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To investigate the altered intrinsic functional connectivity (iFC) of the primary visual cortex (V1) in primary angle-closure glaucoma (PACG) patients before and after surgery using resting-state functional MRI.Twenty-five preoperative PACG (pre-PACG) patients and 25 well-matched healthy controls (HCs) were included in this study, and 9 PACG patients were assessed again at least 3 months after treatment (post-PACG). We generated the iFC maps of the seed regions in the centers of the left and right V1 and conducted group comparisons. Then, the relationships between the altered iFC coefficients and clinical variables were investigated in the pre-PACG patients.Compared with the HCs, the pre-PACG patients showed decreased iFC between the left V1 and right V2 (covering the cuneus, calcarine and lingual gyrus) and increased iFC between the left V1 and left temporal-parietal region, left frontal opercula-insula-basal ganglia region, right insula-basal ganglia region, and right inferior parietal lobule (P < 0.01, corrected). Compared with the pre-PACG patients, the post-PACG patients showed increased iFC between the left V1 and bilateral V2, and between the left V1 and left or right postcentral gyrus; in addition, they showed decreased iFC between the left V1 and the dorsal-attention and frontoparietal-control networks. In the pre-PACG patients, visual activity (VA) was positively correlated with increased iFC between the left V1 and the left temporal-parietal region or the right inferior parietal lobule. Similar patterns of alterations were observed in the right V1-iFC in both the pre- and post-PACG patients.The primary findings have demonstrated a gradual decrease in visual information integration in the left V1-V2 pathway and VA-related functional compensation in the pre-PACG patients, generating further evidence of functional restoration in post-PACG patients.

Obstructive sleep apnea (OSA) has been associated with changes in brain structure and regional function in certain brain areas. However, the functional features of network organization in the whole brain remain largely uncertain. The purpose of this study was to identify the OSA-related spatial centrality distribution of the whole brain functional network and to investigate the potential altered intrinsic functional hubs.Forty male patients with newly confirmed severe OSA on polysomnography, and well-matched good sleepers, participated in this study. All participants underwent a resting-state functional MRI scan and clinical and cognitive evaluation. Voxel-wise degree centrality (DC) was measured across the whole brain, and group difference in DC was compared. The relationship between the abnormal DC value and clinical variables was assessed using a linear correlation analysis.Remarkably similar spatial distributions of the functional hubs (high DC) were found in both groups. However, OSA patients exhibited a pattern of significantly reduced regional DC in the left middle occipital gyrus, posterior cingulate cortex, left superior frontal gyrus, and bilateral inferior parietal lobule, and DC was increased in the right orbital frontal cortex, bilateral cerebellum posterior lobes, and bilateral lentiform nucleus, including the putamen, extending to the hippocampus, and the inferior temporal gyrus, which overlapped with the functional hubs. Furthermore, a linear correlation analysis revealed that the DC value in the posterior cingulate cortex and left superior frontal gyrus were positively correlated with Montreal cognitive assessment scores, The DC value in the left middle occipital gyrus and bilateral inferior parietal lobule were negatively correlated with apnea-hypopnea index and arousal index in OSA patients.Our findings suggest that OSA patients exhibited specific abnormal intrinsic functional hubs including relatively reduced and increased DC. This expands our understanding of the functional characteristics of OSA, which may provide new insights into understanding the dysfunction and pathophysiology of OSA patients.

Using voxel-wise degree centrality (DC), as measured by resting-state fMRI, we aimed to study alterations in the brain functional networks in patients with primary angle-closure glaucoma (PACG) and to reveal the plastic trajectories of surgery.A total of 23 preoperative PACG patients (49.48 ± 14.37 years old) were recruited to undergo a resting-state fMRI scan, and 9 of them were rescanned 3 months after surgery. All PACG patients underwent a complete ophthalmologic examination, including intraocular pressure (IOP), retinal nerve fiber layer (RNFL) thickness, vertical cup to disc ratio (V C/D), and average cup to disc ratio (A C/D). Another 23 gender- and age-matched healthy controls (48.18 ± 9.40 years old) underwent scanning once for comparison. The group difference in DC was calculated in each voxel, and the correlations between the DC value and each of the clinical variables were analyzed in the PACG patients.Preoperative PACG (pre-PACG) patients showed significantly decreased DC in the bilateral visual cortices but increased DC in the left anterior cingulate cortex (ACC) and caudate (p < 0.05, corrected) compared with the controls. Statistical analysis showed a significantly negative correlation between DC in the bilateral visual cortices and the IOP score and between DC in the anterior cingulate cortex (ACC) and both the A C/D and V C/D scores in the pre-PACG patients. Three months after surgery, these postoperative PACG (post-PACG) patients showed a significantly increased DC in both the bilateral visual cortices and the left precentral gyrus compared with the pre-PACG patients.Our results suggest that PACG may contribute to decreased functional centrality in the visual system and to increased degree centrality in cognition-emotional processing regions. Alterations in visual areas seem to parallel the cup to disc ratio, but not the duration of angle closure. The changes of functional centrality in PACG patients after operation may reveal the plasticity or degeneration of the visual-associated brain areas. Our findings may provide further understanding of the pathophysiology of PACG.