Schizophrenia is a complex psychiatric disorder characterized by the presence of reduced ability to motivate effortful behaviour and experience pleasurable events, i.e., amotivation and anhedonia, leading to a wide range of social functioning impairments. However, it is still not clearly known for the putative neurobiological mechanisms for amotivation and anhedonia, and hence, hindering development of effective interventions targeting at amotivation and anhedonia.
Recent theoretical framework suggests that impaired reward functioning may be one of the putative neurobiological mechanisms underpinning amotivation and anhedonia in schizophrenia. According to this theoretical framework, reward processing can be compartmentalized into reward anticipation (ability to anticipate pleasurable events or upcoming reward), reward consumption (ability to experience pleasure at the receipt of the reward), reward learning (ability to sustain and update the inner representation of rewards) and effort computation (decision to make and compute the required effort to approach for the reward).
Recently, Dr. Raymond Chan from the Neuropsychology and Applied Cognitive Neuroscience (NACN) Laboratory, CAS Key Laboratory of Mental Health, Institute of Psychology and his collaborators conducted a meta-analysis to further illustrate the neurobiological mechanisms associating with amotivation and anhedonia in schizophrenia. In so doing, they adopted a “component-based approach” for rewarding processing as well as the ‘whole brain perspective’ for neural mechanisms. Their findings showed that schizophrenia spectrum patients exhibited reduced activation in the striatum, orbital frontal cortex, cingulate cortex, and cerebellar areas.
They also found distinct patterns of brain alterations for different components. Reward anticipation was correlated with decreased activation of the cingulate cortex and striatum. Reward consumption was correlated with decreased activation of the cerebellum IV/V areas, insula and inferior frontal gyri. Regarding reward learning, it was correlated with decreased activation of the striatum, thalamus, cerebellar Crus I, cingulate cortex, orbitofrontal cortex, and some parietal and occipital areas.
Taken together, these findings suggested that both reward anticipation and reward learning components were associated with decreased activation in the dorsal striatum and posterior cingulate cortex in people with schizophrenia spectrum.
Fig. 1. Areas with abnormal activation related to reward anticipation (purple), reward consumption (blue), and reward learning (Red) in SCZ spectrum. Image by Dr. Raymond Chan.
This meta-analysis provides a comprehensive examination of multiple components of reward processing in schizophrenia spectrum disorders. The findings support the compartmentalization of reward processing in schizophrenia spectrum disorders and also highlight the important role of impaired cerebellar connectivity upon the development of amotivation and anhedonia in schizophrenia patients and at-risk individuals for schizophrenia.
The preparation of this systematic review and meta-analysis was supported by the Jiangsu Provincial Key Research and Development Programme, the Scientific Foundation of Institute of Psychology, Chinese Academy of Sciences and the Phillip K.H. Wong Foundation.
This review is now published online in Psychological Medicine:
Wang X, Zhang Y, Huang J, Wang Y, Niu Y, Lui SSY, Hui L, Chan RCK (2023). Revisiting reward impairments in schizophrenia spectrum disorders: a systematic review and meta-analysis for neuroimaging findings. Psychological Medicine 1–15.
Related publications:
Chan, R. C. K.*, Wang, L. L., Lui, S. S. Y. (2022). Theories and models of negative symptoms in schizophrenia and clinical implications. Nature Reviews Psychology, 1, 454–467. DOI: https://doi.org/10.1038/s44159-022-00065-9
LIU Chen
Institute of Psychology Chinese Academy of Sciences
Beijing 100101, China.
E-mail: liuc@psych.ac.cn
