Reduced structural covariance connectivity of defaut mode network and salience network in MRI-normal focal epilepsy. Issue 18 (16th December 2020)

• Record Type: Journal Article
• Authors: Shu, Ting; Xiao, Xinlan; Long, Zhiliang; Zhang, Ran
• Is Part Of: NeuroReport. Volume 31:Issue 18(2020)
• Publication Date: 2020-12-16
• Subjects: default mode network -- focal epilepsy -- MRI-normal -- salience network -- structural covariance connectivity; Neurosciences -- Periodicals; Nervous system -- Periodicals; Neurophysiology -- Periodicals; Nervous System Diseases -- Periodicals; Nervous System Physiological Phenomena -- Periodicals; Neurosciences -- Periodicals; 616.805
• DOI: 10.1097/WNR.0000000000001541
• Languages: English
• ISSNs: 0959-4965

Abstract

Abstract : Neuroimaging studies have found altered functional connectivity of default mode network (DMN) and salience network (SN) in patients with focal epilepsy (FE). However, the structural basis underlying the functional connectivity disturbance in the patients is still unclear. Sixteen MRI-normal FE and 22 healthy controls were included in the current study. The T1 structural image of each participant was obtained. Seed-based structural covariance connectivity was employed to investigate changes of structural covariance connectivity of DMN and SN in FE patients. We further evaluated gray matter volume changes of brain areas showing altered structural connectivity in the patients. We found that patients with FE showed reduced connectivity of posterior cingulate cortex and left medial prefrontal cortex, hippocampus and orbitofrontal cortex, and reduced connectivity of right fronto-insula cortex with left insula, orbitofrontal cortex, opercum part of inferior frontal cortex and right medial prefrontal cortex compared with healthy controls. Moreover, those brain areas showing significant reduced structural covariance connectivity in patients with FE also had a loss of gray matter volume, indicating that reduced structural connectivity of DMN and SN might be associated with gray matter atrophy in the patients. Those results highlight the crucial role of DMN and SN in the pathology of patients with FE, and provided structural basis for the functional disturbance of the two networks in this disease.