Why is Blindsight Blind?

Abstract

Abstract The human retina contains approximately 1.5 million ganglion cells, which convey processed visual information to the brain. About 90% of them project to the lateral geniculate nucleus of the thalamus, from where the signals are relayed in retinotopic order to the striate cortex of the occipital lobe. It is not surprising, therefore, that damaging the striate cortex, or severing its inputs, causes blindness in the corresponding part of the visual field (Holmes, 1945). Some patients with occipital lobe brain damage, however, despite being blind as a result, show signs of being able to process visual stimuli in their field defects (or scotomata), especially during forced choice discrimination tests (Pöppel et al., 1973; Weiskrantz et al., 1974; Weiskrantz, 1986). For example, they have intact pupil light reflexes (small but reproducible changes in pupils diameter brought about by the presentation of visual stimuli such as contrast-modulated gratings, Weiskrantz et al., 1998); they show an effect of priming when unseen targets presented in their scotomata influence the reaction times of their motor responses to seen targets in the intact visual field (Marzi et al., 1986; Rafal et al., 1990); they are able to indicate, verbally or manually, the presence of unseen targets in the scotoma during temporal two-alternative forced choice tests (see Stoerig and Cowey, 1997 for review); they may, when cued, move their eyes towards, or point to, the location of an unseen target in the scotoma (Pöppel et al., 1973), and they may be able to indicate whether or not an unseen target has moved in the scotoma, and perhaps even indicate its direction (reviewed in Chapter 6).