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Anhedonia: A Comprehensive Handbook Volume II pp 125–156Cite as

Anhedonia in Schizophrenia: A Deficit in Translating Reward Information into Motivated Behavior

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Abstract

Anhedonia has long been considered a core clinical feature of schizophrenia, which is thought to be an important predictor of functional outcome and disease liability. However, recent developments in the affective neuroscience of schizophrenia suggest that the traditional understanding of anhedonia as a diminished capacity for pleasure may not correctly characterize the affective abnormalities that occur in this patient population. In the current chapter, literature is reviewed to suggest that anhedonia in schizophrenia primarily reflects a deficit in initiating activities aimed at receiving rewards, rather than a reduced capacity to experience pleasure when patients are exposed to rewards. Multiple psychological and neural mechanisms appear to impair the translation of intact hedonic responses into goal directed behavior in schizophrenia. Several of these mechanisms are reviewed here, including: (1) dopamine-mediated basal ganglia systems that support reinforcement learning and the ability to predict cues that lead to rewarding outcomes; (2) orbitofrontal cortex-driven deficits in generating, updating, and maintaining value representations; (3) aberrant effort-value computations, which may be mediated by disrupted anterior cingulate cortex and midbrain dopamine functioning; (4) altered activation of the prefrontal cortex, which is important for generating exploratory behaviors in environments where reward outcomes are uncertain. Overall, findings suggest that aberrant cortical-striatal interactions are involved with the reduced frequency of pleasurable activities that characterizes schizophrenia. Suggestions are provided for the development of novel behavioral intervention strategies that make use of external cues and reinforcers designed to facilitate goal-directed behavior in light of these various reward-processing deficits. Future directions for examining anhedonia in relation to modern affective neuroscience perspectives are also discussed.

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Abbreviations

ACC:

Anterior cingulate cortex

BG:

Basal Ganglia

BNSS:

Brief Negative Symptom Scale

CAINS:

Clinical Assessment Interview for Negative Symptoms

CBT:

Cognitive Behavioral Therapy

DA:

Dopamine

DLPFC:

Dorsolateral prefrontal cortex

fMRI:

Functional Magnetic Resonance Imaging

OFC:

Orbitofrontal Cortex

PET:

Positron Emission Tomography

PFC:

Prefrontal Cortex

VLPFC:

Ventrolateral Prefrontal cortex

VMPFC:

Ventromedial prefrontal cortex

SANS:

Scale for the Assessment of Negative Symptoms

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Acknowledgments

Work on this chapter was supported in part by funding from NIMH to Dr. Strauss: K23MH0925.

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  1. Department of Psychology, State University of New York at Binghamton, 6000, Binghamton, NY, 13902-6000, USA

    Gregory P. Strauss Ph.D.

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  1. Haifa & Sha'ar Menashe Mental Health Center, Israel Institute of Technology, Hadera, Israel

    Michael S. Ritsner

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Strauss, G.P. (2014). Anhedonia in Schizophrenia: A Deficit in Translating Reward Information into Motivated Behavior. In: Ritsner, M. (eds) Anhedonia: A Comprehensive Handbook Volume II. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-8610-2_5

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