Blindsight Current Biology 2000

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R64 Dispatch

Blindsight: A conscious route to unconscious visionJames Danckert and Melvyn A. Goodale

Damage to the primary visual cortex can leave subjectswith unconscious residual vision, or ‘blindsight’. Newresearch suggests that ‘top-down’ modulation by intactconscious visual processes can improve performance inthe impaired visual domain, even though that domain

still remains quite inaccessible to consciousness.

Address: Vision and Motor Control Group, Department of Psychology,Social Science Centre, University of Western Ontario, London, OntarioN6A 5C2, Canada.E-mail: [email protected]

Current Biology 2000, 10:R64–R67

0960-9822/00/$ – see front matter

© 2000 Elsevier Science Ltd. All rights reserved.

One way to study how the brain works is to look at thebehaviour of individuals who have been unlucky enoughto have suffered brain damage. This neuropsychological approach to the study of brain function has a long history,dating back to at least the early part of the last century.Even today, at a time when neuroscience has becomeincreasingly dominated by molecular biology at one end of the scale and neuroimaging at the other, the study of behavioural deficits in neurological patients continues toprovide important insights into the functional organizationof the brain. This is particularly true of the study of vision,

where neuropsychological research has led to a completerethinking of how the visual pathways in the brain allowus to see the world and control our movements within it.The approach is well illustrated by a new study, publishedrecently in Current Biology [1], which has shown thatconscious visual experience of one type of visual input canmodulate the processing of different visual inputs that areotherwise impaired in certain patients.

Patients with damage to primary visual cortex — area V1,the first place in the cerebral cortex where visual informa-tion arrives — are essentially blind. They can see nothingin the region of the visual field opposite to the damaged

hemisphere (see Box 1). This kind of blindness, as it is notdue to any defect of the eye or the optic nerve, is oftenreferred to as ‘cortical blindness’. Some 25 years ago,however, it was discovered that some individuals whowere cortically blind in a part of their visual field couldnevertheless demonstrate ‘unconscious’ visual processingof stimuli appearing in that field [2]. For example, an indi-vidual might point quite accurately towards a visual targetin their blind field, despite confidently asserting that theyhad seen nothing [3]! Indeed, such individuals wouldsometimes deny that a target had been presented at alland could only be persuaded that they had pointed

accurately by confronting them later with the evidence of their performance. Lawrence Weiskrantz [4] coined theterm ‘blindsight’ to refer to this paradoxical phenomenonin which patients respond to visual stimuli that theycannot see. It is important to note that patients withdamage earlier in the visual pathway, at the level of theeye or the optic nerve, do not show any evidence of blind-sight [5,6] (see Box 1).

The phenomenon of blindsight suggests that other visualpathways — ones that are not entirely reliant on inputfrom primary visual cortex — must continue to function inits absence [2]. After all, without spared visual pathways,

how else could patients demonstrate blindsight? One of the most prominent pathways spared after lesions of primary visual cortex is the one running from the eyedirectly to the superior colliculus in the midbrain. Manyhave suggested that it is this pathway, and its indirect pro-

jections to the cerebral cortex, that mediate much of whathas been called blindsight. But this idea is not universallyaccepted. More sceptical investigators have suggested thatblindsight, such as it is, is carried out by spared ‘islands’ of cortex within the lesion itself. According to this view,blindsight is nothing more than a reduction, albeit a dra-matic one, in the sensitivity of normal vision [7].

But while this possibility is no doubt true in some cases,the weight of evidence suggests that the residual vision ina substantial number of patients does depend on path-ways outside the major projections to primary visualcortex. In fact, it would be surprising if this were not thecase. Although projections from the retina to primaryvisual cortex and beyond represent the major neuralcircuit supporting conscious vision, as we have just seen,this route is not the only way that visual informationreaches the brain. In addition to the projections to thesuperior colliculus, the retina projects directly to at leastten other distinct sites in the thalamus, hypothalamus andmidbrain — and some of these structures send projec-

tions in turn to the cerebral cortex. Processing in all orsome of these pathways could support many of the differ-ent kinds of visually guided behaviour that have beencalled blindsight. What is irrevocably lost in patients withdamage to primary visual cortex is not the ability torespond to visual events, but rather the ability to experi-ence those events consciously [4].

Patients with damage to primary visual cortex are not theonly ones to demonstrate residual visual capacitieswithout visual awareness [8–11]. Patients with more spe-cific visual deficits following damage to the neural outflow



from this region can also show behaviour that is reminis-cent of blindsight. Thus, these patients sometimesdemonstrate remarkable visual abilities within theirimpaired perceptual domain, even though, like the blind-sight patients, they have no conscious appreciation of thevisual cues to which they are responding with suchimpressive accuracy. The specific deficits in visual per-ception can present themselves in a number of different

ways (see Box 1). Patients with visual form agnosia, forexample, lose the ability to discriminate between objectswith different shapes, even though they can perceivecolour and motion. Conversely, patients with corticalcolour blindness (achromatopsia) are quite unable to iden-tify the colours of objects but retain the ability to seemotion and form [12] (see Box 1). Yet both these kinds of patients can demonstrate spared visual processing withinthe very domain that is compromised. Patients with visualform agnosia can pre-shape their fingers and orient theirhand appropriately when picking up objects of differentshapes, even though they cannot tell one shape from

another [11]. Similarly, patients with achromatopsia candifferentiate contours that are defined solely by differ-ences in colour, despite having no conscious appreciationof the colours themselves [12] (see Box 1).

In patients with specific perceptual deficits, there is anopportunity to use what the patient can see consciously toexplore what they process unconsciously. This opportu-

nity, by definition, is not available for the blindsightpatient, at least not within the blind visual field.Humphrey et al. [9] used the intact colour perception inpatients with disturbed form perception to reveal theunconscious processing of form in those patients. To dothis, they took advantage of the fact that some colouraftereffects are dependent on the orientation of thestimuli that are used to adapt the visual system. Forexample, after looking at a pattern of horizontal green andblack lines alternating with a pattern of vertical red andblack lines, people will later see an ‘aftereffect’ of com-plementary colours when shown a display of black and

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The primary visual pathway and effects of lesions.(a) The primary pathway for vision from the retina to the primary visualcortex via the lateral geniculate nucleus of the thalamus and the optic

radiations — the so-called geniculostriate pathway. The numbersprovide a key to the nature of the visual field defect (or portion ofblindness) that would result from a lesion at that particular point in thepathway. 1 Total blindness of the left eye resulting from a completelesion of the optic nerve;2 bitemporal hemianopia resulting from alesion of the optic chiasm; 3 right homonymous hemianopia resultingfrom a lesion of the primary visual cortex in the left hemisphere (notethat there is no macular sparing which is common in patients in whomthe lesion has spared the occipital pole). (b) Conscious andunconscious visual processes in patients with lesions of cortical visualareas. The lesions typically responsible for visual form agnosia occur inthe occipitotemporal cortex, often sparing primary visual cortex and theoptic radiations. Similarly, lesions causing achromatopsia are typicallyconfined to ventromedial occipital cortex, and in addition to sparingprimary visual cortex may spare the regions necessary for form and

motion processing. The top panel in the figure represents an arbitraryvisual stimulus. Panel1 represents a right visual field defect for apatient with blindsight arising from a left primary visual cortex lesion.

Also schematically represented is the patient’s unconsciousexperience, in which he or she can localize stimuli appearing in theblind field. Panel2 schematically represents both conscious andunconscious processing for a patient with visual form agnosia. Thispatient’s conscious experience is not sufficient to accuratelydiscriminate between even simple shapes. However, shape informationis available to the patient at an unconscious level, allowing him or herto accurately grasp the different shapes they cannot consciouslyidentify (note that colour is also available to this patient — see text for adiscussion of this issue). Finally, panel3 indicates the conscious andunconscious experience of a patient with achromatopsia. While thispatient is unable to accurately discriminate between the colour ofdifferent objects consciously, he or she can nevertheless use colourinformation at an unconscious level to discriminate contours and formsof objects, as well as their direction of motion.

Box 1



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white lines. What is interesting, is that the aftereffect isorientation-contingent: in the example just given, thehorizontal lines would look pinkish and the vertical lineswould look greenish.

Even though the patients studied by Humphrey et al. [9]could not discriminate between the different orientationsof the stimuli used in the experiment, they neverthelessshowed an orientation-contingent colour aftereffect. Inother words, the patients experienced colour aftereffectsthat depended on orientations that they could notconsciously perceive [9,13]. This approach to studyingvision in patients with damage to the visual pathwayscould be considered a kind of ‘bootstrapping’ operation, inwhich a conscious visual ability is manipulated in order toreveal the processing of visual input of which the patientremains quite unaware.

There is another way to use this ‘bootstrapping’ approach.Instead of inferring unconscious visual processing bylooking at its effect on a patient’s report of his consciousvisual experience, one can turn the whole thing aroundand attempt to use the patient’s intact conscious visualabilities to enhance his performance in the compromisedvisual domain. This is precisely the approach taken byAglioti et al. [1]. Their patient, SF, had a severe visualform agnosia and could not identify even simple visualforms, including letters of the alphabet. As with manyother cases of visual form agnosia, however, SF had nodifficulty naming colours or discriminating between diff-erent shades of colour. Aglioti et al. [1] investigated

whether or not SF’s spared colour perception could beused to improve his ability to discriminate form. The taskthey used was a variant of the Stroop test, in which normalindividuals take longer to read a colour word like ‘red’when it is printed in green ink (an incongruent trial) thanwhen it is printed in red (a congruent trial). This so-calledStroop effect will work even in the case where only theinitial letter of a colour name is used.

Aglioti et al. [1] asked patient SF to identify the letters ‘R’and ‘V’, the initial letters of the Italian colour words ‘rosso’(red) and ‘verde’ (green). Earlier testing had shown thatSF could not discriminate between single letters, includ-

ing V and R. Yet when given the Stroop test, he was moreaccurate and faster at reading V and R when those letterswere printed in the congruent colours (the letter ‘R’ inred, and the letter ‘V’ in green) than when they wereprinted in the incongruent colours (the letter ‘R’ printedin green and the letter ‘V’ in red). This was true despitethe fact that SF claimed to be completely unaware of theforms of the two letters — like blindsight patients he felthe was simply guessing at the forms presented to him.Although he later claimed to have a ‘feeling’ that he wasperforming above chance level, he maintained that he hadno conscious visual experience of the form of the letters.

What is going on here? Aglioti et al. [1] argue that SF’snormal colour perception, which allowed him to accuratelyidentify the colour of the letters, automatically activatedhis stored memories of the colour names, ‘rosso’ and‘verde’, which in turn produced some sort of internal image

of those colour words. It was the activation of these internalimages that Aglioti et al. [1] believe boosted the weaksignals coming from the damaged form pathway in SF —signals that were quite inaccessible to consciousness.

It is important to note that SF was not simply showingsome mutual interference between his conscious colourperception and his residual, but unconscious, formprocessing. Aglioti et al. [1] are making a stronger claimthan this. They are suggesting that, without the additionof the congruent or incongruent colour cues, therewould be no processing of form at all. Indeed, theyshowed in other tests, that the form of the letters never

affected SF’s naming of colours, as it does in individualswith normal vision. In SF’s case, it was strictly one-waybootstrapping: the conscious visual processing of colourinvoked the unconscious processing of form, but notvice versa.

We began this commentary by pointing out that much of what is called blindsight or unconscious visual processingin patients with brain damage is nothing more than the‘normal’ functioning of spared secondary visual pathways.The initiation of eye movements [14], the constriction of the pupil [15], and even the control of grasping move-ments directed at visual targets [11], all appear to depend

on visual pathways that are quite outside those mediatingour conscious visual perception of the world. It is nosurprise, therefore, to find that patients with profounddeficits in visual perception can sometimes show remark-ably intact, but quite unconscious, visual abilities (seeBox 1). What Aglioti et al. [1] have added to this picture isthe demonstration that it is possible for intact consciousvisual processing to influence how information isprocessed in the impaired domain.

Several challenges arise from their results. First of all, howis the intact ability able to influence processing in theimpaired domain? Is it the case, as Aglioti et al. [1] suggest,

that unconscious residual form processing is enhanced bytop-down cognitive processes that are invoked by colourperception and/or visual imagery? In other words, is itpossible for impaired functions to ‘hitch a ride’ on intactfunctions? Alternatively, do intact visual processes simplyimprove access to the weak signals in the impairedpathway, rather than enhancing the signal within thatimpaired domain? The answers to these questions willhave important implications for our models of normalvisual function, as well as providing insights into whichvisual processes are necessary for conscious vision andwhich are not.



References1. Aglioti S, Bricolo E, Cantagallo A, Berlucchi G:Unconscious letter

discrimination is enhanced by association with conscious colorperception in visual form agnosia. Curr Biol 1999, 9:1419-1422.

2. Poppel E, Held R, Frost D:Residual visual function after brainwounds involving the central visual pathways in man. Nature1973, 243: 295-296.

3. Weiskrantz L, Warrington EK, Sanders MD, Marshall J:Visualcapacity in the hemianopic field following a restricted occipitalablation. Brain 1974, 97: 709-728.

4. Weiskrant L:Blindsight: A case study and implications. Oxford:Oxford University Press; 1986.

5. Danckert J, Maruff P, Kinsella G, de Graaff S, Currie J:Investigatingform and colour perception in blindsight using an interferencetask. Neuroreport 1998, 9:2919-2925.

6. Maruff P, Sanbach J, Danckert J, Yucel M, Currie J:Dissociationbetween perceptual awareness and goal directed action. Evidencefrom hemianopia. InProceedings of the First Perception for ActionConference . Edited by Castiello U, Bennett K. Gippsland, Victoria:Monash University Press; 1996:115-121.

7. Gazzaniga MS, Fendrich R, Wessinger CM: Blindsight reconsidered.Curr Dir Psychol Sci 1994, 3:93-96.

8. Danckert J, Maruff P, Kinsella G, de Graaff S, Currie J:Attentionalmodulation of implicit processing of information in spatial neglect.Neuroreport 1999, 10:1077-1083.

9. Humphrey GK, Goodale MA, Coirbetta M, Aglioti S:The McCollougheffect reveals orientation discrimination in a case of corticalblindness. Curr Biol 1995, 5:545-551.

10. Driver J, Mattingley JB:Parietal neglect and visual awareness. Nat Neurosci 1998, 1:17-22.

11. Goodale MA, Milner AD, Jakobson LS, Carey DP:A neurologicaldissociation between perceiving objects and grasping them.Nature 1991, 349: 154-155.

12. Heywood CA, Kentridge RW, Cowey A:Form and motion from colourin cerebral achromatopsia. Exp Brain Res 1998, 123: 145-153.

13. Humphrey GK, Goodale MA, Gurnsey R:Orientation discriminationin a visual form agnosic: evidence from the McCollough effect.Psychol Sci 1991, 5:331-335.

14. Rafal RD, Smith J, Krantz J, Cohen A, Brennan C:Extrageniculatevision in hemianopic humans: saccade inhibition by signals in theblind field. Science 1990, 250: 118-121.

15. Barbur JL, Weiskrantz L, Harlow JA:The unseen colour aftereffect ofan unseen stimulus: insight from blindsight into mechanisms of

colour afterimages. Proc Natl Acad Sci USA 1999, 96:11637-11641.

Dispatch R67

If you found this dispatch interesting, you might also wantto read the August 1999 issue of

Current Opinion inNeurobiologywhich included the following reviews, editedby Ben A Barres and Louis F Reichardt , onNeuronal and glial cell biology :

Lineages and transcription factors in the specificationof vertebrate primary sensory neuronsDavid J Anderson

Sense and specificity: a molecular identity fornociceptorsMichael J Caterina and David Julius

Glia development in the embryonic CNS of DrosophilaSebastian Granderath and Christian Klämbt

Fringe: defining borders by regulating the Notch pathwayJane Y Wu and Yi Rao

Extracellular-signal-regulated kinase signalling inneuronsSavraj S Grewal, Randall D York and Philip JS Stork

Neurofilament functions in health and diseaseJean-Pierre Julien

Postsynaptic actin and neuronal plasticityAndrew Matus

Polyglutamine diseases: protein cleavage andaggregationHuda Y Zoghbi and Harry T Orr

the same issue also included the followingreviews, edited by Harvey Karten andAndrew Lumsden , on Evolution of thenervous system :

Conservation of neurogenic genes and mechanismsYee-Ming Chan, Yuh Nung Jan

Conserved usage of gap and homeotic genes inpatterning the CNSHeinrich Reichert and Antonio Simeone

Chordate origins of the vertebrate central nervous system

Linda Z Holland, Nicholas D HollandConservation and divergence of axon guidancemechanismsAndrew Chisholm, Marc Tessier-Lavigne

Evolution of the vertebrate neurotrophin and Trk receptor gene familiesFinn Hallböök

The full text ofCurrent Opinion in Neurobiology is in theBioMedNet library athttp://BioMedNet.com/cbiology/jnrb

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