Roots of blindsight.
The chapter reviews the historical background to demonstrations that there is residual visual function in the total absence of striate cortex (V1) in monkey and humans. The late 19th century evidence by Munk and others, as reviewed by William James, was that this was not possible in humans, and doubtful at best in monkeys. It has gradually become realized, starting in the middle of the 20th century, that even total bilateral removal of striate cortex in monkeys does not abolish all visual capacity, including spatial and pattern vision. The situation regarding unilateral or incomplete bilateral lesions in the monkey did not become clarified until Cowey's doctoral work in the 1960s, demonstrating that field defects were not absolute, that sensitivity continued to improve over several months of postoperative testing, that the size of the field defect gradually shrank, that the sensitivity was poorest at the center of the field defect, and that recovery was not spontaneous but depended on sustained practice. In human subjects with unilateral lesions from the 1970s onwards, using forced-choice methodology parallel to animal studies, a wide range of visual discriminations was demonstrated but with alterations or complete absence of acknowledged awareness by subjects (blindsight). Various varieties of skepticism are discussed and rebutted. The gap between humans and animals was diminished by the demonstration by Cowey and Stoerig that monkeys, like humans, classify responses to blind-field stimuli as being 'unseen'. Further recent degrees of closure and developments in human blindsight research are discussed.
Weiskrantz
L
L
Department of Experimental Psychology, University of Oxford, Oxford OX1 3UD, UK. larry.weiskrantz@psy.ox.ac.uk
D000818:Animals; D001364:Awareness / Q000502:physiology*; D005246:Feedback; D006801:Humans; D009435:Synaptic Transmission / Q000502:physiology; D014785:Vision, Ocular / Q000502:physiology*; D014793:Visual Cortex / Q000502:physiology*