Different structural connectivity patterns in the subregions of the thalamus, hippocampus, and cingulate cortex between schizophrenia and psychotic bipolar disorder.

ABSTRACT

OBJECTIVE: Schizophrenia (SCZ) and psychotic bipolar disorder (PBD) are two major psychotic disorders with similar symptoms and tight associations on the psychopathological level, posing a clinical challenge for their differentiation. This study aimed to investigate and compare the structural connectivity patterns of the limbic system between SCZ and PBD, and to identify specific regional disruptions associated with psychiatric symptoms. METHODS: Using sMRI data from 146 SCZ, 160 PBD, and 145 healthy control (HC) participants, we employed a data-driven approach to segment the hippocampus, thalamus, hypothalamus, amygdala, and cingulate cortex into subregions. We then investigated the structural connectivity patterns between these subregions at the global and nodal levels. Additionally, we assessed psychotic symptoms by utilizing the subscales of the Brief Psychiatric Rating Scale (BPRS) to examine correlations between symptom severity and network metrics between groups. RESULTS: Patients with SCZ and PBD had decreased global efficiency (Eglob) (SCZ adjusted P<0.001; PBD adjusted P = 0.003), local efficiency (Eloc) (SCZ and PBD adjusted P<0.001), and clustering coefficient (Cp) (SCZ and PBD adjusted P<0.001), and increased path length (Lp) (SCZ adjusted P<0.001; PBD adjusted P = 0.004) compared to HC. Patients with SCZ showed more pronounced decreases in Eglob (adjusted P<0.001), Eloc (adjusted P<0.001), and Cp (adjusted P = 0.029), and increased Lp (adjusted P = 0.024) compared to patients with PBD. The most notable structural disruptions were observed in the hippocampus and thalamus, which correlated with different psychotic symptoms, respectively. CONCLUSION: This study provides evidence of distinct structural connectivity disruptions in the limbic system of patients with SCZ and PBD. These findings might contribute to our understanding of the neuropathological basis for distinguishing SCZ and PBD.