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Amblyopia is defined as a visual developmental disorder that arises after selective disruption of visual input early in life.  The diagnosis of amblyopia typically focuses on the presence of a selective disruptor (the amblyogenic factors of strabismus and/or anisometropia) in young children which results in a visual disorder (reduced visual acuity) of the amblyopic eye.  Visual acuity becomes the “yardstick” by which treatment progress is measured. However, amblyopic eyes almost always have deficits in many visual functions which can also be measured, such as fixation, accommodation and eye movements, just to name a few.

Although the clinical presentation of amblyopia focuses on one eye, it is a binocular problem.

Between the presence of an amblyogenic factor (the cause) and the reduced visual function (the effect) lies the neurological process of suppression.  The dominant eye dominates and suppresses the amblyopic eye.  Think of big brother bullying his younger sibling, until the younger brother is cowering in the corner.**

A recent review article supports this view of amblyopia as a binocular problem by focusing on deficits in the non-amblyopic eye.  Most of these deficits are subtle and can only be measured in a laboratory, but they enhance our understanding of how amblyopia happens in a developing visual system.

The article considers possible mechanisms for deficits in the non-amblyopic eye.  Are they caused by occlusion (patching) therapy?  slowed maturation of visual functions? atypical development of the binocular cells in the brain’s cortex? or an adaptive mechanism to equate the sensitivity of the two eyes?  The authors conclude that while there isn’t enough evidence to rule out any of these mechanisms, binocular mechanisms are clearly in play.  The idea that the brain is attempting “to equate the sensitivity of the two eyes in order to mitigate the effects of amblyopia on the developing visual system” is very compelling.

What does this mean for treatment?  Traditionally, amblyopia is treated by patching the non-amblyopic eye. Let’s go back to the big brother bullying little brother paradigm. Patching essentially removes big brother from the room and sends little brother to the gym to get stronger.  But eventually, you have to take the patch off, and the amblyopic person has to learn to integrate the information from both eyes.  This requires reducing the suppression.

ashton-bingham-113943New binocular treatments are becoming available which separate the visual information channels to each eye and then decrease the contrast of the information being presented to the non-amblyopic eye.  At what point, will the non-amblyopic eye stop the suppression and allow the amblyopic eye to participate in a binocular view of the world?  Can big brother’s volume be turned down to a point where little brother can be heard?

This review article suggests that the amblyopic brain has already initiated this approach to treatment!  The deficits in the non-amblyopic eye are an expression of having turned down the volume from the non-amblyopic eye, or at least an attempt to do so.  The development of binocular-based treatments that follow the same approach that the amblyopic brain has already undertaken seems very promising. The evidence that amblyopia is a binocular problem requiring binocular treatment is growing. What exactly is this “binocular treatment”? Learn the answer at COVD.org!

** Thank you to Pilar Vergara, who uses this analogy in her book, Crossed and Lazy Eyes — Myths, Misconceptions and Truth. 

Read more about amblyopia:

What is amblyopia?

Amblyopia and suppression

How NOT to treat amblyopia

Eye patching alone is no longer the standard of care

Photo credits to ashton bingham and evan kirby via Unsplash
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