Hyperopia is present in a small proportion of children aged between 6 and 12 months, with ethnicity likely affecting prevalence, and higher prevalences in certain subgroups, especially those with a family history of hyperopia or accommodative esotropia. Around a fifth of children who are hyperopic in infancy go on to develop strabismus, while an unknown proportion develop bilateral ametropic amblyopia; persistent hyperopia appears to be a harbinger of future pathology. Early prophylactic spectacle correction of hyperopia has failed to prevent strabismus in three of four studies, but showed reduced incidence of strabismus in one study, and yielded improved visual acuity outcomes in two studies by one investigator. Currently our ability to detect or measure refractive error with automated instruments easily adaptable to a screening setting has outpaced our knowledge of how best to identify the subset of hyperopes who are really at risk, and how to manage isolated early hyperopia once it has been identified.

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In any endeavor to improve the public health, the first challenge and by no means the least difficult—is to characterize the problem. In the area of early childhood hyperopia there is still considerable uncertainty regarding the prevalence of hyperopia and the frequency with which it is associated with abnormal visual development, either in the absence of or despite optical correction. This paper will review what is currently known about the epidemiology of early hyperopia and associated conditions.

Discussions of the prevalence of hyperopic refractive error are generally plagued by variations in the definition of hyperopia (measurement with or without cycloplegia; diopters of refractive error used as the threshold value; use of the least hyperopic meridian, most hyperopic meridian or spherical equivalent (SE); hyperopia of either eye, right eye, both eyes, or mean SE of both eyes; and inclusion or exclusion of anisometropia). In infants, however, the scarcity of population-based data using cycloplegic refraction is such that one can only wish for the opportunity to compare studies at all. In the first of a series of three studies by the same group of investigators in the UK,1 all 6- to 9-month olds in Cambridge were invited to a screening exam. One thousand ninety-six infants (71% participation) had cycloplegic photorefraction to identify hyperopia >3.5 D in any meridian (meridional hyperopia). Hyperopia without anisometropia was confirmed by cycloplegic retinoscopy in 4.6% of participants (with no photorefraction false negatives among 52 emmetropes tested). In a second study,2 3166 7- to 9-month olds (74% participation) had cycloplegic photorefraction as before, and hyperopia of at least 3.5 D was confirmed in 5.7% of the study population.a In the third study,2 5091 8-month olds (86% participation) were screened using noncycloplegic photoscreening with a criterion of hyperopic focus (accommodative lag) of >1.5 D in any meridian at a distance of 75 cm, and confirmatory exams found at least 3.5 D hyperopia in any meridian in 4.5% of the study population (3.8% if the threshold was raised to 4 D 3). Because screening identified only those hyperopes with accommodative lag, this figure is an underestimate; 280 infants from among the 90%3 with normal screening results were examined under cycloplegia, and hyperopia was found in 7% of these.4

Other estimates of hyperopia prevalence in infants of various ages come from smaller studies that are not population based, and may overestimate prevalence due to participation bias from an association between hyperopia and family history of childhood vision disorders (see below). Newborn infants have quite a wide spread of refractive errors; a classic study 5 using atropine gel cycloplegia in 1000 eyes of newborn infants found that 30% of eyes had at least 3 D of hyperopia, with no significant difference between black and white infants. Mutti et al.6 found that of 221 largely (74%) white 3-month olds, 24.8% had at least 3 D SE hyperopia in the right eye. Ingram 7 screened 6700 6-month olds in the UK (population participation rate unknown), and found 9.2% had at least 3.5 D meridional hyperopia.b The same group of infants that Mutti et al. studied at 3 months had, by 9 months, a reduced prevalence of only 5.4% right eye SE hyperopia of at least 3 D.6 Ingram 9 studied 1648 11- to 13-month olds (58% population participation rate) and found at least 2 D hyperopia in the less hyperopic meridian bilaterally in 11.8% of children. Elsewhere,10 he reports a prevalence of 3.7% for hyperopia of at least 3.5 D in any meridian among close to 800 12-month olds. In a U.S. study of 42 mostly white (85%) 12-month olds,11 over 20% had at least 2 D SE hyperopia.

Some idea of age-related variations in prevalence may best be gleaned from cross-sectional studies that include different age groups. In a review of 376 clinic patients without prematurity or ophthalmic disorders,12 the distribution of right eye SE was reportedly similar in the first, second, and third year of life (overall 8.6% with more than 2.75 D); however, this clinic population may be biased in favor of persistent hyperopia. Refractive error distributions by age among 514 children aged 1 to 48 months 11 show a decrease in prevalence of higher levels of hyperopia with increasing age; however, differential participation bias (e.g., selective participation by families with a history of eye problems among infants more than among older children) could produce an artifactual trend.

Longitudinal studies such as Mutti's 6 seem to support the notion that much infantile hyperopia resolves through emmetropization, at least during the first year of life. Ehrlich et al.13 report longitudinal data between 9 and 20 months of age on a mixed population (enriched for infants with meridional hyperopia) of 254 nonanisometropic children, and similarly describe a decrease of standard deviation and left-shift of the mean SE. On the other hand, Ingram and Barr 14 followed a subset of 148 of 12-month-old hyperopes and found that the percentage with bilateral hyperopia of at least 2 D in the less hyperopic meridian changed little from 10.8% percent at 1 year of age to 11.5% at 3.5 years of age, perhaps suggesting that the efficacy of emmetropization may be age- dependent, or that failures of emmetropization are evident by 1 year of age. Longitudinal studies have the advantage of revealing what happens in individual subjects. Mutti's data show an intriguing split between subjects with more than 4 D hyperopia, who seem to fail to emmetropize, while those with lower levels emmetropize well, despite the evidence that on average, emmetropization is proportional to the initial refractive error.13,15 In other words, there seems to exist a subset of hyperopes with failure to emmetropize normally. Pennie et al.16 show a similar phenomenon, with two of the most hyperopic of 20 infants failing to emmetropize, in contrast to the rest. Dobson and Sebris 17 followed children with moderate (any meridian at least 3 D) or high (at least 4 D) hyperopia before 8 months of age and found that 16/18 moderately hyperopic eyes, but only 8/16 highly hyperopic eyes were less than moderately hyperopic by 3 years of age. Wood et al.18 showed that although mean refractive error becomes less hyperopic over the first year of life, there is a remarkable amount of scatter—for example, between 3 and 6 months of age, more than half the hyperopes are in fact getting more hyperopic. Collectively these data suggest that the average tendency for hyperopia to follow a simple decline from early infancy into early childhood fails to capture the subtleties of emmetropization (or lack of it) in individual children.

Which infants are likely to be hyperopic? Although familial forms of extremely high hyperopia 19 probably represent a distinct entity from most infantile hyperopia, there appears to be a strong genetic component for hyperopia generally. Twin studies showing a high concordance of refractive error between monozygotic when compared with dizygotic twins find that this correlation is especially strong in the hyperopic end of the spectrum, over a range of 1 to 7 D of hyperopia.20 Population-based studies of refractive error in adults, despite the disadvantage of using noncyclopegic refraction, have shown familial aggregation of hyperopia.21,22 For early childhood hyperopia, studies showing the importance of family history have primarily looked at familial clustering of accommodative esotropia rather than hyperopia per se, partly because it is difficult to ascertain hyperopia reliably by history. As will be discussed below, this clustering likely reflects the heritability of hyperopia itself. In a population of 34 newborns having a parent or sibling with esotropia,23 hyperopia of at least 4 D in any meridian was found in 38% of infants at the age of 6 months, a prevalence clearly exceeding the prevalence estimates cited above for the general population at that age.

The genetic component of hyperopia raises the possibility of ethnic differences in hyperopia risk. There are no data comparing hyperopia prevalence in infants of different ethnicities, with the exception of the neonatal data cited earlier,5 but recent World Health Organization-sponsored population-based studies conducted around the globe using standardized methodologies and cycloplegic refraction on children as young as 5 years of age 24–29 do point to possible differences, although it is of course difficult to separate the environmental from the genetic differences between populations of different countries. For example, at least 2 D SE hyperopia in the right eye is seen in 24.4% of 560 5-year olds in Chile, but only 1.9% of 465 5-year olds in Nepal. The prevalence of myopia in these same populations (3.4 and 0.4% respectively) makes it clear that the differences do not simply reflect a myopic shift of otherwise similar refractive error distributions. Figures for non-Hispanic whites are not available for this series of studies, but Finnish population-based data show a 12% prevalence of at least 2 D SE hyperopia in 602 7- to 12-year-old children, and 19% in the subset of 163 7- to 8-year olds.30 Recent population-based data from Australia 31 also show ethnic variations in prevalence in 6-year-old children, with 4.6% of white children having at least 3 D SE hyperopia in the right eye, compared to only 2.4% of nonwhite children. Incidentally, even allowing for the differences in definition, this prevalence in 6-year-old white children suggests that from the 4 to 6% prevalence reported by Atkinson for 6- to 9-month olds 1,2 the reduction in hyperopia prevalence by the age of 6 years is not as marked as might be anticipated from cross-sectional mean refractive error data such as that of Mayer et al.10 Finally, the CLEERE study 32 has also reported ethnic differences in hyperopia, with a 19.3% prevalence of at least 1.25 D hyperopia in the least hyperopic meridian in white children aged 5 to 17 years, compared to 12.7% in Hispanics, and under 7% in Asians and blacks.

Although premature infants are better known for having higher rates of myopia than term children,33 they may also be at increased risk of hyperopia; Larsson et al.34 found right eye SE hyperopia >3 D in only 0.9% of 10-year-old full-term children, but in 4.2% of 213 children born prematurely, present since infancy in two-thirds of cases.35

The most well-characterized consequence of infantile hyperopia is accommodative esotropia.c The overall cumulative incidence of esotropia by the age of 5 years (equivalent to prevalence at age 5, assuming no spontaneous resolution) in the population of Olmsted County, MN has been estimated at 1.9%.36 Of the cases of esotropia, 46.5% were completely or partially accommodative (36% completely), implying a prevalence of accommodative esotropia of around 0.9% (0.7% considering only purely accommodative esotropia). Although these are population-based estimates, they represent a lower limit because they are based on chart review and thus only consider the portion of the population that sought medical attention. Recent population-based and examination-based data from Australia 30 show that among 1739 6-year-old children, between 9 and 14 of 26 cases of esotropia were attributable to hyperopia (depending on the classification of intermittent deviations), giving a prevalence for accommodative esotropia of at least 0.5%.

There is always some difficulty with the retrospective classification of established esotropia that is associated with hyperopia, yet is not completely controlled with full hyperopic correction, because it is impossible to ascertain whether the hyperopia is causal or coincidental. A commonly employed criterion for classifying esotropia as being at least partly accommodative is a difference of 10 prism diopters or more in the angle of deviation between measurements with and without correction.31,37 This definition is problematic, because with a normal stimulus accommodative convergence to accommodation (ACA) ratio of around 5 prism diopters per diopter,38 any esotrope with moderate hyperopia will meet the criterion, regardless of whether the hyperopia is etiologically related to the esotropia. At the same time, it would be wrong to discount all esotropia that is not fully controlled with hyperopic correction, because deviations that start out purely accommodative may increase over time 39–41 and may thus no longer be purely accommodative by the time they come to medical attention. Furthermore, considering the ratio of “partially accommodative” to “acquired nonaccommodative” esotropia in Olmsted County (10:17), it is evident that partially accommodative esotropia is not entirely attributable to a coincidental association of hyperopia with esotropia of nonhyperopic etiology, because it is unlikely (as mentioned earlier) that over a third of 5-year olds have 2 D of hyperopia. Finally, the prevalence of accommodative esotropia may be underestimated if a proportion of esotropes show significant emmetropization of the fixing eye between the onset of esotropia and the age at which it receives medical attention.

The only way to circumvent these difficulties in defining the prevalence of accommodative esotropia is to study the incidence of esotropia prospectively; to date this has only been done in high-risk subsets of the general population, i.e., in hyperopes.

Ingram et al.8 studied children identified by screening at the age of 6 months as having at least 4 D of hyperopia in any meridian; of 285 subjects followed to the age of 3.5 years, 24% became esotropic. In a similar study on 12-month olds with at least 3.5 D hyperopia in any meridian,10 45% subsequently became esotropic, in contrast to under 4% of subjects with less hyperopia. In a related study on a partly overlapping population of 306 12-month olds with at least 2 D hyperopia in the less hyperopic meridian bilaterally,42 15% overall became strabismic, with subgroup rates of 34% in 86 children with at least 3 D meridional hyperopia, and 8% in the remainder.

Atkinson et al.2 studied 6- to 8-month olds with at least 3.5 D meridional hyperopia. Fifteen percentage of 124 hyperopes became strabismic by the age of 3.5 years (23% of the 56 children in the subset not offered treatment in this trial of early spectacle correction). The rate in 123 emmetropes, by contrast, was 1.6%. In a second prospective study looking at children with a similar level of hyperopia, but selected on the basis of showing accommodative lag during screening,4 18% of 76 hyperopes developed strabismus, in contrast to only 1 of 196 emmetropes.

Multiple studies have found an association between accommodative esotropia and a family history of a similar problem. In a prospective study of 34 newborns having a parent or sibling with esotropia,23 six children (all hyperopes) developed esotropia, indicating an 18% chance of having accommodative esotropia for a child or sibling of an esotrope. In a study of individuals with accommodative esotropia,43 26% of their first-degree relatives had esotropia (a prevalence among relatives higher than for any other type of strabismus). Because a given subject has multiple relatives, 67% of subjects in this study had at least one affected first-degree relative. In another study of children with accommodative esotropia,44 22% of the first-degree relatives of 86 subjects had a history of accommodative esotropia,d and 77% of the probands had at least one first- or second-degree relative with the condition.

This familial clustering may in principle reflect either the heritability of hyperopia, as suggested by the data of Aurell and Norsell showing that infantile hyperopia was more than usually frequent in relatives of esotropes and that all the eventual esotropes had been early hyperopes,23 or the existence of another heritable factor which makes children more likely to become strabismic if they happen also to be hyperopic. Abrahamsson et al.45 reported that heredity and hyperopia together were more predictive of accommodative esotropia than either one alone, suggesting that the familial form of hyperopia may differ in some way from hyperopia that does not lead to strabismus—perhaps in the likelihood of emmetropization.

Several studies point to persistence of hyperopia as a distinguishing feature of hyperopia associated with subsequent esotropia. As discussed above, Ingram et al. found higher rates of subsequent strabismus among children who were still hyperopic at 12 months 10 than among children with hyperopia at 6 months,8 and also documented a relative lack of emmetropization before the onset of strabismus in strabismic as opposed to orthotropic hyperopes.46 In a small prospective study of eight infants with at least 4 D meridional hyperopia before 8 months of age,17 of four children with at least 3 D of meridional hyperopia in each eye and 4 D or more in at least one eye persisting at 17 months of age, three subsequently developed large angle esotropia by the age of 3 years, while none of the emmetropizing infants did. Aurell and Norsell 23 found that among family members of individuals with esotropia, who were hyperopic with at least 4 D SE at 6 months, persistence of this level of hyperopia as opposed to emmetropization correlated strongly with the subsequent development of strabismus.

Other factors that have been proposed to influence the outcome of hyperopia are binocular function and anisometropia.44 Among clinic patients with mean (of two eyes) SE hyperopia of at least 2 D and no history of strabismus before 12 months of age, the risk of having anisometropia at the time of presentation is 1.7 times greater in hyperopes with esotropia than in those without, particularly for lower levels of hyperopia (relative risk 7.8 for <3 D, as opposed to 1.5 for at least 3 D mean SE).47 However, it is difficult to know whether the anisometropia is causative, or secondary to strabismus, because nonfixing or amblyopic eyes are known to show abnormal emmetropization relative to the fixing eye, resulting in secondary anisometropia.48–50 It is argued 47 that because the relative risk for anisometropia is 2.1 even in the subset of cases without amblyopia, the anisometropia may precede the strabismus. Furthermore, if it were secondary, one would not necessarily expect the relative risk of anisometropia in strabismic versus orthotropic hyperopes to depend on the level of hyperopia; the fact that the relative risk of finding anisometropia in strabismic versus orthotropic hyperopes is larger for lower degrees of hyperopia seems to point to an additive effect of moderate hyperopia and anisometropia in predisposing to strabismus. On the other hand, it is also worth considering whether the low hyperopes with esotropia might actually have started out with purely anisometropic amblyopia and developed esotropia later, rather than having esotropia of a primarily accommodative etiology, as the study subjects are merely assumed to have accommodative esotropia on the grounds of having hyperopia and acquiring esotropia after the age of 1 year.

Birch et al.44 have also described subnormal binocularity in 41% of children with recent-onset and still intermittent accommodative esotropia and a family history of the condition; they interpret this to mean that the subnormal binocularity preceded the onset of esotropia, although it is difficult to control for the confounding effects of anisometropia and suppression or beginning amblyopia, all of which could be associated with both subnormal binocularity and intermittent esotropia, eliminating the need to invoke a preexisting defect of binocular vision.

Given the ethnicity-related variations in hyperopia prevalence discussed earlier, it becomes important to consider whether a given level of hyperopia has the same predictive value for future esotropia in different populations; data from 6-year olds in Australia 31 suggest that this is indeed the case, because there is no longer any significant difference in esotropia prevalence between whites and nonwhites after adjusting for significant hyperopia.

None of the factors described so far as influencing the likelihood of accommodative esotropia satisfactorily explain why some children with persistent high hyperopia seem to escape strabismus. Von Noorden 51 has pointed out that assuming normal ACA ratios, one would expect to observe large esophorias in these patients. He described nine nonanisometropic high hyperopes with at least 4 D SE bilaterally with good uncorrected visual acuity (20/30 or better in both eyes, suggesting adequate accommodation) and insignificant esophoria (<10 prism diopters), and observed that they had subnormal stimulus ACA ratios when compared with accommodative esotropes, whose ratios were in the normal range. Theoretically, the stimulus ACA ratio could be low despite a normal response ACA ratio in these subjects, if orthotropic hyperopes tended to underaccommodate more than strabismic hyperopes even when wearing full correction. However, assuming von Noorden's finding is not an artifact of using the stimulus ACA ratio, it raises the question of whether accommodative-convergence links were originally (and fortuitously) low in these subjects, or whether the ACA ratio adapted over time as a result of tonic accommodation and fusional vergence.52 Although slow fusional vergence on the time-scale of hours does not appear to alter the ACA in the established visual system,53 the developing visual system may exhibit greater plasticity, and it is conceivable that early accommodative behavior could affect the outcome of hyperopia.

Even among monozygotic twins, there is not always good concordance with regard to accommodative esotropia, even when the level of refractive error is similar.54 Different children may adopt different strategies for dealing with a given level of hyperopia, as proposed by Werner and Scott,55 with some children electing to sacrifice binocularity while others simply elect not to accommodate fully to compensate for their hyperopia, and accept the resulting chronic blur, possibly placing themselves at risk of developing ametropic amblyopia (discussed further below) as a result.

Knowing that hyperopia is a major risk factor for accommodative esotropia, several studies have attempted to determine whether early spectacle correction—optically eliminating the risk factor, would prevent esotropia. The first such trial published was conducted by Ingram et al.42 on 12-month-old infants with at least 2 D hyperopia in every meridian bilaterally. Children were given optical correction with only 0.25 D spherical undercorrection,e and this was discontinued if the child no longer met the entrance criterion and had <1.5 D of astigmatism and <1 D meridional anisometropia. Thirteen percentage of 152 subjects assigned to spectacle treatment developed strabismus by the age of 3.5 years, compared to 18% of 154 subjects not offered treatment (p = 0.17 by Pearson [chi]² test).f Analyzing according to actual treatment received, based on estimates of compliance with spectacle wear, those who were effectively treated developed strabismus in 17% of 87 cases, while those who were effectively untreated became strabismic in 15% of 219 cases. Considering the selected subgroup of 86 subjects with at least 3.5 D of meridional hyperopia, those offered treatment had a 35% strabismus rate, compared to 33% in those not offered treatment, while 50% of those effectively treated became strabismic, compared to 28% of the 64 subjects who were effectively untreated.

Ingram et al.8 conducted a second, similar study on younger infants having hyperopia of at least 3.5 D in any meridian at the age of 6 months. Of the 144 subjects, 24% assigned to treatment developed strabismus, compared to 26% of 141 not offered treatment. Twenty-four percent of those effectively treated became strabismic, compared to 25% of the 215 subjects judged to have been effectively untreated.

In contrast to these findings, Atkinson et al.2,56 found a benefit of early spectacle correction in preventing strabismus in children identified with at least 3.5 D meridional hyperopia (but <6 D and without anisometropia) based on cycloplegic screening at the age of 7 to 9 months. Glasses were given by 10 months of age, with more partial correction than in Ingram's studies: the prescribed spherical component (plus cylinder form) was 1 D less than the refraction of the less hyperopic meridian, and omitted if this was <2.5 D, while only half the cylinder was given, and then only for cylinder over 2.5 D until the child was 2-years old. The authors report 70% compliance with spectacle wear (defined as wearing at least 50% of the time). Of the 68 subjects who were offered treatment, 8.8% became strabismic by 3.5 years of age, as opposed to 23.2% of the 56 subjects not offered teatment. Forty-five compliant subjects showed only a 6.3% incidence of strabismus, compared to 21% in 76 effectively untreated children. In a second, separate study,4 which enrolled hyperopic subjects who had shown accommodative lag on initial screening, 21% of 58 subjects offered treatment developed strabismus when compared with 11% of 18 subjects not offered treatment; among 23 treated and compliant subjects the incidence was 22%, vs. 17% in 53 effectively untreated subjects. The authors note that compliance was lower in the second study (as indeed was the proportion of hyperopes participating in the trial from among the candidates identified during screening), and that initiation of spectacle correction was slightly later (by 11 to 12 months of age); they suggest that this may account for the lack of benefit in the second study. It should be noted that this study also had a power of <0.4 to detect the magnitude of effect seen (using the “intention to treat” analysis) in the earlier study.

Although notable differences between the Ingram and Atkinson studies include more partial correction in Atkinson's, and better compliance with spectacle wear, it is difficult to reconcile the contradictory findings, and the value of early spectacle correction of hyperopia for preventing accommodative esotropia remains uncertain.

In hyperopes, visual deficits other than accommodative esotropia and its downstream consequences, (e.g., unilateral amblyopia, and deficient binocularity despite alignment 57) are not as well-characterized, in part because they are more difficult to evaluate. Mild bilateral ametropic amblyopia, for example, is hard to diagnose early, because of the variability of visual acuity test performance even among young children with normal vision. Bilateral amblyopia is of particular interest in light of the notion, mentioned earlier, that it may result when children adopt a strategy of habitual underaccommodation (relative to their refractive error) to avoid strabismus, thereby experiencing chronically degraded visual input. Numerous studies 55,58–61 have reported on this condition, all in the context of populations presenting for clinical care. It is tempting to ask whether these studies find an inverse correlation between the presence of decreased visual acuity in the better eye and the presence (or early versus late onset) of strabismus, as might be expected based on the above reasoning. However, this can only be assessed in a representative sample of all children with a given level of hyperopia; in clinic-based studies an inverse association can arise spuriously because nonstrabismic hyperopes who present to a clinic are more likely to have decreased vision, as they have no other reason (e.g., strabismus) to seek medical care.

Clinic-based data by the same token cannot yield any meaningful estimate of the overall prevalence of bilateral amblyopic deficits in high hyperopia. The only recent studies in a position to do this would be those of Atkinson et al.2,4,56 Unfortunately, the authors do not make a clear distinction between unilateral and bilateral visual acuity deficits in their analysis. They do, however, comment 2 on the fact that bilateral visual acuity deficits “were common” among untreated hyperopes, and thus did not simply represent unilateral amblyopia secondary to strabismus. This may be surmised also from the fact that in the first study,2 deficits (vision worse than 20/30 either eye) were seen in 68% of effectively untreated hyperopes on crowded letter tests, vs. 11% of emmetropic controls—the excess surpassing the strabismus rate of 21% in this group, implying acuity deficits unrelated to strabismic amblyopia. In the second study,4 visual acuity deficits were similarly seen in 45% of all (treated or untreated) hyperopes, compared to only 1 of 196 emmetropes, while strabismus was present in only 18% of the hyperopes. It should be noted that because Atkinson's hyperopic population is enriched for astigmats, by virtue of using the most hyperopic meridian to define hyperopia, bilateral visual acuity deficits could represent bilateral ametropic amblyopia from astigmatism rather hyperopia per se. The authors tested for selective impairment of acuity in one meridian,2 and concluded that meridional amblyopia could not account for all cases of bilateral visual impairment; however, data from Dobson, Miller and colleagues 62 show that hyperopic astigmats show similar deficiencies in both meridia (presumably from adopting an intermediate focus), so ametropic amblyopia from astigmatism remains a possible explanation for Atkinson's findings. Interestingly, 8% of subjects in the second study 4 who had shown lag on photorefractive screening but turned out not to be hyperopic nonetheless showed visual acuity deficits (compared to 0.5% of emmetropes); this supports the notion that relative hypoaccommodation rather than absolute refractive error may be predictive of future visual acuity deficits.

With regard to spectacle correction, Atkinson et al. found visual acuity benefits of spectacle correction in both studies: acuity deficits (unilateral or bilateral) were seen in only 29% of effectively treated hyperopes in the first study, compared to 67% of those without treatment; in the second study, only 17% of effectively treated hyperopes showed deficits, compared to 68% of effectively untreated subjects. It is tempting to speculate that early optical correction may have prevented bilateral ametropic amblyopia in some subjects.

One additional prospective study 63 followed 16 children identified consecutively, in the course of population-based noncycloplegic retinoscopy screening at the age of 1 to 2.5 years,64 as having 5 D of hyperopia bilaterally (as measured with subsequent cycloplegia) and no strabismus at the time of screening; 25% of subjects went on to have residual bilateral amblyopia (VA of 20/40 or worse at age 7 years) despite early optical treatment. Other studies, however, emphasize relatively good final visual outcomes in clinic populations with high hyperopia 58,60; Edelman and Borchert 60 found that only 8% of 113 mixed strabismic and orthotropic hyperopes with at least 5 D SE bilaterally had 20/40 or worse final acuity in the better eye. An important difference is that Friedman's study 63 selected for hyperopes who were still orthotropic at the age of screening, while Edelman and Borchert's 60 clinic population, conversely, was disproportionately enriched for esotropes (84% esotropia) relative to the presumed source population of hyperopes. It should be noted that because bilateral amblyopic deficits tend to be relatively mild, the frequency of bilateral amblyopia in any group of hyperopes will depend very critically on the threshold used to define a deficit, with much higher rates of impairment reported when the threshold is lowered.59,65

In addition to bilateral amblyopia, several authors have commented on abnormal binocularity in hyperopes even in the absence of strabismus 61,63; such deficits, if unrelated to any co-existing visual acuity deficits, would corroborate the hypothesis that deficient binocularity may precede the onset of esotropia in some hyperopes.44

It seems reasonable to speculate that anisometropia could sometimes result secondarily from hyperopia, as a result of asymmetrical emmetropization. Population-based cross-sectional data on 6-year olds suggest an association between anisometropia and hyperopia,66 but unfortunately in this case the association may simply be an artifact of the refractive error definitions used: use of the refractive error in the more ametropic eye to define hyperopia and myopia will by definition result in a reduced prevalence of anisometropia among children classified as emmetropes.

Finally, there has been debate over whether hyperopia may impact vision-dependent functions such as reading; a discussion of this topic is beyond the scope of this review. In addition to consequences for vision and vision-related activities, hyperopia has also been reported to impact more general measures of development 67,68; however, interpretation of such observations on nonvision outcomes is very much complicated by the difficulty of controlling for confounding factors, and distinguishing between correlations and true causal relationships.

Given the burden of early childhood hyperopia and its sequelae in the population, what are the options for reducing this burden? Two distinct strategies may be delineated. The more conservative approach is to devote resources toward improving early detection of existing strabismus and visual acuity deficits, avoiding unnecessary examinations and/or treatment of children who are not destined to suffer any sequelae of their hyperopia. This strategy does not preclude defining more broadly what is meant by visual acuity deficits, for example, considering habitual hypoaccomodation as a deficit, but the goal remains that of detecting and treating existing disturbances of visual function. Screening programs based on such an approach have shown reduction in the prevalence of severe amblyopia in the general population.69,70 Within this context, refractive error might in principle be used as an easily measured surrogate marker for existing vision problems, identifying a subgroup of children requiring formal assessment of ocular alignment and visual acuity.

A second and different approach is to identify high-risk subsets of the population before they have developed any sequelae, either to single them out for close observation, maximizing the chances of early detection of sequelae when they occur, or to provide them with prophylactic refractive error correction in the hope of forestalling any disturbance of visual development altogether. Again, measurement of refractive error is an obvious candidate for a method of identifying children at risk of future problems.

The difficulty with using refractive error as a screening measure in this way is that currently we do not know enough to determine the optimal timing or referral parameters for such screening. Too large a percentage of hyperopia appears to be benign at very early ages, but the older the age at screening, the more likely we are to miss the window of opportunity for prophylactic interventions should they prove to be effective.

The solution would seem to be some refinement of the concept of detecting refractive error. For example, it has been suggested that hyperopes who demonstrate good accommodation in conjunction with orthotropia are less likely to need spectacle correction,71 and are at lower risk of future problems.46 Consequently, screening instruments designed to evaluate accuracy of focusing in each eye simultaneously in an automated manner 72,73 thus screening only for ocular misalignment or uncompensated refractive error rather than refractive error per se, are very appealing in principle; the biggest challenge with such instruments is likely to be that of distinguishing defocus due to inattentiveness, from real pathology. A simpler variation on the same theme is the notion of exploiting the noncyclopleged state to evaluate residual refractive error in the setting of habitual accommodative behavior; this is in essence the principle behind the photorefraction technique used in the second screening program of Atkinson and colleagues.2 Yet another way to refine refractive error related screening would be to sample a child's refractive status at more than one time point, which would provide information on whether a hyperopic child is demonstrating emmetropization or not, which may help delineate the subset of hyperopes destined for future problems.

Finally, once the optimal method and timing of screening have been determined, there remains the unresolved question of whether prophylactic spectacle correction is in fact beneficial in any subgroup of hyperopes. Even if it is ultimately proven to work in a study setting, would there still be measurable benefits at a population-wide level after taking into account the very real obstacle of poor compliance with spectacle wear in young children? If there is still a benefit at 3.5 years of age even in a real world setting, are final visual and oculomotor outcomes after treatment significantly better with prophylaxis than with the conservative approach of vigilant surveillance for strabismus and amblyopia? And lastly, even if final outcomes are better, what is the overall cost-benefit ratio of a program aimed at prophylaxis, in terms of possible delayed emmetropization 7,74–76 spectacle-dependence, cost of early screening, and cost of prophylactic interventions for children who did not in fact need them, weighed against the improvements in outcome?

Considering these factors does not preclude individual practitioners and patients from adopting a variety of individualized surveillance and management strategies with regard to early childhood hyperopia, as indeed they do at present.77 However, to derive sensible public health policy with regard to minimum acceptable standards of screening for disorders of visual development related to hyperopia, we must recognize that we have insufficient knowledge of the condition currently to either optimize screening guidelines or to guide management following the identification of children at risk.

In conclusion, it is not clear at this stage what strategy is optimal, from a public health perspective, for reducing the burden of pathological manifestations of hyperopia in the pediatric population—indeed, there may be more than one approach, according to the pediatric health care infrastructure present in a given country or even in a given setting within the same country. What is clear, however, is that current knowledge of the natural history of early hyperopia, of the risks associated with hyperopia at given age, and of the benefits of prophylactic interventions are all lagging far behind our technical prowess in detecting and measuring refractive error; the gaps in our knowledge make it difficult to know how most wisely to apply the tools in our possession.

I would like to thank Kurt Simons for first introducing me to the work of Atkinson and Ingram.

Kristina Tarczy-Hornoch

Childrens Hospital Los Angeles

4650 Sunset Blvd., MS#88

Los Angeles, California 90027

e-mail: ktarczyhornoch@chla.usc.edu

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^aPercentage is deduced from graph. [Context Link]

^bThis is determined by applying Ingram's stated 1.75 D working distance correction 8 although the paper reporting prevalence refers, somewhat confusingly, to the value of the neutralizing trial lens. It should be noted for all of Ingram's work that there is a discrepancy between the use of 1.75 D correction for working distance, which would imply a 57 cm working distance, and Ingram's stated working distance of 1 m, which, however, seems rather longer than most arms; if he worked at arm's length, his refractions are probably a quarter to a half diopter more hyperopic than reported, but for the purposes of the present paper we will assume the 1.75 D correction is accurate. [Context Link]

^cAlthough the term accommodative esotropia can be ambiguous, as it may be used to describe esotropia at near resulting from a high accommodative convergence to accommodation ratio even in the absence of any so-called refractive esotropia, I will use this term throughout the paper to refer to esotropia that appears to be etiologically related to hyperopic refractive error. [Context Link]

^dThe text of the article states incorrectly in the results section that 22% of probands had affected first-degree relatives, but from Table 1 it is evident that 22% is instead the prevalence of accommodative esotropia among the first-degree relatives of the probands. [Context Link]

^eNote that he subtracts 2 D not from the refraction, but from the neutralizing trial lens, while using a working distance correction of 1.75 D. [Context Link]

^fStrabismus rates for this study are calculated from raw data in Tables 1 and 2 of the referenced paper. [Context Link]

Key Words: hyperopia; infant; children; prevalence; risk factor; accommodative esotropia

Accession Number: 00006324-200702000-00010