Author’s Disclosure Block: Michael Balas: none; Carmen Balian: none; Chris Hudson: none; Faryan Tayyari: none; Edward Margolin: none; Jonathan Micieli: none; Richard Swartz: none; Ilse Belgraver: none; Efrem Mandelcorn: none; Wendy Lou: none; Wendy Hatch: none

Abstract Body
Purpose: To evaluate longitudinal changes in ganglion cell layer (GCL) thickness in stroke patients and explore associations with stroke volume and vision pathway involvement. Study Design: Prospective cohort study using data from the Ontario Neurodegenerative Research Initiative (ONDRI). Methods: A total of 29 stroke patients (median age: 69.6 years, 72.4% male) were included, all of whom had at least two visits with measurements of GCL thickness via optical coherence tomography (OCT) and stroke volume via magnetic resonance imaging (MRI). Linear mixed-effects modeling was employed to assess thinning of the affected GCL hemiretina (sparing the fovea) over time, adjusted for age, sex, ethnicity, degree of white matter disease, stroke etiology, and vision pathway involvement. Time-adjusted differences in GCL thickness and stroke volume were compared between patients with and without vision pathway involvement using Wilcoxon rank-sum tests, and Spearman’s correlation was used to assess the relationship between GCL thickness and stroke volume. Results: GCL thickness decreased by an estimated 0.12 μm per year (95% CI: -0.29 to 0.04, p=0.15) following stroke. Degree of vision pathway involvement was not significantly associated with GCL thinning, with an estimated 0.01 μm increase in GCL thickness per year for every 1% increase in vision pathway involvement (95% CI: -0.042 to 0.061, p=0.77). Age was a significant predictor, with a reduction of 0.51 μm per year (95% CI: -0.76 to -0.26, p<0.01), indicating greater GCL thinning with advancing age. No significant differences in GCL thickness were observed based on sex, degree of white matter disease, or stroke etiology. Time-adjusted differences in GCL thickness did not significantly differ between patients with and without vision pathway involvement (p=0.20). However, stroke volume decreased significantly more in patients with vision pathway involvement (p<0.05). Spearman’s correlation demonstrated that as stroke volume decreases, GCL thickness also tends to decrease, although this correlation was not statistically significant (Spearman’s ρ=-0.415, p=0.10). Conclusion: In this cohort of stroke patients, GCL thinning was primarily associated with advancing age, while vision pathway involvement, stroke volume, or any of the other studied covariates did not significantly influence GCL loss. These findings highlight the need for further research to better understand the interplay between stroke-related brain changes and retinal degeneration, particularly in larger, more homogenous cohorts.