Motion detection is typically spared in blindsight, which results from damage to the striate cortex (area V1) of the brain that is sufficient to eliminate conscious visual awareness and severely reduce sensitivity to luminance contrast, especially for high spatial and low temporal frequencies. Here we show that the discrimination of motion direction within cortically blind fields is not attributable to feature tracking (the detection of changes in position or shape), but is due instead to the detection of firstorder motion energy (spatiotemporal changes in luminance). The key to this finding was a version of the line motion illusion entailing reverse-phi motion in which opposing motion directions are simultaneously cued by motion energy and changes in stimulus shape. In forced-choice tests, a blindsighted test subject selected the direction cued by shape change when the stimulus was presented in his intact field, but reliably selected the direction cued by motion energy when the same stimulus was presented in his blind field, where relevant position information was either inaccessible or invalid. Motion energy has been characterized as objectless, so reliance on motion energy detection is consistent with impaired access to shape information in blindsight. The dissociation of motion direction by visual field (cortically blind vs. intact) provides evidence that two pathways from the retina to MT/V5 (the cortical area specialized for motion perception) are functionally distinct: the retinogeniculate pathway through V1 is specialized for feature-based motion perception, whereas the retinocollicular pathway, which bypasses V1, is specialized for detecting motion energy.superior colliculus | visual cortex | visual pathway | hemianopia B lindsight is a rare phenomenon caused by damage to the primary visual cortex (striate cortex, or V1) of the brain that is sufficient to eliminate conscious visual awareness (1, 2). Visual sensitivity to luminance contrast is reduced in the corresponding part of the visual field, most severely for high spatial and low temporal frequencies (3). The fact that it is not completely abolished for low spatial and high temporal frequencies accounts for many of the residual visual capacities that have been reported in blindsight, including, in forced-choice tests, the ability to detect and discriminate stimuli presented in the field defect (2, 4). Evidence obtained from monkeys with striate cortex lesions as well as from cortically blind patients suggests that these capacities are mediated by neural pathways that project from the retina to extrastriate visual cortex, which normally bypass the main visual pathway that projects from the retina to the striate cortex via the lateral geniculate nucleus (the retinogeniculate pathway) and involve the superior colliculus of the midbrain and the lateral geniculate and pulvinar nuclei of the thalamus (5-13).Blindsight is not merely normal vision without awareness. In addition to the loss of primary visual cortex, retrograde degeneration of relay neurons ...