August 2015
Volume 56, Issue 9
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Research Highlight  |   August 2015
Amblyopia Reveals the Neuroanatomical Consequences of Prolonged Abnormal Binocular Experience
Author Affiliations
  • Bas Rokers
    Department of Psychology and McPherson Eye Research Institute University of Wisconsin-Madison, Madison, Wisconsin, United States; rokers@wisc.edu
Investigative Ophthalmology & Visual Science August 2015, Vol.56, 5161. doi:10.1167/iovs.15-17626
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    • Get Citation

      Bas Rokers; Amblyopia Reveals the Neuroanatomical Consequences of Prolonged Abnormal Binocular Experience. Invest. Ophthalmol. Vis. Sci. 2015;56(9):5161. doi: 10.1167/iovs.15-17626.

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      © ARVO (1962-2015); The Authors (2016-present)

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Amblyopia is of interest not just as a clinical disorder, but also because it sheds light on the interplay between sensory input and brain development. Duan et al.1 help identify the neuroanatomical consequences of prolonged abnormal binocular experience. 
Electrophysiology and neuroimaging studies have linked amblyopia to reduced neural activity,2 but it has been unclear if this reduction exists purely at the functional level, or has a neuroanatomical basis. 
Diffusion weighted imaging (DWI) can measure the diffusion of water molecules, and makes it possible to investigate the architecture of the living human brain at the millimeter level. Because it is easier for water to diffuse along axons rather than through them, diffusion can reveal the location, integrity, and density of white matter tracts. 
In the current study, the authors used DWI to investigate the properties of white matter tracts in strabismic amblyopia. When compared with age-matched controls, the authors found elevated diffusion within a number of white matter tracts, including the optic radiation. Thus, these results indicate a reduction in the structural integrity of these tracts following long-term abnormal visual experience. 
Clinically, these findings open the way to using neuroanatomical measures to assess the efficacy and impact of novel amblyopia treatments. 
In addition, these findings help clarify the complex interaction between amblyopia, neural activity, and neural architecture. While it is clear that the visual deficits cannot simply be linked to a single underlying neural cause,3 both this paper and a study including strabismic and anisometropic amblyopia now show clear deficits in the optic radiation.4 
An interesting open question concerns whether these deficits depend on neural plasticity during the critical period, or can arise when input to one of the eyes is systematically disrupted later in life, such as in macular degeneration or glaucoma. 
References
Duan Y, Norcia AM, Yeatman JD, Mezer A. The structural properties of major white matter tracts in strabismic amblyopia. Invest Ophthalmol Vis Sci. 2015; 56: 5152–5160.
Shooner C, Hallum LE, Kumbhani RD, et al. Population representation of visual information in areas V1 and V2 of amblyopic macaques [ published online ahead of print January 29, 2015]. Vision Res. doi:10.1016/j.visres.2015.01.012.
Levi DM. Linking assumptions in amblyopia. Vis Neurosci. 2013; 30: 277–287.
Allen B, Spiegel D, Thompson B, Pestilli F, Rokers B. Altered white matter in early visual pathways of human amblyopes [ published online ahead of print January 20, 2015]. Vision Res. doi:10.1016/j.visres.2014.12.021.
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