Childhood Myopia and Ocular Development

Etiology

In myopia, the image forms in front of the retinal photoreceptors. Based on the pathogenesis, myopia can be classified as follows:

• Axial myopia:  Axial myopia results from a rapid increase in axial length. Axial length increases by 0.35 mm for every diopter increase in myopia.[12]
• Curvature myopia: Curvature myopia results from increased corneal curvature. Consequently, the image is focused in front of the retina. Each 1-mm change in the radius of curvature of the cornea causes a myopic shift by 6 diopters.[13]
• Lenticular myopia: Lenticular myopia results from an increase in the refractive index of the crystalline lens. Please see StatPearls' companion reference, "Hyperopia," for further information.
• Positional myopia and other conditions: Myopia may result from anterior shifting of the crystalline lens.[14] Sudden-onset myopia may result from anterior displacement of the lens-iris diaphragm in various conditions, including choroidal effusion and anterior rotation of the ciliary body induced by drugs such as topiramate.[14]

Premyopia is a nonrefractive state in children aged 5 to 7 years with hyperopia less than +0.75 diopter sphere and myopia greater than −0.5 diopter sphere, which helps predict the early development of myopia.[15] Childhood myopia is a complex multifactorial disorder resulting from the interaction among genetic susceptibility, environmental exposures, behavioral factors, visual experiences, and biological mechanisms that regulate ocular growth (see Tabe 1). Contemporary evidence supports that no single etiologic factor is sufficient to induce myopia; rather, disease development occurs through cumulative influences acting on retinal signaling pathways, choroidal modulation, scleral remodeling, and axial elongation. The rapid global increase in myopia prevalence over recent decades strongly indicates that environmental and lifestyle factors have become increasingly important contributors to disease expression in genetically predisposed individuals. Please see StatPearls' companion reference, "Myopia," for further information.

Genetic Predisposition

Genetic susceptibility remains one of the strongest risk factors for childhood myopia. Children with 1 parent with myopia have a significantly increased risk of developing myopia, whereas children with 2 parents with myopia demonstrate an even greater likelihood of earlier onset and faster progression. Results from genome-wide association studies identified hundreds of loci associated with refractive error, axial length regulation, extracellular matrix metabolism, retinal neurotransmission, and scleral biomechanics. Genes involved in collagen synthesis, transforming growth factor signaling, retinal dopamine pathways, and photoreceptor function have all been implicated in myopia susceptibility. However, genetic predisposition alone does not explain the dramatic rise in myopia prevalence observed within a single generation, emphasizing the critical role of environmental influences.[10]

Educational Pressure and Academic Exposure

Educational intensity has emerged as a major environmental determinant of childhood myopia. Children exposed to prolonged academic activities, extensive reading, early educational programs, and high-performance learning environments consistently exhibit higher rates of myopia. Results from several large population-based studies demonstrated a direct relationship between years of education and the progression of refractive error. Educational exposure may contribute through sustained accommodative demand, reduced outdoor activity, increased near work, and alterations in visual behavior. The association remains significant even after adjustment for parental myopia and socioeconomic status, highlighting education as an independent risk factor.[11]

Near-Work Activities

Prolonged near work is strongly associated with the development and progression of myopia. Activities such as reading, writing, tablet use, smartphone viewing, and computer-based learning require sustained accommodation and convergence. Excessive near work may induce hyperopic retinal defocus, accommodative lag, peripheral image blur, and retinal signaling changes that promote axial elongation. Children spending prolonged periods performing near tasks at close viewing distances may experience greater cumulative retinal stress and ocular growth stimulation. Importantly, continuous near work without regular visual breaks appears more strongly associated with myopia progression than total near-work duration alone.[16]

Digital Device Exposure

The widespread adoption of smartphones, tablets, and digital learning platforms has introduced new visual environments during critical periods of ocular development. Digital screens are often viewed at shorter working distances than printed materials and may encourage prolonged uninterrupted visual engagement. Excessive screen exposure has been linked to increased accommodative demand, reduced blink rate, ocular fatigue, and decreased outdoor activity. Although direct causality remains under investigation, digital device use is increasingly recognized as a potential contributor to modern myopia epidemics.[17]

Reduced Outdoor Exposure

Among all modifiable environmental factors, reduced time spent outdoors is one of the most consistently identified risk factors for childhood myopia. Results from numerous longitudinal studies demonstrated that increased outdoor activity lowers the risk of myopia onset. Bright outdoor illumination stimulates retinal dopamine release, which is believed to inhibit excessive axial elongation. Outdoor environments additionally provide greater viewing distances, richer spatial stimuli, and reduced accommodative demand compared with indoor settings. Protective effects appear independent of physical activity itself and are primarily attributed to environmental light exposure.[18]

Urbanization and Lifestyle Changes

Urban populations consistently exhibit higher myopia prevalence than rural communities. Urbanization influences visual behavior through increased educational competition, reduced access to outdoor spaces, greater screen use, and prolonged indoor lifestyles. High population density, limited natural environments, and modern architectural designs may further alter visual experiences during childhood. Socioeconomic development has therefore become closely associated with increasing myopia prevalence across many regions of the world.[19]

Circadian Rhythm and Sleep Disturbances

Emerging evidence suggests that circadian dysregulation may contribute to abnormal ocular growth. Sleep duration, sleep quality, and light exposure patterns influence retinal neurotransmitter activity and ocular physiology. Irregular sleep schedules, excessive nighttime screen exposure, and reduced daytime light stimulation may disrupt normal retinal signaling pathways involved in refractive development. Although the exact mechanisms remain under investigation, circadian influences are increasingly recognized as potential contributors to myopia progression.[20]

Nutritional and Metabolic Factors

Nutrition may indirectly influence ocular development by affecting growth regulation, inflammation, oxidative stress, and extracellular matrix metabolism. Deficiencies in vitamin D, antioxidant nutrients, and essential micronutrients have been investigated as potential risk modifiers, although evidence remains inconsistent. Metabolic disorders associated with obesity, insulin resistance, and altered growth factor signaling have also been explored as possible contributors to excessive axial elongation.[21]

Prenatal and Early-Life Influences

Prenatal and perinatal factors may influence refractive development before the onset of visual maturation. Low birth weight, prematurity, maternal smoking, gestational complications, and abnormal fetal growth patterns have all been associated with altered ocular development. Early childhood visual experiences, environmental stimulation, and developmental exposures may further influence subsequent refractive trajectories. Please see StatPearls' companion reference, "Myopia," for further information.

Environmental Pollution and Emerging Risk Factors

Results from recent studies suggested associations among air pollution, reduced sunlight exposure, urban environmental stressors, and the development of myopia. Chronic exposure to particulate matter and environmental pollutants may influence inflammatory pathways and outdoor activity patterns. Although evidence remains preliminary, environmental health factors are increasingly being investigated as contributors to modern myopia epidemics.[22]

Table 1. Major Etiological Factors Associated with Childhood Myopia

Epidemiology

Myopia has become a public health concern. The rising incidence of myopia can be attributed to reduced outdoor activity, increased screen time, and prolonged near-work, especially during the COVID-19 pandemic.[23] The reported prevalence of myopia in Singapore among children aged 6 to 7 years is 20% to 30%.[24] In China, the prevalence of myopia in children aged 5 to 15 years ranges from 5.7% to 78.4%.[25] 

Myopia is more prevalent in Asian children than in children in European countries, where the prevalence of myopia is lower (17.8%-23.5%).[26] In the US, the prevalence of myopia ranges from 4.6% to 28% in children aged 6 to 12 years.[27] In India, the range varies from 8.5% to 15% among urban children aged 5 to 15 years.[28]

Myopia has emerged as one of the most significant ocular public health challenges worldwide. Over the past few decades, the prevalence of childhood myopia has increased substantially across multiple geographic regions, prompting concerns regarding future burdens of visual impairment and myopia-associated ocular complications. The increasing prevalence has been attributed to a complex interaction between genetic susceptibility and environmental factors, including reduced outdoor exposure, increased educational pressures, prolonged near-work activities, and greater use of digital devices. The COVID-19 pandemic further accelerated these trends due to home confinement, virtual learning, and increased screen exposure among school-aged children.[21]

The prevalence of childhood myopia demonstrates considerable geographic and ethnic variation (see Table 2). East and Southeast Asian countries report the highest rates globally. In Singapore, myopia affects approximately 20% to 30% of children aged 6 to 7 years, with prevalence increasing progressively throughout adolescence. In mainland China, reported prevalence ranges from 5.7% in younger children to more than 78% among adolescents aged 15 years, reflecting both age-dependent progression and regional differences. Urban centers in China, Hong Kong, Taiwan, South Korea, and Japan consistently report some of the highest prevalence rates worldwide, with myopia affecting more than 80% of high-school graduates in certain populations.[11]

Conversely, European populations demonstrate comparatively lower rates of childhood myopia. Results from studies from Northern and Western Europe reported prevalence rates ranging from 17.8% to 23.5% among school-aged children. However, recent epidemiologic data suggest a gradual increase in prevalence even within traditionally low-risk populations, indicating that environmental influences may be overcoming historical geographic differences.[11] In the US, childhood myopia prevalence varies according to age, ethnicity, and study methodology. Reported prevalence ranges from 4.6% to 28% among children aged 6 to 12 years. The condition is more frequently observed in older children and adolescents than in preschool-aged populations. Ethnic disparities have also been documented, with higher prevalence among children of East Asian ancestry compared with Black, Hispanic, or White children.[11]

In India, childhood myopia prevalence ranges from 8.5% to 15% among children aged 5 to 15 years living in urban areas. Urban populations consistently demonstrate higher rates than rural populations, likely reflecting differences in educational intensity, outdoor activity patterns, and digital device use. Results from several Indian epidemiologic studies reported a rising trend in school-based myopia over the last 2 decades, paralleling global observations.[8] Age remains one of the strongest determinants of myopia prevalence. The condition is relatively uncommon before school age but increases steadily during primary and secondary school years, corresponding with periods of rapid ocular growth and increased academic demands. Peak incidence typically occurs between 7 and 15 years of age, with progression often continuing until late adolescence.[29]

Sex-related differences in childhood myopia have been inconsistently reported. Results from several population-based studies demonstrated slightly higher prevalence rates among girls, potentially related to earlier pubertal growth, increased educational engagement, or differences in outdoor activity patterns. However, results from other studies found minimal or no significant sex-related differences after adjusting for environmental and behavioral factors. Recent global estimates suggest that approximately 30% of the world population is currently myopic, with projections indicating that nearly 50% may be affected by 2050 if current trends continue. Childhood-onset myopia is of particular concern because earlier onset is associated with greater progression and a higher risk of developing high myopia in adulthood. High myopia substantially increases the lifetime risk of retinal detachment, myopic maculopathy, glaucoma, cataract, and irreversible visual impairment.[5] The global burden of childhood myopia is therefore expected to continue increasing, emphasizing the importance of early identification, preventive interventions, and public health strategies aimed at reducing modifiable environmental risk factors.

Table 2. Global Prevalence of Childhood Myopia by Geographic Region

Pathophysiology

Myopia and Ocular Development

Refractive error results from a long, complex process of ocular development; hence, myopia cannot be attributed to a single trait. Many factors contribute to the development of childhood myopia, including the extent and effectiveness of emmetropization during the early years of life, environmental influences, genetic factors, and changes in axial length and lens power during adolescence (see Table 3).[30] Myopia develops at the same age as hyperopia correction. Early-onset myopia is usually associated with higher refractive errors and results in progressive thinning of the choroid, staphyloma, and pathologic retinal degeneration.[31] 

Emmetropization

Emmetropization is a process in which the refractive components, including corneal curvature and lenticular curvature, balance with the eye's postnatal development, resulting in the nullification of refractive errors. At birth, the child is hyperopic, with an average refractive error of +2 to +3 diopters.[32] However, with age, the refractive error decreases and may reach emmetropia or myopia, which is more common in the population.[33] The axial length at birth is 16 to 18 mm, increasing to 23 mm by age 3 years. After age 3 years, the axial length growth rate decreases.[34] The rapid increase in axial length should cause a myopic shift; however, other changes in the lens and corneal curvature control this shift, preventing rapid progression.[35]

Sclera and Myopia

The sclera is the outermost coat of the eye and is composed chiefly of collagen types I and III.[36] Proteoglycans modulate collagen assembly. Decorin and biglycan are the most common sulfated proteoglycans present in the sclera.[37] Proteoglycan hydration is considered responsible for age-related changes in the sclera. The interaction between scleral fibroblast cells and the scleral matrix plays a vital role in controlling the distensibility of the sclera during eye growth.[38] During emmetropization, accurate regulation of scleral extracellular matrix growth and remodeling governs eye development.

Embryonic development of sclera: The sclera develops in the sixth week of prenatal life from the cells of the neural crest, or neuroectoderm, and mesoderm.[39] The sclera reaches its adult size by age 10 years. However, the extracellular matrix of the sclera continues to change.[40] In patients with myopia, the sclera is characterized by increased elasticity, which can be attributed to ultrastructural changes of the sclera. The fibroblasts are arranged in a lamellar pattern in patients with myopia and are associated with thinning of collagen bundles.[41] This increased scleral elasticity increases axial length, shifting the image anteriorly.

Emmetropization and scleral remodeling: Scleral extracellular matrix remodeling is regulated by several growth factors, including insulin-like growth factors 1 and 2.[42] Additionally, scleral extracellular matrix remodeling is controlled by locally generated growth factors from the retina and choroid.[43] Results from various experimental models suggest that visual signals in the form of retinal blur induce the production of γ-aminobutyric acid, dopamine, insulin, and glucagon, which in turn elicit a response in the retinal pigment epithelium and choroid, leading to the release of regulatory growth factors and ultimately to scleral extracellular matrix remodeling.[44] 

Choroidal Modulation

The choroid is a highly vascular middle coat of the eyeball. The choroid provides nutrients and oxygen to the outer retinal layers and sclera. Results from various animal models have demonstrated the importance of the choroid in the development of myopia and emmetropization. The choroid regulates its thickness to adjust the retina to the focal plane of the eye, a term known as choroidal accommodation.[45] 

The choroid also delivers growth-stimulating factors to the sclera, thereby regulating the scleral extracellular matrix and axial length.[46] Results from animal models suggested that increased production of choroidal all-trans-retinoic acid is associated with a reduction in scleral proteoglycan and an increase in axial length.[47] With the advent of noninvasive techniques such as enhanced-depth spectral-domain optical coherence tomography, choroidal imaging is now possible. In patients with high myopia, the choroid is usually associated with thinning on optical coherence tomography. A thinner choroid on optical coherence tomography suggests a poorer prognosis and is generally associated with thinner retinal layers.[48] 

Lens Curvature Changes in Childhood

The lens at birth has a spherical contour and eventually flattens.[49] The flattening of the lens can be due to the equatorial expansion and central compaction forces generated by the growing eyeball.[50] As the eyeball grows, the thickness of the lens also decreases along with the increase in the diameter of the ciliary body, which tensions the zonules and causes lens thinning.[51] The thickness of the lens decreases from 4 mm at birth to 3.3 mm by adolescence.[52] This thinning changes the lens dioptric power from 34.4 diopters at birth to 23 diopters at age 3 years and 20 diopters at age 14 years, preventing the myopic shift.[53]  

Factors Affecting Myopia Development and Progression

Family history: Results from various studies suggested that the risk of early-onset myopia development and progression is higher in children if either of the parents has myopia.[54][55]

Birth history: Low birth weight and premature birth associated with retinopathy of prematurity have been suggested to be associated with myopia development.[56] Sunlight exposure or birth during the summer of the perinatal period is also associated with the development of myopia in later life.[57]

Excessive near work: Excessive near work is associated with myopia progression resulting from accommodative lag. Accommodative lag is the difference between the accommodative stimulus, or demand, and the accommodative response.[58] The longer the accommodative lag is, the greater the myopia progression. Excessive near work in patients with myopia causes prolonged retinal defocus, which further stimulates axial length growth.[59]

Higher intelligence quotient: Myopia development may be associated with higher cognitive functions, better education, and a higher intelligence quotient.[60] Results from a population-based study by Mirshahi et al found that higher levels of professional education were associated with higher rates of myopic refractive error compared with participants with lower levels of education.[61] This association can be attributed to defocus signals in the peripheral and central retina with constant accommodative lags.[62]

Outdoor activities: Results from various studies found that outdoor activities reduce myopia progression. One hypothesis suggests that the wavelength of radiant sunlight is 550 nm, the same wavelength focused on a normal observer's retina.[63] Conversely, indoor lights have a longer wavelength and are focused behind the retina.[64] Results from an experimental study found that the spatial features of the indoor environment are similar to those of artificial spatial features created by diffuse filters that induce myopia in animals.[65] Another hypothesis states that sunlight inhibits the increase in axial length by promoting dopamine release.[66]

Increased screen time: Increased screen time can lead to the development of myopia and is attributed to increased time spent indoors.[67] Results from a study by Enthoven et al found that continuous smartphone use for 20 min was associated with a higher risk of developing myopia.[68]

Retinal Defocus Signaling and Peripheral Hyperopic Defocus

Recent evidence suggests that retinal image quality plays a central role in regulating ocular growth. During childhood, the retina continuously monitors the position of the focal plane relative to the photoreceptor layer. When images are focused behind the peripheral retina, a phenomenon known as peripheral hyperopic defocus occurs. Peripheral hyperopic defocus acts as a growth-promoting signal, stimulating axial elongation of the eye in an attempt to move the retina toward the focal plane. Results from experimental studies demonstrated that peripheral retinal signals may exert a stronger influence on ocular growth than central foveal signals, providing the biological rationale for modern myopia-control strategies such as orthokeratology and peripheral-defocus spectacle lenses.[5]

Dopaminergic Regulation of Eye Growth

Dopamine has emerged as one of the most important neurotransmitters involved in ocular growth regulation. Retinal dopamine release increases in response to bright outdoor light exposure and functions as an inhibitory signal against excessive axial elongation. Reduced dopamine activity has been observed in experimental models of form-deprivation myopia and lens-induced myopia. This dopamine-related mechanism may partly explain the protective effect of outdoor activities against the progression of childhood myopia. The interaction between dopamine signaling and circadian rhythms has also been proposed as an important regulator of ocular development.[6]

Circadian Rhythm and Ocular Growth

The eye demonstrates circadian fluctuations in axial length, choroidal thickness, and intraocular pressure. Normal ocular development appears to depend on synchronized circadian regulation of these parameters. Disruption of sleep patterns, excessive nighttime screen exposure, and altered light-dark cycles may interfere with these physiological rhythms, leading to dysregulated ocular growth. Results from recent studies suggest that prolonged evening exposure to artificial light may suppress melatonin secretion and indirectly affect retinal pathways involved in emmetropization.[20]

Retinal Pigment Epithelium as a Signaling Interface

The retinal pigment epithelium (RPE) serves as a critical intermediary between the neural retina and sclera. Visual defocus signals generated within the retina are believed to be transmitted through the RPE via alterations in ion transport, growth factor secretion, and extracellular signaling molecules. The RPE modulates the release of transforming growth factor-β, vascular endothelial growth factor, fibroblast growth factors, and retinoic acid derivatives that ultimately influence scleral remodeling and axial elongation. Consequently, the RPE functions as a key relay station in the retina–choroid–sclera signaling cascade.[5]

Role of Hypoxia and Scleral Metabolism

Emerging evidence indicates that localized scleral hypoxia may contribute to myopia progression. During axial elongation, alterations in choroidal perfusion and scleral oxygenation may activate hypoxia-inducible factor-1α pathways. Activation of these pathways promotes extracellular matrix degradation and reduces collagen synthesis, thereby weakening the scleral wall and facilitating further elongation. Results from experimental studies demonstrated upregulation of hypoxia-related genes in highly myopic eyes, suggesting that metabolic remodeling may be an important component of disease progression.[7]

Matrix Metalloproteinases and Extracellular Matrix Degradation

Scleral remodeling in myopia is associated with increased activity of matrix metalloproteinases, particularly matrix metalloproteinase 2 and matrix metalloproteinase 9. These enzymes degrade collagen fibrils and extracellular matrix components, reducing scleral rigidity. Simultaneously, tissue inhibitors of metalloproteinases are downregulated, shifting the balance toward matrix degradation. This biochemical shift results in progressive scleral thinning and biomechanical weakening, facilitating continued axial elongation.[69]

Biomechanical Failure of the Posterior Pole

Highly myopic eyes exhibit progressive biomechanical instability of the posterior sclera. During axial elongation, mechanical stress becomes concentrated at the posterior pole, resulting in localized stretching, scleral thinning, and deformation. This biomechanical instability contributes to the development of posterior staphyloma, lacquer cracks, chorioretinal atrophy, and myopic maculopathy. Results from modern imaging studies suggested that biomechanical failure of the posterior ocular wall may be a critical determinant of pathologic myopia rather than axial length alone.[70]

Genetic and Epigenetic Regulation

Results from genome-wide association studies identified more than 500 genetic loci associated with refractive development and susceptibility to myopia. Many of these genes are involved in extracellular matrix regulation, neuronal signaling, retinal development, and ocular growth pathways. Additionally, environmental exposures during childhood may induce epigenetic modifications, including DNA methylation and histone alterations, which influence the expression of growth-regulating genes. These findings support the concept that childhood myopia results from complex interactions between inherited susceptibility and environmental triggers.[71]

Neurovascular Changes During Myopia Progression

Progressive axial elongation is associated with alterations in retinal and choroidal microcirculation. Results from optical coherence tomography angiography studies demonstrated reduced choroidal vascularity and decreased retinal perfusion density in highly myopic eyes. These vascular changes may contribute to retinal hypoxia, choroidal thinning, and subsequent degenerative complications. Neurovascular remodeling is increasingly recognized as a component of pathologic myopia rather than merely a consequence of globe enlargement.[72]

Table 3. Pathophysiology of Myopia

Abbreviations: FGF, fibroblast growth factor; HIF-1α, hypoxia-inducible factor 1α; MMP, matrix metalloproteinase; OCTA, optical coherence tomography angiography; RPE, retinal pigment epithelium; TGF-β, transforming growth factor β; TIMP, tissue inhibitor of metalloproteinase; VEGF, vascular endothelial growth factor.

Histopathology

The hallmark histopathologic feature of myopia is progressive axial elongation of the globe, accompanied by remodeling of the sclera, choroid, and retina. Histologic examination demonstrates thinning of the posterior sclera, attributable to reduced collagen fibril diameter, decreased collagen fiber density, and alterations in extracellular matrix composition. The scleral fibroblasts exhibit reduced synthetic activity, leading to diminished production of collagen types I and III and increased susceptibility to biomechanical stretching. These changes are particularly pronounced in eyes with high or pathologic myopia.[5] Table 5 summarizes these features.

The choroid undergoes progressive thinning with loss of vascular and stromal components. Results from histopathologic studies demonstrated attenuation of the choriocapillaris, decreased vascular density, and reduction in melanocyte and connective tissue content. Choroidal thinning contributes to impaired metabolic support of the outer retina and is strongly associated with myopic maculopathy and posterior staphyloma formation.[6] Retinal changes are generally minimal in early childhood myopia but become increasingly evident with greater degrees of axial elongation. Histologic examination may reveal thinning of the neurosensory retina, particularly involving the outer nuclear layer, photoreceptor layer, and retinal pigment epithelium. In pathologic myopia, focal areas of retinal pigment epithelium atrophy, photoreceptor degeneration, and chorioretinal thinning may develop, especially within the posterior pole.[7]

Bruch membrane demonstrates characteristic alterations in highly myopic eyes. Results from histopathologic studies identified thinning, fragmentation, and focal defects of Bruch membrane, which may contribute to the development of lacquer cracks and myopic choroidal neovascularization. These defects are believed to result from chronic mechanical stretching associated with axial elongation. The optic nerve head also exhibits structural changes secondary to globe enlargement. Histologic findings include elongation and thinning of the peripapillary scleral flange, expansion of the parapapillary region, and remodeling of the lamina cribrosa. These alterations contribute to optic disc tilting, peripapillary atrophy, and increased susceptibility to glaucomatous optic neuropathy in individuals with high myopia.[73]

In advanced pathologic myopia, posterior staphyloma represents the most severe histopathologic manifestation. Microscopic examination reveals marked scleral thinning, disorganization of collagen bundles, profound choroidal atrophy, and secondary degenerative changes involving the retina and retinal pigment epithelium. These structural alterations underlie many of the vision-threatening complications associated with high myopia.[74]

Table 5. Characteristic Histopathologic Findings in Myopia

Abbreviations: CNV, choroidal neovascularization; OCT, optical coherence tomography.

Most Common Histopathologic Findings

The most consistently reported microscopic findings in myopia are:

1. Posterior scleral thinning with extracellular matrix remodeling
2. Reduced collagen fibril diameter and density
3. Choroidal thinning with vascular attenuation
4. Retinal pigment epithelium and outer retinal thinning in advanced disease
5. Progressive posterior pole stretching leading to staphyloma formation in pathological myopia

These histopathologic alterations collectively reflect the underlying process of excessive ocular growth and biomechanical remodeling that characterizes childhood-onset and progressive myopia.[75]

Toxicokinetics

Childhood myopia is not a toxicological disorder in the classic sense; however, several environmental exposures, pharmacologic agents, and biochemical signaling pathways influence ocular growth and refractive development (see Table 6). The concept of toxicokinetics in myopia primarily concerns the absorption, distribution, metabolism, and biological effects of endogenous and exogenous substances that modulate retinal, choroidal, and scleral remodeling during emmetropization.[5]

Visual stimuli serve as the principal biological input regulating ocular growth. Retinal photoreceptors detect optical defocus and initiate signaling cascades involving neurotransmitters, growth factors, and metabolic mediators. These signals are transmitted through the retinal pigment epithelium and choroid to the sclera, where extracellular matrix remodeling determines axial elongation. Prolonged exposure to adverse visual environments, including sustained near work, reduced outdoor illumination, and excessive screen use, alters these biochemical pathways and may promote myopia progression.[76]

Dopamine is one of the most extensively studied neurochemical regulators of ocular growth. Increased retinal dopamine release occurs in response to bright outdoor light exposure and functions as an inhibitory signal against excessive axial elongation. Conversely, reduced dopamine activity has been associated with experimental myopia development. Dopamine metabolites are rapidly processed within retinal neurons, and their biological effects influence downstream pathways that regulate scleral remodeling and choroidal thickness.[77]

Retinoic acid, a metabolite of vitamin A, has emerged as an important mediator of ocular growth regulation. Results from experimental studies demonstrated increased concentrations of all-trans-retinoic acid within the choroid during periods of accelerated axial elongation. Retinoic acid influences gene transcription, extracellular matrix turnover, and scleral fibroblast activity, thereby contributing to changes in ocular dimensions during refractive development. Nitric oxide has also been implicated in myopia pathogenesis. Nitric oxide is synthesized locally within retinal and choroidal tissues and modulates vascular tone, neurotransmission, and cellular proliferation. Alterations in nitric oxide signaling have been associated with changes in choroidal thickness and scleral remodeling in animal models of myopia.[7]

Environmental light exposure influences ocular development through circadian and neurochemical pathways. Natural sunlight stimulates retinal dopamine release and supports normal emmetropization, whereas prolonged exposure to artificial indoor lighting and digital displays may alter retinal signaling and circadian regulation. Although direct toxic effects have not been established, cumulative exposure to unfavorable visual environments may contribute to abnormal ocular growth. Pharmacologic agents used for myopia control demonstrate specific ocular pharmacokinetic properties. Low-dose atropine, currently one of the most effective treatments for childhood myopia progression, penetrates ocular tissues following topical administration and acts on muscarinic receptors within the retina, choroid, and sclera. While its precise mechanism remains incompletely understood, atropine appears to modulate retinal neurotransmitter release and inhibit scleral remodeling pathways that promote axial elongation. Please see StatPearls' companion reference, "Lenticonus," for further information.

Oxidative stress has also been proposed to contribute to progressive myopia. Increased production of reactive oxygen species may influence retinal metabolism, extracellular matrix degradation, and vascular homeostasis. Antioxidant defense mechanisms within ocular tissues help maintain normal cellular function, although their precise role in childhood myopia remains under investigation. Overall, the biological pathways influencing childhood myopia involve a complex interplay among retinal neurotransmitters, growth factors, metabolic mediators, circadian regulators, and environmental exposures that collectively determine ocular growth and refractive development.[29]

Table 6. Biochemical Mediators Influencing Childhood Myopia Development

Abbreviations: IGF-1, insulin-like growth factor 1; IGF-2, insulin-like growth factor 2; RPE, retinal pigment epithelium; TGF-β, transforming growth factor β.

Additional Contemporary Concepts

Gut-retina axis and myopia: Emerging studies suggest that systemic metabolic and inflammatory mediators derived from the gut microbiome may influence retinal neurotransmitter pathways involved in ocular growth.

Hypoxia-inducible factor 1α  signaling: Increasing evidence links scleral hypoxia to extracellular matrix degradation and progressive axial elongation.

Mitochondrial metabolism: Altered retinal energy metabolism may contribute to abnormal visual signal processing during emmetropization.

Environmental exposome: The cumulative lifetime exposure to artificial lighting, digital devices, urbanization, and educational pressures is increasingly recognized as an important determinant of childhood myopia risk.[20]

History and Physical

A comprehensive eye examination should be performed, and myopic posterior segment changes should be excluded (see Table 8).[78] Children with myopia typically present with progressive blurring of distance vision while near vision remains relatively preserved. School-aged children commonly report difficulty seeing the classroom board, television screens, road signs, or distant objects during outdoor activities. Parents may notice behaviors such as squinting, sitting closer to the television, holding books very close to the face, frequent eye rubbing, reduced interest in distance-dependent activities, or declining academic performance. Younger children may not verbalize visual difficulties and may instead demonstrate inattentiveness, poor hand-to-eye coordination, or avoidance of visually demanding tasks. Please see StatPearls' companion reference, "Microspherophakia," for further information. 

Associated symptoms may include asthenopia, frontal headaches, brow ache, ocular fatigue, intermittent diplopia during prolonged near work, and difficulty transitioning focus between near and distant targets. Symptoms often worsen after extended reading, use of digital devices, or other near-vision activities. A history of rapid refractive progression, especially during the school years, should raise concern for developing high myopia and warrants closer monitoring.[5]

A detailed history should evaluate age at onset, rate of progression, family history of myopia, educational demands, duration of near work, screen exposure, reading distance, outdoor activity levels, sleep habits, and previous spectacle or contact lens use (see Table 7). Particular attention should be paid to risk factors such as parental myopia, prematurity, low birth weight, retinopathy of prematurity, connective tissue disorders, and syndromic conditions associated with high myopia. Symptoms such as photopsia, floaters, metamorphopsia, visual field defects, or sudden visual loss may indicate complications of pathological myopia and require prompt retinal evaluation.[9]

Visual acuity assessment typically shows reduced uncorrected distance vision, with improvement after refractive correction. Cycloplegic refraction remains the gold standard for diagnosing childhood myopia and determining the true refractive error by eliminating accommodative influences. Manifest refraction alone may underestimate hyperopia or overestimate myopia in children with active accommodation. External examination is usually normal in uncomplicated myopia. Ocular alignment, binocular vision status, accommodative function, convergence ability, and stereopsis should be assessed because binocular vision anomalies may coexist with refractive errors. Children with high myopia may demonstrate larger-appearing globes, deeper anterior chambers, or early vitreous changes.[10]

Anterior segment examination is generally unremarkable in simple myopia. However, slit-lamp evaluation should exclude associated conditions such as lens abnormalities, ectopia lentis, developmental cataracts, or connective tissue disorders that may contribute to excessive axial elongation. Intraocular pressure measurement should be performed as part of a comprehensive ophthalmic examination, particularly in individuals with severe myopia who may have an increased lifetime risk of glaucoma. Please see StatPearls' companion reference, "Lenticonus," for further information.

Dilated fundus examination is essential to evaluate the posterior segment. Mild to moderate myopia may demonstrate a normal fundus appearance or subtle tessellation due to increased visibility of the underlying choroidal vasculature. As axial length increases, characteristic findings may include optic disc tilting, temporal peripapillary atrophy, posterior vitreous degeneration, chorioretinal thinning, and diffuse fundus tessellation. Highly myopic eyes may exhibit posterior staphyloma, lacquer cracks, myopic macular degeneration, choroidal neovascularization, or peripheral retinal degeneration, predisposing to retinal tears and detachment. Biometric evaluation may demonstrate increased axial length, which represents the principal structural correlate of myopia progression. Optical biometry and ocular imaging are increasingly used to monitor axial elongation and assess the risk of future pathologic changes. Optical coherence tomography (OCT) may reveal choroidal thinning, retinal thinning, and early myopic macular alterations in progressive or high myopia.[7]

Table 7. Common History Findings

Table 8. Common Physical Examination Findings

Most Common Findings

The most common clinical findings in childhood myopia are blurred distance vision, reduced uncorrected visual acuity, improvement with minus lens correction, increased axial length, and a normal anterior segment examination. In progressive or high myopia, fundus tessellation, optic disc tilt, peripapillary atrophy, and choroidal thinning may be observed.[5]

Evaluation

Refraction under cycloplegia should be performed up to age 20 years to prevent overestimation of myopia.[79] The commonly used cycloplegic agents are atropine 1%, homatropine 2%, cyclopentolate 1%, tropicamide 1%, tropicamide 0.8%, and phenylephrine 5%. Of these, atropine 1% is the strongest cycloplegic agent, and its effect lasts for 14 days.[80] The onset of action of homatropine starts after one hour and lasts for 1 to 3 days.[81] Cyclopentolate is the preferred cycloplegic for evaluating refractive error in children aged 5 to 13 years. Tropicamide chiefly acts as a mydriatic, but tropicamide is an effective agent for evaluating children with myopia older than 13 years.[82][83] 

Atropine ointment must be instilled cautiously to prevent systemic complications such as facial flushing, fever, and tachycardia. The guidelines for spectacle prescription in children with myopia are summarized in Table 9 (American Academy of Ophthalmology Preferred Practice Pattern on Pediatric Eye Evaluations). Please see StatPearls' companion reference, "Tropicamide," for further information.

Table 9. Diagnostic Evaluation of Childhood Myopia

Abbreviation: DS, diopter sphere.

A complete examination of the anterior segment and fundus evaluation should be performed after refraction. Fundus evaluation in patients with pathologic myopia can reveal degenerative changes, lattice degeneration, peripheral retinal holes, cobblestone degeneration, lacquer cracks, macular hole, and staphyloma.[84] Optical biometry helps with regular monitoring of myopia progression. Optical biometry also helps monitor axial length and provides additional data, including corneal curvature radius, keratometry, central corneal thickness, lens thickness, and white-to-white measurements. Interpretable machine learning tools are now being studied for predicting childhood myopia. Results from a recent study by Feng et al, in a large cohort of 2365 children, showed that axial length-to-corneal curvature radius is a superior parameter for predicting childhood myopia.[85]

Evaluation of childhood myopia should confirm the refractive error, determine the degree and rate of progression, detect amblyopia or binocular vision problems, and rule out posterior segment changes associated with high myopia (see Table 10). The American Academy of Ophthalmology Pediatric Eye Evaluations Preferred Practice Pattern includes age-appropriate visual acuity testing, external and anterior segment examination, cycloplegic refraction, fundus examination, sensorimotor evaluation, intraocular pressure measurement when indicated, and imaging when clinically required.[6] In addition to cycloplegic refraction, baseline assessment should include unaided and best-corrected distance visual acuity, near visual acuity, ocular alignment, stereopsis, accommodation, convergence, pupillary examination, and slit-lamp biomicroscopy. Visual acuity should be measured using age-appropriate standardized charts, and both monocular and binocular acuities should be recorded. In preverbal or developmentally delayed children, fixation preference, red reflex testing, photoscreening, and instrument-based screening may help identify significant refractive error.[8]

Axial length measurement is increasingly important in the evaluation of childhood myopia because refractive error alone may not fully reflect structural progression. Baseline axial length allows objective monitoring of ocular growth, assessment of treatment response, and risk stratification for high myopia. The axial length to corneal curvature ratio may be useful because it reflects the relationship between axial length and corneal power and may identify children at higher risk of incident myopia or faster progression.[9]

Corneal topography or tomography is not mandatory for every child with simple myopia but should be considered when high astigmatism, rapidly changing astigmatism, reduced best-corrected visual acuity, an abnormal retinoscopic reflex, suspected keratoconus, or a family history of corneal ectasia is present. Keratometry obtained from optical biometry may provide additional information, but tomography is preferred when corneal pathology is suspected.[8] Dilated retinal evaluation should document the optic disc, macula, posterior pole, and peripheral retina. In high or progressive myopia, wide-field fundus photography may be useful for baseline documentation of peripapillary atrophy, tilted disc, lattice degeneration, retinal holes, posterior staphyloma, or myopic maculopathy. Optical coherence tomography of the macula and optic nerve is indicated when reduced best-corrected visual acuity, metamorphopsia, suspected macular pathology, an optic disc anomaly, glaucoma suspicion, or high axial myopia is present.[11]

Laboratory testing is not routinely required for uncomplicated childhood myopia. Systemic evaluation or genetic referral should be considered in children with very early-onset high myopia, developmental delay, dysmorphic features, hearing loss, skeletal abnormalities, joint hypermobility, ectopia lentis, congenital cataract, retinal dystrophy, night blindness, or a family history suggesting syndromic myopia. Important associated disorders include Stickler syndrome, Marfan syndrome, Weill-Marchesani syndrome, homocystinuria, Knobloch syndrome, congenital stationary night blindness, and retinopathy of prematurity.[17] A child with simple myopia does not usually require laboratory or radiographic testing. Imaging is ophthalmic rather than radiologic and is directed toward documenting axial length, corneal parameters, and retinal status. Neuroimaging is not indicated for routine myopia but should be considered if reduced vision is unexplained by refractive error, optic nerve pallor or swelling is present, or neurologic symptoms accompany visual concerns.[21]

Table 10. Clinical Evaluation of Myopia

Abbreviation: OCT, optical coherence tomography.

A child with simple myopia does not usually require laboratory or radiographic testing. Imaging is ophthalmic rather than radiologic and is directed toward documenting axial length, corneal parameters, and retinal status. Neuroimaging is not indicated for routine myopia but should be considered if reduced vision is unexplained by refractive error, optic nerve pallor or swelling is present, or neurologic symptoms accompany visual concerns.[5]

Treatment / Management

Management of Myopia in Children

Spectacles: Spectacles are the most commonly advised treatment option for childhood myopia. Refractive error correction should be performed after cycloplegia. Spectacle coverage remains an important issue in resource-limited settings. When prescribing spectacles to children, clinicians should consider factors such as the shape and weight of frames and lenses to improve adherence.[6]

Contact lenses: Soft contact lenses and rigid gas-permeable lenses can be prescribed to correct myopia. However, there is no substantial evidence that these modalities can reduce myopia progression.[86](B2)

Measures for Controlling Myopia Progression

Drugs for myopia control: As of June 2022, the US Food and Drug Administration (FDA) had not approved any pharmacologic agents for the treatment of myopia. However, atropine 0.01% is the most widely studied drug for slowing myopia progression. The Atropine in Myopia 1 (ATOM-1) study was conducted to evaluate the role of atropine 1%.[87] The Atropine in Myopia Study 2 (ATOM-2) examined the roles of atropine 0.5%, 0.1%, and 0.01% in treating myopia and was conducted in 2 phases. The study results found that atropine 0.01% was a safe and effective option for myopia treatment, with minimal adverse effects, including photophobia and loss of accommodation, compared with atropine 1% and 0.5%.[88] (A1)

The Low-Concentration Atropine for Myopia Progression (LAMP) study further evaluated the role of lower concentrations of atropine, including 0.05%, 0.025%, and 0.01%, in slowing myopia progression and found 0.05% to be the optimal concentration.[89] Similar results were also reported by Saxena et al in India.[90] Atropine is an anticholinergic drug that acts nonselectively on acetylcholine receptors, thereby downregulating their function. Acetylcholine regulates eye growth and plays a crucial role in retinal development.[91] Atropine stimulates the synthesis of the scleral extracellular matrix, thereby reducing scleral rigidity and its tendency to elongate.[92] (A1)

At the cellular level, atropine has been found to downregulate the epidermal growth factor receptor pathways.[93] Results from animal models showed that intravitreal atropine promotes dopamine release, thereby further regulating the increase in axial length.[94] Atropine also reduces choroidal thinning caused by hyperopic defocus in myopic eyes.[95] Another hypothesis states that atropine controls myopia progression by regulating excessive accommodation. However, subsequent results showed that myopia induction could not be stopped even after experimental elimination of the accommodation reflex by optic nerve sectioning or destruction of Edinger-Westphal nuclei.[96](B3)

Pirenzapine: Pirenzapine is a selective M1 and M4 muscarinic receptor antagonist. Because of its better safety profile, pirenzapine was studied for the treatment of myopia at concentrations of 0.5% and 2%.[97][98] (A1)

7-Methylxanthine: 7-Methylxanthine is a metabolite of theobromine and caffeine. The possible mechanism of action of the drug is to modulate axial length by increasing collagen fibril diameter and the overall thickness of the posterior sclera.[99](B3)

Intraocular Pressure-lowering drugs: Drugs such as timolol maleate and latanoprost have been used to halt myopia progression.[100] Please see StatPearls' companion reference, "Latanoprost," for further information. Evidence suggests that intraocular pressure causes stretch on the outer scleral wall, leading to enlargement of the eyeball.[101] The biomechanically weaker scleral walls in patients with myopia are at increased risk of stretching due to elevated intraocular pressure. Therefore, a decrease in intraocular pressure can slow elongation of the eye, thereby slowing myopia progression.[102](B2)

Lifestyle modifications, outdoor activities: The risk of myopia decreases by 2% for every 1-hour increase in time spent outdoors.[103] Increasing the duration of outdoor activity to 14 hours per week can reduce the risk of developing myopia by one-third. Outdoor activities reduce myopia progression by promoting the release of dopamine.[104] Dopamine inhibits axial length elongation.[105] Another mechanism could be the difference in spatial frequencies between indoor and outdoor environments. Enhancing spatial frequency can help limit myopia progression.[104][106][105](B2)

Bifocal and multifocal glasses: Myopia progression is thought to result from prolonged accommodation. Treatment with bifocal or multifocal glasses is considered beneficial because these lenses relax accommodation. Results from a study by Cheng et al reported a 40% decrease in myopia progression with bifocal glasses.[107](A1)

Progressive glasses: Progressive glasses have been studied for their effectiveness in controlling myopia progression. Results from a study by Gwiazda et al on progressive additional lenses showed a 20% reduction in myopia progression during the first year of use.[108] Further, the results showed that progressive glasses were more beneficial for children with 2 myopic parents, a larger accommodative lag, or near esophoria.[109]  (B2)

Defocus incorporated multiple segments spectacle (DIMS): Defocus incorporated multiple segments (DIMS) spectacles inhibit myopia progression by inducing myopic defocus. Results from animal studies found that myopic defocus reduces the eye axial length, whereas hyperopic defocus increases axial length.[110][111] DIMS consists of a central zone with a 9-mm diameter and annular zones of 33 mm with a relative positive power of +3.50 diopters. Each segment has a diameter of 1.03 mm.[112] This lens design induces myopic defocus while maintaining clear vision. Results from a study by Lam et al showed that continuous wear of DIMS reduced myopia progression by 52% and axial length progression by 62%.[112]  (A1)

Defocus-incorporated soft contact lenses: Defocus-incorporated soft contact lenses are bifocal lenses with a central correction zone and a sequence of alternating correction and defocus zones in the periphery.[113] This induces myopic defocus while maintaining clear vision.[114] The power of the central zone was customized to the cycloplegic refractive error, while the defocusing zones were set to a relatively negative 2.5 D. Daily use of a defocus-incorporated soft contact lens for 5 to 8 hours has been shown to reduce myopia progression.[113] Similarly, dual-focus soft contact lenses have also been found to reduce myopia progression.[115](A1)

Orthokeratology: Orthokeratology is the only US FDA-approved modality for myopia. Orthokeratology involves wearing overnight contact lenses that reshape the cornea from prolate to oblate, thereby reducing refractive error. Contact lenses appear to be a promising adjunct to other options, but hygiene and maintenance issues need to be addressed and explained to patients and guardians.[116] 

Red light phototherapy: Repeated red light phototherapy is a noninvasive treatment that uses light at 650 nm to slow myopia progression. The therapy is administered for 3 min twice daily. Red light phototherapy acts by increasing choroidal blood perfusion and choroidal thickness.[117][118](A1)

Other therapies explored in the treatment of myopia and reduction of myopia progression include posterior scleral contraction, posterior scleral reinforcement, scleral cross-linking with riboflavin, which can cause loss of photoreceptors, outer nuclear layer, and retinal pigment epithelium; subscleral injection of mesenchymal stem cells and dopamine; intravitreal injection of aquaporin 1; and scleral strengthening using sub-Tenon chemicals such as ethyl acrylate and acrylamide hydrazide.[119][120][121](B3)

Treatment Goals and Risk Stratification

The primary goals of childhood myopia treatment are to provide clear distance vision, prevent amblyopia, maintain binocular function, slow progression of refractive error and axial length, reduce the risk of high myopia, and minimize the risk of future sight-threatening complications. Treatment should be individualized according to age of onset, baseline spherical equivalent, rate of progression, axial length, parental myopia, binocular vision status, lifestyle risk factors, and the child’s ability to adhere to treatment. Children with early-onset myopia, rapid progression, high axial length, or 2 myopic parents should be considered at higher risk and monitored more closely.[20]

Full Correction Versus Undercorrection

Full optical correction is generally preferred in children with myopia to provide clear distance vision and avoid visual disability, poor school performance, and abnormal visual development. Undercorrection is not recommended as a myopia-control strategy because it may increase retinal blur and does not reliably slow progression. Overminus correction should also be avoided, particularly in children with accommodative or binocular vision problems.[122](A1)

FDA-Approved Myopia Control Options in the United States

The earlier statement that no US FDA-approved myopia management drugs existed remains correct for pharmacologic agents, but it should be updated to reflect that no US FDA-approved devices exist. MiSight 1-day soft contact lenses (CooperVision) are FDA-approved for the correction of myopia and slowing progression in children aged 8 to 12 years at initiation, with spherical equivalent refraction from −0.75 D to −4.00 D and astigmatism of less than 0.75 D. In 2025, the FDA also granted de novo authorization for Essilor Stellest spectacle lenses (EssilorLuxottica) for correction of myopia, with or without astigmatism, and slowing progression in children aged 6 to 12 years at initiation, with spherical equivalent refraction from −0.75 D to −4.50 D and astigmatism up to 1.50 D.[123](B2)

Follow-Up and Monitoring

Children undergoing myopia control should be reviewed regularly to assess visual acuity, refractive change, axial length progression, adherence, tolerance, and adverse effects. Follow-up every 6 months is commonly used for stable vision, while 3- to 4-month reviews may be appropriate for children with rapid progression or those recently started on atropine, orthokeratology, or myopia-control contact lenses. Axial length monitoring is preferred when available because it provides an objective measure of structural progression.[124](A1)

Combination Therapy

Combination therapy may be considered in children with rapid progression despite monotherapy. Common approaches include low-dose atropine with orthokeratology, atropine with myopia-control spectacles, or atropine with dual-focus contact lenses. Combination treatment should be individualized, and clinicians should monitor for additive adverse effects, adherence issues, and cost burden.[125]

Counseling and Adherence

Parents should be counseled that myopia control slows progression but usually does not eliminate progression completely. Treatment benefit depends on consistent spectacle or contact lens wear, proper contact lens hygiene, regular follow-up, and lifestyle modification. Families should be educated about warning signs, including sudden floaters, flashes, curtain-like visual field loss, ocular pain, redness, photophobia, or sudden decline in vision.[126]

Safety Considerations

Atropine may cause photophobia, blurred vision, allergic conjunctivitis, periocular dermatitis, and, rarely, systemic anticholinergic symptoms. Contact lens–based treatments require strict hygiene, avoidance of water exposure, and prompt discontinuation if pain, redness, discharge, or photophobia occurs. FDA device data list corneal ulcer, infection, red eye, eye pain, Acanthamoeba keratitis, and keratitis as reported adverse events for daily-wear soft myopia-control contact lenses.[127]

Discontinuation and Rebound

Myopia-control treatment should generally be continued through the active progression years and reassessed during mid-to-late adolescence. Abrupt cessation of higher-dose atropine may be associated with rebound progression; therefore, tapering or step-down therapy may be considered, especially after prolonged treatment or in younger children. Continued monitoring after discontinuation is important to detect recurrence of progression.[128]

Surgical Management

Refractive surgical procedures are not recommended for routine childhood myopia because refractive error and axial length are still changing. Surgical intervention in childhood myopia is generally limited to treatment of complications such as retinal tears, retinal detachment, myopic choroidal neovascularization, macular hole, cataract, or glaucoma in highly myopic eyes. Posterior scleral reinforcement and other scleral procedures remain investigational or selectively used in limited settings and are not standard first-line therapy.[129]

Differential Diagnosis

Other causes of low vision in children should be ruled out, including keratoconus, pediatric cataracts, microspherophakia, pediatric glaucoma, trauma, iridofundal coloboma, nystagmus, congenital optic nerve abnormalities such as optic disc coloboma, large myelinated nerve fibers involving the fovea, and congenital retinal anomalies such as pigmentary retinopathy (see Table 11). Clinicians should also ask about birth history, history of laser treatment for retinopathy of prematurity, delayed cry at birth, and history of intensive care unit hospitalizations. Myopia can also be associated with Down syndrome (8% to 41%).[130] Other differential diagnosis include:

Marfan syndrome and stickler syndrome: Pseudomyopia is the overestimation of myopia resulting from excessive accommodation, typically seen in children. Therefore, refraction without cycloplegia overestimates myopia by −1 to −2 diopters.[131]

Accommodative spasm: Accommodative spasm results from excessive contraction of the ciliary muscle, producing a transient myopic shift. Children typically report fluctuating distance vision, headaches, and visual fatigue. Cycloplegic refraction reveals significantly less myopia than manifest refraction.[132]

Night myopia: Some children and adolescents experience increased myopic refractive error under dim illumination due to accommodative and optical factors. Symptoms are usually limited to reduced distance vision during evening activities and driving, while daytime vision remains relatively unaffected.[133]

Index myopia secondary to metabolic disorders: Transient myopic shifts may occur in systemic metabolic conditions such as uncontrolled diabetes mellitus due to osmotic changes within the crystalline lens. These changes are often reversible following correction of the underlying metabolic disturbance. Please see StatPearls' companion reference, "Collagen Cross Linking for Keratoconus," for further information.

Lens subluxation and ectopia lentis: Displacement of the crystalline lens alters the refractive status and may mimic progressive myopia. Slit-lamp examination may reveal lens decentration, phacodonesis, or zonular weakness. Associated systemic findings may suggest an underlying connective tissue disorder.[5]

Posterior lenticonus: Posterior protrusion of the lens capsule increases lenticular power and may induce unilateral or asymmetric myopia. Affected children frequently present with anisometropia, amblyopia, or an unexplained reduction in visual acuity.[11]

Corneal ectatic disorders other than keratoconus: Conditions such as pellucid marginal degeneration and keratoglobus may produce progressive myopia and irregular astigmatism. Corneal topography or tomography is often required to distinguish these disorders from simple axial myopia. Please see StatPearls' companion reference, "Myopia," for further information.

Retinopathy of prematurity–associated refractive error: Children with a history of prematurity may develop myopia due to altered anterior segment development, lens changes, and abnormal ocular growth. The refractive profile and retinal findings help differentiate this entity from typical school-age myopia.[134]

Congenital stationary night blindness: This inherited retinal disorder may present with childhood myopia before retinal dysfunction becomes apparent. Symptoms include impaired night vision, reduced contrast sensitivity, and characteristic electroretinographic abnormalities.[135]

X-linked juvenile retinoschisis: Affected boys may present with reduced vision and myopia during childhood. Fundus examination and optical coherence tomography typically demonstrate foveal schisis and splitting of the retinal layers.[136]

Ocular albinism: Children with ocular albinism may exhibit refractive errors, reduced visual acuity, nystagmus, and photophobia. Iris transillumination defects and foveal hypoplasia distinguish the condition from uncomplicated myopia.[137]

Leber congenital amaurosis: High refractive errors, including severe myopia, may occur in association with this inherited retinal dystrophy. Profound visual impairment, oculodigital behavior, and markedly abnormal electroretinography aid diagnosis.[138]

Achromatopsia: Children may initially be thought to have refractive blur due to reduced visual acuity. However, severe photophobia, color vision deficiency, and pendular nystagmus are characteristic findings.[139]

Optic nerve hypoplasia: Reduced visual acuity and poor visual development may be mistaken for uncorrected refractive error. Fundus examination reveals a small optic disc, often accompanied by visual field defects and variable endocrine abnormalities.[140]

Septo-optic dysplasia: Visual impairment in affected children may initially prompt evaluation for refractive error. Neuroimaging and endocrine assessment often reveal associated midline brain and pituitary abnormalities.[141]

Cerebral visual impairment: Children with neurologic injury may demonstrate poor visual performance despite relatively normal ocular findings. Visual dysfunction is related to impaired cortical processing rather than refractive error.[142]

Cone-rod dystrophy: Progressive central visual loss, photophobia, and color vision abnormalities may initially be attributed to refractive causes. Electroretinography and retinal imaging are helpful in establishing the diagnosis.

Juvenile open-angle glaucoma: Axial elongation and myopic refractive error may coexist with elevated intraocular pressure in susceptible children. Optic nerve evaluation and gonioscopy are essential when glaucoma is suspected.[143]

Familial exudative vitreoretinopathy: This inherited retinal vascular disorder may present with high myopia, retinal dragging, or peripheral retinal abnormalities. Careful peripheral retinal examination and family history are often diagnostic.[144]

Wagner syndrome: Wagner syndrome is an inherited vitreoretinopathy characterized by high myopia, vitreous degeneration, and progressive retinal changes. This disorder may mimic simple myopia during early childhood before retinal manifestations become apparent.[145]

Knobloch syndrome: High myopia may be the earliest ocular finding in this rare hereditary condition. Occipital skull defects, vitreoretinal degeneration, and retinal detachment help establish the diagnosis.[146]

Table 11. Differential Diagnosis of Childhood Myopia

Abbreviations: ERG, electroretinography; IOP, intraocular pressure; OCT, optical coherence tomography; ROP, retinopathy of prematurity.

Pertinent Studies and Ongoing Trials

The evidence base for childhood myopia management is strongest for low-dose atropine, myopia-control spectacle lenses, dual-focus or multifocal soft contact lenses, orthokeratology, and outdoor-time interventions. Most randomized trials use cycloplegic spherical equivalent refraction and axial length progression as the primary outcome measures (see Table 12).[5]

Table 12. Key Trials in Myopia

Abbreviations: ATOM-2, Atropine in Myopia Study 2; BLINK, Bifocal Lenses in Nearsighted Kids; DIMS, defocus incorporated multiple segments; FDA, Food and Drug Administration; LAMP, Low-Concentration Atropine for Myopia Progression; PEDIG, Pediatric Eye Disease Investigator Group; RLRL, repeated low-level red-light.

Several randomized trials support active myopia-control therapy rather than simple refractive correction alone. The ATOM and LAMP studies established low-concentration atropine as an effective pharmacologic option, with LAMP demonstrating a concentration-dependent response and the greatest 1-year efficacy at 0.05% atropine.[68] However, a US randomized trial found that atropine 0.01% was not superior to placebo, suggesting that very-low-dose atropine may not be equally effective across all populations.[128]

Optical myopia-control interventions are supported by randomized clinical trial evidence. DIMS spectacle lenses reduce myopia progression and axial elongation by imposing simultaneous clear central vision and peripheral myopic defocus. Multifocal and dual-focus soft contact lenses, including high-add multifocal designs and MiSight 1-day lenses, have demonstrated a clinically meaningful reduction in refractive progression and axial elongation in school-aged children.[147]

School-based randomized trials support increased outdoor time as a preventive strategy, particularly for reducing the incidence of myopia in children without myopia or with premyopia. Orthokeratology has shown consistent benefit in slowing axial elongation but requires careful patient selection, contact lens hygiene, and monitoring for microbial keratitis. Repeated low-level red-light therapy has shown encouraging short-term outcomes, including reduced axial elongation in randomized trials, but longer-term safety, rebound after cessation, optimal dosing, and retinal safety remain to be evaluated.[148]

Ongoing and Emerging Areas

Current research focuses on combination therapy, personalized atropine dosing, newer spectacle designs, the long-term safety of red-light therapy, rebound after treatment discontinuation, and artificial intelligence–based prediction of progression. Future trials should include standardized axial length outcomes, longer follow-up after cessation of treatment, safety reporting, quality-of-life measures, and subgroup analyses by age, ethnicity, baseline refraction, parental myopia, and axial length.[149]

Treatment Planning

Treatment planning for childhood myopia should be individualized based on the child's age, baseline refractive error, axial length, rate of progression, family history, environmental risk factors, binocular vision status, and risk of developing high myopia (see Table 13). The primary goals are to provide optimal visual correction, slow axial elongation, preserve binocular visual development, and reduce the lifetime risk of pathological myopia and its associated complications.[5] All children diagnosed with myopia should undergo baseline documentation of cycloplegic refraction, visual acuity, ocular alignment, binocular vision status, and, where available, axial length measurement. Risk stratification should be performed at the initial visit. Children with early-onset myopia (younger than 8 years), rapid progression (> 0.50 D/year), significant axial elongation, parental myopia, or high baseline refractive error require closer surveillance and consideration of active myopia-control interventions. The International Myopia Institute recommends a structured approach consisting of risk assessment, education, optical correction, environmental modification, initiation of myopia-control therapy when indicated, and longitudinal monitoring. Parents and caregivers should be informed that myopia progression is typically most rapid during the early school years and that treatment effectiveness should be evaluated over time rather than at a single visit.[6]

Table 13. Risk-Based Treatment Planning

Initial Management Strategy

At diagnosis, full refractive correction should be prescribed to ensure optimal visual development and academic performance. Environmental interventions should be recommended for all children regardless of refractive status. Current evidence supports increasing outdoor activity to at least 2 h/d (approximately 10 to 14 h/wk), limiting prolonged uninterrupted near work, maintaining appropriate reading distance, and encouraging regular visual breaks during digital device use.

Children demonstrating progressive myopia should be considered for evidence-based myopia-control therapy. Treatment selection depends on patient age, refractive status, lifestyle, ocular characteristics, treatment availability, and family preference. Options include low-dose atropine, defocus-incorporated multiple-segment or highly aspherical lenslet spectacle lenses, dual-focus or multifocal soft contact lenses, and orthokeratology.[124]

Monitoring Treatment Response

Successful treatment planning requires objective monitoring. Refractive progression should ideally be assessed using cycloplegic refraction, while axial length measurement provides a more sensitive indicator of ocular growth. Treatment effectiveness should be evaluated at regular intervals, typically every 6 months.

The following parameters should be documented at follow-up:

• Uncorrected and corrected visual acuity
• Cycloplegic spherical equivalent
• Axial length (if available)
• Binocular vision and accommodative status
• Treatment adherence
• Adverse effects
• Rate of progression compared with baseline [150]

Criteria for Treatment Escalation

Treatment escalation should be considered when any of the following occur:

• Progression exceeding 0.50 D/year
• Significant axial elongation despite treatment
• Development of high myopia
• Poor treatment adherence
• Intolerance to current therapy
• Strong family history with ongoing progression

Escalation strategies may include increasing atropine concentration, switching to an alternative optical intervention, or implementing combination therapy.[151]

Long-Term Management

Myopia control is a long-term process extending throughout the active growth period of childhood and adolescence. Treatment is generally continued until refractive stability is achieved, typically in the mid-to-late adolescent years. After treatment cessation, continued monitoring is recommended because rebound progression may occur, particularly following atropine discontinuation.

Suggested Treatment Planning Algorithm for Childhood Myopia

1. Confirm the diagnosis with cycloplegic refraction and, when available, axial length measurement.
2. Stratify the child as low, moderate, or high risk based on age at onset, baseline refractive error, axial length, rate of progression, parental myopia, and posterior segment findings.
3. Recommend lifestyle modification for all children, including increased outdoor activity, reduced prolonged uninterrupted near work, appropriate reading distance, and regular visual breaks during digital device use.
4. Select an appropriate myopia-control strategy based on risk category, ocular findings, family preference, treatment availability, and ability to adhere to therapy. Options include spectacle correction, low-dose atropine, myopia-control spectacle lenses, myopia-control contact lenses, and orthokeratology.
5. Monitor response at regular intervals, typically every 6 months, using visual acuity, cycloplegic refraction, axial length measurement when available, treatment adherence, and adverse effects.
6. Continue the current therapy if myopia remains stable. Escalate or combine treatments if refractive progression or axial elongation continues despite therapy.
7. Continue follow-up through adolescent stabilization and provide long-term surveillance for children with high or pathologic myopia.

Key Clinical Pearl

The most effective treatment planning strategy is early identification of children at risk for rapid progression and timely initiation of evidence-based myopia-control interventions before significant axial elongation occurs, because prevention of high myopia remains more effective than treatment of its complications later in life.[152]

Toxicity and Adverse Effect Management

The management of childhood myopia is generally safe; however, adverse effects may occur depending on the treatment modality used. Clinicians should counsel children and caregivers about potential complications, monitor treatment tolerance at follow-up visits, and promptly address treatment-related adverse events to optimize adherence and long-term outcomes (see Table 14).

Atropine-Associated Adverse Effects

Topical atropine is the most widely studied pharmacologic therapy for myopia control. The frequency and severity of adverse effects are concentration-dependent. Higher concentrations (0.5% to 1%) are associated with photophobia, glare, reduced accommodation, near blur, and pupillary dilation, whereas lower concentrations (0.01% to 0.05%) generally demonstrate a more favorable safety profile. Patients experiencing photophobia may benefit from photochromic or tinted lenses, ultraviolet protection, and avoidance of excessive sunlight exposure. Near-vision blur can be treated with temporary near additions or by reducing atropine concentration when clinically appropriate. Ocular surface irritation, allergic conjunctivitis, and periocular dermatitis should prompt evaluation for preservative sensitivity or drug intolerance. Rare systemic anticholinergic adverse effects include facial flushing, fever, tachycardia, dry mouth, constipation, urinary retention, behavioral changes, confusion, and central nervous system toxicity. Caregivers should be instructed to perform punctal occlusion following instillation and store medications securely to prevent accidental ingestion. Significant systemic toxicity requires immediate medical evaluation.[153]

Contact Lens–Related Complications

Soft multifocal contact lenses, dual-focus contact lenses, and orthokeratology lenses may cause contact lens–associated complications. Common adverse effects include dry eye symptoms, foreign body sensation, lens discomfort, superficial punctate keratopathy, allergic conjunctivitis, and giant papillary conjunctivitis. Microbial keratitis remains the most serious complication associated with contact lens wear, particularly orthokeratology. Risk factors include overnight lens wear, poor hygiene, water exposure, improper lens storage, and inadequate follow-up. Patients presenting with pain, redness, photophobia, discharge, or sudden visual deterioration should discontinue lens wear immediately and undergo urgent ophthalmic evaluation. Corneal staining, epithelial defects, corneal infiltrates, and sterile inflammatory reactions may require temporary discontinuation of lens wear, lubrication, modification of lens parameters, or treatment of associated ocular surface disease.[154]

Orthokeratology-Specific Adverse Effects

Orthokeratology may be associated with corneal molding irregularities, lens decentration, induced astigmatism, corneal staining, epithelial iron deposition, and transient visual disturbances such as halos and glare. Most complications are reversible following lens discontinuation. Regular corneal topography is recommended to monitor treatment response and detect early complications. Please see StatPearls' companion reference, "Cycloplegic and Noncycloplegic Refraction," for further information.

Spectacle-Related Issues

Although spectacles are among the safest interventions, adaptation difficulties, image distortion, peripheral aberrations, frame intolerance, and adherence issues may occur. Children should undergo periodic reassessment to ensure appropriate refractive correction and proper frame fit. Please see StatPearls' companion reference, "Contact Lens–Related Complications," for further information.

Defocus and Multifocal Spectacle Lens Adverse Effects

Children using DIMS lenses, highly aspherical lenslet designs, or progressive addition lenses may initially report peripheral blur, altered depth perception, mild dizziness, or adaptation difficulties. Symptoms typically improve during the adaptation period. Persistent visual discomfort may require reassessment of lens centration, prescription accuracy, or treatment selection.[155]

Repeated Low-Level Red-Light Therapy Adverse Effects

Repeated low-level red-light therapy has generally demonstrated favorable short-term safety profiles in clinical studies. Reported adverse effects include transient afterimages, mild visual discomfort, temporary glare phenomena, and visual fatigue. Because long-term retinal safety data remain limited, periodic retinal evaluation and adherence to recommended treatment protocols are essential. Excessive exposure or unsupervised use should be avoided.[156]

Monitoring for Myopia Progression Despite Therapy

Treatment failure represents an important treatment challenge rather than a direct adverse effect. Continued progression despite therapy may result from poor adherence, inadequate treatment intensity, inappropriate patient selection, or individual variability in treatment response. These patients may require escalation of atropine concentration, transition to an alternative modality, or combination therapy.[157]

Rebound Following Treatment Discontinuation

Rebound progression may occur following cessation of myopia-control therapy, particularly after higher-concentration atropine treatment. Children undergoing treatment discontinuation should be monitored closely with periodic cycloplegic refraction and axial length measurements. Gradual tapering strategies may reduce the risk of rebound in selected patients.[158]

Table 14. Management of Treatment-Related Adverse Effects

Clinical Monitoring Recommendations

Children receiving active myopia-control therapy should undergo periodic evaluation of:

• Visual acuity
• Cycloplegic refractive error
• Axial length progression
• Ocular surface status
• Corneal integrity (for contact lens users)
• Treatment adherence
• Drug-related adverse effects
• Fundus status in high myopia

Key Clinical Pearl

Most adverse effects associated with childhood myopia interventions are mild, reversible, and manageable with appropriate monitoring. The greatest vision-threatening complication is contact lens–associated microbial keratitis, while the most common pharmacologic adverse effects are photophobia and reduced accommodation with atropine therapy. Early recognition and management of complications improve treatment adherence and long-term outcomes.[159]

Staging

For Childhood Myopia and Ocular Development, there is no universally accepted formal staging system analogous to those used in cancer staging or diabetic retinopathy grading. However, several clinically relevant classification systems categorize myopia by refractive error, axial length, age of onset, progression rate, and the presence of pathological changes (see Table 15).[6]

Staging

Although childhood myopia lacks a universally accepted staging system, classification based on refractive magnitude, age of onset, progression characteristics, and structural ocular changes is useful for clinical management, prognosis, and risk stratification. The International Myopia Institute recommends distinguishing between simple myopia, high myopia, and pathological myopia because the risk of ocular complications increases substantially with increasing axial length and refractive error.[160]

Table 15. Classification Based on Refractive Error

Premyopia refers to a refractive state in which a child is not yet myopic but has a high likelihood of developing myopia due to age, family history, environmental risk factors, or excessive axial elongation.

Classification Based on Axial Length

Axial length is increasingly recognized as a more reliable indicator of myopia progression and future pathological risk than refractive error alone (see Table 16).[8]

Table 16. Myopia Classification by Axial Length

Eyes with axial lengths exceeding 26 mm demonstrate substantially increased risks of retinal detachment, myopic maculopathy, glaucoma, and choroidal neovascularization.

Table 17. Classification Based on Age of Onset

Earlier onset is strongly associated with greater lifetime axial elongation and increased risk of pathological myopia.

Table 18. Classification Based on Progression Rate

Children exhibiting rapid progression require closer monitoring and consideration of active myopia-control interventions (Table 18).

Pathological Myopia Classification (META-PM Classification)

The Meta-Analysis for Pathologic Myopia (META-PM) Study Group developed the most widely accepted grading system for myopic maculopathy (Table 19).

Table 19. Classification by Fundus Findings

Plus lesions include:

• Lacquer cracks
• Myopic choroidal neovascularization
• Fuchs spot

The presence of plus lesions significantly increases the risk of irreversible visual impairment.[161]

Suggested Clinical Staging for Childhood Myopia

For practical pediatric use, childhood myopia can be staged as follows (Table 20):

Table 20. Childhood Staging of Myopia

Prognostic Significance

The most important prognostic indicators in childhood myopia are:

• Younger age at onset
• Faster annual progression
• Increasing axial length
• Positive parental history
• Development of high myopia
• Presence of posterior segment abnormalities

Children who develop myopia before 8 years of age are significantly more likely to progress to high myopia during adolescence and therefore benefit most from early intervention and longitudinal monitoring.[160]

Prognosis

School-aged children with early-onset myopia usually have greater axial length and higher refractive error. Conversely, the progression in children with congenital myopia, defined as myopia greater than 5 diopters before age 6 years, differs. Results from a study by Shih et al found faster rates of myopia progression in children with lower grades of myopia (5.0 to 7.75 D) compared with those with higher grades (maximum of 11.0 D).[162] Patients with pathologic myopia, choroidal thinning, and posterior staphyloma have worse long-term visual outcomes.[163]

The prognosis of childhood myopia is highly variable and depends on the age of onset, baseline refractive error, rate of progression, axial length growth, genetic predisposition, environmental influences, and the development of pathological ocular changes. Most children with low-to-moderate myopia achieve excellent visual outcomes with appropriate optical correction and regular follow-up. However, children who develop myopia at an earlier age are at substantially greater risk of progressing to high myopia and experiencing vision-threatening complications later in life.[9]

Early-onset myopia is one of the strongest predictors of future high myopia. Children who become myopic before age 8 years typically exhibit longer periods of ocular growth and refractive progression, resulting in greater cumulative axial elongation. With increasing axial length, the risk of developing pathologic myopia rises significantly, independent of refractive error alone. Consequently, early identification and implementation of evidence-based myopia-control strategies may improve long-term outcomes. Please see StatPearls' companion reference, "Lenticonus," for further information.

The annual rate of progression is another important prognostic indicator. Children exhibiting rapid progression, particularly greater than 0.50 D per year, are more likely to develop high myopia during adolescence. Monitoring axial length may provide additional prognostic information because structural ocular growth often precedes measurable refractive changes. Excessive axial elongation is associated with increased risks of retinal detachment, myopic maculopathy, glaucoma, cataract, and choroidal neovascularization in adulthood.[17]

Family history strongly influences prognosis. Children with one parent with myopia demonstrate an increased risk of developing myopia, whereas those with 2 parents with myopia often experience earlier onset and greater progression. Environmental factors such as reduced outdoor activity, intensive educational demands, prolonged near work, and excessive screen exposure may further accelerate progression in genetically susceptible individuals. Please see StatPearls' companion reference, "Myopia," for further information.

Most children with uncomplicated myopia retain excellent corrected visual acuity throughout childhood and adolescence. Visual prognosis is generally favorable when refractive errors are recognized early, corrected appropriately, and monitored regularly. In contrast, children with high myopia, syndromic myopia, or secondary myopia associated with ocular developmental abnormalities may experience greater visual morbidity.[11]

The prognosis becomes less favorable when structural ocular complications develop. Progressive choroidal thinning, diffuse or patchy chorioretinal atrophy, posterior staphyloma, lacquer cracks, myopic traction maculopathy, macular hole formation, and myopic choroidal neovascularization are associated with irreversible visual impairment. The presence of pathological myopia substantially increases the lifetime risk of legal blindness and visual disability.[21]

Advances in myopia-control therapies have improved the long-term outlook for many children. Low-dose atropine, myopia-control spectacle lenses, multifocal contact lenses, orthokeratology, and behavioral interventions have been shown to slow refractive progression and axial elongation. Although these treatments do not cure myopia, they may reduce the likelihood of developing high myopia and its associated complications.[11]

Complications

Pathologic myopia can be associated with retinal complications such as retinal detachment, myopic traction maculopathy, macular hole, and choroidal neovascular membrane formation. High myopia can also be associated with subluxated lenses and a higher risk of primary open-angle glaucoma (see Table 21).[164][165] Although most children with low to moderate myopia maintain good visual function with appropriate correction, progressive axial elongation may predispose affected individuals to a spectrum of ocular complications. The risk of complications increases substantially with increasing refractive error, longer axial length, earlier age of onset, and the development of pathologic myopia (see Table 22). Many of these complications may not become clinically apparent until adolescence or adulthood, highlighting the importance of long-term surveillance.[6] Pathological myopia can be associated with retinal complications such as retinal detachment, myopic traction maculopathy, macular hole formation, myopic choroidal neovascularization, and progressive chorioretinal atrophy. High myopia is also associated with lens subluxation and an increased lifetime risk of primary open-angle glaucoma.[9]

Additional Retinal Complications

Progressive axial elongation may lead to peripheral retinal degenerations, including lattice degeneration, snail-track degeneration, retinal thinning, atrophic retinal holes, and retinal tears. These abnormalities increase the risk of rhegmatogenous retinal detachment, particularly in eyes with high myopia. Symptoms such as flashes, floaters, or a curtain-like visual field defect warrant urgent retinal evaluation. Myopic foveoschisis, also known as myopic traction maculopathy, may develop because of vitreoretinal traction and progressive posterior scleral deformation. Untreated myopic foveoschisis can progress to foveal detachment, full-thickness macular hole formation, or severe central vision loss.[9]

Choroidal and Macular Complications

Progressive choroidal thinning may result in diffuse and patchy chorioretinal atrophy. Advanced stages can culminate in macular atrophy and irreversible visual impairment. Myopic choroidal neovascularization may arise from breaks in Bruch membrane, or lacquer cracks, and can lead to hemorrhage, fibrosis, and permanent central vision loss if untreated. Posterior staphyloma represents a hallmark complication of pathologic myopia and results from localized outpouching of the weakened posterior sclera. The resulting structural deformation contributes to macular dysfunction, retinal stretching, and progressive visual decline.[9]

Optic Nerve Complications

High myopia is associated with optic disc tilting, peripapillary atrophy, and structural remodeling of the optic nerve head. These changes may complicate glaucoma diagnosis and increase susceptibility to glaucomatous optic neuropathy. Individuals with high myopia demonstrate a higher lifetime risk of developing primary open-angle glaucoma compared with individuals with emmetropia.[9]

Vitreous Complications

Excessive axial elongation accelerates vitreous liquefaction and posterior vitreous degeneration. Premature posterior vitreous detachment may occur and increase the likelihood of retinal tears and retinal detachment. Vitreomacular interface abnormalities may also contribute to tractional macular disease.[9]

Anterior Segment Complications

Eyes with high myopia often exhibit deeper anterior chambers and altered ocular biomechanics. In addition to lens subluxation, individuals with high myopia have an increased risk of earlier cataract development, particularly nuclear sclerosis and posterior subcapsular cataract. Surgical planning for cataract extraction may be more challenging due to long axial length and increased retinal vulnerability.[9]

Ocular Surface and Contact Lens–Related Complications

Children undergoing contact lens–based myopia control may experience lens intolerance, allergic conjunctivitis, dry eye symptoms, giant papillary conjunctivitis, corneal staining, corneal infiltrates, and microbial keratitis. Although uncommon, infectious keratitis remains the most serious treatment-related complication and requires prompt intervention.[9]

Psychosocial and Functional Complications

Uncorrected or inadequately corrected myopia may adversely affect academic performance, educational participation, sports activities, self-esteem, and quality of life. Children with significant visual impairment from pathological myopia may require low-vision rehabilitation, educational accommodations, and psychosocial support.[9]

Table 21. Complications of Childhood Myopia

Table 22. Risk Factors for Complications

Key Clinical Pearls

• The likelihood of complications correlates more strongly with axial length than refractive error alone.
• Retinal detachment risk remains elevated throughout life in individuals with severe myopia.
• Myopic maculopathy is among the leading causes of irreversible visual loss in pathological myopia.
• Posterior staphyloma is a major predictor of future retinal and macular complications.
• Early myopia-control interventions may reduce the risk of future complications by limiting excessive axial elongation.
• Lifelong ophthalmic surveillance is recommended for patients with high or pathological myopia, even after refractive stability has been achieved.[9]