Established 1998 ISBN 978-969-7690-00-8

EDITORIALREFRACTIVE ERRORS:A CLINICAL PERSPECTIVEThe human eye is similar to an optical instrument1.A clear cornea allow slight to enter the eye and focus ata spot on the centre of retina, the foveal pit, which has amaximum concentration of cones, (the photoreceptorsthat are stimulated by light). Their maximal stimulationsends impulses via the optic nerve to the occipital cortex(a three neuronal pathway) to perceive a perfect imagewhich is further analyzed by the prefrontal cortex. Thisperfect optical system has certain imperfections calledaberrations as well as refractive errors; their additiveaffect not only degrades the retinal image but limits itsclarity and spatial resolution.The aberrations in the optical system of the eye:2,3The curved shape of the cornea, which is steeper at thecentre, allows a straight beam of light to pass throughwhile its flat periphery bends the light rays; the anteriorand posterior surfaces of the cornea refract and bendlight rays further. The bi-convex shaped lens has asimilar affect (with minimal bending of light rays at thecentre and more towards the periphery) and alterationsin the size of pupil, all add up to defocus the retinalimage. In bright light, the pupil constricts and its smallaperture blocks the divergent, peripheral rays fromboth the cornea and lens, thus minimizing the affect ofspherical aberration. However, as the pupil enlargesin dim light or at night, more divergent rays from theperiphery of cornea and lens enter the eye and focusanterior to the straight beam of light passing throughthe centre of both these structures, not only producingglare but a defocused, blurred image4.The affect of spherical aberrations increases asthe fourth power of the diameter of the pupil i.e. if thepupillary diameter doubles, it increases the sphericalaberration by 16 times. This results in haloes aroundpoint images and produces the condition of “NightMyopia”, the affect of which is exaggerated after LASIKor surface ablation for myopia. In young eyes, the lensis an elastic structure and by altering its thickness, itplays a significant role in compensating for cornealaberrations by neutralizing them and improving theOphthalmology Update Vol. 14. No. 4, October-December 2016quality of retinal image5,6. But with age, it hardens,loses its elasticity and this compensatory mechanismstarts failing; rather it adds to the optical aberrations bythe cornea, resulting in an image of poor quality.Impact of refractive errors: all babies are born withsome degree of refractive errors due to a mismatchbetween the optical components of the eye so thatthe resultant retinal image is out of focus to varyingdegrees. About 90-95% of babies are born with somedegree of hypermetropia. Emmetropia, as describedby Grosvenor7 is the “normal” state of an eye inwhich parallel light rays focus on the retina when theaccommodation is fully relaxed. Others consider thestate of emmetropia to range between hypermetropiaof 0.50 to 1.50 diopters8.The Process of Emmetropization: It starts duringthe first 12-18 months after birth and by the first 5 yearsof life, 80% of both myopic and hypermetropic childrenbecome emmetropic9.This process has been postulatedto result from an active as well as a passive ---------Uncorrected refractive errors in children resultin Amblyopia and Strabismus, interferingchild’s development which can be avoided byearly appropriate spectacle. Strabismus surgeryis mostly required in congenital strabismus,while it can also be avoided in other types ofstrabismus by appropriate glasses. They not onlyrestore a normal vision in either eye but also themuscular -----The active mechanism10 is a neural processregulated by the degree of blurring of the retinal image:the eye analyses the degree of retinal blur and shortensor elongates proportionately, by changing the axiallength of the eye, till both the image and retina areconjugate.A critical factor that regulates the axial elongationof eyeball is the alteration in the composition andamount of extracellular matrix of the sclera. The clarity115

Editorialor defocus of an image at the neuroretina results inrelease of neurotransmitters (Dopamine and VIP)by retinal amacrine cells11; Dopamine increases theproduction of DNA and promotes the synthesis ofproteins and proteoglycans in the sclera12,13,14 making itthick and less stretchable thus reducing its elongation.On the other hand, Vaso-active Intestinal Peptidesecretion (VIP)15 stimulates choroidal blood flow andthickens the spongy choroid while at the same time,stretches, thins and elongates the sclera. Hence, theaxial length of eyeball increases posteriorly. The sclerais also capable of altering its growth in a sector withoutaltering the remainder. If a defocused image is presenton one portion of the retina, only that part continuesto grow to become myopic while the remainder witha clear image remains unaltered and emmetropic,resulting in myopic astigmatism.This active neural control operates via a feedbackmechanism from the brain, the evidence of whichwas provided by Troilo and Wallman16. They founda reversal of the original refractive error by severingthe optic nerves of chicks: hypermetropic eyes becamemyopic, while myopic eyes became hypermetropic; withan intact optic nerve, the process of emmetropizationwas more accurate. This proved the theory that anactive feedback provided by the brain regarding thequality of perceived image is essential for regulatingemmetropization process. They further noted thatby severing the Edinger Westphall nucleus (whichcontrols accommodation), process of emmetropizationslowed but it was not a prerequisite for it. Sorsby17 hassuggested that an increase in axial length occurringunder genetic influence in high levels of ametropia;if one parent is myopic, the chance of a myopic child22.5% while it increases to 42% if both parents aremyopic18.Similarly, visual deprivation in neonates dueto severe congenital ptosis19,20,21, corneal opacity22,congenital cataract, vitreous opacification orhaemorrhage23, and retinopathy of prematurity24,25causes the eye to elongate and become increasinglymyopic. Another observation suggesting thatemmetropization has an active component is theassociation of myopic progression in response tosustained near vision26.This active mechanism works in close associationwith a passive process of emmetropization in whichappropriate and proportional interactive changes occurin refractive components of the eye in response to achange in its axial length27. In a study on chicks, Troiloand Wallman28 concluded that corneal curvature wasa major contributor of astigmatic emmetropization.116Gernet and Olbrich30 suggested lenticular changes wereresponsible for spherical emmetropization as myopicchildren have thin crystalline lenses, suggestinga mechanical relationship between growth of theeyeball and lens compensation. Larger eyes have alarger equatorial diameter, causing more tension andstretching of the zonular fibers. These stretched fibersconsequently flatten the lens and reduce its opticalpower. The third factor is the changing choroidalthickness during active emmetropization processresulting in altering the vitreous chamber depth (a passivephenomenon)39. In myopia, the choroid is thin so retinamoves backwards with it, resulting in an increaseddepth of vitreous chamber; in hypermetropia, thechoroid thickens (active phenomenon) and pushes theretina forwards, thereby reducing the depth of vitreouschamber passively. Hence, the ocular structuresresponsible for causing large changes in refractive errorare cornea, lens and the depth of vitreous chamber40,which is determined by the posterior growth of sclera.2-The Natural History of Refractive Errors: Infants areborn with a mild hypermetropia of 2.00D but a smallnumber may have it in a moderate to high range of 3.5D. This is due to a relatively smaller size of eyeballas compared to the rest of the body. By the age of 4years, the eyeballs and the brain attain 85% of theiradult size while the rest of the body has grown to only20%41.The continued growth of eyeballs during these firstfew years of life results in a shift towards emmetropiaand a gradual decrease in the level of hypermetropiain most individuals42 so by the age of 5-6 years, 80%of the children are found to be emmetropic43. Ingramand Barr44,45 stated that a child born with hypermetropiaof less than 2.50 diopters of is likely to becomeemmetropic, whereas a child born with more than2.50 dioptes is likely become more hypermetropic bythe age of 3.5 years46,47. By the age of 5 years, thoughthe prevalence of refractive errors is reduced, itsdistribution still peaks towards a mild hypermetropia48.Over the next 10-15 years of life, the prevalence ofhypermetropia is very much reduced though myopia isseen more frequently49,50.Infants, with a family history of myopia ( 5%), areborn myopic which increases further as the axial lengthof eyeball continues to increase under the geneticinfluence. Some of them may exhibit a shift towardsemmetropia by the age of 6 months but infants bornwith high myopia retain most of it in later years of life.Therefore, it is possible to predict refractive status inolder children based on their earliest manifest refraction,with one year being optimal51. Myopic progression hasOphthalmology Update Vol. 14. No. 4, October-December 2016

Editorialbeen found to be associated with other factors likeethnicity, female gender, younger age of onset, highIQ score, and prolonged study hours (by increasingthe accommodative demand and eye strain)52,53. Theevidence has been provided by Chua et al.54,who foundthat elongation of axial length and myopic progressioncan be slowed down by reducing accommodation with0.1% atropine eye drops once a day.At birth, the average amount of astigmatismis 2.00 D which decreases to 1.00 D by the age of 2.55 years55,56 as a part of emmetropization process; 1/3of spherical equivalent and 2/3 of the astigmatismreduces due to flattening of cornea during the firsttwo years of life. This has been found in 90% of thechildren57in most races. Astigmatism of more than 1.50D results in amblyopia if not corrected with glasses.Emmetropization process corrects “With”-the-ruleastigmatism more than “Against”-the-rule astigmatismwhich is also a risk factor for becoming myopic at anearlier age and amblyopia. According to Abrahamsonand Sjostrand57, low amounts of anisometropia ( 2.50D) is commonly found during the normal growth periodof the eye58; children with 3.00 D or more anisometropiaat one year of age have a 90% chance of retaining it atthe age of 10, and a 60% risk of developing amblyopia59.The emmetropization process cannot correct 5.00 D ofanisometropia60 and may result in juvenile microtropia.Optics of Hypermetropia: In emmetropia, parallel raysof light from a distant object are focused by the lens(without the need for accommodation) onto the retina(fovea) to form a clear image. In hypermetropia, becauseof a short axial length, they are focused behind the retinaresulting in a blurred image. Therefore, accommodationis called upon to increase the curvature and thicknessof the lens in order to increase its refractive power andfocus the distant light rays upon the retina. The rayscoming from a near object are more divergent and moreaccommodative effort is needed to see it clearly. Dueto the phenomenon of accommodation/convergencesynkinesis in the brain, the eyes converge as wellresulting in an Esotropia (ET). According to Ingram, etal.61, infants with an esotropia or a microtropia do notshow a spontaneous reduction of hypermetropia by theemmetropization process and were more likely to haveaccommodative problems. Both fixing and non-fixingeyes demonstrated accommodative abnormalities withpoor convergence, showing that the underlying defectwas congenital rather than refractive.Children have a sufficient accommodativereserve to maintain a clear retinal image withoutproducing asthenopia62. However a constant needfor accommodative effort for near work results inOphthalmology Update Vol. 14. No. 4, October-December 2016watery eyes, squinting and facial contortions duringreading, frequent blinking, constant or intermittentblurring of vision, focusing problems, difficulty withor aversion to reading, decreased binocularity and eyehand coordination. The presence and severity of thesesymptoms is variable and depends upon the degree ofhypermetropia. Hypermetropia usually stabilizes bythe age of 6-8 years63 and starts reducing in amplitudewith time. However, in children, who are constantlyreading or doing close work for long periods, constantaccommodation results in spasm of ciliary muscle andartificial myopia.Impact of Uncorrected Hypermetropia on Vision &Strabismus:1) A mild to moderate degree of hypermetropia orastigmatism is present in 90% cases of infantileesotropia and should be fully corrected as it may lead toamblyopia. A child with true, essential infantile ETshould have a surgical correction of strabismus by18 months age so that stereopsis can develop. Anyastigmatic error should be corrected by glasses.2) Anisometropic hypermetopia ( 1.5D) orhypermetropic astigmatism of 1D, persistingbeyond 2 years of age, results in amblyopia 64.3) If both eyes have the same degree of hypermetropia,then an alternating ET develops. Since the childfixates alternately with either eye, amblyopia doesnot develop.4) If one eye is more hypermetropic, it accommodatesmore and converges more resulting in a unilateral,constant ET. A constantly in-turned eye losesfoveal fixation, the child tends to prefer theemmetropic or less hypermetropic eye for seeingand the more hypermetropic eye (with a blurredimage) is neglected by the brain. It is suppressedby the good eye, its neuronal connections to thebrain shrink and it becomes amblyopic.5) A large, constant ET results in an eccentric fixationas it never straightens to focus image on the fovea.6) In a constantly esotropic eye, the MR never relaxesas the eye never assumes a primary position; itsconstant contraction results in its hypertrophyand contracture. Even if such an eye is givenfull hypermetropic correction, the hypertrophicmuscle does not relax fully, a small amount ofET still persists and is erroneously labeled as apartially accommodative ET.7) Uncorrected hypermetropia ( 3.5 D in onemeridian) results in blurring of vision, reducedbinocular vision, constant accommodative effort,fatigability. These factors contribute to poor motorand cognitive development in younger children117

Editorial(9 months to 5.5 years) and poor performance atschool in older children. Screening by visual acuitytesting in all preschool children is very important.Full optical correction of significant hypermetopiaduring infancy in the absence of strabismus, mayinterfere with the process of emmetropization 65but partial spectacle correction is safe and reducesthe incidence of subsequent strabismus.8) In the presence of an esophoria or ET, no matterof how small a magnitude, full hypermetropiccorrection is mandatory to achieve a fovealfixation binocularly. This can only be achievedby full cycloplegia with atropine eyedrops as itneutralises even the latent hypermetropia (due tothe tone of ciliary muscle 1-1.50D). Cycloplegiawith cyclopentolate eye drops does not neutralizethe latent hypermetropia but only the manifesthypermetropia which an individual can correctby accommodating and is called FacultativeHypermetropia. If the error is large, then evenby fully accommodating, the objects are not seenclearly, especially for near. This remaining amountof Hypermetropia that still remains uncorrectedby accommodation is called Absolute andneeds correcting glasses (Manifest facultative absolute).Optics of Myopia: The term myopia means “Iclose eyes”, a myopic person sees distant objects withhalf closed eyes. Because of a large axial length, parallelrays of light from a distant object are focused in frontof the retina resulting in a blurred distant image.Half-closed eyes create the affect of a pinhole, therebyreducing the extent of blurred image. Since the raysfrom a near object are divergent, they focus on theretina, producing a clear image. Hence a myopic personcan see near objects clearly (short-sightedness); thefarthest distance at which the vision is clear is called theFar Point (Punctum Remotum). In an emmetrope, thefar point is at infinity while in a myopes, the higher thedegree of myopia, shorter is this distance e.g. in myopiaof 1D, far point is at 1 meter, in myopia of 2D, far pointis ½ meter.Impact of Myopia on Vision & Strabismus:1) Myopia is mostly due to an increase in axiallength of the eyeball; an increase in axial lengthof 1 mm produces myopia of 3D. Increase incorneal curvature by 1mm results in a myopia of6D but this is seen less frequently as the normalemmetropization process encourages cornealflattening. It is seen in pathological conditions likekeratoconus, keratoglobus. Index myopia (dueto increased refractive index of lens) is seen in1182)3)4)5)diabetes and nucleus sclerosis.Myopes usually have a limited horizon as they cansee clearly till the far point, as their whole worldis limited to that distance. This results in psychosocial problems in children with uncorrectedmyopia.Eyestrain and diplopia for near work in myopes:The eyes normally converge when focused at a nearobject during reading, writing; convergence causesaccommodation because of accommodation/convergence synkinesis in the brain (both reflexesoperate together). The divergent rays from nearobjects focus clearly on the retina without theneed for accommodation, but because of thesynkinetic reflex, this extra accommodative effortfocuses the light rays in front of retina producinga blurred near image. Hence the myope gives upthe effort to converge allowing one eye to deviateoutwards intermittently, resulting in diplopia fornear and an exophoria initially, progressing laterto an exotropia (XT), when the effort to convergeis totally abandoned. In a study by Noha et.al.66,myopia was associated with intermittent XT in90% cases by the age of 20 years. Intermittent XTis seen in 1% of healthy children in USA whileesodeviation is more common, though the reverseis seen in Asian populations. Another study alsoshowed a strong association between myopia andXT. The explanation given by the authors is thatintermittent XT promotes the development ofmyopia through an increase in accommodativedemand, as the reduction

Dr. Jahanzeb Durrani Ophthalmic Section . Dr. Syed Sikandar Hasnain (USA) Prof. Marianne L. Shahsuvaryan (Armenia) Prof. Emeritus Diljeet Singh (India) Dr. Sakkaf Ahmed Aftab (UK) Dr. Madiha Durrani (Canada) Dr. Anam Arshad (USA) Editors Prof. Syed Imtiaz Ali, Prof. Hafeez ur Rehman Prof. Jahangir Akhtar, Dr