Abstract

The article by Prakash et al.1 presents the case of a 25-year-old man with idiopathic unilateral amblyopia possibly due to asymmetry in the pattern of higher-order aberrations (HOAs) between the eyes. Wavefront error is one of the key components that determine retinal image quality. Allowing for neural factors, the retinal image is a key element in determining visual perception. It is possible to calculate how any given single point is imaged on the retina by knowing the wavefront error of the eye. This image is known as the point spread function (PSF). In light of this, the possible role of interocular asymmetry in wavefront error in the development of idiopathic amblyopia, as postulated by Prakash et al., is very relevant. In a study currently in press,2 we examined 60 eyes of 30 children between 6 and 17 years of age who had unilateral amblyopia due to strabismus in 15 children and anisometropia in 15. Eyes with deprivation or bilateral amblyopia were excluded from the study. Aberrometry was performed using the iTrace visual function analyzer (Tracey Technologies). No difference in total, 3rd-, 4th-, or 5th-order aberrations or in any individual term was found between the amblyopic eyes and the normal fellow eyes. We concluded that HOAs did not play a role in the development of amblyopia in these patients in whom the cause of amblyopia was known. Keratorefractive surgery has been shown to be an effective treatment for children with unilateral amblyopia due to myopic anisometropia. Significant postoperative improvement in amblyopia has been reported.3,4 This form of surgery alters aberrations and the PSF. It follows that surgery in 1 eye in children with unilateral amblyopia results in significant postoperative asymmetry in the pattern of HOAs. Yet, despite this, improvement in amblyopia occurs. In an ongoing study of HOAs, we examined 46 eyes of 23 patients from 20 to 28 years of age. All eyes had a best corrected Snellen visual acuity of 6/6 and aberrometry was performed using the Zywave Hartmann-Shack aberrometer. The maximum observed interocular difference in root mean square (RMS) HOAs were as follows: total = 0.69 μm, vertical trefoil = 0.29 μm, vertical coma = 0.24 μm, horizontal coma = 0.73 μm, and horizontal trefoil = 0.61 μm. These differences were present in the absence of amblyopia. The patient presented by Prakash et al.1 had low levels of total RMS HOAs that were lower in the amblyopic eye. The interocular difference in 3rd-order coma and trefoil was low compared with our findings in age-matched patients. In addition, the aberrations were lowest in the amblyopic eye. Amblyopia due to myopic and hyperopic anisometropia affects the eye with the greatest refractive error. If HOAs induced amblyopia, would it not be more likely to develop in the eye with the highest levels of aberrations? Significant anisometropia at a critical age in childhood may lead to idiopathic amblyopia in later life if the degree of anisometroia decreases. This important point was raised by Prakash et al. Interestingly, the patient in question had 0.5 diopters more hyperopia and a greater level of hyperopic defocus in the amblyopic eye than in the normal fellow eye. Overall, these findings indicate that anisometropia at a young age and not asymmetry in the pattern of HOAs could have been responsible for amblyopia in this case.

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