Primary angle-closure glaucomas disturb regional spontaneous brain activity in the visual pathway: An fMRI study

Abstract

Objective: To explore the underlying regional brain activity deficits in the visual cortex in patients with primary angle-closure glaucoma (PACG) relative to normal controls (NCs) using regional homogeneity (ReHo) method, and its relationship with behavioral performances. Patients: Twenty PACG patients (10 females, 10 males; mean age ± standard deviation [SD]: 54.42±9.46 years) and 20 age-, and sex status-matched NCs (10 females, 10 males; mean age ± SD: 53.75±9.16 years) were included in this study. Measurements and results: Compared with NCs, patients with PACG showed significant atrophic peripapillary retinal nerve fiber layer (pRNFL) and neuroretinal rim area, increased optic disk cup-to-disc ratio (CDR) and optic disk volume (P,0.05), higher ReHo value in the left fusiform gyrus, left cerebellum anterior lobe, right frontal-temporal space, and right insula, and lower ReHo value in the bilateral middle occipital gyrus, left claustrum, and right paracentral lobule lobe. The receiver operating characteristic analysis revealed these different areas with high value of area under curve, and high degree of sensitivity and specificity. The mean beta values of these different areas were extracted. In PACG, the duration of disease showed a negative correlation with the mean beta value of left cerebellum anterior lobe (r=−0.453, P=0.045) and a positive correlation with right middle occipital gyrus (r=0.586, P=0.007); left middle occipital gyrus showed positive correlations with duration of disease (r=0.562, P=0.01) and left pRNFL (r=0.49, P=0.028); left claustrum had a positive correlation with left CDR (r=0.515, P=0.02); and right paracentral lobule lobe demonstrated a positive correlation with left pRNFL (r=0.623, P=0.003). Conclusion: PACG is involved in abnormal spontaneous brain activity in multiple brain areas, and such changes are associated with clinical performances, which may reflect the underlying pathologic mechanism and play important roles in the initiation and progression of PACG.