Myopia

Overview

Myopia, or nearsightedness, is a refractive error in which the eye's optical power is mismatched to its axial length — most commonly because the eye is too long relative to its focusing power — so that parallel light rays from distant objects converge in front of the retina rather than on it, producing blurred distance vision that improves with minus-power lens correction. Myopia is not simply a nuisance refractive error: axial elongation, particularly in high myopia, is associated with a lifelong elevated risk of sight-threatening complications, which has made pediatric myopia control a growing clinical and public health priority.¹

Epidemiology & Risk Factors

Myopia prevalence and severity vary substantially by ancestry and geography: myopia, and especially high myopia, is more prevalent and more severe among East Asian populations — particularly individuals of Chinese, Japanese, and Korean ancestry — than among individuals of Caucasian ancestry.² Genetic architecture is complex and polygenic: more than 400 gene loci have been mapped to myopia and refractive error through family linkage studies, candidate-gene studies, genome-wide association studies, and next-generation sequencing.² Lifestyle and environmental factors — most consistently, greater near-work and reduced outdoor time — are considered the primary external factors influencing myopia onset and progression, though the specific mechanism by which outdoor time is protective (proposed to relate to light exposure) is still debated, and the claim that the effect is specifically attributable to daylight itself is identified as lacking robust supporting evidence.³ Because gene-environment interaction shapes both onset and progression, polygenic risk scores are an active area of research aimed at identifying children likely to progress to high myopia who might benefit most from early intervention.²

Pathophysiology

Myopia develops through axial elongation of the eye during a period of active ocular growth in childhood, driven by a combination of genetic predisposition and environmental exposures (principally near-work and reduced outdoor time). The precise visual signaling mechanisms that translate near-work and light exposure into a growth signal favoring axial elongation remain incompletely understood and are an active area of investigation; the once-common hypothesis that relative peripheral hyperopia specifically drives central myopia onset and progression in children is explicitly identified as lacking a robust evidence base.³

Clinical Presentation

Children and adults with myopia typically report blurred distance vision — difficulty seeing the whiteboard, street signs, or faces across a room — while near vision (reading, close work) remains clear or is even subjectively easier. Pediatric myopia often first becomes apparent through school vision screening, parental observation of squinting, or sitting unusually close to screens/books. High myopes may additionally report floaters or, in advanced cases, symptoms of the myopia-associated complications described below (metamorphopsia, peripheral visual field loss).

Exam Findings

• Reduced uncorrected distance visual acuity that improves with minus-lens correction on refraction
• Elongated axial length on biometry, correlating with the degree of myopia in axial (as opposed to purely refractive) myopia
• In high myopia: peripapillary atrophy, tilted or myopic-crescent optic discs, posterior staphyloma, and lattice degeneration or other peripheral retinal thinning on dilated fundus exam
• Progressive myopic shift on serial refraction is the key finding distinguishing active progression from stable, corrected myopia

Classification

• Simple/school-age myopia: onset in childhood, typically progressive during the growth years and stabilizing in early adulthood
• High myopia: generally defined as a spherical equivalent at or beyond a threshold commonly set around -6.00 D (thresholds vary by source), associated with the greatest risk of axial-elongation-related complications
• Pathologic (degenerative) myopia: high myopia accompanied by structural chorioretinal changes (posterior staphyloma, myopic maculopathy, lacquer cracks) that carry independent risk of vision loss beyond the refractive error itself
• Axial vs. refractive myopia: distinguishing whether the mismatch between optical power and focal length is primarily due to increased axial length (axial myopia, most common and most relevant to progression/complications) or increased corneal/lenticular power relative to a normal axial length (refractive myopia)

Differential Diagnosis

• Pseudomyopia (accommodative spasm), which can mimic true myopia on manifest refraction but resolves with cycloplegic refraction
• Lenticular myopia from early nuclear cataract changes in adults
• Other causes of pediatric vision complaints (amblyopia, strabismus) that may coexist with or be mistaken for uncorrected refractive error
• Keratoconus or other corneal ectasia, which can present with progressive myopic astigmatism rather than pure spherical myopia (see the Astigmatism entry for irregular-astigmatism red flags)

Management

Optical correction (spectacles or contact lenses) addresses the refractive error itself but does not slow axial elongation. For children with progressive myopia, several evidence-based myopia control strategies exist, each with a growing but variable evidence base and none completely halting progression: increased time outdoors, low-concentration atropine eye drops, dual-focus and multifocal soft contact lenses, orthokeratology lenses, and specialized myopia-control spectacle lenses.¹ As of a comprehensive evidence review commissioned for a National Academies consensus study, dual-focus contact lenses were the only myopia treatment approved by the US Food and Drug Administration specifically for myopia control, despite growing international evidence supporting several other interventions.¹

Clinicians should be aware that several commonly repeated claims in myopia management lack a robust evidence base as characterized by a critical review of the field, including: that low-dose (0.01%) atropine reliably slows progression; that undercorrection of myopia slows progression (evidence instead suggests undercorrection may worsen progression); that the percentage treatment effect of an intervention remains constant over time or applies uniformly across the full range of progression; and that handheld digital device use independently contributes to the myopia epidemic.³ This underscores the importance of counseling families using current, specific evidence for a given intervention rather than generalized assumptions.

Complications

High myopia carries meaningfully elevated lifetime risk of:

• Retinal detachment (see the dedicated entry on this topic)
• Myopic macular degeneration/maculopathy, including lacquer cracks and myopic choroidal neovascularization
• Posterior staphyloma
• Primary open-angle glaucoma
• Earlier-onset cataract and increased surgical complexity of cataract surgery in highly myopic eyes

Clinical Pearls

• Myopia prevalence and severity are strongly influenced by ancestry, with East Asian populations at disproportionately higher risk of high myopia — a relevant consideration when counseling families about progression risk and monitoring intensity.²
• No current intervention completely halts myopia progression; the goal of myopia control is slowing progression to reduce the lifetime risk of high-myopia-associated complications, not achieving zero further change.¹
• Be skeptical of confidently stated "facts" about myopia causation and treatment effect size — a number of widely repeated claims in the field, including specific claims about low-dose atropine, undercorrection, and screen time, are identified as lacking robust supporting evidence.³

Common Pitfalls

• Assuming all myopia in a child is simple refractive myopia without considering pseudomyopia (which requires cycloplegic refraction to unmask) or an underlying corneal ectasia presenting as progressive myopic astigmatism.
• Treating unproven myopia-control claims (e.g., the specific efficacy of low-dose 0.01% atropine, or that daylight exposure itself — rather than outdoor time generally — is protective) as established fact when counseling families.³
• Overlooking that dilated fundus exam for peripapillary atrophy, staphyloma, and peripheral retinal thinning is particularly important in high myopes, given their elevated risk of retinal complications.
• Assuming a myopia-control intervention's treatment effect is constant over time or applies equally across all levels of baseline progression, when the evidence for this assumption is specifically called into question.³