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      Reconceptualizing anhedonia: novel perspectives on balancing the pleasure networks in the human brain

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          Abstract

          Anhedonia, the lack of pleasure, has been shown to be a critical feature of a range of psychiatric disorders. Yet, it is currently measured primarily through subjective self-reports and as such has been difficult to submit to rigorous scientific analysis. New insights from affective neuroscience hold considerable promise in improving our understanding of anhedonia and for providing useful objective behavioral measures to complement traditional self-report measures, potentially leading to better diagnoses and novel treatments. Here, we review the state-of-the-art of hedonia research and specifically the established mechanisms of wanting, liking, and learning. Based on this framework we propose to conceptualize anhedonia as impairments in some or all of these processes, thereby departing from the longstanding view of anhedonia as solely reduced subjective experience of pleasure. We discuss how deficits in each of the reward components can lead to different expressions, or subtypes, of anhedonia affording novel ways of measurement. Specifically, we review evidence suggesting that patients suffering from depression and schizophrenia show impairments in wanting and learning, while some aspects of conscious liking seem surprisingly intact. Furthermore, the evidence suggests that anhedonia is heterogeneous across psychiatric disorders, depending on which parts of the pleasure networks are most affected. This in turn has implications for diagnosis and treatment of anhedonia.

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          Twelve-month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States.

          Estimates of 12-month and lifetime prevalence and of lifetime morbid risk (LMR) of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) anxiety and mood disorders are presented based on US epidemiological surveys among people aged 13+. The presentation is designed for use in the upcoming DSM-5 manual to provide more coherent estimates than would otherwise be available. Prevalence estimates are presented for the age groups proposed by DSM-5 workgroups as the most useful to consider for policy planning purposes. The LMR/12-month prevalence estimates ranked by frequency are as follows: major depressive episode: 29.9%/8.6%; specific phobia: 18.4/12.1%; social phobia: 13.0/7.4%; post-traumatic stress disorder: 10.1/3.7%; generalized anxiety disorder: 9.0/2.0%; separation anxiety disorder: 8.7/1.2%; panic disorder: 6.8%/2.4%; bipolar disorder: 4.1/1.8%; agoraphobia: 3.7/1.7%; obsessive-compulsive disorder: 2.7/1.2. Four broad patterns of results are most noteworthy: first, that the most common (lifetime prevalence/morbid risk) lifetime anxiety-mood disorders in the United States are major depression (16.6/29.9%), specific phobia (15.6/18.4%), and social phobia (10.7/13.0%) and the least common are agoraphobia (2.5/3.7%) and obsessive-compulsive disorder (2.3/2.7%); second, that the anxiety-mood disorders with the earlier median ages-of-onset are phobias and separation anxiety disorder (ages 15-17) and those with the latest are panic disorder, major depression, and generalized anxiety disorder (ages 23-30); third, that LMR is considerably higher than lifetime prevalence for most anxiety-mood disorders, although the magnitude of this difference is much higher for disorders with later than earlier ages-of-onset; and fourth, that the ratio of 12-month to lifetime prevalence, roughly characterizing persistence, varies meaningfully in ways consistent with independent evidence about differential persistence of these disorders. Copyright © 2012 John Wiley & Sons, Ltd.
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            The neural basis of drug craving: an incentive-sensitization theory of addiction.

            This paper presents a biopsychological theory of drug addiction, the 'Incentive-Sensitization Theory'. The theory addresses three fundamental questions. The first is: why do addicts crave drugs? That is, what is the psychological and neurobiological basis of drug craving? The second is: why does drug craving persist even after long periods of abstinence? The third is whether 'wanting' drugs (drug craving) is attributable to 'liking' drugs (to the subjective pleasurable effects of drugs)? The theory posits the following. (1) Addictive drugs share the ability to enhance mesotelencephalic dopamine neurotransmission. (2) One psychological function of this neural system is to attribute 'incentive salience' to the perception and mental representation of events associated with activation of the system. Incentive salience is a psychological process that transforms the perception of stimuli, imbuing them with salience, making them attractive, 'wanted', incentive stimuli. (3) In some individuals the repeated use of addictive drugs produces incremental neuroadaptations in this neural system, rendering it increasingly and perhaps permanently, hypersensitive ('sensitized') to drugs and drug-associated stimuli. The sensitization of dopamine systems is gated by associative learning, which causes excessive incentive salience to be attributed to the act of drug taking and to stimuli associated with drug taking. It is specifically the sensitization of incentive salience, therefore, that transforms ordinary 'wanting' into excessive drug craving. (4) It is further proposed that sensitization of the neural systems responsible for incentive salience ('for wanting') can occur independently of changes in neural systems that mediate the subjective pleasurable effects of drugs (drug 'liking') and of neural systems that mediate withdrawal. Thus, sensitization of incentive salience can produce addictive behavior (compulsive drug seeking and drug taking) even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family. We review evidence for this view of addiction and discuss its implications for understanding the psychology and neurobiology of addiction.
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              Reconsidering anhedonia in depression: lessons from translational neuroscience.

              Anhedonia is a core symptom of major depressive disorder (MDD), the neurobiological mechanisms of which remain poorly understood. Despite decades of speculation regarding the role of dopamine (DA) in anhedonic symptoms, empirical evidence has remained elusive, with frequent reports of contradictory findings. In the present review, we argue that this has resulted from an underspecified definition of anhedonia, which has failed to dissociate between consummatory and motivational aspects of reward behavior. Given substantial preclinical evidence that DA is involved primarily in motivational aspects of reward, we suggest that a refined definition of anhedonia that distinguishes between deficits in pleasure and motivation is essential for the purposes of identifying its neurobiological substrates. Moreover, bridging the gap between preclinical and clinical models of anhedonia may require moving away from the conceptualization of anhedonia as a steady-state, mood-like phenomena. Consequently, we introduce the term "decisional anhedonia" to address the influence of anhedonia on reward decision-making. These proposed modifications to the theoretical definition of anhedonia have implications for research, assessment and treatment of MDD. Copyright © 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Front Behav Neurosci
                Front Behav Neurosci
                Front. Behav. Neurosci.
                Frontiers in Behavioral Neuroscience
                Frontiers Media S.A.
                1662-5153
                11 March 2015
                2015
                : 9
                : 49
                Affiliations
                [1] 1Center of Functionally Integrative Neuroscience (CFIN), University of Aarhus Aarhus, Denmark
                [2] 2Department of Psychiatry, Warneford Hospital, University of Oxford Oxford, UK
                [3] 3Centre for Alcohol and Drug Research, School of Business and Social Sciences, University of Aarhus Aarhus, Denmark
                [4] 4Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, LA, USA
                Author notes

                Edited by: Raymond C. K. Chan, Institute of Psychology, Chinese Academy of Sciences, China

                Reviewed by: Siri Leknes, University of Oslo, Norway; Nuno Sousa, ICVS, University of Minho, Portugal; Predrag Petrovic, Wellcome Trust Centre for Neuroimaging, UK

                *Correspondence: Morten L. Kringelbach, Department of Psychiatry, Warneford Hospital, University of Oxford, Oxford, OX3 7JX, UK e-mail: morten.kringelbach@ 123456psych.ox.ac.uk

                This article was submitted to the journal Frontiers in Behavioral Neuroscience.

                Article
                10.3389/fnbeh.2015.00049
                4356228
                25814941
                8ef9f54d-29bc-4da3-b19d-dfd6f88329a7
                Copyright © 2015 Rømer Thomsen, Whybrow and Kringelbach.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 21 November 2014
                : 11 February 2015
                Page count
                Figures: 4, Tables: 0, Equations: 0, References: 252, Pages: 23, Words: 22141
                Categories
                Neuroscience
                Review Article

                Neurosciences
                wanting,liking,learning,dopamine,opioids,orbitofrontal cortex,depression,schizophrenia
                Neurosciences
                wanting, liking, learning, dopamine, opioids, orbitofrontal cortex, depression, schizophrenia

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