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Amblyopia?
Editorial Amblyopia? Steven M. Archer, MD
I
n his article “Optic Nerve Hypoplasia and Small Eyes in Presumed Amblyopia” in this issue of the Journal of AAPOS, Lempert convincingly shows that subclinical optic disc anomalies (hypoplasia and dysversion) are associated with eyes that have clinically diagnosed amblyopia. Certainly, there are human clinical examples that cleanly demonstrate amblyopia caused by deprivation, but it appears from Lempert’s work that most of what we call amblyopia in the general population is associated with subclinical disc anomalies. This challenges our fundamental beliefs about amblyopia. It also raises questions about the rationale behind screening programs for early detection, prevention, and treatment of amblyopia. Should we be screening for amblyopia with fundus photographs? How could early spectacle correction of hyperopia and anisometropia prevent amblyopia if organic optic nerve pathology is actually the problem? Have clinicians been deluding themselves about the efficacy of treating an intractable organic optic nerve problem by occluding the sound eye? The crucial question left unanswered by this study is whether the association between subclinical disc anomalies and “amblyopia” is a causal relationship. Lempert found that amblyopic eyes, in addition to having smaller discs, have statistically shorter axial lengths than control eyes (hyperopia) and their fellow eyes (anisometropia). Both hyperopia (indirectly, by causing strabismus) and anisometropia are traditionally believed to cause amblyopia. Lempert suggests that these factors may only be concurrent findings associated with disc anomalies, which are the true cause of decreased vision in presumed amblyopia. However, it seems equally likely that it is the other way around—small disc area is statistically associated with amblyopia by being correlated with hyperopia and anisometropia rather than itself being the cause of decreased vision. Instead of being revolutionary, this study may be no more than the interesting but less remarkable observation that small eyes have small discs.
Further study is needed to show which of these factors— disc anomalies, hyperopia, or anisometropia—is causative. Unfortunately, the degree of correlation between these three factors will make it difficult to statistically implicate any one of them as an independent predictor of amblyopia. Of course, they may all be causative to a degree, further complicating the interpretation of these studies. Even if we accept Lempert’s premise that clinically undetectable variations in disc size are a frequent cause of reduced vision, our traditional views of amblyopia may not need to be dramatically altered. Small disc areas tend to be a bilateral problem. The disc areas of amblyopic eyes were significantly less than those of control eyes, but so were the disc areas of fellow sound eyes. Although an amblyopic eye was likely to have a smaller disc area than its fellow eye in an individual, the disc areas of the population of amblyopic eyes as a whole show considerable overlap with the population of fellow eyes. This suggests that decreased vision attributable entirely to variations in disc area should be roughly comparable in the two populations. In other words, the subtle vision abnormalities described in the sound eye of amblyopes are probably the extent of what we can attribute directly to disc anomalies in amblyopic eyes as well. The greater visual deficits found in amblyopic eyes would then be the result of competitive binocular interaction between slightly mismatched small eyes. The traditional mechanism for amblyopia production is still in play and could reasonably be expected to respond to traditional treatment methods. It is uncertain at this point how the implications from this study will affect the diagnosis and management of amblyopia. Regardless, we owe thanks to Lempert for an unconventional view and a reminder, as large-scale vision screening projects are being planned, that with amblyopia things are not always what they appear to be.
From the Department of Ophthalmology, W. K. Kellogg Eye Center, University of Michigan, Ann Arbor. J AAPOS 2000;4:257. Copyright © 2000 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/2000/$12.00 + 0 75/1/110552 doi:10.1067/mpa.2000.110552
Journal of AAPOS
October 2000
257
I
n his article “Optic Nerve Hypoplasia and Small Eyes in Presumed Amblyopia” in this issue of the Journal of AAPOS, Lempert convincingly shows that subclinical optic disc anomalies (hypoplasia and dysversion) are associated with eyes that have clinically diagnosed amblyopia. Certainly, there are human clinical examples that cleanly demonstrate amblyopia caused by deprivation, but it appears from Lempert’s work that most of what we call amblyopia in the general population is associated with subclinical disc anomalies. This challenges our fundamental beliefs about amblyopia. It also raises questions about the rationale behind screening programs for early detection, prevention, and treatment of amblyopia. Should we be screening for amblyopia with fundus photographs? How could early spectacle correction of hyperopia and anisometropia prevent amblyopia if organic optic nerve pathology is actually the problem? Have clinicians been deluding themselves about the efficacy of treating an intractable organic optic nerve problem by occluding the sound eye? The crucial question left unanswered by this study is whether the association between subclinical disc anomalies and “amblyopia” is a causal relationship. Lempert found that amblyopic eyes, in addition to having smaller discs, have statistically shorter axial lengths than control eyes (hyperopia) and their fellow eyes (anisometropia). Both hyperopia (indirectly, by causing strabismus) and anisometropia are traditionally believed to cause amblyopia. Lempert suggests that these factors may only be concurrent findings associated with disc anomalies, which are the true cause of decreased vision in presumed amblyopia. However, it seems equally likely that it is the other way around—small disc area is statistically associated with amblyopia by being correlated with hyperopia and anisometropia rather than itself being the cause of decreased vision. Instead of being revolutionary, this study may be no more than the interesting but less remarkable observation that small eyes have small discs.
Further study is needed to show which of these factors— disc anomalies, hyperopia, or anisometropia—is causative. Unfortunately, the degree of correlation between these three factors will make it difficult to statistically implicate any one of them as an independent predictor of amblyopia. Of course, they may all be causative to a degree, further complicating the interpretation of these studies. Even if we accept Lempert’s premise that clinically undetectable variations in disc size are a frequent cause of reduced vision, our traditional views of amblyopia may not need to be dramatically altered. Small disc areas tend to be a bilateral problem. The disc areas of amblyopic eyes were significantly less than those of control eyes, but so were the disc areas of fellow sound eyes. Although an amblyopic eye was likely to have a smaller disc area than its fellow eye in an individual, the disc areas of the population of amblyopic eyes as a whole show considerable overlap with the population of fellow eyes. This suggests that decreased vision attributable entirely to variations in disc area should be roughly comparable in the two populations. In other words, the subtle vision abnormalities described in the sound eye of amblyopes are probably the extent of what we can attribute directly to disc anomalies in amblyopic eyes as well. The greater visual deficits found in amblyopic eyes would then be the result of competitive binocular interaction between slightly mismatched small eyes. The traditional mechanism for amblyopia production is still in play and could reasonably be expected to respond to traditional treatment methods. It is uncertain at this point how the implications from this study will affect the diagnosis and management of amblyopia. Regardless, we owe thanks to Lempert for an unconventional view and a reminder, as large-scale vision screening projects are being planned, that with amblyopia things are not always what they appear to be.
From the Department of Ophthalmology, W. K. Kellogg Eye Center, University of Michigan, Ann Arbor. J AAPOS 2000;4:257. Copyright © 2000 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/2000/$12.00 + 0 75/1/110552 doi:10.1067/mpa.2000.110552
Journal of AAPOS
October 2000
257