Anhedonia in schizophrenia: Deficits in both motivation and hedonic capacity

Wang, Jiao; Huang, Jia; Yang, Xinhua; Lui, Simon S.Y.; Cheung, Eric F.C.; Chan, Raymond C. K.

doi:10.1016/j.schres.2015.06.019

Cited by 62 publications

(65 citation statements)

References 45 publications

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“…Of the 23 studies that included schizophrenia and control samples, 11 have found lower anticipatory pleasure in individuals with schizophrenia than controls [67–69, 9, 70–75, 52]; however, these findings may be specific to patients with severe negative symptoms [76]. Ten studies found no group differences in anticipatory pleasure [77–79, 39, 80–85]. Eight studies found lower consummatory pleasure in schizophrenia patients than controls [78, 71, 72, 74, 81–83, 75], while 12 found no group differences in consummatory pleasure [52, 85, 84, 80, 39, 79, 73, 70, 9, 69, 77, 67].…”

Section: Anticipatory Affect Affective Forecasting and Prospectionmentioning

confidence: 99%

“…Ten studies found no group differences in anticipatory pleasure [77–79, 39, 80–85]. Eight studies found lower consummatory pleasure in schizophrenia patients than controls [78, 71, 72, 74, 81–83, 75], while 12 found no group differences in consummatory pleasure [52, 85, 84, 80, 39, 79, 73, 70, 9, 69, 77, 67]. Eleven studies have reported group means for the TEPS subscales in patient and control groups, which provide evidence for numerically lower consummatory and anticipatory pleasure in schizophrenia: Schizophrenia anticipatory = 4.17; Control anticipatory = 4.54; Schizophrenia consummatory = 3.99; Control consummatory = 4.35.…”

Section: Anticipatory Affect Affective Forecasting and Prospectionmentioning

confidence: 99%

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A Review of Anticipatory Pleasure in Schizophrenia

Frost

Strauss

2016

Curr Behav Neurosci Rep

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Purpose of Review Anhedonia, traditionally defined as a diminished capacity to experience pleasure, has long been considered a core symptom of schizophrenia. However, recent research calls into question whether individuals with schizophrenia are truly anhedonic, suggesting intact subjective and neurophysiological response to rewarding stimuli in-the-moment. Despite a presumably intact capacity to experience pleasure, people with schizophrenia still engage in fewer reward-seeking behaviors. This discrepancy has been explained as a dissociation between “liking” and “wanting”, with dopaminergic and prefrontal influences on incentive salience leading hedonic responses to not effectively translate into motivated behavior. In the current review, the literature on a key aspect of the wanting deficit is reviewed, anticipatory pleasure. Recent Findings Results provide consistent evidence for impairment in some aspects of anticipatory pleasure (e.g., prospection, associative learning between reward predictive cues and outcomes), and inconsistent evidence for others (e.g., anticipatory affect and affective forecasting). Summary Mechanisms underlying anticipatory pleasure abnormalities in schizophrenia are discussed and a new model of anticipatory pleasure deficits is proposed. Findings suggest that anticipatory pleasure may be a critical component of impairments in wanting that impact motivated behavior in schizophrenia.

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Section: Anticipatory Affect Affective Forecasting and Prospectionmentioning

confidence: 99%

Section: Anticipatory Affect Affective Forecasting and Prospectionmentioning

confidence: 99%

A Review of Anticipatory Pleasure in Schizophrenia

Frost

Strauss

2016

Curr Behav Neurosci Rep

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“…Nucleus accumbens DA signalling modulates behavioural responsiveness to stimuli in terms of stimulus-stimulus learning, response-stimulus (operant) learning, and the motivation underlying behaviour directed at positive and negative stimuli (Salamone and Correa, 2012;Wise, 2004). Altered processing of positive-and negative-valence stimuli is characteristic of various psychiatric disorders, including depression and schizophrenia (Eshel and Roiser, 2010;Wang et al, 2015). For example, low motivation for reward underlies the core loss-of-interest symptom in depression and the core negative symptoms in schizophrenia; low motivation to cope with aversive stimuli likely contributes to both the perceived loss of control underlying helplessness (Nunes et al, 2013;Pryce et al, 2011;Treadway and Zald, 2011) and to fatigue (Demyttenaere et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Depletion of nucleus accumbens dopamine leads to impaired reward and aversion processing in mice: Relevance to motivation pathologies

et al. 2016

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Dopamine (DA) neurotransmission, particularly the ventral tegmental area-nucleus accumbens (VTA-NAcc) projection, underlies reward and aversion processing, and deficient DA function could underlie motivational impairments in psychiatric disorders. 6-hydroxydopamine (6-OHDA) injection is an established method for chronic DA depletion, principally applied in rat to study NAcc DA regulation of reward motivation. Given the increasing focus on studying environmental and genetic regulation of DA function in mouse models, it is important to establish the effects of 6-OHDA DA depletion in mice, in terms of reward and aversion processing. This mouse study investigated effects of 6-OHDAinduced NAcc DA depletion using the operant behavioural test battery of progressive ratio schedule (PRS), learned non-reward (LNR), learned helplessness (LH), treadmill, and in addition Pavlovian fear conditioning. 6-OHDA NAcc DA depletion, confirmed by ex vivo HPLC-ED, reduced operant responding: for gustatory reward under effortful conditions in the PRS test; to a stimulus recently associated with gustatory non-reward in the LNR test; to escape footshock recently experienced as uncontrollable in the LH test; and to avoid footshock by physical effort in the treadmill test. Evidence for specificity of effects to NAcc DA was provided by lack of effect of medial prefrontal cortex DA depletion in the LNR and LH tests. These findings add significantly to the evidence that NAcc DA is a major regulator of behavioural responding, particularly at the motivational level, to both reward and aversion. They demonstrate the suitability of mouse models for translational study of causation and reversal of pathophysiological DA function underlying motivation psychopathologies.

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“…Familial risk for depression is also associated with altered neural responses during reward and punishment processing (Foti et al, 2011; Gotlib et al, 2010; Luking et al, 2015; McCabe et al, 2012). However, it is also clear that dysfunctional reward processing is also observed in other psychiatric disorders, including schizophrenia (Barch et al, 2014; Wang et al, 2015) and bipolar disorder (Di Nicola et al, 2013; Pizzagalli et al, 2008b). Indeed, anhedonia has been reported to be a stable clinical feature in schizophrenic illness (Herbener and Harrow, 2002) and a trait-like feature in bipolar disorder, occurring across euthymic and depressive illness states (Di Nicola et al, 2013); although the similarities in motivational symptoms could conceivably be driven by different pathological mechanisms in different disorders (Whitton et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Anhedonia is associated with blunted reward sensitivity in first-degree relatives of patients with major depression

Liu

Roiser

Wang

et al. 2016

Journal of Affective Disorders

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Background Anhedonia is a cardinal feature of major depression and is hypothesized to be driven by low motivation, in particular blunted reward sensitivity. It has been suggested to be a marker that represents a genetic predisposition to this disorder. However, little is known about the mechanisms underlying this heightened risk in unaffected first-degree relatives of patients with major depression. We previously demonstrated abnormal reward biases in acutely depressed patients. The present study aimed to examine the development of reward bias in first-degree relatives of patients with major depression. Methods Forty-seven first-degree relatives of patients with major depression (26 females, age 18-52) and 60 healthy controls with no family history of depression (34 females, age 21-48) were recruited. A probabilistically rewarded difficult visual discrimination task, in which participants were instructed about the contingencies, was used to assess blunted reward sensitivity. A response bias towards the more frequently rewarded stimulus (termed “reward bias”) was the primary outcome variable in this study. Participants also completed self-reported measures of anhedonia and depressive symptoms. Results Compared with the control group, relatives of patients with major depression with sub-clinical depressive symptoms displayed a blunted reward bias. Relatives without symptoms displayed largely intact motivational processing on both self-report and experimental measures. The degree of anhedonia was associated with attenuated reward bias in first-degree relatives of patients with major depression, especially in those with sub-clinical symptoms. Limitations The study did not include a depressed patient group, which restricted our ability to interpret the observed group differences. Conclusions Blunted reward sensitivity may be largely manifested in a subgroup of relatives with high levels of depressive symptoms.

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Anhedonia in schizophrenia: Deficits in both motivation and hedonic capacity

Cited by 62 publications

References 45 publications

A Review of Anticipatory Pleasure in Schizophrenia

A Review of Anticipatory Pleasure in Schizophrenia

Depletion of nucleus accumbens dopamine leads to impaired reward and aversion processing in mice: Relevance to motivation pathologies

Anhedonia is associated with blunted reward sensitivity in first-degree relatives of patients with major depression

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