Anhedonia: A Concept Analysis

doi:10.1016/j.apnu.2013.02.001

Archives of Psychiatric Nursing

Volume 27, Issue 3, June 2013, Pages 121-129

https://doi.org/10.1016/j.apnu.2013.02.001 Get rights and content

Anhedonia presents itself in a myriad of disease processes. To further develop our understanding of anhedonia and effective ways to manage it, the concept requires clear boundaries. This paper critically examined the current scientific literature and conducted a concept analysis of anhedonia to provide a more accurate and lucid understanding of the concept. As part of the concept analysis, this paper also provides model, borderline, related, and contrary examples of anhedonia.

Section snippets

Method

A concept analysis method described by Walker and Avant (2010) was chosen for its ability to provide a conceptual framework for research and practice. It aids in the clarification of concepts through a set of eight demarcated steps (see Table 2). Consistent with this method, case examples (model, borderline, related, and contrary) will be presented and compared to highlight the fundamental features of the concept. For the purposes of clarity, the authors will present the case examples last,

Literature search

The authors conducted a search of the key term “anhedonia” in PubMed and CINAHL databases. Search limits included: human studies published in the English language. When the search was restricted to the last 10 years, there were over 1000 hits. Thus, the authors decided to focus on the most recent articles, published in 2011–2012, for this concept analysis. A total of 96 articles, with the term “anhedonia” in the title and/or abstract, were used to analyze the concept of anhedonia. Frequently

Select Concept and Determine the Purpose of Analysis

Concept selection or isolating the concept is the first step in the concept analysis process. The authors chose to analyze anhedonia because of its relevance to depression. Depressed patients with anhedonia typically do not respond to first-line medication therapies for major depressive disorder (McMakin et al., 2012, Steffenhagen et al., 2011, Tran et al., 2012, Treadway and Zald, 2011). Additionally, compared to other depressive symptoms, anhedonia is usually the last to resolve (Rubin, 2012

Discussion

Prior to delving into the discussion, it should be noted that concept analyses results are always tentative. The understanding of anhedonia will likely evolve over time as additional knowledge about the concept is generated through rigorous scientific inquiry. Additionally, different people will likely generate different results for the same concept. Even when the same analyst revisits a concept, she/he will likely produce different results. As the analyst changes over time, the understanding

Conclusions

The result of this concept analysis summarizes the critical features of anhedonia as the subjective lowered ability to experience pleasure, especially when compared to similar experiences that were perceived as pleasurable in the past (Agrawal et al., 2012, Rubin, 2012, Shomaker et al., 2012). As discussed, anhedonia occurs on a continuum and is closely related to the concept of pleasure (Gabbay, Mao, et al., 2012, Horan et al., 2011, Kirkpatrick et al., 2011). This dependence on the complex

Acknowledgment

Writing of this publication was supported in part by National Institute of Health grant F31-NR010853.

References (99)

L. Aguera-Ortiz et al.
Pain as a symptom of depression: Prevalence and clinical correlates in patients attending psychiatric clinics
Journal of Affective Disorders
(2011)
C.G. Ahnallen et al.
The relationship between reward-based learning and nicotine dependence in smokers with schizophrenia
Psychiatry Research
(2012)
M. Bencherif et al.
Alpha7 nicotinic cholinergic neuromodulation may reconcile multiple neurotransmitter hypotheses of schizophrenia
Medical Hypotheses
(2012)
W.V. Bobo et al.
The effect of adjunctive armodafinil on cognitive performance and psychopathology in antipsychotic-treated patients with schizophrenia/schizoaffective disorder: A randomized, double-blind, placebo-controlled trial
Schizophrenia Research
(2011)
R.S. Calabro et al.
Levetiracetam-associated loss of libido and anhedonia
Epilepsy & Behavior
(2012)
H.L. Chapman et al.
Going beyond students: An association between mixed-hand preference and schizotypy subscales in a general population
Psychiatry Research
(2011)
A.S. Cohen et al.
Neuropsychological functioning and social anhedonia: Three-year follow-up data from a longitudinal community high risk study
Journal of Psychiatric Research
(2012)
A.S. Cohen et al.
The state-trait disjunction of anhedonia in schizophrenia: Potential affective, cognitive and social-based mechanisms
Clinical Psychology Review
(2011)
M.T. Compton et al.
Mental health concerns among Canadian physicians: Results from the 2007–2008 Canadian Physician Health Study
Comprehensive Psychiatry
(2011)
S.M. Couture et al.
Negative expectancy appraisals and defeatist performance beliefs and negative symptoms of schizophrenia
Psychiatry Research
(2011)

A. Der-Avakian et al.

The neurobiology of anhedonia and other reward-related deficits

Trends in Neurosciences

(2012)

H. D'Haenen

Measurement of anhedonia

European Psychiatry

(1996)

S.A. Dinovo et al.

Reactive and self-regulatory dimensions of temperament: Interactive relations with symptoms of general distress and anhedonia

Journal of Research in Personality

(2011)

L.T. Germine et al.

Social anhedonia is associated with neural abnormalities during face emotion processing

NeuroImage

(2011)

L. Grillo

Might the inability to feel pleasure (anhedonia) explain the symptoms of major depression and schizophrenia, including unmotivated anxiety, delusions and hallucinations?

Medical Hypotheses

(2012)

J. Hannestad et al.

Citalopram reduces endotoxin-induced fatigue

Brain, Behavior, and Immunity

(2011)

N. Ho et al.

Depressive phenotypes evoked by experimental diabetes are reversed by insulin

Physiology and Behavior

(2012)

W.P. Horan et al.

Development and psychometric validation of the Clinical Assessment Interview for Negative Symptoms (CAINS)

Schizophrenia Research

(2011)

P.A. Keedwell et al.

The neural correlates of anhedonia in major depressive disorder

Biological Psychiatry

(2005)

H. Kober et al.

Regulation of emotion in major depressive disorder

Biological Psychiatry

(2011)

J.M. Koolhaas et al.

Stress revisited: A critical evaluation of the stress concept

Neuroscience and Biobehavioral Reviews

(2011)

J.S. Lee et al.

Neuroanatomical correlates of trait anhedonia in patients with schizophrenia: A voxel- based morphometric study

Neuroscience Letters

(2011)

S.N. Light et al.

Reduced right ventrolateral prefrontal cortex activity while inhibiting positive affect is associated with improvement in hedonic capacity after 8 weeks of antidepressant treatment in major depressive disorder

Biological Psychiatry

(2011)

E.A. Martin et al.

Differential associations between schizotypy facets and emotion traits

Psychiatry Research

(2011)

G. Martinotti et al.

Acetyl-l-carnitine in the treatment of anhedonia, melancholic and negative symptoms in alcohol dependent subjects

Progress in Neuro-Psychopharmacology & Biological Psychiatry

(2011)

D.L. McMakin et al.

Anhedonia predicts poorer recovery among youth with selective serotonin reuptake inhibitor treatment-resistant depression

Journal of the American Academy of Child and Adolescent Psychiatry

(2012)

J.W. Messinger et al.

Avolition and expressive deficits capture negative symptom phenomenology: Implications for DSM-5 and schizophrenia research

Clinical Psychology Review

(2011)

S. Miura et al.

Anhedonia in Japanese patients with Parkinson's disease: Analysis using the Snaith- Hamilton Pleasure Scale

Clinical Neurology and Neurosurgery

(2012)

G. Nefs et al.

Suboptimal glycemic control in type 2 diabetes: A key role for anhedonia?

Journal of Psychiatric Research

(2012)

G. Nefs et al.

Type D (distressed) personality in primary care patients with type 2 diabetes: Validation and clinical correlates of the DS14 assessment

Journal of Psychosomatic Research

(2012)

L. Ossewaarde et al.

Two-week administration of the combined serotonin–noradrenaline reuptake inhibitor duloxetine augments functioning of mesolimbic incentive processing circuits

Biological Psychiatry

(2011)

S.G. Park et al.

Screening for negative symptoms: Preliminary results from the self-report version of the Clinical Assessment Interview for Negative Symptoms

Schizophrenia Research

(2012)

D.A. Pizzagalli et al.

Toward an objective characterization of an anhedonic phenotype: A signal-detection approach

Biological Psychiatry

(2005)

E.J. Rose et al.

Chronic exposure to nicotine is associated with reduced reward-related activity in the striatum but not the midbrain

Biological Psychiatry

(2012)

D.H. Rubin

Joy returns last: Anhedonia and treatment resistance in depressed adolescents

Journal of the American Academy of Child and Adolescent Psychiatry

(2012)

S.A. Shankman et al.

The effect of pre- vs. post-reward attainment on EEG asymmetry in melancholic depression

International Journal of Psychophysiology

(2011)

L.B. Shomaker et al.

Depressive symptoms and cardiorespiratory fitness in obese adolescents

Journal of Adolescent Health

(2012)

M.J. Smoski et al.

fMRI of alterations in reward selection, anticipation, and feedback in major depressive disorder

Journal of Affective Disorders

(2009)

A. Soliman et al.

Limbic response to psychosocial stress in schizotypy: A functional magnetic resonance imaging study

Schizophrenia Research

(2011)

G.P. Strauss et al.

Deficits in positive reinforcement learning and uncertainty-driven exploration are associated with distinct aspects of negative symptoms in schizophrenia

Biological Psychiatry

(2011)

G.P. Strauss et al.

Patterns of emotional experience in schizophrenia: Differences in emotional response to visual stimuli are associated with clinical presentation and functional outcome

Schizophrenia Research

(2011)

G.P. Strauss et al.

Anticipatory vs. consummatory pleasure. What is the nature of hedonic deficits in schizophrenia?

Psychiatry Research

(2011)

P. Tran et al.

Efficacy and tolerability of the novel triple reuptake inhibitor amitifadine in the treatment of patients with major depressive disorder: A randomized, double-blind, placebo-controlled trial

Journal of Psychiatric Research

(2012)

M.T. Treadway et al.

Reconsidering anhedonia in depression: Lessons from translational neuroscience

Neuroscience and Biobehavioral Reviews

(2011)

L.M. Tully et al.

Impaired executive control of emotional information in social anhedonia

Psychiatry Research

(2012)

E. Velthorst et al.

The association between social anhedonia, withdrawal and psychotic experiences in general and high-risk populations

Schizophrenia Research

(2012)

B.P. Winterstein et al.

Brief assessment of schizotypy: Developing short forms of the Wisconsin Schizotypy Scales

Personality and Individual Differences

(2011)

A. Agrawal et al.

Cannabinoid receptor genotype moderation of the effects of childhood physical abuse on anhedonia and depression

Archives of General Psychiatry

(2012)

American Psychiatric Association

Diagnostic and statistical manual of mental disorders (4th ed., Text Revision)

(2000)

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Prevalent models of sexual desire, arousal and orgasm postulate that they result from an excitatory process, whereas disorders of sexual desire, arousal and orgasm result from an inhibitory process based on psychosocial, pharmacological, medical, and other factors. But neuronal excitation and active neuronal inhibition normally interact at variable intensities, concurrently and continuously. We propose herein that in conjunction with neuronal excitation, neuronal inhibition enables the generation of the intense, non-aversive pleasure of orgasm. When this interaction breaks down, pathology can result, as in disorders of sexual desire, arousal, and orgasm, and in anhedonia and pain. For perspective, we review some fundamental behavioral and (neuro-) physiological functions of neuronal excitation and inhibition in normal and pathological processes.
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We selected studies from searches on PubMed, Google Scholar, Dialnet, and SciELO for terms including orgasm, neuronal development, Wallerian degeneration, prenatal stress, parental behavior, sensorimotor, neuronal excitation, neuronal inhibition, sensory deprivation, anhedonia, orgasmic disorder, hypoactive sexual desire disorder, persistent genital arousal disorder, sexual pain.
We provide evidence that the intensity of neuronal inhibition dynamically covaries concurrently with the intensity of neuronal excitation. Differences in these relative intensities can facilitate the understanding of orgasm and disorders of orgasm.
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Komisaruk BR, Rodriguez del Cerro MC. Orgasm and Related Disorders Depend on Neural Inhibition Combined With Neural Excitation. Sex Med Rev 2022;10:481–492.
An evolutionary investigation of depressed mood: The relationship between daily stressors and patterns of depressive symptoms
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Citation Excerpt :
Keller and Nesse (2006), using the same measure of depressive symptoms, also found that anhedonia did not correlate significantly with the stressors hypothesized to elicit that response. In examining the specific anhedonia symptoms assessed in our study, it is noteworthy that all five symptoms relate to a lack of positive affect (e.g., “Nothing could make me smile; ” see Keller & Nesse, 2006, p. 321) and none of the symptoms relate to a lack of motivation to engage in pleasurable activities, which is also typically associated with anhedonia (Ho & Sommers, 2013). It may be that the absence of positive affect is a ubiquitous depressive response to all adverse situations while a lack of motivation to engage in pleasurable activities is a specific response to specific adverse situations.
The situation-symptom congruence hypothesis (SSCH; (Keller & Nesse, 2006), grounded in evolutionary theory, argues that different types of adversity should lead to distinct patterns of depressive symptoms that help individuals deal with adaptive challenges. Situation-symptom congruence hypotheses were tested in this study using experience sampling methodology.
Two hundred and sixty-five individuals, including 54% who scored at least 16 on the Center for Epidemiologic Studies Revised Depression Scale, responded to text prompts daily for up to 9 days, reporting depressive symptoms as well as the most stressful event or issue they had experienced or focused on within the past 24 h.
Multilevel modeling analyses indicated that the relationships between stressors and depressive symptom patterns were largely consistent with SSCH predictions. All stressors were significantly associated with symptoms hypothesized to be adaptive in response to those stressors. Moreover, in separate analyses, nine of the ten symptoms examined were either predicted by the stressors hypothesized to lead to that symptom or negatively related to stressors hypothesized to not elicit those symptoms.
It is unclear whether the results generalize to those diagnosed with a major depressive disorder; the study did not assess actual life events.
Findings suggest that depressive symptoms may, in part, be adaptations that have evolved through natural selection to help individuals cope with adverse situations.
Validation of the Oxford Depression Questionnaire: Sensitivity to change, minimal clinically important difference, and response threshold for the assessment of emotional blunting
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Citation Excerpt :
Emotional blunting presents as emotional indifference, ‘numbing’ or ‘flattening’ of emotions, and reduced responsiveness to emotionally significant positive or negative stimuli (Goodwin et al., 2017). In contrast, anhedonia manifests as the inability to anticipate and experience pleasure and is not associated with a lack of emotional responsiveness (Franken et al., 2007; Ho and Summers, 2013; Watson et al., 2020). Indeed, patients with anhedonia are able to experience negative emotions, the perception of which is typically heightened rather than blunted.
The Oxford Depression Questionnaire (ODQ) is a patient-reported scale for assessing emotional blunting in patients with major depressive disorder (MDD). This analysis was undertaken to further validate the scale in patients experiencing emotional blunting while receiving antidepressant treatment.
Patients with MDD who experienced inadequate depressive-symptom resolution and emotional blunting on selective serotonin reuptake inhibitor or serotonin-noradrenaline reuptake inhibitor monotherapy (adequate dose for ≥6 weeks) were switched to vortioxetine 10–20 mg/day. ODQ total scores were assessed excluding and including the “antidepressant-as-cause” domain (ODQ-20 and ODQ-26, respectively). Anchor- and distribution-based methods were used to determine the minimal clinically important difference in ODQ scores in terms of change from baseline to week 8 of antidepressant treatment.
After 8 weeks of vortioxetine treatment, the mean change in ODQ-20 and ODQ-26 scores from baseline was −24.8 and −30.1 points, respectively. Greater mean changes from baseline in ODQ-20 and ODQ-26 scores were seen in patients reporting no emotional blunting vs those still experiencing emotional blunting after 8 weeks of vortioxetine treatment (ODQ-20: −27.0 vs −22.6 points; ODQ-26: –32.8 vs –27.5 points, respectively). In patients considered clinically minimally improved (Clinical Global Impression–Improvement score, 3) after 8 weeks of vortioxetine treatment, respective mean (standard deviation) change in ODQ-20 and ODQ-26 score from baseline was −15.5 (18.1) and –20.0 (20.5) points.
Short study duration.
These results provide further validation of the clinical utility of the ODQ for assessing emotional blunting in patients with MDD. The suggested minimal clinically important difference for change in ODQ-20 and ODQ-26 scores is 16 and 20 points, respectively, after 8 weeks of antidepressant treatment.
ClinicalTrials.gov identifier: NCT03835715.
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Serotonin transporter gene variance has long been considered an essential factor contributing to depression. However, meta-analyses yielded inconsistent findings recently, asking for further understanding of the link between the gene and depression-related symptoms. One key feature of depression is anhedonia. While data exist on the effect of serotonin transporter gene knockout (5-HTT^−/−) in rodents on consummatory and anticipatory anhedonia, with mixed outcomes, the effect on decisional anhedonia has not been investigated thus far. Here, we tested whether 5-HTT^−/− contributes to decisional anhedonia. To this end, we established a novel touchscreen-based go/go task of visual decision-making. During the learning of stimulus discrimination, 5-HTT^+/+ rats performed more optimal decision-making compared to 5-HTT^−/− rats at the beginning, but this difference did not persist throughout the learning period. During stimulus generalization, the generalization curves were similar between both genotypes and did not alter as the learning progress. Interestingly, the response time in 5-HTT^+/+ rats increased as the session increased in general, while 5-HTT^−/− rats tended to decrease. The response time difference might indicate that 5-HTT^−/− rats altered willingness to exert cognitive effort to the categorization of generalization stimuli. These results suggest that the effect of 5-HTT ablation on decisional anhedonia is mild and interacts with learning, explaining the discrepant findings on the link between 5-HTT gene and depression.
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Citation Excerpt :
It is defined as an inability to enjoy experiences and activities that normally would be pleasurable (American Psychological Association [APA], 2013) and is associated with low pleasure derived from positive activities, low positive affect (PA; e.g., feeling happy or joyful) and increased negative affect (NA; e.g., feeling gloomy or nervous). Anhedonia is experienced in different domains such as social situations or physical experiences (Ho and Sommers, 2013) and linked to deficits in the appetitive system of the brain, which motivates action towards goals and rewards and elicits positive emotions (Michel-Chávez et al., 2015). People suffering from anhedonia are more likely to experience persistent mental health problems (Spijker et al., 2001), to benefit less from pharmacological treatment (McMakin et al., 2012) and to become suicidal (Hawes et al., 2018).
Anhedonia is a common symptom of several disorders, but cost-effective treatments that focus on anhedonia specifically have been lacking. Therefore, personalized lifestyle advice has recently been investigated as a suitable means of enhancing pleasure and positive affect (PA) in young adults with anhedonia. This intervention provided individuals with a personalized lifestyle advice which was based on observed individual patterns of lifestyle behaviors and experienced pleasure in daily life. The present study extends this previous work by examining a potential mechanism of treatment success, affective reactivity.
We explored changes in affective reactivity to events in daily life from pre- to post-intervention in a subclinical sample of young adults with anhedonia (N = 69). Using the Experience Sampling Method (ESM), participants answered questions on their activities, their pleasure levels, PA and negative affect (NA) before and after the intervention.
Multilevel analysis revealed that participants did not experience an altered affective reactivity to positive events after the intervention. The affective reactivity to negative events depended on the level of improvement in mean-PA after the lifestyle advice intervention.
The present study used a subclinical sample with the majority of participants being female which limited the generalizability of the findings.
This study suggests that an altered affective reactivity to negative events is an underlying mechanism of the effectiveness of a personalized lifestyle advice.

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Anhedonia: A Concept Analysis

Section snippets

Method

Literature search

Select Concept and Determine the Purpose of Analysis

Discussion

Conclusions

Acknowledgment

Journal of Affective Disorders

Psychiatry Research

Medical Hypotheses

Schizophrenia Research

Epilepsy & Behavior

Psychiatry Research

Journal of Psychiatric Research

Clinical Psychology Review

Comprehensive Psychiatry

Psychiatry Research

Trends in Neurosciences

European Psychiatry

Journal of Research in Personality

NeuroImage

Medical Hypotheses

Brain, Behavior, and Immunity

Physiology and Behavior

Schizophrenia Research

Biological Psychiatry

Biological Psychiatry

Neuroscience and Biobehavioral Reviews

Neuroscience Letters

Biological Psychiatry

Psychiatry Research

Progress in Neuro-Psychopharmacology & Biological Psychiatry

Journal of the American Academy of Child and Adolescent Psychiatry

Clinical Psychology Review

Clinical Neurology and Neurosurgery

Journal of Psychiatric Research

Journal of Psychosomatic Research

Biological Psychiatry

Schizophrenia Research

Biological Psychiatry

Biological Psychiatry

Journal of the American Academy of Child and Adolescent Psychiatry

International Journal of Psychophysiology

Journal of Adolescent Health

Journal of Affective Disorders

Schizophrenia Research

Biological Psychiatry

Schizophrenia Research

Psychiatry Research

Journal of Psychiatric Research

Neuroscience and Biobehavioral Reviews

Psychiatry Research

Schizophrenia Research

Personality and Individual Differences

Cannabinoid receptor genotype moderation of the effects of childhood physical abuse on anhedonia and depression

Archives of General Psychiatry

Diagnostic and statistical manual of mental disorders (4th ed., Text Revision)