Myopia

Myopia (nearsightedness) is a refractive error in which the eye's optical power exceeds its axial length, so parallel light rays from distant objects converge in front of the retina rather than on it, producing blurred distance vision correctable with minus-power lenses. Childhood-onset myopia is a growing public health concern because axial elongation, particularly progression to high myopia, carries lifelong risk of sight-threatening complications.¹ Categories include simple/school-age myopia (progressive during growth years, stabilizing in adulthood), high myopia (generally ≥-6.00 D, greatest complication risk), pathologic/degenerative myopia (high myopia with structural chorioretinal changes carrying independent vision-loss risk), and axial versus refractive myopia (axial being most common and most relevant to progression and complications).

Myopia prevalence and severity vary substantially by ancestry: myopia, and especially high myopia, is more prevalent and severe among East Asian populations — particularly Chinese, Japanese, and Korean ancestry — than Caucasian populations.² Genetic architecture is complex and polygenic, with more than 400 gene loci mapped to myopia and refractive error.² Myopia develops through axial elongation during childhood ocular growth, driven by genetic predisposition and environmental exposures, principally near-work and reduced outdoor time — though the specific mechanism linking outdoor time to protection remains debated, and the claim that the effect is attributable specifically to daylight exposure itself is identified as lacking robust supporting evidence, as is the older hypothesis that relative peripheral hyperopia specifically drives central myopia progression.³

Patients report blurred distance vision with preserved near vision. Pediatric myopia often first becomes apparent through school vision screening, parental observation of squinting, or sitting close to screens. High myopes may report floaters or, in advanced cases, symptoms of complications (metamorphopsia, peripheral visual field loss).

Key differentials: pseudomyopia (accommodative spasm, resolves with cycloplegic refraction), lenticular myopia from early nuclear cataract, other pediatric vision complaints (amblyopia, strabismus) coexisting with refractive error, and keratoconus or corneal ectasia presenting as progressive myopic astigmatism.

Refraction shows reduced uncorrected distance acuity that improves with minus-lens correction. Biometry shows elongated axial length correlating with degree of myopia in axial myopia. High myopia shows peripapillary atrophy, tilted or myopic-crescent optic discs, posterior staphyloma, and lattice degeneration or peripheral retinal thinning on dilated exam. Progressive myopic shift on serial refraction distinguishes active progression from stable, corrected myopia.

Optical correction addresses the refractive error but does not slow axial elongation. For progressive pediatric myopia, evidence-based control strategies include increased outdoor time, low-concentration atropine, dual-focus/multifocal contact lenses, orthokeratology, and specialized myopia-control spectacles — each with a growing but variable evidence base, and none completely halting progression.¹ As of a review commissioned for a National Academies consensus study, dual-focus contact lenses were the only FDA-approved myopia control treatment in the US, despite broader international evidence for other interventions.¹ Clinicians should be cautious about several widely-repeated claims specifically identified as lacking robust evidence: that low-dose (0.01%) atropine reliably slows progression; that undercorrection slows progression (evidence instead suggests it may worsen it); that a given intervention's percentage treatment effect remains constant over time or applies uniformly across the progression range; and that handheld digital device use independently drives the myopia epidemic.³

High myopia carries meaningfully elevated lifetime risk of retinal detachment, myopic macular degeneration/maculopathy (including lacquer cracks and myopic choroidal neovascularization), posterior staphyloma, primary open-angle glaucoma, and earlier-onset, more surgically complex cataract.

• No current intervention completely halts myopia progression; the goal is slowing progression to reduce lifetime complication risk¹
• Be skeptical of confidently stated claims about myopia causation and treatment effect size — several widely repeated claims lack robust supporting evidence³
• Common pitfall: assuming all pediatric myopia is simple refractive myopia without considering pseudomyopia or corneal ectasia
• Common pitfall: treating unproven myopia-control claims (e.g., low-dose atropine efficacy, daylight-specific benefit) as established fact when counseling families³
• Common pitfall: overlooking dilated fundus exam for peripapillary atrophy, staphyloma, and peripheral retinal thinning in high myopes