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.

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