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Amblyopia is a fairly common disease affecting between 1% and 2% of the population of most developed countries.1Amblyopia is the unilateral or, less commonly, bilateral loss of vision caused by abnormal visual inputs during a critical period of visual development. The critical period is seen as the period of time during which abnormal visual inputs can result in amblyopia, but it is also the time during which amblyopia can be reversed by eliminating the abnormal visual inputs and, usually, occluding the normal eye for some periods of time.
However, there are now reasons to believe that these critical periods for development and treatment of amblyopia cannot be rigidly defined. Firstly, it is clear that visual acuity of the amblyopic eye is not always firmly established even after amblyopia therapy has been terminated, because the age of the patient is beyond what is generally considered to be the critical period.2-4 Scott and Dickey reported a short term follow up study of amblyopic patients after patching therapy was stopped. Seventeen per cent of patients lost a line of visual acuity and 8% lost two lines or more.3 In a study of patients 10 years after amblyopia therapy was stopped, Gregersen and Rindziunski reported that 14% of patients lost all of the previously improved visual acuity in the amblyopic eye5; 67% of patients lost at least one line of visual acuity in the amblyopic eye.
Secondly, improvement in visual acuity and changes in the neurophysiological substrates of amblyopia can be demonstrated in some adult experimental animal models.6-8 This is most dramatic when the non-amblyopic eye is enucleated in the adult animal. In the case of amblyopic cats, a sixfold increase in cells in the visual cortex responding to the amblyopic eye can be demonstrated after enucleation of the non-amblyopic eye.6 7 Similar but less dramatic effects have been reported in adult primate amblyopes.8
Finally, several clinical reports have demonstrated improved visual acuity in the amblyopic eye of human adults following loss of central vision in the non-amblyopic eye.9-14 In a retrospective multicentre report, Vereecken and Brabant reported at least three lines of visual acuity improvement in 28.5% of patients with visual loss in the good eye.9 Typically, improvement occurred in the first few weeks after visual loss in the non-amblyopic eye. Api and coworkers reported eight adult strabismic amblyopes with visual loss in the non-amblyopic eye.11 There were more than two lines of visual acuity improvement in the amblyopic eye in all patients. It is noteworthy that in three cases enucleation of the non-amblyopic eye was performed. Klaeger-Manzanell and coworkers documented a case of a man with strabismic amblyopia who experienced a two step recovery of vision in the amblyopic eye after loss of vision and then subsequent enucleation of the non-amblyopic eye.12
In this issue of the BJO (p 952) El Mallah and coworkers detail amblyopic patients who exhibited increased visual acuity following loss of vision in the non-amblyopic eye due to macular degeneration. It is not clear if, in this 465 patient study group with age related macular degeneration, there were any amblyopic patients who lost vision in the non-amblyopic eye but did not experience visual acuity improvement in the amblyopic eye. This information would be of interest. By 12 months after the vision loss in the non-amblyopic eye, visual acuity had improved by an average of three lines in the non-amblyopic patients. Improvement of visual acuity seems to have occurred primarily in the first 6 months following visual loss in the non-amblyopic eye. So, if visual acuity can improve in the adult amblyope following visual loss in the non-amblyopic eye, why should we spend so much time trying to treat amblyopia in children with the purpose of creating a “spare tyre” in case the non-amblyopic eye is lost in adulthood?
In the case of strabismus amblyopia, improving visual acuity in the amblyopic eye is critical since the long term stability of the ocular motor alignment is directly affected by the degree to which the amblyopic eye is effectively treated in childhood.
Not all adult amblyopes experience visual acuity improvement in the amblyopic eye after visual loss in the non-amblyopic eye. We do not yet know what percentage of amblyopes can anticipate improvement if they are unfortunate enough to lose visual function in the non-amblyopic eye as an adult. Certainly, there is no evidence that form deprivation will improve in an adult who loses vision in a non-amblyopic eye. Moreover, there is good reason to believe from primate studies that this would not be expected.15
In most cases, the improvement in the adult amblyopic eye following loss of vision in the non-amblyopic eye is reasonably modest. In addition, studies to date have limited their assessment of these patients to measuring resolution visual acuity. No reports have studied the other many abnormalities that occur in amblyopia, in particular, motion processing, ocular motor stability and efficiency, or orientation discrimination. In my experience, these adult amblyopic patients with improved visual acuity are still much more visually impaired than the resolution acuity measurement would suggest. In particular, their motion processing seems to be still severely affected even when the recognition acuity is by all measures quite good.
Finally, it is not yet clear how much of the improved visual acuity reported in adult amblyopes with visual loss in the non-amblyopic eye is nothing more than recapturing the “slipped” visual acuity that occurs in so many “successfully” treated amblyopes.3 4
Nevertheless, this group of patients is of obvious interest to ophthalmologists. What are the biochemical and cellular correlates for changes in visual acuity that occur in adult amblyopes? If these were better understood, would they lead us to pharmacological forms of amblyopia therapy? We look forward to more detailed studies of adult amblyopes with improvement of visual acuity following loss of vision in the non-amblyopic eye.
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