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Why is the adult amblyopic eye unstable?
  1. C S Hoyt
  1. Correspondence to: Creig S Hoyt University of California San Francisco, Department of Ophthalmology, 10 Kirkham Street, K301, San Francisco, CA 94143, USA;

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Surely, understanding the mechanisms that account for improvement and “slippage” in the acuity of the adult amblyopic eye should be more thoroughly studied

In 1981, David Hubel and Torsten Wiesel were awarded the Nobel Prize in Physiology or Medicine. Their elegant animal models of various deprivation studies in infancy have provided invaluable information to practising ophthalmologists.1,2 Hubel and Wiesel described the potentially irreversible anatomical consequences of early monocular occlusion.3 The profound and specific cellular loss that occurred in layer IVc of the visual cortex and the laminae of the lateral geniculate nucleus subserving the deprived eye was interpreted as a model of form deprivation amblyopia.4 The fact that permanent cellular changes occurred within weeks of initiating occlusion (eyelid closure) in an infant animal prompted ophthalmologists to consider early surgery in the management of congenital cataracts.5,6 That the strategy was successful in some cases of monocular congenital cataracts was seen as clinical validation of Hubel and Wiesel’s experimental studies.6,7 Many of us could imagine that if understanding the neural anatomical alterations resulting from experimental visual deprivation states resulted in improved visual outcomes in infants with cataracts surely neuropharmacological studies would be even more enlightening and might provide “medical” therapies to replace the traditional patching therapy for amblyopia.

The subsequent years have proved how elusive a complete understanding of amblyopia is. Human necropsy studies of anisometropic and strabismic amblyopia have demonstrated that layer IVc of the visual cortex does not appear to be adversely affected in these types of amblyopia.8,9 The early maturation of layer IVc makes it an unlikely site for changes caused by any type of unequal visual inputs other than occlusion.8 Appropriate models of anisometropic and strabismic amblyopia to define the neuroanatomical consequences of these types of amblyopia remain unavailable. Moreover, early but careful studies to treat amblyopia in children with pharmacological agents have been thought provoking but disappointing.10 Yet, in a broader sense we must ask the question—can neuroanatomical and neuropharmacological studies address all of the clinical behaviours of the amblyopic eye? For example, it is now recognised that patients with strabismic amblyopia may show a “slippage” of visual acuity in the amblyopic eye well after the so called “sensitive” age (6–8 years of age).11 This acuity loss can be reversed with occlusion of the non-amblyopic eye even in adults, although it may subsequently “slip” again with cessation of occlusion therapy. Surely this phenomenon of unstable visual acuity in the older strabismic amblyope is not likely to be explained by anatomical changes in the brain stem or visual cortex.

Equally puzzling is the ability of some strabismic or anisometropic amblyopes to show spontaneous improvement in the amblyopic eye if injury or disease reduces the acuity of the non-amblyopic eye. Although this has been the subject of numerous case reports there are now two good epidemiological studies that agree that this is not a rare occurrence.12,13 Rahi and coworkers, in the United Kingdom, reported that 10% of adult amblyopes who suffered visual loss in the non-amblyopic eye exhibited spontaneous visual improvement in the amblyopic eye.12 In this issue of the BJO (p 1119) Chua and Mitchell report their findings from the Blue Mountains Eye Study in Australia. Their findings are strikingly similar to those of Rahi and coworkers. In all, 9.1% of adults with amblyopia showed significant improvement in the amblyopic eye after a two line or more visual loss in the non-amblyopic eye. The underlying inhibitory influence of the non-amblyopic eye on the amblyopic eye that apparently counts for this is undefined. However, there may be more than one potential mechanism responsible. Although most, but not all, forms of amblyopia are uniocular it is an important disability. Chua and Mitchell also point out in their study that amblyopes have an incident 5 year visual impairment risk in the non-amblyopic eye of 33%. This compares with the 12.5% risk in non-amblyopes. Unsuccessfully detected or treated amblyopia does have its consequences. Early detection of amblyopia remains a practical goal. Appropriate treatment of children with amblyopia is effective.14 Yet, surely understanding the mechanisms that account for improvement and “slippage” in the acuity of the adult amblyopic eye should be more thoroughly studied. Newer, more effective treatments of amblyopia may be the result of such studies.

We are indebted to Hubel and Wiesel for their pioneer modelling of visual deprivation states. Yet, the pathophysiology of amblyopia remains to be fully delineated. The dream of direct pharmacological treatments for amblyopia (not penalisation of the non-amblyopic eye) remains largely a dream. The mysterious ways of the adult amblyopic eye merit better study. Better treatment of amblyopia could be the result.

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Surely, understanding the mechanisms that account for improvement and “slippage” in the acuity of the adult amblyopic eye should be more thoroughly studied


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