Contact Lens Correction and Myopia Progression

This chapter gives a review of the literature which provides evidence that myopia control can be effective and beneficial. Clinical practice can be found on p. 502 of this chapter and in Chapter 19 .

Contact lenses have been an effective method of correction for myopia for many decades during which time the prevalence of myopia has increased markedly and reflects the worldwide increase evident in all industrialised nations, particularly those in East Asia. Studies of myopia progression indicate that for juvenile-onset myopia the notional optimum age range for intervention would be 8–10 years. As it represents a substantial proportion of myopia, early adult-onset myopia is also a candidate for intervention.

Animal studies have demonstrated that the optical basis for myopia control with contact lenses is to reduce the degree of relative peripheral hypermetropic refractive error while maintaining optimum correction for central vision ( ). However, a consensus has yet to emerge on the aetiological significance of peripheral refraction in the onset and progression of human myopia. Instruments are available to measure the peripheral refraction for example the Shin-Nippon binocular open-field infrared autorefractor ( ).

Prevalence of Myopia

The prevalence of myopia has increased since the middle of the twentieth century, and it has been predicted that myopia and high myopia will show a significant increase in prevalence globally by 2050, affecting nearly 5 billion people (49.8%, up from 22.9% in 2000) and 1 billion people (2.7%, up from 9.8% in 2000), respectively ( ). Studies show this trend worldwide including the following:

▪
Northern Ireland (UK) – Longitudinal data collected since 2006 by the UK Northern Ireland Childhood Errors of Refraction study (NICER) showed that the proportion of children with myopia increases significantly from 6 to 7 years (1.9%) and 12 to 13 years (14.6%) to reach a level more than double that reported for children 10 to 16 years of age in the 1960s (7.2%) ( ).
▪
Aston (metropolitan area of England) – Cross-sectional data collected since 2005 by the UK Aston Eye Study (AES) showed that the prevalence of myopia in a multi-racial sample of children (South Asian, black African Caribbean and white European) had increased significantly. Increases in the 6–7 year age group was 9.4% and in the 12–13 years age group, it was 24.9%. In the older group, South Asian children had substantially higher levels of myopia than white European children (36.8% vs 18.6%) ( ).
▪
Europe – A population-based cohort cross-sectional study of the prevalence of refractive error in adults of predominantly European ancestry (98%) found the prevalence of myopia and high myopia to be 30.6% adn 2.7% respectively. Age-specific estimates revealed a high prevalence of myopia in younger participants (47.2%) 25 to 29 years of age ( ).
▪
USA – Prevalence of myopia in the USA has increased from 25% to 41% over a 30-year period ( ).
▪
Singapore – Systematic studies on global prevalence of myopia indicate that East Asians have exhibited marked increases in prevalence over time, reaching 69% at 15 years of age (86% among Singaporean-Chinese) ( ).

Urban areas

Children residing in predominantly urban environments are approximately 2.6 times more likely to be myopic than children residing in rural settings (a consistent picture across different ethnic groups).

Ethnic groups

In white and East Asian children, differences in myopia prevalence emerge at about 9 years of age; by late adolescence, females are twice as likely as males to be myopic ( ).

Given the likelihood of an inexorable rise in its incidence, myopia is now considered a major public health concern in all industrialised societies as even relatively modest levels constitute a significant risk of ocular pathology, in particular myopic maculopathy and retinal detachment ( Table 28.1 ; ).

Table 28.1

Odds Ratios of Increased Risk for Ocular Pathology With Increasing Levels of Myopia *

	Glaucoma	Cataract (PSCC)	Retinal Detachment	Myopic Maculopathy
–1.00 to –3.00	2.3	2.1	3.1	2.2
–3.00 to –5.00	3.3	3.1	9.0	9.7
–5.00 to –7.00	3.3	5.5	21.5	4.6
> –7.00	–	–	44.2	126.8

* Summarised from . The complex interactions of retinal, optical and environmental factors in myopia aetiology. Prog. Ret. Eye Res. 31, 622–660.

Most myopes seen in practice are the juvenile-onset or ‘school myopia’ type. These represent around 70% of myopia, which typically has an onset between 7 and 11 years of age and stabilises between 15 and 18 years of age at around 3–4 dioptres ( ).

Earlier presentation, around 5 years of age, is less common and accounts for around 3% of myopes. It is likely to progress to levels in excess of 6 dioptres with an increased probability of myopic pathology ( ). Presentation of high myopia at this early age also may be associated with systemic syndromes such as Marfan or Stickler syndrome (see Chapters 21 and 24 ). It has been estimated that approximately 25% of myopia can be categorised as early adult-onset (i.e. onset generally between 18 and 40 years of age) that rarely reaches levels in excess of 2 dioptres ( , ). The use of contact lenses to regulate early adult-onset myopia is not well-documented despite it being particularly apposite to existing wearers where compliance and financial commitment are less significant ( ).

Progression of Myopia

This chapter addresses specifically the effect of contact lens correction on progression of myopia rather than onset of myopia. Emmetropisation is essentially complete by 6 years of age; hence myopia developing in later years cannot be attributed per se to a failure to emmetropise ( ). Intricate gene-environment interactions characterise the onset and progression of juvenile-onset myopia ( , ) and involve several factors:

▪
intense urbanisation combined with education that imposes high levels of visual and cognitive demand ( )
▪
reduced time spent outdoors ( )
▪
a predisposing polygenetic profile ( ).

However, the prospective therapeutic use of contact lenses in a child who is ostensibly emmetropic introduces significant ethical constraints.

Key point

Low hypermetropic refractive errors (<+0.75 D) at 6 years of age have a highly predictive power for future myopia ( ).

, in a comprehensive longitudinal study, considered the age at which intervention might be considered as relevant. They analysed changes in ocular structures contributing to the progression of myopia over an 8-year period in 247 children aged 6 years and older of mainly White and East Asian ethnicity. The changes were compared with those in 194 children who remained emmetropic over the same period. Mean spherical errors at age 14 years were +0.44 D and –3.17 D in emmetropes and myopes, respectively. No significant differences were apparent between the two groups in corneal power and anterior chamber depth over the measurement period. However, although lens power became progressively less in myopic eyes than in emmetropic eyes, it was not sufficient to compensate for the concomitant elongation of vitreous chamber depth in myopic eyes, which significantly exceeded that found in emmetropic eyes.

The study also showed that the rate of change of posterior chamber depth elongation in myopia increased significantly, relative to emmetropia at around 10 years of age and was maintained through to 14 years of age. They suggested therefore that an optimum age range to consider intervention would be 8 to 10 years of age, when it is likely that contact lenses could be managed on a day-to-day basis.

Key point

The principal structural correlate of myopia is excessive elongation of the posterior vitreous chamber ( ).

Contemporary Approaches to Myopia Control

selected randomised controlled trials (RCTs) with a treatment duration of at least 1 year to evaluate 16 interventions for controlling the progression of myopia in children. The primary outcomes were mean annual change in refraction (in dioptres/year) and mean annual change in axial length (in millimeters/year). Thirty RCTs were identified and involved four principal categories of intervention: 13 spectacle lens studies, 9 contact lens studies, 1 outdoor activity study, and 7 pharmacological intervention studies. They compared the relative efficacy of the procedures in terms of statistically significant reductions in dioptric error or inhibition of axial elongation.

Those judged as ineffective were:

▪
rigid gas-permeable contact lenses
▪
conventional soft contact lenses
▪
the ophthalmic drug timolol (a nonselective beta-receptor antagonist)
▪
undercorrection of distance vision with single-vision spectacle lenses.

Those judged as effective were:

▪
the ophthalmic muscarinic receptor antagonist drugs atropine and pirenzepine (the former nonselective, the latter selective for M ₁ receptors)
▪
orthokeratology
▪
soft contact lenses that incorporate optical designs to modulate peripheral defocus (see Multifocal Lenses, p. 503 )
▪
progressive addition spectacle lenses.

In a review of strategies to regulate myopia progression specifically with contact lenses, orthokeratology was identified as the procedure providing greatest efficacy across ethnic groups ( , ).

Low doses of atropine (i.e. 0.01%) are particularly significant in slowing myopia progression in Chinese children and induce only modest increases in pupil size (~0.8 mm) and reduction in amplitude of accommodation (2.00–3.00 D), although the precise basis for its effect is presently unclear ( ). A literature search by found that 0.01% atropine produced the lowest rebound effect. *

* Rebound effect – where the myopia starts to increase once the treatment has stopped.

Peripheral refraction and myopia control (see also Section 9 , Addendum, available at: https://expertconsult.inkling.com/ )

The optical basis for the reported inhibition of axial elongation with contact lenses emanates principally from investigations that disrupt the process of emmetropisation in neonate monkey eyes ( ). The investigations demonstrate that ocular growth and refractive development are regulated by retinal defocus. For example, when monocular hyperopia is produced by a negatively powered lens placed in front of a monkey's right eye, the central defocus induces compensatory myopic growth relative to the left eye (which acts as the control eye) – that is, the right eye elongates axially to eliminate the imposed hyperopic defocus and therefore becomes myopic rather than emmetropic. Conversely, when monocular myopia is produced by a positively powered lens placed in front of the right eye, the central defocus inhibits ocular growth relative to the left eye – that is, axial elongation of the right eye is inhibited such that it is constrained to hyperopia ( ). Importantly, subsequent work, again on monkey eyes, demonstrated that the regulation of axial growth similar to that described earlier could be achieved when optical defocus was restricted to peripheral regions of the retina.

Key point

Studies show that, in the presence of an in-focus central image:

hyperopic peripheral defocus promotes axial growth and
conversely, myopic peripheral defocus inhibits axial growth ( ).

As axial growth is the principal structural correlate of myopia progression, these studies indicate therefore that contact lenses designed to inhibit progression should reduce the degree of relative peripheral hyperopic refractive error – to an extent that might be either conjugate with the retina or anterior to the retina – while simultaneously maintaining optimum correction for central vision ( ).

A consensus has not yet emerged on the aetiological significance of peripheral refraction in the onset and progression of human myopia ( , ).

Current and prospective methods of myopia control with contact lenses demonstrate that they provide a feasible procedure for eye care practitioners to manage effectively a ubiquitous condition that represents a significant risk to ocular health ( , ). However, evidence is needed of the potentially detrimental effects of cessation of therapy and possible rebound effect * because cessation of long-term therapy commenced in the young, developing eye may have pathological consequences should it provoke reversion to a predetermined myopic state, as structural change may be induced in a fully developed adult eye.

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