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Abstract

Visual information transmission flows from the retinal ganglion cells to the lateral geniculate nucleus and then to the primary visual cortex (V1), the chief cortical relay of visual information to ldquo;higherrdquo; extrastriate areas. Beyond area V1, visual processing is distributed across multiple interconnected brain areas, the precise role of which and their interactions are not yet, completely understood. To add to the dynamic complexity of the system, feedback from higher areas and modulation by top-down processes, such as attention, are often critical in the
formation of visual percepts (Deco and Lee; 2004; Olhausen, 2003; Kastner and Ungerleider, 2000; Mumford, 1994; Hubel and Weisel, 1977).
Impairment of visual function can occur at any point along the visual pathway from the eye to the cortex. We focus our discussion here on lesions of the primary visual cortex (area V1), which result in dense contralateral visual field defects known as ldquo;scotomasrdquo;. Scotomas resulting from area V1 lesions often involve the contralateral half of the visual field resulting in hemianopia, or a contralateral visual field quadrant resulting in quadrantanopia. V1 lesions are the most prevalent injury of the visual cortex, often occurring as a result of posterior cerebral artery (PCA) stroke, hemorrhage, or traumatic brain injury (TBI) (
Pambakian and Kennard, 1997; Zhang et al., 2006; Ajina and Kennard, 2012). Twenty to thirty percent of stroke
survivors experience visual disability (Taylor, 1997; Gilhotra et al., 2002; Giorgi et al., 2009).