Placebo effects in laser-evoked pain potentials

Wager, Tor D.; Matre, Dagfinn; Casey, Kenneth L.

doi:10.1016/j.bbi.2006.01.007

Cited by 125 publications

(99 citation statements)

References 53 publications

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“…6). Before scanning, warm and noxious temperatures were chosen on an individualized basis for each subject (3,26,46). Warm temperatures (44-46.5°C) were chosen at calibration level 2.…”

Section: Methodsmentioning

confidence: 99%

“…After calibration, placebo and control treatments were applied to two regions of the volar forearm of each volunteer. As in previous work, before scanning, subjects also underwent an expectancy manipulation phase in which belief in the placebo was strengthened (3,26,46). The manipulation involves surreptitiously presenting reduced temperatures during stimulation on placebo-treated skin (using different skin areas from those used in scanning).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Placebo effects on human μ-opioid activity during pain

Wager

Scott

Zubieta

2007

Proc. Natl. Acad. Sci. U.S.A.

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528

427

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Placebo-induced expectancies have been shown to decrease pain in a manner reversible by opioid antagonists, but little is known about the central brain mechanisms of opioid release during placebo treatment. This study examined placebo effects in pain by using positron-emission tomography with [ 11 C]carfentanil, which measures regional -opioid receptor availability in vivo. Noxious thermal stimulation was applied at the same temperature for placebo and control conditions. Placebo treatment affected endogenous opioid activity in a number of predicted -opioid receptorrich regions that play central roles in pain and affect, including periaqueductal gray and nearby dorsal raphe and nucleus cuneiformis, amygdala, orbitofrontal cortex, insula, rostral anterior cingulate, and lateral prefrontal cortex. These regions appeared to be subdivided into two sets, one showing placebo-induced opioid activation specific to noxious heat and the other showing placeboinduced opioid reduction during warm stimulation in anticipation of pain. These findings suggest that a mechanism of placebo analgesia is the potentiation of endogenous opioid responses to noxious stimuli. Opioid activity in many of these regions was correlated with placebo effects in reported pain. Connectivity analyses on individual differences in endogenous opioid system activity revealed that placebo treatment increased functional connectivity between the periaqueductal gray and rostral anterior cingulate, as hypothesized a priori, and also increased connectivity among a number of limbic and prefrontal regions, suggesting increased functional integration of opioid responses. Overall, the results suggest that endogenous opioid release in core affective brain regions is an integral part of the mechanism whereby expectancies regulate affective and nociceptive circuits.neuroimaging ͉ periaqueductal gray ͉ expectancy ͉ affective neuroscience

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“…6). Before scanning, warm and noxious temperatures were chosen on an individualized basis for each subject (3,26,46). Warm temperatures (44-46.5°C) were chosen at calibration level 2.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Placebo effects on human μ-opioid activity during pain

Wager

Scott

Zubieta

2007

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

528

427

View full text Add to dashboard Cite

show abstract

“…4). Electroencephalography (EEG) studies have further confirmed that placebo analgesia is associated with reduced amplitudes of event-related potentials to experimental pain stimuli (Wager et al, 2006;Watson et al, 2007;Aslaksen et al, 2011). Evidence from spinal cord forced magnetic resonance imaging (fMRI), which only recently became technically feasible in both humans and animals, has revealed that pain-related activity in the ipsilateral dorsal horn, corresponding to painful stimulation, is substantially reduced under placebo (Eippert et al, 2009b) and rises under expectations of increased pain (nocebo) .…”

Section: A Painmentioning

confidence: 98%

Neuro-Bio-Behavioral Mechanisms of Placebo and Nocebo Responses: Implications for Clinical Trials and Clinical Practice

Schedlowski¹,

Enck²,

Rief³

et al. 2015

Pharmacol Rev

263

257

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“…It has been shown that this may occur through both expectation and conditioning mechanisms, although expectations and emotions seem to play a fundamental role (Benedetti et al, 2003;Price et al, 2005). Most of our knowledge about the placebo effect comes from the field of pain, in which both a neuropharmacological approach with opioid antagonists (Levine et al, 1978;Grevert et al, 1983;Levine and Gordon, 1984;Amanzio and Benedetti, 1999;Benedetti et al, 1999;Hoffman et al, 2005) and, more recently, brain imaging techniques (Petrovic et al, 2002(Petrovic et al, , 2005Wager et al, 2004Wager et al, , 2006Zubieta et al, 2005;Keltner et al, 2006;Kong et al, 2006) have been used.…”

Section: Introductionmentioning

confidence: 99%

The Biochemical and Neuroendocrine Bases of the Hyperalgesic Nocebo Effect

Benedetti¹,

Amanzio²,

Vighetti³

et al. 2006

J. Neurosci.

366

247

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Despite the increasing research on placebos in recent times, little is known about the nocebo effect, a phenomenon that is opposite to the placebo effect and whereby expectations of symptom worsening play a crucial role. By studying experimental ischemic arm pain in healthy volunteers and by using a neuropharmacological approach, we found that verbally induced nocebo hyperalgesia was associated to hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, as assessed by means of adrenocorticotropic hormone and cortisol plasma concentrations. Both nocebo hyperalgesia and HPA hyperactivity were antagonized by the benzodiazepine diazepam, suggesting that anxiety played a major role in these effects. The administration of the mixed cholecystokinin (CCK) type-A/B receptor antagonist proglumide blocked nocebo hyperalgesia completely but had no effect on HPA hyperactivity, which suggests a specific involvement of CCK in the hyperalgesic but not in the anxiety component of the nocebo effect. Importantly, both diazepam and proglumide did not show analgesic properties on basal pain, because they acted only on the nocebo-induced pain increase. These data indicate a close relationship between anxiety and nocebo hyperalgesia, in which the CCKergic systems play a key role in anxiety-induced hyperalgesia. These results, together with previous findings showing that placebo analgesia is mediated by endogenous opioids, suggest that the analgesic placebo/ hyperalgesic nocebo phenomenon may involve the opposite activation of endogenous opioidergic and CCKergic systems.

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Placebo effects in laser-evoked pain potentials

Cited by 125 publications

References 53 publications

Placebo effects on human μ-opioid activity during pain

Placebo effects on human μ-opioid activity during pain

Neuro-Bio-Behavioral Mechanisms of Placebo and Nocebo Responses: Implications for Clinical Trials and Clinical Practice

The Biochemical and Neuroendocrine Bases of the Hyperalgesic Nocebo Effect

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