Functional and Metabolic Abnormalities in Primary Visual Cortex and Frontal Eye Fields and Candidate Biomarkers of Acute Acquired Comitant Esotropia

Purpose: To investigate functional and metabolic changes in the primary visual cortex (V1) and frontal eye fields (FEFs) of patients with acute acquired comitant esotropia (AACE), identify potential biomarkers, and explore their associations with clinical features. Methods: Fifteen patients with AACE and 15 healthy controls underwent resting-state functional magnetic resonance imaging and single-voxel ¹H-magnetic resonance spectroscopy. Regional homogeneity (ReHo) and amplitude of low-frequency fluctuation (ALFF) in V1 and FEF, as well as the absolute concentrations of N-acetylaspartate (NAA), aspartate (Asp), glutamate (Glu), and glutathione (GSH) in V1 and FEF, were compared between the two groups and selected via LASSO regression. Results: Compared with controls, the AACE group exhibited significantly increased ReHo and ALFF in both V1 and FEF (all false discovery rate [FDR] q < 0.05). ReHo levels in V1 and FEF significantly discriminated patients with AACE from controls in receiver operating characteristic (ROC) analysis (area under the curve = 0.77-0.83, all FDR q < 0.05). Asp and NAA levels in V1 were significantly lower in the AACE group than those in the control group and had significant discrimination by ROC analysis (all q < 0.05). Logistic least absolute shrinkage and selection operator regressions identified ReHo in FEF and V1, ALFF in FEF, NAA and Asp levels in V1, and GSH and NAA levels in FEF as potential biomarkers of AACE. Conclusions: The pathogenesis of AACE might involve dual neural mechanisms: neuronal metabolism alteration and adaptive function upregulation within the visual cortex and oculomotor cortical regions. ReHo in V1 and FEF could serve as core functional biomarkers, and NAA and Asp levels in V1 and NAA and GSH levels in FEF might serve as core metabolic biomarkers of AACE.