The development of Amblyopia and Strabism

 

For many animals with multiple eyes, their brains combine the electrical signals from each eye into a “master” (cyclopic) image which gives them stronger environmental awareness.  Sometimes physical problems seem to prevent the emergence of binocular vision, and sometimes it simply never emerges due to poorly understood neurological issues.

How does binocular vision emerge? Nature or nurture?

Babies first develop the ability to control their eyes (to bring them together and apart in order to look at the same object), before they develop binocular vision (the ability to get a sense of depth/distance).

 

By comparing how these two different sets of abilities develop in premature babies, as opposed to babies born normally, it has been possible to answer whether they are dependent on the biological age of the child (relative to the point of conception) or on the amount of “experience” the child has had (chronological age) defined relative to the moment of birth.

 

It transpires that the development of eye control is related to biological maturity (nature). Contrastingly, the development of binocular vision is dependent very heavily on real world experience (nurture) – such as the brain connecting the feeling of distance through touch with the feeling in the eye muscles reflecting eye position, leading to an interpolated feeling of distance just by looking at something.

Which develops first, amblyopia or strabismus?

In different scenarios, either can occur first.

Strabism first

It has been suggested that the higher likelihood of strabismus in premature babies is linked to differing rates of maturation between the visual processing system (neurological) and the ability of the baby to control and develop its eye muscles. This posits that the basic maturation of the visual system (such as the ability to control accommodation/vergence) finishes before the necessary muscular control is in place which would allow these two connected systems to coordinate.  

 

Recent research suggests that premature birth alone has no significance on the likelihood of strabismus, but there is a very strong connection to the premature birth of underweight babies – whose physical development is delayed even longer, strengthening the argument that strabismus can be triggered by these two biological systems developing “out of step” with one another.

 

At the point where the baby’s visual system is ready to receive physical sensations to help it establish biocular and binocular vision, these are missing. It does not learn to adequately control and coordinate its eyes (strabism-like), leading to double vision which in turn causes the brain to choose to suppress one of the eyes.  In this case, therefore, strabismus proceeds amblyopia.

Amblyopia first

Amblyopia remains a fascinating area of research, precisely because it seems more questions are still being raised than answered. Typically, amblyopia is broken down into three different categories:

• Strabismic amblyopia
  • Misalignment of the eyes results in abnormal binocular interaction.
  • Eventual unconscious suppression of visual stimulation to an affected eye creates amblyopia.
• Deprivation amblyopia
  • Eyes fail to receive clearly formed images on the retina
  • Due to a cataract, other opacity, or obstruction (hemangioma of lid)
• Refractive (anisometropic) amblyopia
  • Difference in refractive error between the two eyes
  • Clearer image favored
  • Visual loss (amblyopia) in eye with higher refractive error

 

For the moment, let us consider just two categories – when the brain does not receive a signal (Deprivation amblyopia) and when it does (Strabismic and Refractive amblyopia).

 

What happens if one eye is physically unable to deliver any signal to the developing brain?

Perhaps one eye is missing, its retina is detached, a cataract is completely blocking light from entering the eye, the optical nerve is damaged – or anyone of a number of physical issues are completely preventing a signal from reaching the brain. One consequence seems to be that ocular dominance columns for the damaged eye completely waste away,. In this scenario, the brain is using a structure used to prefer one eye over another, to favour that eye completely.

What happens in the situation that an eye can deliver some signal, but without enough similarity between the eyes to allow the brain to compare and integrate (fuse) them?

 

When the brain is receiving input from both eyes which are so different it cannot bring them together (e.g. they are looking in different directions, or at focal points, or physical blockers such as cataracts have been removed and the brain simply doesn’t know what to do with the signal) it suppresses the non-functioning (or in the case of both eyes having no physical problems, the non-dominant) eye chemically.  This is known, as various pharmaceutical compounds can remove this suppression, even in adults with amblyopia. This also shows that suggestions that the eyes of adults with amblyopia are no longer neurologically connected to the brain are incorrect.

 

Furthermore, the nature of this eye suppression (GABAergic inhibition) has the consequence of reducing brain plasticity (the ability of the brain to learn). These same pharmaceutical compounds are being assessed as to whether or not their removal of suppression also helps patients learn to use that eye again.

 

It was suggested for many years that the differences in ocular dominance columns might lie behind such amblyopic suppression, but work on a recently deceased person with refractive amblyopia showed that his ocular dominance columns were unaffected. So, what is happening?  

 

More recent research implies that it is not an issue of neurons connected to the amblyopic eye being degraded or damaged, but that there are in fact, neurons dedicated to detecting interocular conflict.  Once this conflict is detected, they actively trigger suppression. This may herald a significant change in direction.  What if we can reduce interocular conflict, helping the brain choose to lift suppression, and proceed from this point in training for straighter eyes?

Muscular consequences

In both of the previous cases, the brain is now left with input from only one eye. Perhaps to preserve energy, or perhaps because it doesn’t know where to point the eye without any visual feedback, the damaged eye falls to one side as one of the two main groups of eye muscles relaxes more than the other, no longer receiving any neurological stimulus. Long term muscle relaxation can then result in muscular atrophy as the eye muscle degrades and wastes away.

The fix is part of the problem

Even if the original impediment to achieving binocular vision has been removed (which might also include the body having fully matured), the reaction of the development system to preserve at least monocular vision will have introduced its own obstacles – namely strabism and amblyopia.  If we can circumnavigate these obstacles in a special environment, we may be able to allow some people to re-visit and re-live the process of initialising/paramaterising/connecting their visual system in such a way that they are then able to re-establish binocular vision.

 

EyeSkills does not have the skills or resources or hubris to think it can definitively decipher strabismus, amblyopia. Nor do we believe we can provide some form of “out-of-the-box ultimate training environment” which could help all suffers recover.

 

What we can do, and are doing, it to try to provide tools which enable members of the research and sufferer community to experiment with developing and comparing different training approaches among a wide range of sufferers.

Next: Read about our philosophy for tackling strabism and amblyopia