Somatotopy of placebo analgesia is independent of spatial attention

Abstract

Placebo analgesia is being increasingly appraised as an effective support of pharmacological and surgical treatments of pain. The understanding of its neurobiological and psychological basis is therefore of high clinical relevance. It has been shown that placebo analgesia is somatotopically organized and relies on endogenous opioids. However, it is not clear whether temporal fluctuations of cue-dependent spatial attention account for the site specificity of placebo analgesia or whether a somatotopic placebo effect is possible without an attentional focus on the respective location. To address this issue we induced placebo expectations for one specific foot in healthy subjects, the other foot serving as a control location. The feet were stimulated in random order by painful laser stimuli. Half of the pulses were cued for stimulus location, whereas in the other half of trials the subjects were naïve about the location. We found that about half of the subjects exhibited a somatotopic placebo effect that was statistically independent of the spatial cue. We suggest that, after the induction of an initial expectation, placebo analgesia is spatially specific but does not necessarily depend on momentary fluctuations of spatial attention. This result rather suggests that the somatotopy of placebo analgesia relies on the creation of spatially guided expectations or conditioning, but can be maintained without ongoing monitoring of the affected body part.

The Placebo Effect: Advances from Different Methodological Approaches

“…These findings are reminiscent of studies in the field of placebo analgesia, where pain reduction was observed only in the placebo-treated part of the body (Montgomery and Kirsch, 1996; Benedetti et al, 1999; Domnick et al, 2011) and could be reversed by the opioid-antagonist naloxone, suggesting a somatotopic activation of endogeneous opioid systems (Benedetti et al, 1999). Placebo effects on inner organ functions may likewise be mediated by organotopic activation of visceromotor representations in the insular and medial prefrontal cortices (Meissner, 2000, 2009, 2011; Meissner and Ziep, 2011).…”