Some patients with lesions in the geniculostriate pathway (GSP) can respond to visual stimuli in the blind field without conscious acknowledgement. The substrate for this “blind-sight” is controversial: whether it is the uninjured extrastriate pathway (EXP), which bypasses the lesion site, or residual fibers within damaged visual cortex (“islands of vision”). Using stimulus detection, localization, and spatial summation tasks, we have found blindsight in patients with damage both in the optic nerve (ON) and EXP. The prevalence and functional characteristics of their blindsight are indistinguishable from that in patients with GSP lesions, so blindsight does not require a completely intact EXP. The present findings support the view that a few surviving ON axons within an area of primary damage are sufficient to mediate blindsight: Several combinations of partially intact pathways can transmit information to the extrastriate cortex and the sum of activation of all visual fibers surviving the injury determines if and to what extent blindsight occurs.

In a previously conducted randomized placebo-controlled trial, we were able to demonstrate significant visual field enlargement induced by restitution therapy in patients with cerebral lesions [Kasten, E., Wuest, S., Behrens-Bamann, W., & Sabel, B. A. (1998c). Computer-based training for the treatment of partial blindness. Nature Medicine, 4 , 1083-1087.]. Visual field training was performed on a computer monitor for 1 hr per day over a period of 6 months. Since the procedure included only stimulation with white light, in the present study we investigated if this simple detection training had a transfer effect on color or form recognition in the trained area (i.e., in the absence of modality specific training). Answering this question would be crucial for planning optimal restitution therapy: In case there is no transfer of training effects to other visual modalities, a specific treatment of each visual function must be performed in order to achieve maximum benefit. Therefore, we analyzed the data from 32 patients with visual field defects who had participated in the original trial and whose form and color recognition had been investigated. The experimental group ( n = 19, restitution training) experienced not only an increase of 12.8% correctly detected stimuli (PeriMa program, p < .05), but also an improvement of 5.6% in pattern recognition (PeriForm) and of 6.1% in color perception (PeriColor), respectively. In contrast, the placebo group ( n = 13, fixation training) showed no significant changes from baseline to final outcome in any of the visual modalities (PeriMa: 0.3%; PeriForm: -0.3%; PeriColor: 0.4%). Conventional perimetry yielded an increase of 7.8% detected stimuli in the experimental group, but only of 1.2% in the placebo group ( p < .05). For form recognition and color perception, the differences between the results of the experimental and the placebo groups narrowly missed significance. However, correlations of diagnostic results showed that mainly those patients who had achieved visual field enlargement also improved in color and form perception: r = .67 ( p < .05) between PeriMa and PeriForm and r = .32 between PeriMa and PeriColor. We conclude that visual restitution training using a simple white light stimulus has at least some influence on improving other visual functions such as color and pattern recognition. This result supports the “bottleneck theory” of visual restitution, i.e., training effects can be explained as a process of perceptual learning and increased processing of information by residual structures surviving lesions of the primary visual pathways.