Core Thesis The autistic brain operates under heightened predictive coding error weighting (Pellicano & Burr, 2012). When the visual input is degraded by uncorrected strabismus, amblyopia, or accommodative dysfunction, this weighting generates chronic low-level sensory noise that consumes cognitive resources otherwise available for compensation strategies pattern thinking, structured analysis, social masking. The result is a measurable shift in expressed severity that correlates with the timing of ophthalmological screening across national health systems. Empirical Foundation (5 converging axes) Ophthalmological infrastructure: strabismus prevalence in ASD reaches OR 4.72 (Perna et al., 2023, Molecular Psychiatry, 49 studies, 15.6M individuals) Critical window: stereopsis recovery after infantile esotropia drops from 77% (surgery ≤ 8 months) to 13% (surgery > 24 months) Birch 2009 Retinal signature: PhNR photopic markers distinguish primary ADHD from secondary visual-deficit ADHD (Constable 2022) International comparison: stratified prevalence gradients across US (ADDM), UK (NHS), Germany (KiGGS), Canada (PHAC), and France (INSERM) correlate with pediatric screening architecture Cascade model: sensory noise vs. sensory silence produces opposite neurodevelopmental trajectories, unifying ASD, visual dyslexia (Meares-Irlen/Stein), and secondary ADHD under a single chronological framework Falsifiability The CSC model defines explicit falsification criteria and proposes a three-study prospective research program. No strong causal claim is made. The framework is offered as a testable, refutable explanatory model compatible with existing genetic, neurochemical, and connectivity models. Citation and Usage Any academic or commercial work replicating, adapting, or building upon the CSC framework, its tripartite partition model, or its clinical recommendations must cite this foundational deposit.