Neuro-ophthalmic review on pediatric myopia: Advancing from refraction to a brain-centric model of axial growth

Abstract

Pediatric myopia is conventionally characterized as a refractive anomaly influenced by optical defocus and environmental factors. Emerging evidence suggests that axial elongation during childhood may be usefully reframed through a neuro-ophthalmic perspective, integrating retinal signaling, visual cortex maturation, and neuroplasticity. This minireview examines myopia within an eye–brain axis framework, emphasizing the roles of retinal neurotransmitters, dopaminergic pathways, and visual processing networks in regulating eye growth. Here, “brain-centric” denotes a clinically integrative model in which neurodevelopmental state and brain-governed behaviors (e.g., sleep/circadian timing, viewing habits, outdoor exposure) shape the visual inputs that engage established intraocular growth pathways, rather than implying that post-retinal processing is required for emmetropization. Advances in high-resolution imaging, electrophysiology, and functional neuroimaging have reported structural and functional differences in the retina and central visual pathways that may be detectable early during myopia development; however, evidence that such alterations consistently precede refractive error remains limited, and causal direction is not fully established. We examine how early visual experiences, sleep, digital viewing behaviors, and neurodevelopmental factors may influence these pathways in children. Reconceptualizing pediatric myopia within an eye–brain axis framework may support targeted prevention, individualized monitoring, and treatment selection, as well as hypothesis-driven predictive work to identify higher-risk trajectories, while avoiding causal overinterpretation when evidence remains primarily associative.

Keywords: Myopia; Child; Axial length; Eye; Visual pathways; Retina; Neuroplasticity; Dopamine

Core Tip: Pediatric myopia is not simply a refractive state, but a disorder of visually driven axial elongation shaped by neuroretinal signaling and developmental visual experience. Evidence supports prioritizing axial length as a core endpoint and integrating intermediate biomarkers (e.g., choroid and optical coherence tomography angiography or optical coherence tomography angiography metrics) to refine risk phenotyping and monitor response. A brain-informed “eye-brain axis” model can guide earlier prevention and individualized escalation, while avoiding overclaiming when central mechanisms remain only partially causal.