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Exciting developments in understanding amblyopia are shaping how we can approach treatment in previously inconceivable ways. That there is considerable neuroplasticity in the visual system, and that amblyopia is a binocular (two-eyed) problem, are two important realizations that allow us to think about amblyopia and its treatment in different ways. The fact that the system is neuroplastic is great news, because it means that amblyopia can be treated much later in life than we used to believe possible. Where we once believed that there was a critical period in childhood, after which amblyopia could no longer be treated, we now have evidence that people even more senior in years can be successfully be treated. Numerous clinical studies have reported significant improvement in visual acuity in older people up to age 60 with amblyopia.
Amblyopia usually involves reduced vision in one eye compared with the other, and this has traditionally been thought of as a monocular (one-eye) problem, not a binocular (two-eye) problem. It has been conceptualized as a problem with the development of one eye, which prevented that eye from making the necessary connections to the brain. It was thought that binocular cells were physically lacking in the brain; meaning cells that process information from both eyes were thought not to exist in the brain with amblyopia. For this reason, traditional amblyopia treatment has taken a monocular approach, involving patching (or occluding) one eye in an attempt to build supposed missing connections from the amblyopic eye to the brain.
New and exciting research is showing that even in amblyopia the system is structurally binocular. The proper cells and connections do exist to process visual information from both eyes. However, in amblyopia the system functions as though it is monocular (using only one eye). There is a lack of binocular responsiveness of brain cells in amblyopia, but we now know that this is due to a functional suppression of the amblyopic eye’s input, rather than a loss of cells driven by that eye’s input. The visual system is behaving monocularly through an active suppression mechanism, in which one of the eyes is actively shutting down the ability of the other eye to contribute to the visual process. The fact that the lack of binocular responsiveness of brain cells can be corrected by antisuppression techniques, supports a functional rather than structural defect.
Understanding that amblyopia is a binocular problem rather than a monocular problem, opens the door to different approaches for treating amblyopia binocularly. A new treatment of amblyopia, one that is purely binocular, is aimed at reducing suppression as a first step, rather than using patching as a first step.
Hess, Mansouri, and Thompson have developed a binocular procedure that has been shown to improve the vision loss in amblyopia. This treatment is aimed at creating a viewing experience that prevents the one eye from suppressing the other. This antisuppression technique allows the information from each eye to combine normally. After prolonged periods of viewing under antisuppression conditions, there is a strengthening of binocular vision and eventual combination of binocular information under natural viewing conditions. The result is favorable in that monocular vision is improved, and there is development of three-dimensional depth perception. Although treatment that relies on patching one eye often improves monocular eyesight for amblyopic children younger than 12 years, this does not always result in binocular function or three-dimensional depth perception.
Another consideration is that assessment of amblyopia, and success in treatment, should consider broader measures of visual function beyond visual acuity. Since amblyopia has been primarily thought of as a loss of vision in one eye, the criteria for improvement is almost solely based on visual acuity measurements. We now recognize that amblyopia is a syndrome of visual processing abnormalities. Active optometric vision therapy is designed to improve visual performance in amblyopia in many deficient areas of visual skill such as: eye movements, fixation, spatial perception, accommodative focusing efficiency, and binocular function. This therapy requires the active involvement of the person using a series of specific, controlled visual procedures that provide feedback to the person about their performance. Once an automatic response is learned, it is expected that the person will apply their improved performance abilities to everyday visual tasks. This ultimately changes the underlying visual process. Treatment in the elderly population requires a more lengthy, rigorous approach, and extent of recovery can be reduced when compared with younger people.
Since establishing binocular function in cases of monocular amblyopia, significantly reduces the underlying binocular inhibition, it increases the probability of maintaining visual acuity improvements. When amblyopia recurs it is usually because, normal binocular function was not established when final visual acuity was attained, or the person discontinues wearing corrective lenses. Since there is no guarantee that amblyopia will not recur, it is important to continue monitoring closely even after successful treatment.
- Hess RF, Mansouri B, Thompson B. A binocular approach to treating amblyopia: antisuppression therapy. Optom Vis Sci 2010;87:697–704.
- Sale, A. et al., Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition, Nature Neuroscience Advanced On line publication (2007). Published online 29 April 2007; doi:10.1038/nn1899.
- Bonneh, Y. S. et al., Spatial and temporal crowding in amblyopia, Vision Research (2007), doi:10.1016/j.visres.2007.02.
- Thompson, B. et al., Brain plasticity in the adult: modulation of function in amblyopia with rTMS. Current Biology (2008) 18, 1067–1071, doi:10.1016/j.cub.2008.06.052
- Press LJ. Amblyopia. J Optom Vis Dev 1988; 19(1):2-15.
- McKee SP, Schor CM, Steinman SB, et al. The classification of amblyopia on the basis of visual and oculomotor performance. Trans Am Ophthalmol Soc 1992; 90:123-48.
- American Optometric Association.Definition of optometric vision therapy. St. Louis: AOA, June, 1991.
- Caloroso EE, Rouse MW. Clinical management of strabismus. Boston: Butterworth-Heinemann, 1993.
- Cornsweet TN, Crane HD. Training the visual accommodation system. Vision Res 1973; 13:713-5.
- Liu JS, Lee M, Jang J, et al. Objective assessment of accommodative orthoptics. I. Dynamic insufficiency. Am J Optom Physiol Opt 1979; 56:285-94.
- North RV, Henson DB. Effects of orthoptics upon the ability of patients to adapt to prism induced heterophoria. Am J Optom Physiol Opt 1982; 59:983-6.
- Ciuffreda KJ. Visual system plasticity in human amblyopia. In: Hilfer SR, Sheffield B, eds. Development of order in the visual system. New York: Springer-Verlag, 1986:211-44.
- Ham O, Claramunt M, Diaz T. Strabismic amblyopia: final results of occlusion treatment in 205 cases. Binoc Vis 1985; 1:195-202.