ABSTACT Placebo analgesia is defined as a psychobiological phenomenon triggered by the information surrounding an antalgic drug instead of its inherent pharmacological properties. Placebo analgesia is hypothesized to be formed through either verbal suggestions or conditioning. The present study aims at disentangling the neural correlates of expectations effects with or without conditioning through prior experience using the model of placebo analgesia. We will address this question by recruiting two groups of individuals holding comparable verbally-induced expectations regarding morphine analgesia but either (i) with or (ii) without prior experience with opioids. We will then contrast the two groups’ neurocognitive response to acute heat-pain induction following the injection of sham morphine using electroencephalography (EEG). Topographic ERP analyses of the N2 and P2 pain evoked potential components will allow to test the hypothesis that placebo analgesia involves distinct neural networks when induced by expectations with or without prior experience.

ABSTACT Placebo analgesia is defined as a psychobiological phenomenon triggered by the information surrounding an antalgic drug instead of its inherent pharmacological properties. Placebo analgesia is hypothesized to be formed through either verbal suggestions or conditioning. The present study aims at disentangling the neural correlates of expectations effects with or without conditioning through prior experience using the model of placebo analgesia. We will address this question by recruiting two groups of individuals holding comparable verbally-induced expectations regarding morphine analgesia but either (i) with or (ii) without prior experience with opioids. We will then contrast the two groups’ neurocognitive response to acute heat-pain induction following the injection of sham morphine using electroencephalography (EEG). Topographic ERP analyses of the N2 and P2 pain evoked potential components will allow to test the hypothesis that placebo analgesia involves distinct neural networks when induced by expectations with or without prior experience.

ABSTACT Placebo analgesia is defined as a psychobiological phenomenon triggered by the information surrounding an antalgic drug instead of its inherent pharmacological properties. Placebo analgesia is hypothesized to be formed through either verbal suggestions or conditioning. The present study aims at disentangling the neural correlates of expectations effects with or without conditioning through prior experience using the model of placebo analgesia. We will address this question by recruiting two groups of individuals holding comparable verbally-induced expectations regarding morphine analgesia but either (i) with or (ii) without prior experience with opioids. We will then contrast the two groups’ neurocognitive response to acute heat-pain induction following the injection of sham morphine using electroencephalography (EEG). Topographic ERP analyses of the N2 and P2 pain evoked potential components will allow to test the hypothesis that placebo analgesia involves distinct neural networks when induced by expectations with or without prior experience.

ABSTACT Placebo analgesia is defined as a psychobiological phenomenon triggered by the information surrounding an antalgic drug instead of its inherent pharmacological properties. Placebo analgesia is hypothesized to be formed through either verbal suggestions or conditioning. The present study aims at disentangling the neural correlates of expectations effects with or without conditioning through prior experience using the model of placebo analgesia. We will address this question by recruiting two groups of individuals holding comparable verbally-induced expectations regarding morphine analgesia but either (i) with or (ii) without prior experience with opioids. We will then contrast the two groups’ neurocognitive response to acute heat-pain induction following the injection of sham morphine using electroencephalography (EEG). Topographic ERP analyses of the N2 and P2 pain evoked potential components will allow to test the hypothesis that placebo analgesia involves distinct neural networks when induced by expectations with or without prior experience.

ABSTRACT Placebo effects (PE) are defined as the beneficial psychophysiological outcomes of an intervention that are not attributable to its inherent properties; PE thus follow from individuals’ expectations about the effects of the intervention. The present study aims aimed at examining how expectations influence neurocognitive processes. We will addressed this question by contrasting three double-blinded within-subjects experimental conditions in which participants are were given decaffeinated coffee, while being told they have had received caffeinated (condition i) or decaffeinated coffee (ii), and given caffeinated coffee while being told they have had received decaffeinated coffee (iii). After each of these three interventions, performance and electroencephalogram will bewas recorded at rest as well as during sustained attention Rapid Visual Information Processing task (RVIP) and a Go/NoGo motor inhibitory control task. We first aimed to confirm previous findings for caffeine-induced enhancement on these executive components and on their associated electrophysiological indexes (attentional P3 component, response conflict N2 and inhibition P3 components (ii vs iii contrast); and then to test the hypotheses that expectations also induce these effects (i vs ii), although with a weaker amplitude (i vs iii). Related to the behavioral findings, wWe didn’t not confirm any of our hypotheses for behavioral improvement induced by caffeine intakeon either of the investigate tasks’ measures. Regarding the neurophysiological findingsAt the electrophysiological level, however, we confirmed that caffeine effects on increased the attentional P3 and inhibition P3 components amplitude, but not on the response conflict N2 component. Additionally, wWe dodid not confirm provide evidence that expectations do not influence any of the investigate electrophysiological indexeices. Finally, we confirm that that expectations effects are smaller compared to caffeine effects but only for the Global Field Power parameter related to the attentional P3 component. only for one of the investigated the attentional P3 component’s parameters, and that this effect was smaller than that of We conclude that Hence, previously identified caffeine effects at the behavioral level may have been overestimated and that if while expectations effects have any no influence on sustained attention and inhibitory control, they are small. XXCaffeine effects at the electrophysiological level indicate that it tends to modulate brain areas underlying attentional mechanisms in both RVIP and Go/NoGo tasks rather than being specific to inhibitory control processes.

ABSTRACT Placebo effects (PE) are defined as the beneficial psychophysiological outcomes of an intervention that are not attributable to its inherent properties; PE thus follow from individuals’ expectations about the effects of the intervention. The present study aims aimed at examining how expectations influence neurocognitive processes. We will addressed this question by contrasting three double-blinded within-subjects experimental conditions in which participants are were given decaffeinated coffee, while being told they have had received caffeinated (condition i) or decaffeinated coffee (ii), and given caffeinated coffee while being told they have had received decaffeinated coffee (iii). After each of these three interventions, performance and electroencephalogram will bewas recorded at rest as well as during sustained attention Rapid Visual Information Processing task (RVIP) and a Go/NoGo motor inhibitory control task. We first aimed to confirm previous findings for caffeine-induced enhancement on these executive components and on their associated electrophysiological indexes (attentional P3 component, response conflict N2 and inhibition P3 components (ii vs iii contrast); and then to test the hypotheses that expectations also induce these effects (i vs ii), although with a weaker amplitude (i vs iii). Related to the behavioral findings, wWe didn’t not confirm any of our hypotheses for behavioral improvement induced by caffeine intakeon either of the investigate tasks’ measures. Regarding the neurophysiological findingsAt the electrophysiological level, however, we confirmed that caffeine effects on increased the attentional P3 and inhibition P3 components amplitude, but not on the response conflict N2 component. Additionally, wWe dodid not confirm provide evidence that expectations do not influence any of the investigate electrophysiological indexeices. Finally, we confirm that that expectations effects are smaller compared to caffeine effects but only for the Global Field Power parameter related to the attentional P3 component. only for one of the investigated the attentional P3 component’s parameters, and that this effect was smaller than that of We conclude that Hence, previously identified caffeine effects at the behavioral level may have been overestimated and that if while expectations effects have any no influence on sustained attention and inhibitory control, they are small. XXCaffeine effects at the electrophysiological level indicate that it tends to modulate brain areas underlying attentional mechanisms in both RVIP and Go/NoGo tasks rather than being specific to inhibitory control processes.