Neuroimaging of amblyopia and binocular vision: a review

Abstract

Amblyopia is a cerebral visual impairment considered to derive from abnormal visual experience (e.g., strabismus, anisometropia). Amblyopia, first considered as a monocular disorder, is now often seen as a primarily binocular disorder resulting in more and more studies examining the binocular deficits in the patients. The neural mechanisms of amblyopia are not completely understood even though they have been investigated with electrophysiological recordings in animal models and more recently with neuroimaging techniques in humans. In this review, we summarize the current knowledge about the brain regions that underlie the visual deficits associated with amblyopia with a focus on binocular vision using functional magnetic resonance imaging. The first studies focused on abnormal responses in the primary and secondary visual areas whereas recent evidence shows that there are also deficits at higher levels of the visual pathways within the parieto-occipital and temporal cortices. These higher level areas are part of the cortical network involved in 3D vision from binocular cues. Therefore, reduced responses in these areas could be related to the impaired binocular vision in amblyopic patients. Promising new binocular treatments might at least partially correct the activation in these areas. Future neuroimaging experiments could help to characterize the brain response changes associated with these treatments and help devise them.

Altered white matter structure in the visual system following early monocular enucleation

“…In contrast, relative to early blind and visually impaired individuals (e.g., amblyopia, glaucoma), who demonstrate significant bilateral reductions in FA and associated increases in MD and RD in the optic radiations [Shimony et al, ; Shu et al, 2009a, 2009b; Xie et al, ; Zhang et al, ], our results in the ME group are considerably less severe. Instances of monocular vision loss, such as amblyopia, which continue to send degraded visual input to the brain, have widespread detrimental effects on the visual system both behaviorally and structurally [Joly and Frankó, ; Levi, ]. While the neural mechanisms of amblyopia are not fully understood, it seems that some aspect of the continued interactions between the affected and normal eyes, or the known functional abnormalities of visual cortex [Kiorpes et al, ], result in more disruptive changes compared to the complete deafferentation of visual input that occurs following enucleation.…”

Covert spatial attention is functionally intact in amblyopic human adults

“…The two types of attention are subserved by highly interactive and partially overlapping yet distinct neural substrates; the neural basis of exogenous attention is hypothesized to primarily be subcortical, and the top-down modulatory signals of endogenous attention are thought to originate from within a distributed dorsal frontoparietal network (for reviews, see Corbetta, Patel, & Shulman, 2008; Patel et al, 2015; Petersen & Posner, 2012; Serences & Kastner, 2014). Furthermore, neurophysiology and neuroimaging studies suggest that the neural anomalies of amblyopia intensify as one moves progressively further along the dorsal and ventral streams (for reviews, see Asper et al, 2000b; Joly & Franko, 2014; Kiorpes, 2006; Levi, 2006). …”

The Structural Properties of Major White Matter Tracts in Strabismic Amblyopia

“…1,2 Functional neuroimaging has revealed changes in patterns of brain activation in patients with amblyopia compared with control subjects. 3 Early in the visual pathway, the lateral geniculate nucleus (LGN) shows reduced activation when driven by the amblyopic compared with the fellow eye. 4,5 Downstream from the LGN, reduced activation has also been found in the primary visual cortex (V1), [6][7][8][9] as well as in highorder cortical areas involved in face perception, 10 multiobject tracking, 11 and visual-guided actions.…”