Dynamic Functional Connectivity Strength Within Different Frequency-Band in Schizophrenia.

As a complex psychiatric disorder, schizophrenia is interpreted as a "dysconnection" syndrome, which is linked to abnormal integrations in between distal brain regions. Recently, neuroimaging has been widely adopted to investigate how schizophrenia affects brain networks. Furthermore, some studies reported frequency dependence of the abnormalities of functional network in schizophrenia, however, dynamic functional connectivity with frequency dependence is rarely used to explore changes in the whole brain of patients with schizophrenia (SZ). Therefore, in the current study, dynamic functional connectivity strength (dFCS) was performed on resting-state functional magnetic resonance data from 96 SZ patients and 121 healthy controls (HCs) at slow-5 (0.01–0.027 Hz), slow-4 (0.027–0.073 Hz), slow-3 (0.073–0.198 Hz), and slow-2 (0.198–0.25 Hz) frequency bands and further assessed whether the altered dFCS was correlated to clinical symptoms in SZ patients. Results revealed that decreased dFCS of schizophrenia were found in salience, auditory, sensorimotor, visual networks, while increased dFCS in cerebellum, basal ganglia, and prefrontal networks were observed across different frequency bands. Specifically, the thalamus subregion of schizophrenic patients exhibited enhanced dynamic FCS in slow-5 and slow-4, while reduced in slow-3. Moreover, in slow-5 and slow-4, significant interaction effects between frequency and group were observed in the left calcarine cortex, the bilateral inferior orbitofrontal gyrus, and anterior cingulum cortex (ACC). Furthermore, the altered dFCS of insula, thalamus (THA), calcarine cortex, orbitofrontal gyrus, and paracentral lobule were partial correlated with clinical symptoms of SZ patients in slow-5 and slow-4 bands. These results demonstrate the abnormalities of dFCS in schizophrenia patients is rely on different frequency bands and may provide potential implications for exploring the neuropathological mechanism of schizophrenia. [ABSTRACT FROM AUTHOR]