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Sophie Wuerger, Joanne Powell, Anshoo Chaudhoury, Laura Parkes; Comparison of fMRI measurements in LGN and Primary Visual cortex with visual deficits in Glaucoma. Journal of Vision 2015;15(12):257. doi: 10.1167/15.12.257.
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© ARVO (1962-2015); The Authors (2016-present)
Experimental primate glaucoma demonstrates that the retinal ganglion cell (RGC) loss is associated with atrophies in the lateral geniculate nucleus (LGN) and the primary visual cortex (V1). The purpose of our study was to determine whether, in glaucoma patients, selective behavioural deficits in the three main visual pathways (magnocellular, parvocellular, koniocellular) are associated with selective changes in the neural activity in LGN and V1. A POAG group (n=20) and a matched control group (n=20) were examined using the following tests: Visual field loss was assessed using standard automated perimetry (SAP); the Cambridge Colour Vision test (CCT) was used to assess colour deficiencies; visual thresholds along the three cardinal directions of colour space were measured (achromatic; red-greenish; lime-violet). For a subset of the participants (n=9 in either groups), functional Magnetic Resonance Imaging (fMRI) was used to obtain BOLD signals in the LGN and V1 in response to supra-threshold modulations along these three cardinal directions. We report the following results: (1) There are significant visual threshold differences between patients with Glaucoma and controls, in particular along the yellowish-violet (YV) cardinal direction. (2) The average BOLD signal in primary visual cortex (V1) is lower in the Glaucoma group compared to the control group. High thresholds along the yellowish-violet colour direction are associated with low V1 activity. (3) In contrast, the BOLD signal in the LGN is higher in Glaucoma patients compared to the controls. Within the Glaucoma group, more severe visual field defects are associated with higher LGN activity. In conclusion and contrary to our expectations, the LGN signal is increased in glaucoma patients compared to the controls. We speculate that this may reflect feedback from primary visual cortex.
Meeting abstract presented at VSS 2015
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