This study sheds some light on the lazy eye.

According to it there's a brain region called

the binocular zone. And there's an additional

brain circuit that inhibits the binocular zone,

and this circuit might be a solution.

http://www.eurekalert.org/pub_releases/2013-08/nei-rfe082313.php

Other:

http://www.eurekalert.org/pub_releases/2012-10/ip-aie101612.php

http://www.eurekalert.org/pub_releases/2013-04/muhc-ed041913.php

https://www.mcgill.ca/newsroom/channels/news/lazy-eye-disorder-promising-therapeutic-approach-226011

http://www.eurekalert.org/pub_releases/2015-10/ehs-wmh101315.php

http://nautil.us/blog/how-utter-darkness-could-heal-lazy-eye

Regards,

Joachim

Yes, indirectly.

A retinal desease that reduce the vision in one eyes can induce a strong dominance of the other eye taking de facto to a single eye vision. In these conditions it can easily happen amblyopia.

It was really helpful but I still want more details about the condition of the retina especially neuro retina in amblyopic eye due to strabismus.

By definition, an amblyopic  eye suffers no organic disease in the eye itself.

Retinal cause of amblyopia can only be  secundaer, a cosequence of some retinal or optic nerve damage/ disease. We use monocular  and binocular VEP test. When we find some binocular facilitation,wich means, that the binocular VEP amplitude is larger, than that of the monocular one on the worth eye,then we say, no consecutive amblyopia,  

Hi,

The text that follows is from a book, Binocular Single Vision and Ocular Motility.

(With minor edits)

You will find it useful!

The first to suggest a specific cause for an organic anomaly resulting in  non reversible amblyopia was Enoch, who demonstrated that in some amblyopic eyes a malorientation of the retinal receptors exists. He did this by measuring the Stiles-Crawford effect, that is, the directional sensitivity of the retinal elements by means of a pencil of light moved across the pupil. He found not only various types of malorientation of the retinal elements but also some amblyopic eyes in

which the retinal elements appeared to be properly oriented. The question arose in connection with Enoch’s work whether the well-known and frequent retinal hemorrhages of neonates might be an etiologic factor in a malorientation of the foveal receptors if such hemorrhages occurred in the central retinal regions. To cite just one example from a rather extensive literature, Sachsenweger found retinal hemorrhages in as many as 24% of 1025 neonates. However, several studies have failed to establish a correlation between neonatal

foveal hemorrhages and the appearance of amblyopia later in life.

Over the years, Enoch further developed and broadened his work on receptor amblyopia, treating the retina as a fiberoptic bundle and investigating the optical characteristics of retinal receptors in normal and pathologic states. He has now concluded that in most patients with amblyopia the loss of central retinal resolution capability is not caused by disturbances in the physical or optical properties or in the malorientation of the retinal fiberoptic bundle. The same conclusions were reached by Bedell, who reinvestigated the role of photoreceptor misalignment in Enoch’s laboratory, and were recently reiterated by Enoch.

Findings from animal experiments and histologic studies of brains from human amblyopes  have added a different dimension to organic amblyopia and have placed its seat more centrally than in the retina. One can reasonably assume that recovery of visual acuity depends on reversibility of the neurophysiologic and histologic anomalies that have been shown to exist in the striate cortex and lateral geniculate nucleus of cats and monkeys with experimental amblyopia and in the lateral geniculate nuclei (LGN) of human patients with anisometropic and strabismic amblyopia.

So-called bilateral congenital amblyopia has always been regarded as being organic, a theory confirmed by Goodman and coworkers, who showed that these patients have low vision, nystagmus, poor color vision (achromatopsia), and defective photopic elements in their electroretinograms (ERGs). All these findings point to an irreversible, generally defective cone function, and these investigators therefore suggested that the older term congenital amblyopia be abandoned in favor of the term cone deficiency syndrome.

Thank you!

Hi,

some years ago I was looking for reasons why amblyopic eyes do get  AMD and DR to lesser degree then "normal eyes" and came to these conclusions that might be of use here:

Clinically, it is usually considered that amblyopia is only a result of lacking or not-established synapses in visual cortex and that the eye itself is morphologically normal. Using high resolution OCT, several studies have shown though that central retina in adult patients with monocular amblyopia is thicker. It is not surprising that in very deep amblyopia central retinal thickness is greater, as in this case the forming of macula with migration of ganglia cells from the center doesn’t take place in early infancy. However, the effect was detectable in shallow amblyopia too. In myopic anisometropic amblyopia, beside attenuation of peripheral retina, increased central retinal thickness was observed. These observations seem to be more pronounced in adult patients with amblyopia – there were only slight variations in macular retinal thickness and NFL thickness found in children, which suggests that it is more an effect of the preservation of the retina from thinning with age (Kanai et al.,2002), then early thickening of its central part. In the Kanai˙s study however, it was found that foveola itself, in normal eyes, is spared from thinning with age.  

There seems to be a top-down mechanism in amblyopia that affects retinal changes with age. But still, except in bilateral congenital amblyopia, there is little evidence that retina itself might be the primary cause for amblyopia.

Try  read Unilateral amblyopia: Optical coherence tomography findings at at http://www.saudiophthaljournal.com/article/S1319-4534(11)00085-3/pdf and  Analysis of retinal nerve fibre layer changes in anisometropic amblyopia by Heidelberg retina tomographhttp://jpma.org.pk/full_article_text.php?article_id=5508

The retina is normal in strabismic amblyopia.  The studies done by Hubel & Wiesel (for example) demonstrate a normal retina (on disection and staining) after induced strabismic and anisometropic amblyopia.

I hope that these new References will be helpful.

Good luck !

Choroidal and peripapillary retinal nerve fiber layer thickness in adults with anisometropic amblyopiaKantarci, Feride Aylin et al., Eur J Ophthalmol, 2015

Comparison of normal and amblyopic retinas by optical coherence tomography in children.Fernando Aguirre et al., Eur J Ophthalmol, 2009

BOLD responses to different temporospatial frequency stimuli in V1 and V2 visual cortex of anisometropic amblyopia.Hua Li et al., Eur J Ophthalmol, 2012

Retinal nerve fibre layer and macular thickness in amblyopia as measured by spectral-domain optical coherence tomography.Christiane E Al-Haddad et al., Br J Ophthalmol, 2011

Macular ultrastructural features in amblyopia using high-definition optical coherence tomography.Christiane Elias Al-Haddad et al., Br J Ophthalmol, 2012

Choroidal thickness in children with hyperopic anisometropic amblyopia.Tomo Nishi et al., Br J Ophthalmol, 2013

ambliopia  is usually for pediaric type, but in adults patient history (retinal detachment may be a cause. good luck

Amblyopia can be organic, meaning that it can occur secondary to a structural abnormality, including retinal disorders. However, reduced visual acuity in organic amblyopia cannot be solely attributed to the primary defect, but rather to a combination of both the structural defect and an added functional factor. That is, the loss of vision is more profound than would be expected from the structural defect alone.