Blindsight

In 1905, the Swiss neurologist L. Bard demonstrated residual visual functions, in particular an ability to locate a source of light, in cortically blind patients. The phenomenon was termed blindsight by Weiskrantz and colleagues (1974) and has been extensively studied both in human patients and in monkeys with lesions of the primary VISUAL CORTEX (V1, striate cortex). The cortical blindness that results from the visual cortex's destruction or deafferentation is complete if the lesion destroys V1 in both hemispheres. The more common partial blindness (a field defect) always affects the contralesional visual hemifield. Its extent ("quadrantanopia," "hemianopia"), position ("to the left"), and density ("relative," "absolute") is perimetrically assessed. Density refers to the degree to which conscious vision is lost: in a relative defect, conscious vision is reduced and qualitatively altered; often, only fast-moving, high-contrast stimuli are seen (Riddoch 1917). In an absolute defect, no conscious vision remains.

Cortical blindness differs from blindness caused by complete destruction of the eye, the RETINA, or the optic nerve: the latter lesions destroy the visual input into the brain, while destruction of the striate cortex spares the retinofugal pathways that do not project (exclusively or at all) to this structure. These pathways form the extra-geniculo-striate cortical visual system that survives the effects of the V1-lesion and the ensuing degeneration of the lateral geniculate nucleus and the partial degeneration of the retinal ganglion cell layer. Physiological recordings in monkeys and functional neuroimaging in patients has shown that this system, which includes extrastriate visual cortical areas, remains visually responsive following inactivation or destruction of V1 (Bullier, Girard, and Salin 1993; Stoerig et al. 1997).

The discovery of residual visual functions that were demonstrable in patients who consistently claimed not to see the stimuli they nevertheless responded to (Pöppel, Frost, and Held 1973; Richards 1973; Weiskrantz et al. 1974) was met with a surprise that bordered on disbelief. It seemed inconceivable that human vision could be blind, nonphenomenal, and not introspectable. At the same time, the remaining visual responsivity of extensive parts of the visual system renders remaining visual functions likely to the point where one wonders how to explain that the subjects are blind.

These puzzling residual functions that have increasingly attracted attention from philosophers (e.g., Nelkin 1996; see CONSCIOUSNESS) include neuroendocrine and reflexive responses that can even be demonstrated in unconscious (comatose) patients. In contrast, the nonreflexive responses that are the hallmark of blindsight are only found in conscious patients with cortical visual field defects. They have been uncovered with two types of approach that circumvent the blindness the patients experience. The first approach requires the patient to respond to a stimulus presented in the normal visual field, for instance by pressing a response key or by describing the stimulus. In part of the trials, unknown to the patient, the blind field is additionally stimulated. If the additional stimulus significantly alters the reaction time to the seen stimulus (Marzi et al. 1986), or if it alters its appearance, for instance by inducing perceptual completion (Torjussen 1976), implicit processing of the unseen stimulus has been demonstrated. The second type of approach requires the patients to respond directly to stimulation of the blind field. Commonly, forced-choice guessing paradigms are used, and the patients are asked to guess where a stimulus has been presented, whether one has been presented, or which one of a small number of possible stimuli has been presented. Saccadic and manual localization, detection, and discrimination of stimuli differing in dimensions ranging from speed and direction of motion to contrast, size, flux, spatial frequency, orientation, disparity, and wavelength have been demonstrated in this fashion (see Stoerig and Cowey 1997 for review). Whether a patient's performance is at chance level, moderately significant, or close to perfect depends on many variables. Among others they include (a) the stimulus properties: changes in on- and off-set characteristics, size, wavelength, adaptation level, and speed can all cause significant changes in performance (Barbur, Harlow, and Weiskrantz 1994); (b) the stimulus position: when the stimulus is stabilized using an eye-tracking device, at least in some patients stimuli are detectable at some positions and not at others (Fendrich, Wessinger, and Gazzaniga 1992); (c) the response: a spontaneous grasping response may yield better discriminability than a verbal one (Perenin and Rossetti 1996); (d) the training: performance in identical conditions may improve dramatically with practice (Stoerig and Cowey 1997); (e) the lesion: although a larger lesion does not simply imply less residual function (Sprague 1966), evidence from hemidecorticated patients indicates that at least the direct responses require extrastriate visual cortical mediation (King et al. 1996).

Monkeys with striate cortical ablation show very similar residual visual responses. In both humans and monkeys, compared to the corresponding retinal position in the normal hemifield, the residual sensitivity is reduced by 0.4-1.5 log units (Stoerig and Cowey 1997). It is important to note that detection based on straylight, determined with the stimulus positioned on the optic disc of normal observers or in the field defects of patients who are asked to respond by indicating whether they can notice light emanating from this area, requires stimulus intensities 2 - 3 log units above those needed in the normal field. Blindsight is thus considerably more sensitive and cannot be explained as an artifact of light scattered into the normal visual field (Stoerig and Cowey 1991). The relatively small loss in sensitivity that distinguishes blindsight from normal vision is remarkable in light of the patients' professed experience of blindness. Interestingly, hemianopic monkeys, when given the chance to indicate "no stimulus" in a signal detection paradigm, responded to stimuli they detected perfectly in a localization task as if they could not see them (Cowey and Stoerig 1995). This indicates that it may not just be the patients who deny seeing the stimuli and claim that they are only guessing, but that both species have blindsight: nonreflexive visual functions in response to stimuli that are not consciously seen.

That the visual functions that remain in absolute cortical blindness are indeed blind is one of the most intriguing aspects of the phenomenon. Like other implicit processes that have been described in patients with amnesia, achromatopsia, or prosopagnosia, they may help us understand which neuronal processes and structures mediate implicit as opposed to consciously represented processes. As ipsilesional as well as contralesional extrastriate cortical responsivity to visual stimulation remains in patients and monkeys with blindsight, it appears insufficient to generate the latter (Bullier, Girard, and Salin 1993; Stoerig et al. 1997). This hypothesis gains further support from a recent functional MAGNETIC RESONANCE IMAGING study that compared within the same patient with a relative hemianopia the activation patterns elicited with a consciously perceived fast moving stimulus and a slow moving one that the patient could only detect in an unaware mode: in both modes, extrastriate visual cortical areas were activated (Sahraie et al. 1997). Further exploration along these lines may help pin down the neuronal substrate(s) of conscious vision, and studies of what can and cannot be done on the basis of blind vision alone can throw some light on the function as well as the nature of conscious representations.

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-- Petra Stoerig

References

Barbur, J. L., A. J. Harlow, and L. Weiskrantz. (1994). Spatial and temporal response properties of residual vision in a case of hemianopia. Phil.Trans. R. Soc. Lond. B 343:157-166.

Bard, L. (1905). De la persistance des sensations lumineuses dans le champ aveugle des hemianopsiques. La Semaine Medicale 22:253-255.

Bullier, J., P. Girard, and P.-A. Salin. (1993). The role of area 17 in the transfer of information to extrastriate visual cortex. In A. Peters and K. S. Rockland, Eds., Cerebral Cortex. New York: Plenum Press, pp. 301-330.

Cowey, A., and P. Stoerig. (1995). Blindsight in Monkeys. Nature 373:247-249.

Fendrich, R., C. M. Wessinger, and M. S. Gazzaniga. (1992). Residual vision in a scotoma. Implications for blindsight. Science 258:1489-1491.

King, S. M., P. Azzopardi, A. Cowey, J. Oxbury, and S. Oxbury. (1996). The role of light scatter in the residual visual sensitivity of patients with complete cerebral hemispherectomy. Vis. Neurosci. 13:1-13.

Marzi, C. A., G. Tassinari, S. Aglioti, and L. Lutzemberger. (1986). Spatial summation across the vertical meridian in hemianopics: a test of blindsight. Neuropsychologia 30:783-795.

Nelkin, N. (1996). Consciousness and the Origins of Thought. Cambridge: Cambridge University Press.

Perenin, M. T., and Y. Rossetti. (1996). Grasping without form discrimination in a hemianopic field. NeuroReport 7:793-797.

Pöppel, E., D. Frost, and R. Held. (1973). Residual visual function after brain wounds involving the central visual pathways in man. Nature 243:295-296.

Richards, W. (1973). Visual processing in scotomata. Exp. Brain Res. 17:333-347.

Riddoch, G. (1917). Dissociation of visual perceptions due to occipital injuries, with especial reference to appreciation of movement. Brain 40:15-57.

Sahraie, A., L.Weiskrantz, J. L. Barbur, A. Simmons, S. C. R. Williams, and M. J. Brammer. (1997). Pattern of neuronal activity associated with conscious and unconscious processing of visual signals. Proc. Natl. Acad. Sci. USA 94:9406-9411.

Sprague, J. M. (1966). Interaction of cortex and superior colliculus in mediation of visually guided behavior in the cat. Science 153:1544-1547.

Stoerig, P., and A. Cowey. (1991). Increment-threshold spectral sensitivity in blindsight. Brain 114:1487-1512.

Stoerig, P., and A. Cowey. (1997). Blindsight in man and monkey. Brain 120:120-145.

Stoerig, P., R. Goebel, L. Muckli, H. Hacker, and W. Singer. (1997). On the functional neuroanatomy of blindsight. Soc. Neurosci. Abs. 27: 845.

Torjussen, T. (1976). Residual function in cortically blind hemifields. Scand. J. Psychol. 17:320-322.

Weiskrantz, L., E. K. Warrington, M. D. Sanders, and J. Marshall. (1974). Visual capacity in the hemianopic field following a restricted cortical ablation. Brain 97:709-728.

Blindsight

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