Abstract

Deficit schizophrenia (DS), which is marked by stable negative symptoms, is regarded as a homogeneous subgroup of schizophrenia. While DS patients have structurally altered nucleus accumbens (NAcc) compared to non-deficit schizophrenia (NDS) patients and healthy individuals, the investigation of NAcc functional connectivity (FC) with negative symptoms and neurocognition could provide insights into the pathophysiology of schizophrenia. 58 DS, 93 NDS, and 113 healthy controls (HCs) underwent resting-state functional magnetic resonance (rsfMRI). The right and left NAcc were respectively used as seed points to construct the functional NAcc network in whole-brain FC analysis. ANCOVA compared the differences in NAcc network FC and partial correlation analysis explored the relationships between altered FC of NAcc, negative symptoms and neurocognition. Compared to HCs, both DS and NDS patients showed decreased FC between the left NAcc (LNAcc) and bilateral middle cingulate gyrus, and between the right NAcc (RNAcc) and right middle frontal gyrus (RMFG), as well as increased FC between bilateral NAcc and bilateral lingual gyrus. Moreover, the FC between the LNAcc and bilateral calcarine gyrus (CAL) was lower in the DS group compared to NDS patients. Correlation analysis indicated that FC value of LNAcc-CAL was negatively correlated to negative symptoms. Furthermore, aberrant FC values within the NAcc network were correlated with severity of clinical symptoms and neurocognitive impairments in DS and NDS patients. This study demonstrated abnormal patterns of FC in the NAcc network between DS and NDS. The presence of altered LNAcc-CAL FC might be involved in the pathogenesis of negative symptoms in schizophrenia.

Highlights

  • The reward network is usually implicated in schizophrenia, especially in the regulation of negative symptoms [1,2,3]

  • Post-hoc comparisons indicated that both Deficit schizophrenia (DS) (p < 0.05) and non-deficit schizophrenia (NDS) (p < 0.05) patients had lower education compared to healthy controls (HCs)

  • Our findings demonstrated that there were altered functional connectivity (FC) of the nucleus accumbens (NAcc) network in both DS and NDS patients

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Summary

Introduction

The reward network is usually implicated in schizophrenia, especially in the regulation of negative symptoms [1,2,3]. The nucleus accumbens (NAcc), which is a core node of the reward network, modulates information flow from the amygdaloid complex to the basal ganglia, mesolimbic dopaminergic regions, mediodorsal thalamus, and prefrontal cortex. Structural abnormalities of the NAcc were consistently demonstrated in schizophrenia. Two metaanalyses with large sample size showed significant volume reductions of the NAcc in schizophrenia patients [8, 9]. Another study indicated that there were lower NAcc volumes when antipsychotic medication therapy was discontinued in patients with schizophrenia [10]. While previous neuroimaging studies of NAcc in schizophrenia were primarily focused on structural alterations, functional neuroimaging studies via functional magnetic resonance imaging (fMRI) analyses are scarce

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