Background and objective Keratoconus is a chronic, progressive corneal disease that occurs primarily in people of working age and significantly affects visual function. However, its broader impact on vision-related quality of life (VRQoL), work productivity, and functional capacity remains poorly investigated. The primary objective of this study was to assess the impact of keratoconus on VRQoL and work productivity. Secondary objectives included the evaluation of daily activity impairment and the investigation of associations between these outcomes and demographic, clinical, and economic factors. Methods A cross-sectional study was conducted in patients with keratoconus, who completed the National Eye Institute Visual Function Questionnaire-25 (VFQ-25) and the Work Productivity and Activity Impairment (WPAI) Questionnaire. Demographic and clinical data, including Amsler-Krumeich staging and type of treatment, were collected. Associations were assessed using univariate and multivariate analyses. Results Reduced VRQoL was significantly associated with increased presenteeism, overall work productivity loss, and functional disability. The VFQ-25 subscales for near and distance vision activities, mental health, and caregiver dependence showed the strongest associations. Higher age, advanced stages of keratoconus, especially in the worse eye, and surgical treatment were associated with lower VRQoL. No independent association was observed between VRQoL and annual treatment costs. Conclusions Keratoconus imposes a substantial functional and psychosocial burden, significantly impairing VRQoL and work productivity. Reduced VRQoL was strongly associated with increased presenteeism, overall productivity loss, and activity impairment, highlighting its role as a key indicator of disease burden. Disease severity, older age, and surgical treatment were identified as important determinants of poorer outcomes. These findings underscore the importance of early detection and comprehensive, patient-centered management strategies, including the routine assessment of VRQoL and functional outcomes in clinical practice.

Background: Post-traumatic stress disorder (PTSD) exhibits heterogeneous clinical trajectories: while many affected individuals achieve remission, a substantial proportion develop a chronic, persistent form. The neuroanatomical mechanisms distinguishing these divergent outcomes remain poorly defined. This study aimed to elucidate the structural network organisation of persistent PTSD using structural covariance network analysis.Methods: Participants included trauma-unexposed healthy controls (HC; n = 112), individuals with remitted PTSD (n = 32), and those with persistent PTSD (n = 78). High-resolution T1-weighted magnetic resonance imaging data were analyzed using independent component analysis to extract spatially independent morphometric networks. Gray matter volumes within these networks were subsequently compared across groups.Results: Linear trend analysis revealed a stepwise reduction in gray matter volume within the frontal-cognitive control and visual networks across groups (HC > remitted PTSD > persistent PTSD). Further examination of inter-network connectivity demonstrated heightened connectivity between the frontal-cognitive control and temporo-insular-limbic networks in the persistent PTSD group, compared with both the remitted PTSD and HC groups. Notably, the remitted PTSD group exhibited inter-network connectivity levels comparable to those of HC. This hyperconnectivity in persistent PTSD reflects compensatory recruitment of cognitive control mechanisms to regulate interoceptive and emotional processing systems, thereby sustaining symptom modulation.Conclusion: Persistent PTSD is characterised by progressive gray matter volume reductions and compensatory hyperconnectivity between cognitive control and limbic-interoceptive networks, indicative of sustained engagement of regulatory mechanisms to modulate enduring symptoms. These findings provide novel neurobiological insights into the mechanisms of PTSD chronicity and highlight potential network-level targets (particularly prefrontal-limbic interactions) for future investigation of personalised interventions in treatment-resistant cases.

Diabetic retinopathy (DR) is a leading cause of vision loss worldwide and represents a complex neurovascular complication of diabetes mellitus driven by chronic hyperglycemia. Increasing evidence identifies oxidative stress-defined as an imbalance between reactive oxygen species (ROS) production and antioxidant defenses-as a central pathogenic mechanism linking metabolic dysregulation to retinal injury. The retina is particularly vulnerable to oxidative damage due to its high metabolic demand, elevated oxygen consumption, and abundance of polyunsaturated fatty acids. Hyperglycemia activates multiple interconnected biochemical pathways, including the polyol and hexosamine pathways, protein kinase C signaling, advanced glycation end-product formation, and lipid peroxidation, all of which converge on excessive ROS production and mitochondrial dysfunction. Growing attention has focused on oxidative stress biomarkers as tools to characterize DR severity and progression. Elevated systemic markers of lipid, protein, and DNA oxidation, together with impaired antioxidant capacity, correlate with disease stage, while oxidative biomarkers detected in aqueous and vitreous humor reflect localized retinal injury. Importantly, oxidative stress biomarkers are also associated with functional outcomes, including best-corrected visual acuity and diabetic macular edema. Integration of systemic and ocular oxidative biomarkers with clinical staging may improve risk stratification and support personalized therapeutic strategies in DR.

Leber hereditary optic neuropathy (LHON) is a mitochondrial optic neuropathy that typically causes severe bilateral central vision loss. Although several natural-history studies have reported visual outcomes, long-term trajectories beyond 5 years remain incompletely quantified, particularly in Asian cohorts. We performed a single-center retrospective cohort study at a tertiary eye hospital in Japan. Among 174 genetically confirmed LHON patients, we identified 27 patients (53 eyes) who presented within 6 months of onset and were followed continuously for ≥10 years. Best-corrected visual acuity (BCVA, logMAR) was collected from onset to 120 months. Piecewise linear mixed-effects models with patient- and eye-level random effects were fitted over three phases (Acute, < 12 months; Chronic, 12-60 months; Late Chronic, 60-120 months). Kaplan-Meier analyses estimated time to achieving BCVA ≤1.6 and ≤1.3 logMAR. BCVA worsened rapidly after onset, followed by gradual improvement and then an approximately horizontal course. During the Chronic phase, BCVA showed a small but statistically significant improvement (overall -0.030 logMAR/year, 95% confidence interval (CI) -0.045 to -0.015; -0.025 logMAR/year, 95% CI -0.044 to -0.007 in a pre-specified m.11778G > A subgroup). In the Late Chronic phase, estimated slopes were close to zero (+0.003 logMAR/year, 95% CI -0.007 to +0.013 overall), with wide CIs compatible with small long-term improvement or deterioration. By 10 years, the cumulative probabilities of achieving BCVA ≤1.6 and ≤1.3 logMAR were approximately 45% and 26%, respectively. In this Japanese LHON cohort with ≥10 years of continuous follow-up, BCVA showed limited improvement during the early chronic period, and we did not detect a clear directional trend thereafter. Given the modest sample size and selection of long-term attendees, these estimates should be interpreted as descriptive, phase-specific benchmarks rather than definitive evidence of long-term stability or ethnic differences.