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      Reward Processing under Chronic Pain from the Perspective of “Liking” and “Wanting”: A Narrative Review

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          Abstract

          The therapeutic goals of patients with chronic pain are not only to relieve pain but also to improve the quality of life. Chronic pain negatively affects various aspects of daily life, such as by decreasing the motivation to work and reward sensitivity, which may lead to difficulties in daily life or even unemployment. Human and animal studies have shown that chronic pain damages reward processing; the exploration of associated internal mechanisms may aid the development of treatments to repair this damage. Incentive salience theory, used widely to describe reward processing, divides this processing into “liking” (reward-induced hedonic sensory impact) and “wanting” (reward-induced motivation) components. It has been employed to explain pathological changes in reward processing induced by psychiatric disorders. In this review, we summarize the findings of studies of reward processing under chronic pain and examine the effects of chronic pain on “liking” and “wanting.” Evidence indicates that chronic pain compromises the “wanting” component of reward processing; we also discuss the neural mechanisms that may mediate this effect. We hope that this review aids the development of therapies to improve the quality of life of patients with chronic pain.

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          The debate over dopamine's role in reward: the case for incentive salience.

          Debate continues over the precise causal contribution made by mesolimbic dopamine systems to reward. There are three competing explanatory categories: 'liking', learning, and 'wanting'. Does dopamine mostly mediate the hedonic impact of reward ('liking')? Does it instead mediate learned predictions of future reward, prediction error teaching signals and stamp in associative links (learning)? Or does dopamine motivate the pursuit of rewards by attributing incentive salience to reward-related stimuli ('wanting')? Each hypothesis is evaluated here, and it is suggested that the incentive salience or 'wanting' hypothesis of dopamine function may be consistent with more evidence than either learning or 'liking'. In brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic 'liking' for sensory pleasures. Other recent evidence indicates that dopamine is not needed for new learning, and not sufficient to directly mediate learning by causing teaching or prediction signals. By contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. Dopamine appears necessary for normal 'wanting', and dopamine activation can be sufficient to enhance cue-triggered incentive salience. Drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Such drugs interact with incentive salience integrations of Pavlovian associative information with physiological state signals. That interaction sets the stage to cause compulsive 'wanting' in addiction, but also provides opportunities for experiments to disentangle 'wanting', 'liking', and learning hypotheses. Results from studies that exploited those opportunities are described here. In short, dopamine's contribution appears to be chiefly to cause 'wanting' for hedonic rewards, more than 'liking' or learning for those rewards.
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            Goal constructs in psychology: Structure, process, and content.

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              Addiction.

              The development of addiction involves a transition from casual to compulsive patterns of drug use. This transition to addiction is accompanied by many drug-induced changes in the brain and associated changes in psychological functions. In this article we present a critical analysis of the major theoretical explanations of how drug-induced alterations in psychological function might cause a transition to addiction. These include: (a) the traditional hedonic view that drug pleasure and subsequent unpleasant withdrawal symptoms are the chief causes of addiction; (b) the view that addiction is due to aberrant learning, especially the development of strong stimulus-response habits; (c) our incentive-sensitization view, which suggests that sensitization of a neural system that attributes incentive salience causes compulsive motivation or "wanting" to take addictive drugs; and (d) the idea that dysfunction of frontal cortical systems, which normally regulate decision making and inhibitory control over behavior, leads to impaired judgment and impulsivity in addicts.
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                Author and article information

                Contributors
                Journal
                Pain Res Manag
                Pain Res Manag
                PRM
                Pain Research & Management
                Hindawi
                1203-6765
                1918-1523
                2019
                21 April 2019
                : 2019
                : 6760121
                Affiliations
                1CAS Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing 100101, China
                2Department of Psychology, University of Chinese Academy of Sciences, Beijing 100049, China
                Author notes

                Academic Editor: Monika I. Hasenbring

                Author information
                http://orcid.org/0000-0003-2814-4017
                http://orcid.org/0000-0002-2879-3386
                http://orcid.org/0000-0002-7477-7547
                http://orcid.org/0000-0002-1662-928X
                Article
                10.1155/2019/6760121
                6501242
                f8eec920-66fd-4fc6-916d-f5626be18d83
                Copyright © 2019 Xinhe Liu et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 3 January 2019
                : 6 March 2019
                : 4 April 2019
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 31671140
                Award ID: 31271092
                Award ID: 31471061
                Funded by: Chinese Academy of Sciences
                Award ID: KLMH 2014G01
                Award ID: KLMH2016K02
                Funded by: CAS/SAFEA International Partnership Program for Creative Research Teams
                Award ID: Y2CX131003
                Categories
                Review Article

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