Comparison of fMRI measurements in LGN and Primary Visual cortex with visual deficits in Glaucoma

Abstract

Purpose Primary open angle glaucoma (POAG) is a major cause of visual morbidity and blindness. Experimental primate glaucoma demonstrates that the retinal ganglion cell (RGC) loss is also 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 are associated with selective changes in the neural activity in LGN and V1. Methods 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 defficiencies; visual detection thresholds along the three cardinal directions of colour space were measured (achromatic - BW; red-greenish - RG; yellowish-violet - YV). For a subset of the participants (n=9 in either groups), functional Magnetic Resonance Imaging (fMRI) was used to obtain BOLD (Blood-oxygen-level dependent) signals in the LGN and V1 in response to suprathreshold modulations along the cardinal directions. Results (1) There are significant visual threshold differences between patients with Glaucoma and controls, in particular along the yellowish-violet (YV) cardinal direction. This is confirmed by the Cambridge Colour Vision Test (CCT) which shows differential deficits along the tritanopic confusion line. (2) The average BOLD signal in primary visual cortex (V1) is lower in the Glaucoma group compared to the control group. Within the glaucoma group, high visual thresholds along the yellowish-violet colour direction are associated with low V1 activity. (3) In contrast, the BOLD signal in the lateral geniculate nucleus (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. Conclusions The BOLD signal in V1 is reduced in patients with POAG, consistent with their loss in visual sensitivity along the cardinal colour directions. Contrary to our expectations, the LGN signal is increased in POAG patients. We speculate that this may reffect feedback from primary visual cortex. (Figure presented).