Emmetropisation & Development of Ref Error

Question 1

How do we define emmetropisation?

Answer 1

“The coordination of the power of the cornea, crystalline lens and axial length to process a sharp retinal image of a distant object” in the absence of accommodation
Adlers Physiology of the Eye, 11th Ed

Question 2

What structures are involved in Emmetropisation and how are they involved?

Answer 2

• Cornea (curvature of anterior and posterior surfaces, refractive index and thickness)
• Anterior Chamber (depth and refractive index of aqueous humour)
• Lens (curvature of anterior and posterior surfaces, refractive index and thickness)
• Posterior Chamber (depth and refractive index of vitreous humour)

Question 3

What is the average refractive error at birth?

Answer 3

+2D

Question 4

At birth how are refractive errors distributed?

Answer 4

At birth refractive errors are normally distributed across population. (Mutti et al 2018; 222 ppts)

Question 5

How are the ocular components distributed at birth?

Answer 5

The individual components are normally distributed across population at birth.

Question 6

What is leptokurtosis?

Answer 6

Leptokurtosis in itself is just a narrowing of the distribution (away from normally distributed)

Question 7

By the age of 6 how does the distribution of refractive error look?

Answer 7

By age 6, distribution is no longer normal but shows leptokurtosis and is also positively skewed.

Question 8

By adulthood how does the distribution of refractive error look?

Answer 8

In adult populations, distribution is still leptokurtic but skew becomes negative

Question 9

How do the ocular components grow? Passively or actively?

Answer 9

Ocular components remain normally distributed at 6 years old and 18yo but the output is no longer normally distributed except for one parameter. The fact ocular components remain normal dist. suggests that most ocular components are passively changing according to genetics which is a natural growth (passive changes). The axial length (total size of the eye) departs from a normal distribution which is evidence of an active process.

Question 10

What did Hubel & Weisel find in the 70’s about emmetropisation? (think cats)

Answer 10

Active emmetropisation requires visual feedback as a neonatal (cats eyes sutured shut, the sutured eye grows uncontrollably). Increased axial length as a result of a lack of visual feedback.

Question 11

What’s the most common orientation of astigmatism in 3mo compared to 36mo? (Mutti et al., 2004)

Answer 11

The most common orientation was with-the-rule at 3 months (37.0% compared with 2.7% for against-the-rule) but against-the- rule at 36 months (3.2% compared with 0.9% for with-the-rule

Question 12

How might astigmatism be related to emmetropisation?

Answer 12

Some have suggested that the presence of astigmatism provides a necessary cue for the emmetropisation process but the evidence for this is not conclusive.

Presence of astigmatism ?is related to the grow and stop conditions of the retina

Question 13

What ocular pathology can interfere the most with the emmetropisation process?

Answer 13

Retinopathy of prematurity

Question 14

What systemic condition ca influence the rate of change and the effective end-point of emmetropisation?

Answer 14

These include Down’s syndrome (Doyle et al, 1998), albinism (Flitcroft, 2014) and cerebral palsy (Saunders, 2010)

Question 15

Can spectacle correction during emmetropisation interfere with the process?

Answer 15

Use dynamic RET to ensure they’re accommodating normally = doesn’t interfere
(Chang, 2017)

Question 16

What age does emmetropisation end?

Answer 16

6yrs old

Question 17

What is change in refractive error after 6yo known as?

Answer 17

It’s not emmetropisation as after 6yrs!

It’s a process called ………………

Question 18

What is Myopigenesis?

Answer 18

The development of myopia

Question 19

What is the prevalence of myopia expected to do between 2000 - 2050? (Holden et al., 2016)

Answer 19

Prevalence rates are expected to increase from 23% to 54% in the time period 2000 to 2050.

Question 20

Why are we experiencing an increase in myopic prevalence?

Answer 20

This increase can not be explained by genetic factors and points to an environmental contribution to myopigenesis. (Morgan, I. & Rose, K., 2019). Increased urbanisation, intensive schooling, increased near work, not spending time outdoors.

Question 21

What changes to make a person myopic?

Answer 21

The posterior 1/3rd of the eye, the vitreous chamber elongates which stretches the retina, choroid and sclera and thus increases the risk of eye disease. Greater myopia = greater risk; no safe level of myopia (retinal detachment, primary angle glaucoma, cataracts). 9x greater to be at risk of myopia if you have myopic parents.

Question 22

What are high myopes at risk of specifically?

Answer 22

Myopic myopathy (macular degeneration specific to myopes) for which there is no treatment (leading cause of blindness in Chinese populations)

Question 23

What can provide protection against myopia development?

Answer 23

Time spent outdoors (suggest to children to do it 2 hours per day)

Question 24

How are schools trying to reduce myopic prevalence?

Answer 24

Interventions are taking place which include ensuring take their school breaks outside and the creation of classrooms which are 100% glass, or mimic outdoor scenery to try to reduce myopia prevalence. (Zhou et al, 2017, Yi et al, 2023)

Question 25

What is Relative Peripheral Hyperopia (RPH)?

Answer 25

What’s happening in the peripheral refractive error (because we correct central refractive error)? If we leave the periphery with a refractive error e.g. hypermetropic, then this can stimulate the growth signal for the eye to grow causing the central refraction to become myopic. If we correct this again then we make the periphery hypermetropic again which continues the cycle (Wallman & Winawer, 2004)

Question 26

What happens in RPH if the defocus/periphery of the eye is myopic?

Answer 26

You stay emmetropic (eye can’t shrink)

Question 27

What is optical control of myopia?

Answer 27

The optical control is based on correcting peripheral hyperopia using bifocal or multifocal soft contact lenses, by Ortho-K or by using spectacles which utilise Defocus Incorporated Multiple Segments (DIMS), eg Hoya MiyoSmart.

These interventions have been shown to reduce myopic progression by approximately 50% when compared to single vision correction.

More importantly, they have been shown to reduce axial elongation by up to 62% when compared with single vision correction.

Question 28

What are MiSight soft contact lenses?

Answer 28

Used in myopia therapy – use this lens instead of single vision lenses, they have half the axial expansion compared to the control group. Hasn’t removed the myopia progression but has halved it (has zones of lens and others not). Corrects central distance and then has extra zones of plus to correct the relative peripheral hyperopia.

Question 29

What are MiyoSmart Spectacle Lenses?

Answer 29

Lenses that add extra plus into the periphery. Distance correction of centre but extra plus in the periphery.

60% slowing of myopia progression.

Hoya Vision (2021)

Question 30

What is Ortho-K?

Answer 30

Ortho-Keratology - relies on treatment in ancient China/Japan by placing weights on eyes when myopic which flattens the cornea to see in the distance.
Fit contact lenses flat to wear at night which affects the corneal surface and flattens them. This stops myopic individuals getting worse as increasing the plus in the periphery by flattening the cornea.

Question 31

What are the Pharmacological Controls of myopia?

Answer 31

The pharmacological approach involves the use of atropine, in particular low-dose atropine. (Chia et al, 2012)

Concentrations as low as 0.01% are currently being used in myopia control and have been shown to reduce myopic progression by 50% compared with a placebo drop.

0.05% is looking most effective (Yam et al., 2023) for controlling axial elongation and having minimal side effects but there are disputes to low doses (Lee et al., 2022)

But there is a rebound phenomenon in terms of their myopia and elongation when using HIGH atropine doses that is not seen in MiSight soft contact lenses.

Be aware these results are based only on Chinese populations.

Question 32

How does atropine have an effect on reducing axial elongation?

Answer 32

The exact mechanism by which atropine reduces axial elongation is still under investigation but it has been shown not to be due to the cycloplegic action at the ciliary muscle. (McBrien et al, 1993)

Question 33

Why have they reduced the dosage rate for atropine for reducing axial length?

Answer 33

Because there is a rebound phenomenon in terms of their myopia and elongation when using HIGH atropine doses that is not seen in MiSight soft contact lenses

Question 34

How might R/G colourblindness affect the growth signal in axial elongation?

Answer 34

Observed difference in myopia between colour vision normal and R/G colour deficient groups where the latter have a reduced prevalence and severity of myopia in comparison with the former. (Gan et al, 2022)

Question 35

Why do we need to be cautious in applying studies on growth signalling re: axial length that are based solely on Chinese populations?

Answer 35

The ratio of Long to Medium cones in the retinal mosaic has been shown to be different between North Americans and Asians (2.7:1 v 1:1). (Hagen et al 2019)

Question 36

What is the red light therapy principle based on?

Answer 36

The ratio of Long to Medium cones in the retinal mosaic has been shown to be different between North Americans and Asians (2.7:1 v 1:1). (Hagen et al 2019). Different cones worldwide might be affecting signalling routes for axial length control.

Not yet recommended as no safety tests but it seems to reduce myopia (found 3 minutes per session, twice daily with a minimum interval of 4 hours, 5 days per week caused a 69.4% reduction of axial elongation)