Wavelength sensitivity in blindsight

Abstract

BLINDSIGHT—the residual visual functions observed in visual-field defects resulting from destruction of part of the primary visual cortex (striate cortex) even though visual stimuli presented in the field defect are not consciously perceived—has generated new insights into the nature of consciousness and the role of the extrastriate pathways in visual processing. Some patients can detect and localize unseen stimuli when they are required to guess^1–4. Discrimination of movement^5,6, flicker^5,7 and orientation^4,8 may also be present, but residual colour discrimination is controversial. Negative results (see ref. 9 for review) imply that only the pathways from eye to striate cortex can transmit information about colour in primates. By measuring sensitivity to light of different wavelengths in patients with blindsight we show that spectral sensitivity in the blind fields is surprisingly high, with a reduction of only 1 log unit or less across the visible spectrum. It is also essentially normal in form, whether the patients are adapted to light or dark. The shift in peak sensitivity from medium to shorter wavelengths in adaptation to the dark (the Purkinje shift) and the presence of discontinuities in the light-adapted curve together show that blindsight involves both rod and cone contributions, and that some colour opponency remains. As colour opponency requires input from primate beta retinal ganglion cells, two-thirds of which degenerate transneurally after a striate cortical lesion in juvenile monkeys¹⁰, our results show that the surviving subpopulation of primate beta cells is functional.