Online research in philosophy

Blindsight, the ability to blindly discriminate wavelength and other aspects of stimuli in a blind field, sometimes occurs in people with lesions to striate (V1) cortex. There is currently no consensus on whether qualitative color information of the sort that is normally computed by double opponent cells in striate cortex is indeed computed in blindsight but doesn?t reach awareness, perhaps owing to abnormal neuron responsiveness in striate or extra-striate cortical areas, or is not computed at all. The existence of primesight, the experience of colored afterimages in blindsight, has been taken to suggest that qualitative color information is computed either in pre-striate or striate cortical areas but is not broadcast to working memory. I argue here that a recent study in which color phosphenes were induced in a blindsighter using bilateral transcranial magnetic stimulation indicates that computations necessary for conscious color vision are lost in blindsight. Owing to this loss, the neural responsiveness in extrastriate cortical areas is abnormal and hence is unable to give rise to color awareness. Blindsight is thus degraded vision in which the computations necessary for conscious color vision have been lost.

Blindsight is the ability of patients with an impaired visual cortex to perform visually in their blind field without acknowledging that performance. This ability has been interpreted as a sign of the absence of phenomenal consciousness, and neuroscientific studies have extensively studied cases of it. Different proposals separate visual form recognition from motion perception, and attempt to show that either the former or the latter is solely responsible for blindsight performance. However, a review of current experimental evidence shows that a poor performance (on both form and motion) is accompanied by poor awareness. Blindsight cases do not influence the qualia debate, because they denote a severe visual performance deficit, and not because of a purportedly non-phenomenal nature of consciousness.

A lesion of striate cortex, area V1, produces blindness in the retinotopically corresponding part of the visual field, although in some cases visual abilities in the blind field remain that are paradoxically devoid of conscious visual percepts ("blindsight"). Here we demonstrate that the blindsight subject GY can experience visual sensations of phosphenes in his blind field induced by transcranial magnetic stimulation (TMS). Such blind field percepts could only be induced when stimulation was applied bilaterally, i.e. over GY's area V5/MT in both hemispheres. Consistent with an earlier report [Cowey, A., & Walsh, V. (2000). Magnetically induced phosphenes in sighted, blind and blindsighted observers. Neuroreport, 11, 3269-3273], GY never experienced phosphenes when stimulation was restricted to his ipsilesional V5/MT. To the best of our knowledge this is the first time GY has experienced visual qualia in his blind hemifield. The present report characterizes the necessary conditions for such conscious experience in his hemianopic visual field and interprets them as demonstrating that only via a contribution from GY's intact hemisphere can activation in the damaged hemisphere reach visual awareness.

Some patients with a lesion to the striate cortex (V1), when assessed through forced-choice paradigms, are able to detect stimuli presented in the blind field, despite reporting a complete lack of visual experience. This phenomenon, known as blindsight, strongly implicates V1 in visual awareness. However, the view that V1 is indispensable for conscious visual perception is challenged by a recent finding that the blindsight subject GY can be aware of visual qualia in his blind field, implying that V1may not be critical under all circumstances. This apparent contradiction raises the following question: if V1 is not always necessary for phenomenal awareness, why do V1 lesions have such a detrimental effect on conscious perception? It is suggested here that this contradiction can be resolved by considering the impact of V1 lesions on the functioning of the whole visual cortex.

Stoerig links blindsight to lesions between the primary visual cortex and the extravisual cortex. A parallel 'blindsight' occurs when input from the primary visual cortex is blocked during eye movements, convergence and blinks. At such moments (i) conscious vision based upon retinal input is blocked, (ii), however, like in blind sight retinal input can be used in motor tasks. The main difference to blindsight is that we are not only blind but cannot even with deliberate attention bring this blindness into awareness. We are doubly unaware: unaware of being blind and unaware that in spite of this that what we can see is created by the posterior parietal cortex substituting output (for that temporarily not coming from the primary visual cortex) for higher areas of the cerebral cortex.

The filling-in process proposed as a cover up for the existence of the blind spot has some conceptual similarities to blindsight. The perceptual operation of a hypothetical mechanism responsible for filling in represents a logical paradox. The apparent indeterminacy of the percept in the optic-disc region can be tested experimentally by viewing the grating test pattern below.