A new 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 behavior and engaging goal-directed behavior, 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. While previous research has largely focused on cortical and subcortical areas of the brain, the role of the cerebellum in these symptoms has remained underexplored.

Emerging evidence has increasingly implicated the cerebellum and its broader functional networks in emotion regulation and motivation processing. However, whether cerebellar-related connectivity disruptions directly contribute to anhedonia and amotivation in schizophrenia has remained unclear—until now.

In this study, Dr. Raymond Chan from the Institute of Psychology of the Chinese Academy of Sciences and his collaborators conducted a study designed to clarify the role of cerebellar functional connectivity in motivational and hedonic processing. 

They recruited two independent cohorts: a main sample consisting of 62 patients with schizophrenia and 61 healthy controls, and a validation sample of 53 patients and 55 controls. All participants underwent resting-state functional magnetic resonance imaging (fMRI).

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 schizophrenia, 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. 

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