A recent study published in Schizophrenia Bulletin on June 13 shows that cerebellum-basal ganglia functional connectivity plays an important role to the development of anhedonia and amotivation in patients with schizophrenia. 

Schizophrenia is a complex mental disorder characterized by a significant reduction in initiating effortful behaviour and engaging goal-directed behaviour, collectively known as anhedonia and amotivation, leading to a wide range of social functioning impairments. These impairments contribute to the core negative symptoms that have been closely linked to dysfunctions in the reward processing system. 

Conventional work on neurobiological mechanisms associating with anhedonia and amotivation has primarily limited to the study of the cortical and subcortical areas without examining the role of cerebellum. Accumulating evidence has suggested that cerebellum and its functional connectivity may be associated with emotion regulation and motivating processing. However, it is unclear whether cerebellar-related functional connectivity may be one of the underpinning neural mechanisms contributing to the development of anhedonia and amotivation in patients with schizophrenia. 

In this current study, Dr. Raymond Chan from the Neuropsychology and Applied Cognitive Neuroscience (NACN) Laboratory, Institute of Psychology and his collaborators have designed at study to specifically examine the important role of cerebellar-related functional connectivity in motivational and hedonic processing in patients with schizophrenia. They recruited two independent samples to answer this question. In the main sample, they recruited 62 schizophrenia patients and 61 healthy controls. All of them undertook a resting-state functional connectivity scan. Their results showed that there was a disrupted subnetwork between the cerebellum and basal ganglia in schizophrenia patients. More importantly, amotivation was found to be correlated with these functional connectivity alterations, especially with cerebellar-pallidal connectivity. These altered functional connectivity and corresponding associations with amotivation were replicated in the validation sample consisting of 53 schizophrenia patients and 55 healthy controls. 

Taken together, these findings highlight the important role of disrupted cerebellum-basal ganglia connectivity in the pathophysiology of SCZ, particularly in relation to anhedonia and amotivation. This functional connectivity may be a putative target for neuromodulation to ameliorate negative symptoms of schizophrenia patients. Dr. Chan’s team is now running a clinical trial to examine whether neuromodulation on cerebellum would improve negative symptoms in general, and amotivation and anhedonia in particular in schizophrenia patients. 

The study was supported by the STI2030-Major Projects, the National Key Research and Development Programme, and the Philip K. H. Wong Foundation. 

This review was published online in Schizophrenia Bulletin

Wang X, Guo X.D., Cai, X. L., Huang, B. J., Wang, Y., Pu, C. C., Yu, X., Lui, S. S. Y., Chan, R. C. K.* (2025). Cerebellar-basal ganglia dysconnectivity in schizophrenia: Insights into motivational deficits. Schizophrenia Bulletin