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Neuroscience and Biobehavioral Reviews Jun 2016The resurgence of interest in anhedonia within major depression has been fuelled by clinical trials demonstrating its utility in predicting antidepressant response as... (Review)
Review
The resurgence of interest in anhedonia within major depression has been fuelled by clinical trials demonstrating its utility in predicting antidepressant response as well as recent conceptualizations focused on the role and manifestation of anhedonia in depression. Historically, anhedonia has been understood as a "loss of pleasure", yet neuropsychological and neurobiological studies reveal a multifaceted reconceptualization that emphasizes different facets of hedonic function, including desire, effort/motivation, anticipation and consummatory pleasure. To ensure generalizability across studies, evaluation of the available subjective and objective methods to assess anhedonia is necessary. The majority of research regarding anhedonia and its neurobiological underpinnings comes from preclinical research, which uses primary reward (e.g. food) to probe hedonic responding. In contrast, behavioural studies in humans primarily use secondary reward (e.g. money) to measure many aspects of reward responding, including delay discounting, response bias, prediction error, probabilistic reversal learning, effort, anticipation and consummatory pleasure. The development of subjective scales to measure anhedonia has also increased in the last decade. This review will assess the current methodology to measure anhedonia, with a focus on scales and behavioural tasks in humans. Limitations of current work and recommendations for future studies are discussed.
Topics: Anhedonia; Depression; Humans; Motivation; Reward
PubMed: 26959336
DOI: 10.1016/j.neubiorev.2016.03.004 -
Trends in Neurosciences Jan 2012Anhedonia, or markedly diminished interest or pleasure, is a hallmark symptom of major depression, schizophrenia and other neuropsychiatric disorders. Over the past... (Review)
Review
Anhedonia, or markedly diminished interest or pleasure, is a hallmark symptom of major depression, schizophrenia and other neuropsychiatric disorders. Over the past three decades, the clinical definition of anhedonia has remained relatively unchanged, although cognitive psychology and behavioral neuroscience have expanded our understanding of other reward-related processes. Here, we review the neural bases of the construct of anhedonia that reflects deficits in hedonic capacity and also closely linked to the constructs of reward valuation, decision-making, anticipation and motivation. The neural circuits subserving these reward-related processes include the ventral striatum, prefrontal cortical regions, and afferent and efferent projections. An understanding of anhedonia and other reward-related constructs will facilitate the diagnosis and treatment of disorders that include reward deficits as key symptoms.
Topics: Anhedonia; Animals; Humans; Mental Disorders; Neural Pathways; Neurobiology; Prefrontal Cortex; Reward
PubMed: 22177980
DOI: 10.1016/j.tins.2011.11.005 -
Psychiatria Danubina Jun 2019The perception of reward exerts a powerful influence on human behavior. While anhedonia might occur in healthy individuals, its prevalence and severity are much higher... (Review)
Review
The perception of reward exerts a powerful influence on human behavior. While anhedonia might occur in healthy individuals, its prevalence and severity are much higher in psychiatric patients, particularly those with depression and schizophrenia. Anhedonia is a negative symptom, and presumably a trait marker in schizophrenia. Recent research confirmed that anhedonia is a complex construct, consisting of anticipatory, consummatory, and reward learning components. In general, schizophrenia patients show anticipation deficits, and a substantial portion of them have physical (PA) and social anhedonia (SA). The relationship between anhedonia and psychopathology appears bidirectional. While gene-environment interactions affect reward circuity, anhedonia modulates clinical features, such as suicidality and nicotine consumption. Future clinical research employing longitudinal designs may shed more light on the dynamics and treatment of anhedonia in schizophrenia.
Topics: Anhedonia; Depression; Humans; Reward; Schizophrenia; Schizophrenic Psychology
PubMed: 31158114
DOI: No ID Found -
Current Topics in Behavioral... 2022Neurodegenerative diseases are increasingly recognised to be an important cause of brain disorders, particularly in late age. Associated with a wide range of... (Review)
Review
Neurodegenerative diseases are increasingly recognised to be an important cause of brain disorders, particularly in late age. Associated with a wide range of pathologies, they lead to progressive loss of neurons in different regions of the nervous system. Although anhedonia is common in a variety of neurodegenerative diseases, to date it has not been extensively studied in most of these conditions. Here we review the current literature on studies assessing the association between anhedonia and neurodegenerative diseases including Parkinson's Disease, Dementia with Lewy Bodies, Parkinson's Plus Syndromes, Alzheimer's Disease, Vascular Dementia, Frontotemporal Dementia, Amyotrophic Lateral Sclerosis and Huntington's Disease. Much of the research has been conducted in Parkinson's disease where it is evident that there are strong links between apathy (loss of motivation) and anhedonia, although the two syndromes can be dissociated. Intriguingly, drugs that improve apathy can also lead to amelioration of anhedonia in some cases. Overlaps between the two syndromes may also exist across other neurodegenerative conditions, including Frontotemporal Dementia in which imaging has revealed atrophy of both common brain regions associated with anhedonia and apathy, as well as a set of unique brain regions associated with anhedonia. A transdiagnostic perspective might be helpful to investigate whether a common network of brain regions is dysfunctional with anhedonia across neurodegenerative conditions.
Topics: Alzheimer Disease; Anhedonia; Brain; Humans; Neurodegenerative Diseases; Parkinson Disease
PubMed: 35435648
DOI: 10.1007/7854_2022_352 -
Depression and Anxiety Oct 2016Anhedonia, or loss of interest or pleasure in usual activities, is characteristic of depression, some types of anxiety, as well as substance abuse and schizophrenia....
Anhedonia, or loss of interest or pleasure in usual activities, is characteristic of depression, some types of anxiety, as well as substance abuse and schizophrenia. Anhedonia is a predictor of poor long-term outcomes, including suicide, and poor treatment response. Because extant psychological and pharmacological treatments are relatively ineffective for anhedonia, there is an unmet therapeutic need for this high-risk symptom. Current psychological and drug treatments for anxiety and depression focus largely on reducing excesses in negative affect rather than improving deficits in positive affect. Recent advances in affective neuroscience posit that anhedonia is associated with deficits in the appetitive reward system, specifically the anticipation, consumption, and learning of reward. In this paper, we review the evidence for positive affect as a symptom cluster, and its neural underpinnings, and introduce a novel psychological treatment for anxiety and depression that targets appetitive responding. First, we review anhedonia in relation to positive and negative valence systems and current treatment approaches. Second, we discuss the evidence linking anhedonia to biological, experiential, and behavioral deficits in the reward subsystems. Third, we describe the therapeutic approach for Positive Affect Treatment (PAT), an intervention designed to specifically target deficits in reward sensitivity.
Topics: Affect; Anhedonia; Anticipation, Psychological; Anxiety Disorders; Appetitive Behavior; Brain; Depressive Disorder; Humans; Motivation; Psychotherapy; Reward
PubMed: 27699943
DOI: 10.1002/da.22490 -
The International Journal of... Feb 2019Pleasure and motivation are important factors for goal-directed behavior and well-being in both animals and humans. Intact hedonic capacity requires an undisturbed... (Review)
Review
Pleasure and motivation are important factors for goal-directed behavior and well-being in both animals and humans. Intact hedonic capacity requires an undisturbed interplay between a number of different brain regions and transmitter systems. Concordantly, dysfunction of networks encoding for reward have been shown in depression and other psychiatric disorders. The development of technological possibilities to investigate connectivity on a functional level in humans and to directly influence networks in animals using optogenetics among other techniques has provided new important insights in this field of research.In this review, we aim to provide an overview on the neurobiological substrates of anhedonia on a network level. For this purpose, definition of anhedonia and the involved reward components are described first, then current data on reward networks in healthy individuals and in depressed patients are summarized, and the roles of different neurotransmitter systems involved in reward processing are specified. Based on this information, the impact of different therapeutic approaches on reward processing is described with a particular focus on deep brain stimulation (DBS) as a possibility for a direct modulation of human brain structures in vivo.Overall, results of current studies emphasize the importance of anhedonia in psychiatric disorders and the relevance of targeting this phenotype for a successful psychiatric treatment. However, more data incorporating these results for the refinement of methodological approaches are needed to be able to develop individually tailored therapeutic concepts based on both clinical and neurobiological profiles of patients.
Topics: Anhedonia; Connectome; Depressive Disorder, Major; Humans; Nerve Net; Reward
PubMed: 30239748
DOI: 10.1093/ijnp/pyy081 -
The American Journal of Psychiatry Jul 2022Anhedonia-the loss of pleasure or lack of reactivity to pleasurable stimuli-remains a formidable treatment challenge across neuropsychiatric disorders. In major... (Review)
Review
Anhedonia-the loss of pleasure or lack of reactivity to pleasurable stimuli-remains a formidable treatment challenge across neuropsychiatric disorders. In major depressive disorder, anhedonia has been linked to poor disease course, worse response to psychological, pharmacological, and neurostimulation treatments, and increased suicide risk. Moreover, although some neural abnormalities linked to anhedonia normalize after successful treatment, several persist-for example, blunted activation of the ventral striatum to reward-related cues and reduced functional connectivity involving the ventral striatum. Critically, some of these abnormalities have also been identified in unaffected, never-depressed children of parents with major depressive disorder and have been found to prospectively predict the first onset of major depression. Thus, neural abnormalities linked to anhedonia may be promising targets for prevention. Despite increased appreciation of the clinical importance of anhedonia and its underlying neural mechanisms, important gaps remain. In this overview, the author first summarizes the extant knowledge about the pathophysiology of anhedonia, which may provide a road map toward novel treatment and prevention strategies, and then highlights several priorities to facilitate clinically meaningful breakthroughs. These include a need for 1) appropriately controlled clinical trials, especially those embracing an experimental therapeutics approach to probe target engagement; 2) novel preclinical models relevant to anhedonia, with stronger translational value; and 3) clinical scales that incorporate neuroscientific advances in our understanding of anhedonia. The author concludes by highlighting important future directions, emphasizing the need for an integrated, collaborative, cross-species, and multilevel approach to tackling anhedonic phenotypes.
Topics: Anhedonia; Depressive Disorder, Major; Humans; Magnetic Resonance Imaging; Reward; Ventral Striatum
PubMed: 35775159
DOI: 10.1176/appi.ajp.20220423 -
Current Topics in Behavioral... 2022Anhedonia, a loss of interest or pleasure in activities, is a transdiagnostic symptom that characterizes many individuals suffering from depression and anxiety. Most... (Review)
Review
Anhedonia, a loss of interest or pleasure in activities, is a transdiagnostic symptom that characterizes many individuals suffering from depression and anxiety. Most psychological interventions are designed to decrease negative affect rather than increase positive affect, and are largely ineffective for reducing anhedonia. More recently, affective neuroscience has been leveraged to inform treatments for anhedonia by targeting aspects of the Positive Valence Systems, including impairments in reward anticipation, reward responsiveness, and reward learning. In this chapter, we review the efficacy of treatments and, when possible, highlight links to reward constructs. Augmented behavioral approaches and targeted cognitive interventions designed to target reward anticipation, responsiveness, and learning show preliminary efficacy in reducing anhedonia, while there is a relative lack of treatments that target positive emotion regulation and reward devaluation. In addition to developing treatments that address these targets, the field will benefit from establishing standardized measurement of anhedonia across units of analysis, mapping mechanisms of change onto aspects of reward processing, and examining anhedonia outcomes in the long-term.
Topics: Anhedonia; Anxiety Disorders; Humans; Learning; Reward
PubMed: 34935116
DOI: 10.1007/7854_2021_291 -
Current Topics in Behavioral... 2022Anhedonia, or the decreased ability to experience pleasure, is a cardinal symptom of major depression that commonly occurs within other forms of psychopathology.... (Review)
Review
Anhedonia, or the decreased ability to experience pleasure, is a cardinal symptom of major depression that commonly occurs within other forms of psychopathology. Supportive of long-held theory that anhedonia represents a genetically influenced vulnerability marker for depression, evidence from twin studies suggests that it is moderately-largely heritable. However, the genomic sources of this heritability are just beginning to be understood. In this review, we survey what is known about the genomic architecture underlying anhedonia and related constructs. We briefly review twin and initial candidate gene studies before focusing on genome-wide association study (GWAS) and polygenic efforts. As large samples are needed to reliably detect the small effects that typically characterize common genetic variants, the study of anhedonia and related phenotypes conflicts with current genomic research requirements and frameworks that prioritize sample size over precise phenotyping. This has resulted in few and underpowered studies of anhedonia-related constructs that have largely failed to reliably identify individual variants. Nonetheless, the polygenic architecture of anhedonia-related constructs identified in these studies has genetic overlap with depression and schizophrenia as well as related brain structure (e.g., striatal volume), providing important clues to etiology that may usefully guide refinement in nosology. As we await the accumulation of larger samples for more well-powered GWAS of reward-related constructs, novel analytic techniques that leverage GWAS summary statistics (e.g., genomic structural equation modeling) may currently be used to help characterize how the genomic architecture of anhedonia is shared and distinct from that underlying other constructs (e.g., depression, neuroticism, anxiety).
Topics: Anhedonia; Depressive Disorder, Major; Genome-Wide Association Study; Genomics; Humans; Reward
PubMed: 35152374
DOI: 10.1007/7854_2021_293 -
Current Topics in Behavioral... 2022Drug addiction has been defined as a chronically relapsing disorder that is characterized by a compulsion to seek and take a drug or stimulus, the loss of control in... (Review)
Review
Drug addiction has been defined as a chronically relapsing disorder that is characterized by a compulsion to seek and take a drug or stimulus, the loss of control in limiting intake, and the emergence of a negative emotional state when access to the drug or stimulus is prevented, a component of which is anhedonia. The present review explores a heuristic framework for understanding the role of anhedonia in addiction, in which anhedonia is a key component of hyperkatifeia (conceptualized as the potentiated intensity of negative emotional/motivational symptoms during drug withdrawal) and negative reinforcement in addiction. The neural substrates that mediate such anhedonia and crosstalk between elements of hyperkatifeia that contribute to anhedonia are then explored, including crosstalk between physical pain and emotional pain systems. The present review explores current knowledge of neurochemical neurocircuitry changes that are associated with conditioned hyperkatifeia/anhedonia. The overall hypothesis is that the shift in motivation toward negative reinforcement in addiction reflects the allostatic misregulation of hedonic tone, such that drug taking makes anhedonia worse during the process of seeking temporary relief by compulsive drug taking, thereby perpetuating the addiction cycle and hedonic comorbidities that are associated with addiction.
Topics: Anhedonia; Brain; Humans; Pain; Reinforcement, Psychology; Substance-Related Disorders
PubMed: 35112332
DOI: 10.1007/7854_2021_288