PURPOSE: To further the understanding of wound healing anomalies affecting visual function after myopic photorefractive keratectomy (PRK). METHOD: Analysis of a clinical database of PRK on 133 eyes with myopia of -1.5 to -7.0 D and 43 eyes with myopia of -6.0 to -12.0 D. Visual function was analyzed by subgroups of 1) no topographic anomalies; 2) topographic central islands; and 3) topographic keyhole patterns. The natural course of healing was documented over 6 months with visual acuity measurements, clinical observation, and corneal topography. In vivo clinical-pathologic correlations were made by scanning confocal microscopy. RESULTS: Topographic anomalies were identified 1 month post-PRK in 48 eyes (40.3%) with low-moderate myopia and in 14 eyes (32.5%) with moderate-high myopia. For patients with 6 month follow-up, these rates declined to 25% and 23%, respectively. At 1 month post-PRK, topographic anomalies significantly reduced uncorrected and best-corrected visual acuity and refractive predictability. By 6 months post-PRK, the small number of eyes with persistent anomalies had visual outcomes similar to patients with normal topography. A simple approach to anti-island pre-treatment reduced islands slightly and keyhole anomalies significantly (anti-island pre-treatment vs no pretreatment: islands 25% vs 31.8%; keyholes 2.3% vs 17.6%; p = 0.021) but with decreased predictability of induced refractive change at 1 month post-PRK. Confocal microscopy in vivo demonstrated prominent deposition of subepithelial extracellular material 1 to 2 months after PRK that diminished by 6 to 8 months, but persisted in the presence of central islands. Scar formation appeared to represent an elevated plaque of new collagen with active keratocytes. CONCLUSIONS: Topographic anomalies of wound healing are common after PRK. Vision and predictability are reduced by anomalies 1 month post-PRK but anomalies often resolve by 6 months. Marked improvement of vision occurs even when anomalies persist. Central islands appear to consist of persistent dense subepithelial extracellular deposits. Local scars are caused by new collagen deposition.