Expectation to feel more pain disrupts the habituation of laser-pain rating and laser-evoked potential amplitudes

Pazzaglia, Costanza; Testani, Elisa; Giordano, Rocco; Padua, Luca; Valeriani, Massimiliano

doi:10.1016/j.neuroscience.2016.07.027

Cited by 19 publications

(16 citation statements)

References 34 publications

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“… 52 , 58 , 63 For example, the mere expectation to feel more pain after the administration of an inert medication affects a laser-induced pain experience and related laser-evoked potential amplitude in the treated hand. 62 The magnitude of nocebo effects were not potentiated by conditioning as occurs for the positive placebo effects. 34 Changes in EEG activity, namely, an enhancement of low alpha (8–10 Hz) activity have been linked to nocebo manipulations that increase intensity and unpleasantness of heat-induced pain.…”

Section: Biochemical and Neurophysiological Mechanismsmentioning

confidence: 93%

Nocebo and pain: an overview of the psychoneurobiological mechanisms

Blasini

Corsi

Klinger

et al. 2017

PR9

107

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Introduction Nocebo effects are defined as adverse events related to negative expectations and learning processes that are involved in the modulation of the descending pain pathways. Research over the last couple of decades has illustrated that behavioral, psychoneurobiological and functional changes occur during nocebo-induced pain processing. Objectives We aimed to review published human and non-human research on algesia and hyperalgesia resulting from negative expectations and nocebo effects. Methods Herein, we searched and comprehensively reviewed scientific literature providing informative knowledge about the psychoneurobiological bases of the nocebo effect in the field of pain with an emphasis on how pain processes are shaped by both cognitive and non-cognitive factors. Results Negative expectations are formed through verbal suggestions of heightened pain, prior nociceptive and painful experiences and observation of pain in others. Susceptibility to the nocebo effect can be also influenced by genetic variants, conscious and nonconscious learning processes, personality traits and psychological factors. Moreover, providers’ behaviors, environmental cues and the appearance of medical devices can induce negative expectations that dramatically influence pain perception and processing in a variety of pain modalities and patient populations. Conclusion Importantly, we concluded that nocebo studies outline how individual expectations may lead to physiological changes underpinning the central integration and processing of magnified pain signaling. Further research is needed to develop strategies that can identify nocebo-vulnerable pain patients in order to optimize the psychosocial and therapeutic context in which the clinical encounter occurs, with the ultimate purpose of improving clinical outcomes.

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Section: Biochemical and Neurophysiological Mechanismsmentioning

confidence: 93%

Nocebo and pain: an overview of the psychoneurobiological mechanisms

Blasini

Corsi

Klinger

et al. 2017

PR9

107

View full text Add to dashboard Cite

show abstract

“…When inducing placebo hypoalgesia or nocebo hyperalgesia by verbal suggestions alone, results are inconsistent, sometimes resulting only in weak [ 24 ] or even no effects [ 25 , 29 , 30 ] and at other times leading to robust pain reduction [ 10 , 31 ] or increase [ 10 , 32 ]. Some studies indicate that learning is less important in nocebo hyperalgesia compared to placebo hypoalgesia, but direct comparisons are rare [ 24 , 33 ]. Interestingly, while placebo effects induced by expectation can be antagonized by the opioid antagonist naloxone, conditioned placebo effects can be antagonized by naloxone when the pharmacological conditioning had been performed with an opioid and by cannabinoid receptor antagonists when it had been performed with ketorolac, a nonsteroidal anti-inflammatory drug [ 34 , 35 ].…”

Section: Development Of Placebo and Nocebo Effectsmentioning

confidence: 99%

The Underestimated Significance of Conditioning in Placebo Hypoalgesia and Nocebo Hyperalgesia

Bräscher

Witthöft

Becker

2018

Pain Research and Management

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Placebo and nocebo effects are intriguing phenomena in pain perception with important implications for clinical research and practice because they can alleviate or increase pain. According to current theoretical accounts, these effects can be shaped by verbal suggestions, social observational learning, and classical conditioning and are necessarily mediated by explicit expectation. In this review, we focus on the contribution of conditioning in the induction of placebo hypoalgesia and nocebo hyperalgesia and present accumulating evidence that conditioning independent from explicit expectation can cause these effects. Especially studies using subliminal stimulus presentation and implicit conditioning (i.e., without contingency awareness) that bypass the development of explicit expectation suggest that conditioning without explicit expectation can lead to placebo and nocebo effects in pain perception. Because only few studies have investigated clinical samples, the picture seems less clear when it comes to patient populations with chronic pain. However, conditioning appears to be a promising means to optimize treatment. In order to get a better insight into the mechanisms of placebo and nocebo effects in pain and the possible benefits of conditioning compared to explicit expectation, future studies should carefully distinguish both methods of induction.

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“…Not only the way in which the information is given but also the words that are used can prepare subject to expect something. For that reason in our protocol we did not mention the words “pain” or “analgesia,” as we demonstrated that the mere verbal suggestion in healthy subject was able to produce either placebo or nocebo effects ( Colloca et al, 2008 ; Pazzaglia et al, 2016 ). Seen in this light, Tamura’ results could have been influenced by nocebo mechanisms which possibly affected laser-pain rating and LEP amplitude more than rTMS.…”

Section: Discussionmentioning

confidence: 99%

Low-Frequency rTMS of the Primary Motor Area Does Not Modify the Response of the Cerebral Cortex to Phasic Nociceptive Stimuli

et al. 2018

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Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive technique of cortical stimulation. Although the exact mechanism of action is not clearly understood, it has been postulated that rTMS action on pain depends most on stimulation sites and stimulation parameters. Most studies concern high-frequency rTMS of the primary motor cortex (M1). High-frequency rTMS over motor cortex seems to induce an analgesic effect while contrasting results were reported after low-frequency rTMS. The aim of the current study was to investigate the effects of 1 Hz rTMS stimulation over the left primary motor cortex on subjective laser pain rating and laser evoked potential (LEP) amplitudes in healthy subjects. Subjects underwent two different sessions (real and sham rTMS) according to a cross-sectional design. In each session, LEPs and laser-pain rating to stimulation of both right and left hand dorsum were collected before 1 Hz rTMS over the left M1 area (baseline), which lasted 20 min. Then, LEPs and laser-pain rating were measured immediately after rTMS (T0), after 20 min from T0 (T0+20), and after 40 min from T0 (T0+40). We could not find any modification of both laser-pain rating and LEP parameters (latencies and amplitudes) following 1 Hz rTMS. Therefore, our results show that the low-frequency rTMS of the M1 area does not change the response of the cerebral cortex to pain.

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Expectation to feel more pain disrupts the habituation of laser-pain rating and laser-evoked potential amplitudes

Cited by 19 publications

References 34 publications

Nocebo and pain: an overview of the psychoneurobiological mechanisms

Nocebo and pain: an overview of the psychoneurobiological mechanisms

The Underestimated Significance of Conditioning in Placebo Hypoalgesia and Nocebo Hyperalgesia

Low-Frequency rTMS of the Primary Motor Area Does Not Modify the Response of the Cerebral Cortex to Phasic Nociceptive Stimuli

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