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Nocebo

About: Nocebo is a research topic. Over the lifetime, 648 publications have been published within this topic receiving 27953 citations. The topic is also known as: nocebo.


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Journal ArticleDOI
20 Feb 2004-Science
TL;DR: fMRI experiments found that placebo analgesia was related to decreased brain activity in pain-sensitive brain regions, including the thalamus, insula, and anterior cingulate cortex, and was associated with increased activity during anticipation of pain in the prefrontal cortex, providing evidence that placebos alter the experience of pain.
Abstract: The experience of pain arises from both physiological and psychological factors, including one's beliefs and expectations Thus, placebo treatments that have no intrinsic pharmacological effects may produce analgesia by altering expectations However, controversy exists regarding whether placebos alter sensory pain transmission, pain affect, or simply produce compliance with the suggestions of investigators In two functional magnetic resonance imaging (fMRI) experiments, we found that placebo analgesia was related to decreased brain activity in pain-sensitive brain regions, including the thalamus, insula, and anterior cingulate cortex, and was associated with increased activity during anticipation of pain in the prefrontal cortex, providing evidence that placebos alter the experience of pain

1,820 citations

Journal ArticleDOI
TL;DR: Promotion and integration of laboratory and clinical research will allow advances in the ethical use of placebo mechanisms that are inherent in routine clinical care, and encourage the use of treatments that stimulate placebo effects.

1,040 citations

Journal ArticleDOI
TL;DR: The demonstration of the involvement of placebo mechanisms inclinical trials and routine clinical practice has highlighted interesting considerations for clinical trial design and opened up opportunities for ethical enhancement of these mechanisms in clinical practice.
Abstract: Our understanding and conceptualization of the placebo effect has shifted in emphasis from a focus on the inert content of a physical placebo agent to the overall simulation of a therapeutic intervention. Research has identified many types of placebo responses driven by different mechanisms depending on the particular context wherein the placebo is given. Some placebo responses, such as analgesia, are initiated and maintained by expectations of symptom change and changes in motivation/emotions. Placebo factors have neurobiological underpinnings and actual effects on the brain and body. They are not just response biases. Other placebo responses result from less conscious processes, such as classical conditioning in the case of immune, hormonal, and respiratory functions. The demonstration of the involvement of placebo mechanisms in clinical trials and routine clinical practice has highlighted interesting considerations for clinical trial design and opened up opportunities for ethical enhancement of these mechanisms in clinical practice.

1,022 citations

Journal ArticleDOI
10 Aug 2001-Science
TL;DR: In vivo evidence is provided for substantial release of endogenous dopamine in the striatum of PD patients in response to placebo, indicating that the placebo effect in PD is powerful and is mediated through activation of the damaged nigrostriatal dopamine system.
Abstract: The power of placebos has long been recognized for improving numerous medical conditions such as Parkinson's disease (PD). Little is known, however, about the mechanism underlying the placebo effect. Using the ability of endogenous dopamine to compete for [11C]raclopride binding as measured by positron emission tomography, we provide in vivo evidence for substantial release of endogenous dopamine in the striatum of PD patients in response to placebo. Our findings indicate that the placebo effect in PD is powerful and is mediated through activation of the damaged nigrostriatal dopamine system.

908 citations

Journal ArticleDOI
TL;DR: The findings show that cognitive factors and conditioning are balanced in different ways in placebo analgesia, and this balance is crucial for the activation of opioid or nonopioid systems.
Abstract: We investigated the mechanisms underlying the activation of endogenous opioids in placebo analgesia by using the model of human experimental ischemic arm pain. Different types of placebo analgesic responses were evoked by means of cognitive expectation cues, drug conditioning, or a combination of both. Drug conditioning was performed by means of either the opioid agonist morphine hydrochloride or the nonopioid ketorolac tromethamine. Expectation cues produced placebo responses that were completely blocked by the opioid antagonist naloxone. Expectation cues together with morphine conditioning produced placebo responses that were completely antagonized by naloxone. Morphine conditioning alone (without expectation cues) induced a naloxone-reversible placebo effect. By contrast, ketorolac conditioning together with expectation cues elicited a placebo effect that was blocked by naloxone only partially. Ketorolac conditioning alone produced placebo responses that were naloxone-insensitive. Therefore, we evoked different types of placebo responses that were either naloxone-reversible or partially naloxone-reversible or, otherwise, naloxone-insensitive, depending on the procedure used to evoke the placebo response. These findings show that cognitive factors and conditioning are balanced in different ways in placebo analgesia, and this balance is crucial for the activation of opioid or nonopioid systems. Expectation triggers endogenous opioids, whereas conditioning activates specific subsystems. In fact, if conditioning is performed with opioids, placebo analgesia is mediated via opioid receptors, if conditioning is performed with nonopioid drugs, other nonopioid mechanisms result to be involved.

811 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202347
202297
202161
202054
201973
201853