Due to the orderly retinotopic mapping of the visual field across the surface of the primary and extrastriate visual cortex (Dougherty et al.,
2003; Engel, Glover, & Wandell,
1997; Wandell, Dumoulin, & Brewer,
2007), it is possible to precisely relate specific retinal locations to their corresponding representations within the visual cortex. Using this approach, it has been suggested that monocular and binocular focal retinal lesions in adult primates result in changes to the receptive fields of cells at the borders of the lesion projection zone (LPZ; the area of cortex corresponding to the lesioned retinal location) in the primary visual cortex (Baseler, Gouws, & Morland,
2009; Gilbert & Wiesel,
1992; Heinen & Skavenski,
1991; Kaas et al.,
1990; Schmid, Rosa, Calford, & Ambler,
1996). It should be noted that this effect is not universally accepted and may reflect the presence of existing long range connections rather than changes in the size of receptive fields (Botelho, Ceriatte, Soares, Gattass, & Fiorani,
2012; Calford et al.,
2005; Wandell and Smirnakis,
2009). A number of functional magnetic resonance imaging (fMRI) studies of humans with macular degeneration have also found evidence for remapping of the visual cortex whereby regions of the cortex within the LPZ became responsive to visual stimuli falling upon undamaged regions of the retina (Baker, Dilks, Peli, & Kanwisher,
2008; Baker, Peli, Knouf, & Kanwisher,
2005; Schumacher et al.,
2008). The interpretation of these findings has been disputed. Specifically it has been proposed that the functional activation within the LPZ is due to an unmasking of task-dependent feedback signals from higher cortical areas and not due to low-level changes in cortical function (Liu et al.,
2010; Masuda, Dumoulin, Nakadomari, & Wandell,
2008). In addition, a complete absence of visual field remapping has recently been reported in groups of participants with age-related or juvenile macular degeneration (Baseler et al.,
2011). Therefore it is still unclear whether functional plasticity occurs within the adult human visual cortex following peripheral damage to the visual system. Further, the human studies conducted in this area to date have focused primarily on macular degeneration, which affects photoreceptors in the retina. The effects of neurodegenerative diseases of the optic nerve such as glaucoma on visual cortex plasticity have not yet been investigated using fMRI. This is important as neurodegeneration is common to a large number of neurological disorders and therefore understanding the impact of neurodegeneration on the visual cortex could provide information that is relevant to understanding the impact of neurodegeneration on the brain in general (Gupta and Yücel,
2007a).