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Abstract
In advanced retinitis pigmentosa with retinal lesions, the lesion projection zone (LPZ) in the early visual cortex can be driven during visual tasks, while it remains unresponsive during passive viewing. We tested whether this finding translates to advanced glaucoma, a major cause of acquired blindness. During visual stimulation, 3T fMRI scans were acquired for participants with advanced glaucoma (n = 4; age range: 51–72) and compared to two reference groups, i.e., advanced retinitis pigmentosa (n = 3; age range: 46–78) and age-matched healthy controls with simulated defects (n = 7). The participants viewed grating patterns drifting in 8 directions (12 s) alternating with uniform gray (12 s), either during passive viewing (PV), i.e., central fixation, or during a one-back task (OBT), i.e., reports of succeeding identical motion directions. As another reference, a fixation-dot task condition was included. Only in glaucoma and retinitis pigmentosa but not in controls, fMRI-responses in the lesion projection zone (LPZ) of V1 shifted from negative for PV to positive for OBT (p = 0.024 and p = 0.012, respectively). In glaucoma, these effects also reached significance in V3 (p = 0.006), while in V2 there was a non-significant trend (p = 0.069). The general absence of positive responses in the LPZ during PV underscores the lack of early visual cortex bottom-up plasticity for acquired visual field defects in humans. Trends in our exploratory analysis suggesting the task-dependent LPZ responses to be inversely related to visual field loss, indicate the benefit of patient stratification strategies in future studies with greater sample sizes. We conclude that top-down mechanisms associated with task-elicited demands rather than visual cortex remapping appear to shape LPZ responses not only in retinitis pigmentosa, but also in glaucoma. These insights are of critical importance for the development of schemes for treatment and rehabilitation in glaucoma and beyond.
Highlights
Glaucoma, a progressive degeneration of retinal ganglion cells (RGCs), results in an irreversible loss of vision, eventually leading to blindness (Jonas et al, 2017)
The fMRI-responses in the visual cortex of a representative participant with glaucoma (GL1) and a healthy control (HC1) with simulated peripheral visual field (VF)-defect are shown in Figure 3 for three different stimulation conditions (PV, one-back task (OBT), fixation-dot task (FDT))
lesion projection zone (LPZ) responses in the glaucoma patient resulted in positive coherenceps and BOLD modulations for OBT, while negative coherenceps and negative BOLD modulations, as for the control, were obtained only for passive viewing (PV) and FDT
Summary
A progressive degeneration of retinal ganglion cells (RGCs), results in an irreversible loss of vision, eventually leading to blindness (Jonas et al, 2017). A substantial proportion of glaucoma patients will become severely visually impaired and eventually bilaterally blind during their lifetime (Quigley and Broman, 2006; Kapetanakis et al, 2016) This motivates current research initiatives, to focus on better disease treatment tools, and to further our understanding of the management of visual impairment in advanced glaucoma. The ultimate goal is to explore effective avenues for the restoration of visual input, which is motivated by ongoing research progress, ranging from cell-based therapies at the retinal level to interventions at the cortical level (reviewed in Jutley et al, 2017; Roska and Sahel, 2018) For this purpose, knowledge about the state and functionality of the deafferented visual cortex in glaucoma is instrumental. In addition to the retinal damage caused by glaucoma, the concomitant deprivation of visual input from the retina to the cortex has been shown to result in structural and functional changes at the cortical level, in particular in the primary (V1) and extra-striate (V2 and V3) visual cortex (Duncan et al, 2007; Dai et al, 2013; Frezzotti et al, 2014; Boucard et al, 2016; Wang et al, 2016; Zhou et al, 2017)
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