Deficient responses from the lateral geniculate nucleus in humans with amblyopia

Abstract

Amblyopia or lazy eye is the most common cause of uniocular blindness in adults. It is caused by a disruption to normal visual development as a consequence of unmatched inputs from the two eyes in early life, arising from a turned eye (strabismus), unequal refractive error (anisometropia) or form deprivation (e.g. cataract). Animal models based on extracellular recordings in anesthetized animals suggest that the earliest site of the anomaly in the primate visual pathway is the primary visual cortex (corresponding to the striate cortex, cytoarchitectonic area 17 and area V1), which is where inputs from the two eyes are first combined in an excitatory fashion, whereas more distal and monocular processing structures such as the retina and lateral geniculate nucleus (LGN) are normal. Using high-field functional magnetic resonance imaging in a group of human adults with amblyopia, we demonstrate that functional deficits are first observable at a thalamic level, that of the LGN. Our results suggest the need to re-evaluate the current models of amblyopia that are based on the assumption of a purely cortical dysfunction, as well as the role for the LGN in visual development.

The contrast dependence of the cortical fMRI deficit in amblyopia; a selective loss at higher contrasts

“…This being the case, the model is particularly relevant to V1 as it receives all its input from the LGN and where at the input level the Mand P-inputs from the geniculate are segregated by layer (i.e. 4cB and 4Ca) and have been shown to exhibit reduced responses when driven by the AE [Hess et al, 2009a].…”

Effective connectivity anomalies in human amblyopia

“…Brain imaging studies with functional Magnetic Resonance Imaging (fMRI) revealed reduced regional cerebral blood flow and blood-oxygen-level dependent (BOLD) response in the lateral geniculate nucleus (Hess et al, 2009), the striate (Barnes et al, 2001;Conner et al, 2007;Demer, 1997;Demer et al, 1988;Kabasakal et al, 1995;Li et al, 2007) and extra-striate cortex (Barnes et al, 2001;Li et al, 2007;Muckli et al, 2006) in amblyopia. There is also a literature from the numerous psychophysical studies that have been carried out on humans with amblyopia where striate and extra-striate cortical processing anomalies have been inferred.…”

The Structural Properties of Major White Matter Tracts in Strabismic Amblyopia

“…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. 12 In addition to changes in neural responses, structural neuroimaging has helped us understand the biological underpinnings of the behavioral differences in terms of changes in the structure of either grey matter [13][14][15][16][17][18][19] or white matter.…”