuates shock-induced hypoal
gesia. If fear-inducin
g shocks are represented by a limited capacity workin
g memory system, then a distractor should speed the decay of the hypoal
gesia. Healthy men were randomly assi
gned to 1 of 4
groups: shock-distraction, shock-no distraction, no shock-distraction, and no shock-no distraction. Followin
g baseline pain tests, participants in the shock
groups were presented with 3 brief shocks. Immediately followin
g shock, an unexpected vibration stimulus was presented to participants in the distraction
groups. Both self-report and physiolo
gical (SCL, HR) measures indicated that shock exposure resulted in fear, arousal, and decreased pain sensitivity. Consistent with prior animal studies, presentation of a post-shock distractor sped the decay of shock-induced hypoal
gesia. Specifically, the distraction
group exhibited si
gnificantly less shock-induced hypoal
gesia compared to the no-distraction
group. These findin
gs provide additional evidence for the involvement of memory processes in the activation of descendin
g pain inhibitory pathways.
Perspective
This study demonstrated that the presentation of a distracting stimulus immediately following 3 brief shocks attenuated shock-induced hypoalgesia in healthy human subjects. Understanding the impact of post-pain distraction on pain processing may have important clinical implications because it may influence patients' willingness to undergo future painful medical procedures.