The utility of occlusion for binocular dysfunction is limited to patients for whom binocular vision is too confusing due to constant or variable diplopia. Oft times these patients will be responsive to vision therapy, lenses, prisms, syntonics or other therapeutic interventions but, in those rare instances when it is not, the tradeoff of losing half of one’s visual field in occlusion is worth the relief to the brain of trying to suspend or de-tune the troublesome second image. In many instances diplopia can be sufficiently alleviated by spot or sector occlusion rather than total occlusion, thereby preserving peripheral vision in both eyes.
This does not apply to amblyopia, for which occlusion leads to con-fusion, as our colleague Dr. Dan Fortenbacher demonstrated in his presentation on advanced treatment of amblyopia six years ago.
By con-fusion we mean that any time the patient is patched, we’re sending the brain a negative message counter to binocular vision. That is illogical now that the consensus in vision science is that the source of amblyopia itself is a disruption to binocular vision and, as recently reviewed by Kraus and Culican, the depth of amblyopia is positively correlated to the degree of binocular imbalance. Can you think of another form of therapy for which the mainstay of treatment is the source of the problem? Neither can I, and that is the fundamental reason why the paradigm in amblyopia therapy has shifted from a focus on the amblyopic eye to emphasis on binocular integration.
In 2012 Dr. Daniel Press and I co-authored a paper that followed the methodology of Dr. Anrold Sherman who who reverse engineered hyperopic anisometropic refractive amblyopia. Dr. Sherman originally termed the condition Adaptive Refractive Error Syndrome which he considered to be the origin of refractive amblyopia. In a subsequent paper that provided his rationale for undercorrecting the eye with more ametropia, and treating the condition without occlusion, Dr. Sherman writes: “If binocular interference is the major etiological factor in amblyopia development, treatment must be designed to eliminate it and achieve binocular cooperation.”
As reviewed by Zhao et al in Scientific Reports, visual acuity is widely used in the diagnosis of amblyopia and has traditionally been the metric most valued by clinicians. They demonstrate that although occlusion can aid in the recovery of some visual functions including visual acuity, stereo vision, and binocular rivalry at low spatial frequency, many other binocular visual functions remain deficient including binocular rivalry at high spatial frequencies, interocular summation, and interocular phase combination. While their results support the observation that occlusion treatment is not sufficient to recover all the visual functions in amblyopia, and that additional treatment is necessary, the new paradigm goes a step further in stating that for many forms of amblyopia, occlusion is actually counterproductive. If occlusion has any remaining application, it may reside in rapid alternating occlusion and flicker therapy as published by Vera-Diaz and colleagues.
The final nail in the coffin of occlusion therapy may be emanating from research at the SUNY College of Optometry addressing the brightness deficit in amblyopia.
Published this month in the Journal of Neuroscience, the SUNY research shows that amblyopia increases visual dark dominance by three to ten times, and that the increase in dark dominance is strongly correlated with the severity of amblyopia. The implication of this research is that one of the keys to effective amblyopia therapy involves ameliorating the brightness deficit in amblyopia. In that regard, occlusion is counterproductive because it reduces brightness. One of the reasons that two eyes are better than one, even on a task as basic as visual acuity (for example OU acuity vs. OD or OS on the Snellen Chart) is a boost in brightness perception due to binocular summation.
How do we boost brightness perception through the amblyopic eye? Bear in mind that Claud Worth, over a hundred years ago, invented the Amblyoscope as a device that emphasized ways to improve vision through the amblyopic eye. He didn’t call it a Strabismoscope or a Troposcope, which placed emphasis on the motor misalignment in strabismic amblyopia. He was interested in rehabilitating the sensory deficits in amblyopia which, as it turns out, occur at the neural or cortical levels. Clement Clarke did a better job than American Optical with terminology in that regard, changing the name of its device to Synoptophore, the “Syn” signaling togetherness of the eyes, parenthetically calling it the Major Amblyoscope. The major advancement over Worth’s device was the ability to boost brightness to the amblyopic eye, and engage in what more recently has been termed the “push-pull” balance between the amblyopic and fellow eye.
On a final note, in bypassing occlusion we may be trading off a final outcome that in select cases would be better if occlusion were “judiciously applied”, much as one would judiciously apply lenses or prisms. The patient with unilateral strabismic amblyopia typically has some degree of eccentric fixation. Monocular activities such as Haidinger Brush done while the non-amblyopic eye is occluded are usually necessary to adequately stimulate foveal fixation that provides 20/20 rather than something a bit less. But the patient or parent who is compromised by amblyopia and has improved considerably not only in visual acuity, but in many aspects of life really doesn’t care whether they end up with 20/20 unless we make that the sine qua non of a “cure”. Much as the patient with strabismus really doesn’t know or care if she has anomalous or normal correspondence, the patient with amblyopia doesn’t know or care if she has eccentric or central fixation. As a wise patient said to me many years ago: “You don’t have to make it perfect, doc. You just have to make it better.”