In recent years there has been a growing call in the industry for eye care professionals to address the problem of myopia. According to the International Myopia Institute, we can expect to see the prevalence of myopia to have reached 50% of the global population by 20501. This has significant implications due to the increased risk of pathology leading to visual impairment, negative impact on education and quality of life, not to mention the effect this will have on economic impact, with an estimated $250bn loss in productivity due to myopia in 20151.
Most children are born hyperopic before undergoing the process of emmetropisation which usually stabilises around the age of six. Traditionally, children were thought to become or remain myopic because of genetics based on the increased incidence of myopia in those with myopic parents and data from certain ethnic groups. This view changed following numerous studies which demonstrate that the eye’s growth is homeostatic in nature2 (i.e., it adjusts to the conditions, with visual input being the primary driver of growth).
With research continuing in this area to ascertain the exact mechanisms by which myopia develops and progresses, there is evidence to show that there are changes to the peripheral retina which are linked to myopia.
Peripheral defocus
Multiple studies3,4,5,6 have demonstrated that myopic eyes have a prolate shape, with a hyperopic tendency in the periphery. If the eye develops homeostatically, then for myopic patients the peripheral retina is being stimulated to elongate (which will place the focal plane on the retina), while the central retina corrected with a negative correction will have no such stimulation.
Foveal vision has always been key in finding the best correction for patients, in myopes this could lead to an exaggerated elongation effect in the peripheral retina.
This can be seen by the cumulative distribution of neurones in the central and peripheral retina. Although the fovea has a denser concentration, it is over a much smaller region. A direct comparison shows there are far more parasol ganglion cells and dopaminergic amacrine cells in the periphery than at the fovea. Additionally, there are around 300% more ganglion cells and 40-50% more cones in the nasal retina compared to the temporal region7.
The consequence is that the peripheral signals dominate, stimulating growth and an increase in the elongation in the peripheral retina. Therefore, it is important to not only correct the myopia in the central retina, but to also correct the hyperopic defocus in the peripheral retina.
My-Nor
Backed by a five-year study, My-Nor is a rear surface, peripheral defocus myopia management solution. Delivering optimal myopic correction in the centre of the lens, the horizontal peripheral defocus in My-Nor begins at 4mm temporally compared to 6mm nasally, inducing positive spherical power in the form of a progressive addition in the horizontal meridian to maximise the chances of inhibiting the homeostatic signal which stimulates elongation. The progression is higher temporally to coincide with the increased cell distribution in the nasal retina (figures 1 and 2).
Figure 1 & 2 (right to left): Power map of the My-Nor len; and horizontally located progressive power additions nasally and temporally
Trial results
My-Nor has been rigorously tested to ensure its efficacy. In a comparative study, My-Nor was shown to reduce myopia progression on average by 40%, with a reduction in myopic refractive error after 18 months of 34% and a reduction in axial length of 56%. These results were maintained after five years with a reduction of 40% in mean power and 31% in axial length compared to the control group (figure 3).
Figure 3: Refractive error (left) and axial length (right) progressions with and without test lenses
As My-Nor is a rear surface freeform design using a spherical blank, it has a vast range of powers and materials at an affordable price for suitable patients, giving practitioners a myopia management solution that they can recommend with confidence.
At Norville, we take our responsibility as a premier supplier of Rx lenses seriously, which is why we have ensured we can offer our customers a myopia management solution fully backed with clinical evidence of its success and unique flexibility in the power and material ranges, at a fair price.
Dispensing guidelines
Once a patient has been identified as a suitable candidate for myopia management using the standard clinical guidelines, dispensing My-Nor is a very simple process.
Beginning with the frame selection, care should be taken to ensure the lens is centred correctly with at least 5mm above the pupil centre, and 12mm below (figure 4, below). To maximise the chance of success in the slowing down of the myopic progression, we advise a minimum boxed size of 37mm x 17mm, which ensures the correct placement of the defocus zones.
Once the frame has been adjusted, the centration distance and heights should be measured and supplied with the order.
On collection, both child and parent should be advised of the defocus in the periphery and the need to look centrally through the lenses. This advice can also help to speed up the adaptation time (a maximum of two weeks, although during the trial 90% of participants adapted in less than a day). It is important to highlight how changes to the fit, such as slipping forward or misalignment, must be remedied with an adjustment as soon as possible. We advise that patients always wear their My-Nor lenses, except when participating in dynamic or aggressive sports.
Any practice interested in offering My-Nor as part of their myopia management solutions portfolio will receive comprehensive training on the recommended refraction and dispensing guidelines, with ongoing support available from our trained team of lens specialists.
References
- Sankaridurg P, Tahhan N, Kandel H, et al. IMI Impact of myopia. Invest Ophthalmol Vis Sci. 2021;62(5):2. https://doi.org/10.1167/iovs.62.5.2
- Wallman J, Winawer J,. Homestasis of Eye Growth and the Question of Myopia. Neuron, Vol. 43, 447-468, August 19, 2004
- Logan, N.S., Gilmartin, B., Wildsoet, C.F., and Dunne, M.C. (2004). Mutti, D.O., Sholtz, R.I., Friedman, N.E., and Zadnik, K. (2000). PePosterior retinal contour in adult human anisomyopia. Invest. Ophthalmol. Vis. Sci. 45, 2152–2162
- Millodot,M. (1981). Effect of ametropia on peripheral refraction. Am. J. Optom. Physiol. Opt. 58, 691–695.
- Mutti, D.O., Sholtz, R.I., Friedman, N.E., and Zadnik, K. (2000). Peripheral refraction and ocular shape in children. Invest. Ophthalmol. Vis. Sci. 41, 1022–1030
- Schmid, G. (2003). Variability of retinal steepness at the posterior pole in children 7–15 years of age. Curr. Eye Res. 27, 61–68.
- Curcio, Christine & Allen, Kimberly. (1990). Topography of ganglion cells in human retina. The Journal of comparative neurology. 300. 5-25. 10.1002/cne.903000103.