Abstract
Placebo analgesia (PA) is accompanied by decreased activity in pain-related brain regions, but also by greater prefrontal cortex (PFC) activation, which has been suggested to reflect increases in top-down cognitive control and regulation of pain. Here we test whether PA is associated with altered prefrontal monitoring functions that could adjust nociceptive processing to a mismatch between expected and experienced pain. We recorded event-related potentials to response errors in a go/nogo task during placebo vs. a matched control condition. Error commission was associated with two well-described components, the error-related negativity (ERN) and the error positivity (Pe). Results show that the Pe, but not the ERN, was amplified during placebo analgesia compared to the control condition, with neural sources in the lateral and medial PFC. This Pe increase was driven by participants showing a placebo-induced change in pain tolerance, but was absent in the group of non-responders. Our results shed new light on the possible functional mechanisms underlying PA, suggesting a placebo-induced transient change in prefrontal error monitoring and control functions.
Highlights
Placebo analgesia (PA) refers to a reduced pain sensation due to the belief in an otherwise non-effective treatment [1,2]
Several authors have suggested that LPFC activations during PA reflect a recruitment of cognitive control mechanisms that could in turn trigger opioidergic changes in the descending pain inhibitory system (e.g. [6,9,10,11,12])
Questionnaire results revealed a strong effect of placebo versus control condition on analgesia expectation (Placebo mean = 4.61, SD = 1.69, Control mean = 1.33, SD = 0.77; t(17) = 8.1, p,0.001) and on subjectively experienced pain relief (Placebo mean 4.44, SD = 1.04, Control mean = 1.44, SD = 0.51; t(17) = 13.1, p,0.001), confirming that participants experienced a subjective pain-relieving effect of the capsule in the placebo compared to the control session
Summary
Placebo analgesia (PA) refers to a reduced pain sensation due to the belief in an otherwise non-effective treatment [1,2]. Converging neuroimaging evidence demonstrates that placebo effects are accompanied by decreases of pain-related brain activation in the so-called ‘pain matrix’ [3,4,5,6]. Such decreases are consistently paralleled by increased activity in other regions, such as lateral and medial prefrontal cortex (LPFC and MPFC) – both during PA [3,4,7,8] and as early as during expectation of relief, before actual pain stimulation [4,6].
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