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The term "blindsight" describes a condition in which patients who are cortically and perceptually blind nevertheless demonstrate residual visual abilities within their scotomas, or areas of blindness (Radoeva et al. 2008). Though these patients have no conscious vision due to damage to the striate corticex (or primary visual corticex, area V1), they still respond to certain visual stimuli as though they are able to see them. The condition was first formally identified by psychologist Lawrence Weiskrantz and his colleagues at Oxford, when they were studying a cortically blind patient who had no conscious visual awareness of a light stimulus presented in his blind field, and yet was able to point to it with 99% accuracy when told to "guess" where the light was (Ramachandran 2004). Weiskrantz has categorized blindsight in humans as being either Type I, in which the patient has no conscious recognition of stimuli, or Type II blindsight, in which they have some awareness that something has happened in their blind field, without having any visual precept. Humans have shown evidence of blindsight in their ability to discriminate various types of visual stimuli, including those involving motion, color, simple shapes, orientations of lines, emotions of faces, etc. (De Gelder 2010). Though the mechanisms underlying blindsight are still uncertain, scientists are investigating several potential central pathways which would make unconscious processing and responding to visual information possible.
The video below documents a patient known as TN, who is completely blind due to damage to both striate cortices, as he walks down a hallway with no help. Though he cannot see where he is going and has no conscious vision of the obstacles cluttering the hallway, he somehow manages and avoid them all, without being aware that he is doing so.
Review of the Visual Processing System
In order to more fully understand and explain the phenomenon of blindsight, it is important to have an understanding of the normal visual processing structures and pathways in a healthy brain. Visual information is initially processed in the retina, and is then sent on to subcortical brain structures. These project to higher brain areas like the primary visual cortex, or to other areas which make use of visual information, like those which coordinate visual and motor reflexes.
Structures and Pathways
Visual processing begins when light enters the eye through the lens, which inverts the image and projects it onto the retina. There, light is detected by photoreceptors (rods and cones), and is then transduced into an electrical neural signal. This neural signal is passed through the layers of the retina to the ganglion cells, where an action potential is generated. There are multiple types of ganglion cells, which each respond to different aspects of visual information, including M-cells (responsive to depth, and are rapidly adapting), P-cells (color and shape); and K-cells (color). The ganglion cells project their axons into the brain through the
optic disks of each eye, forming the optic nerves.
At the optic chiasm, projections from the temporal portions of the retina remain ipsilateral, while information from the nasal retina decussate and project contralaterally. As a result, information from one’s right hemifield is projected to the left hemisphere via the left optic tract, and vice versa.
From there, the retinal axons travel along pathways to various subcortical regions in the brain, especially the thalamus, superior colliculus, and pretectum. The primary projection site for these axons is the lateral geniculate nucleus (LGN) of the thalamus, where approximately 90% of the ganglion cells terminate (Kandel et al. 2000). The LGN segregates the information into magnocellular, parvocellular, and intralaminar layers for processing, and then relays the visual information to the primary visual cortex. In a healthy person, V1 engages in thorough intracortical connections, and also projects to areas like the extrastriate visual cortices, the superior colliculus, the pons, the pulvinar, the LGN, etc. (Kandel et al. 2000). This processing ultimately gives rise to conscious visual perception.
Major structures involved in visual processing.
Most of the retinal ganglion cell axons which do not project to the LGN terminate in the superior colliculus, or the pretectum in the midbrain. The superior colliculus (SC) is involved in integrating visual and motor information, and therefore coordinates oculomotor functions like reflexive saccadic eye movements (De Gelder 2010). In addition to receiving retinal input, the SC receives input from V1, the frontal eye fields, pre-striate regions, middle temporal, parietal cortices, etc. (Kandel et al. 2000). By integrating all of this information, the SC is able to create a sort of neural map of the visual field and the motor actions necessary to respond to it. Neurons in the SC fire before contralateral saccades, driving long-lead burst neurons of the PPRF to excite or inhibit the appropriate burst neurons, and ultimately the motor neurons innervating eye muscles, to initiate saccades.
Retinal projections to the pretectal region of the midbrain are used to trigger pupillary light reflexes, in which the pupils constrict or dilate in response to light stimuli. The pretectum projects information bilaterally to the accessory oculomotor nucleus (also called the Edinger-Westphal nucleus), which relays it along the oculomotor nerve to the ciliary ganglion. From there, neurons innervate smooth muscles controlling the constriction and dilation of the pupils.
The Neurobiology of Blindsight
Blindsight has proved difficult to study extensively, due to the fact that cortical blindness (without excessive damage to other brain functions) is a rare condition. Further, because blind patients do not realize when they have unconscious visual function, they insist that they can see nothing, and therefore are only identified as possessing blindsight when they answer correctly in forced-choice responses to stimuli. Because of this, the existence of blindsight was initially doubted by many scientists. Now, however, it is widely accepted by many as a legitimate condition, and it has been shown that residual vision is probably present to some degree in most patients with occipital damage (Rees 2008). However, because the nature and extent of brain damage varies greatly across individuals, so do the visual impairments and remaining abilities manifested in those with blindsight. For example, depending on whether V1 lesions are bilateral or unilateral, and whether it is all of V1 or just parts of it that are damaged, a patient may be totally blind, or only blind in certain areas of their visual field.
Because of the variability between blindsighted individuals, researchers have investigated patients’ responses to multiple types of visual stimuli, attempting to understand the extensiveness of their abilities within their scotomas. Testing takes many forms, but typically involves the researcher presenting a visual stimulus (ie., of a particular shape, color, orientation, movement type, etc.) in the blind field of the patient, where he has no conscious vision of it. Though the patient is unaware of having seen anything, the researcher urges them to “guess” about the nature of the stimuli, according to the designated response method (ie, pointing, verbally answering, etc. to discriminate between types of stimuli). In other cases, the researcher may measure the patients’ reflexive or unconscious behaviors, such as withdrawal from stimuli, saccadic eye movements, pupillary constriction, avoidance of obstacles, etc. A variety of visual abilities have been observed in patients with blindsight, including the ability to detect moving stimuli (this function is often especially prominent), and to locate objects with saccades, pointing, or verbal responses (Radoeva et al. 2008). Patients have also been shown to discriminate between shapes, orientation of objects/lines, colors/wavelengths, facial emotions, etc. (De Gelder 2010). Perceptually blind patients may exhibit any or all of these abilities, and to varying degrees. Individuals often respond best to certain types of stimuli, and in certain ways, depending on the nature of their brain damage and the neural mechanisms being utilized in their personal experience of blindsight.
A conceptual chart of the visual processing involved in blindsight.
Neural Mechanisms Underlying Blindsight
Because the characteristics of a person’s blindsight depend upon the nature of his brain damage, there are probably multiple possible neural pathways involved in the condition, which vary across individuals. In fact, blindsight has even been observed in brain-damaged patients with a degree of V1 funtioning and retinotopic organization still intact, indicating that the condition takes many forms, and is not even specific to V1 lesions (Radoeva et al. 2008). Blindsight, therefore, may be most accurately described as a behavioral phenomenon in which a person is unaware of engaging in some amount of visual processing, as a result of brain damage. Radoeva et al. (2008) have noted that, “…there is the intriguing possibility that what appears to be the same behavioral phenotype (low confidence but accurate detection of moving stimuli in a perimetrically blind field) may be mediated by different neural mechanisms in different patients,” (p. 1937).
Blindsight patients usually have damage in area V1 of the occipital lobe.
Still, blindsight is most often observed in patients with damage to part or all of V1 areas, and though scientists aren’t certain of the pathways involved, they do have a few well-supported theories. The major propositions being considered as underlying blindsight involve the use of subcortical structures projecting to extrastriate regions, or the functioning of “islands” of preserved striate cortices. These theories can be understood in terms of three possible pathways underlying blindsight (Ro and Rafal 2006):
Extrageniculate subcortical pathways
Perhaps the most widely accepted explanation of blindsight is that visual input is sent to subcortical structures (other than the LGN), which bypass the primary visual cortex in processing and relaying the information. In the retinotectal tract, information from the retina projects to the superior colliculus in the midbrain, and then on through the pulvinar to the dorsal stream of the extrastriate cortex. The superior colliculus in the midbrain plays a significant role in this pathway and has been shown to be highly active during visual processing in cortically blind patients (De Gelder 2010). As mentioned earlier, the superior colliculus is involved in using visual information for motor actions without awareness, like saccades or reflexive orienting of attention—behaviors which are commonly present in blindsight. One study found that while cells of the middle temporal area (MT) remain active after striate lesions, MT cells become unresponsive to visual stimuli when both V1 and the superior colliculus are destroyed (Radoeva et al. 2008). Because the superior colliculus sends visual information to MT, this is evidence that the superior colliculus acts as a relay to extrastriate areas after V1 lesions.
2.) Geniculoextrastriate pathways
An alternative pathway for processing visual info in the absence of striate cortex functioning involves the LGN of the thalamus. Though the LGN is the main relay sight for visual input to V1 in healthy brains, it is thought to also have direct projections to the extrastriate cortex. This is supported by the fact that interlaminar layers of the LGN remain intact after V1 destruction, even though magnocellular and parvocellular layers (which project mainly to V1) suffer from rapid and widespread degeneration. Presumably, LGN interlaminar layers continue to function because they have projections to extrastriate cortices (Cowey 2010). Indeed, one study of blindsighted and normally sighted individuals revealed the existence of such pathways. In both groups, a pathway from the LGN to ipsilateral motion area V5/MT was identified. Furthermore, in the blind patient, additional tracts were observed, including connections from the LGN to the contralateral V5/MT, as well as transcallosal connections between V5/MT areas bilaterally (Rees 2008). Geniculoextrastriate pathways would explain the ability of blindsight patients to respond to orientation and color, since the superior colliculus cannot discriminate these types of stimuli (Ro and Rafal 2006).
3.) Partial functioning in the striate cortex
A final major theory for blindsight is that patients have “islands” of remaining V1 function which, though inadequate for complete conscious vision, are able to engage in some degree of processing. Because some patients have been shown to have total bilateral destruction of striate cortices, and yet still exhibit residual vision, this theory cannot account for all cases of blindsight. However, because many patients
seem to have functioning portions of V1 after damage, it is likely that they contribute to blindsight in some patients. This would help explain the broad scope of visual abilities in cortically blind patients. Since one might expect somewhat uniform blindsight symptoms in patients if one specific subcortical pathway were at work, it is reasonable to believe that the varying degrees of striate cortex damage account for the variability in blindsight behavior (Radoeva et al. 2008).
The image above and the accompanying caption were taken from Cowey (2009).
Blindsight is a fascinating phenomenon which paradoxically involves the ability of cortically blind patients to respond to visual stimuli with stunning accuracy, despite being unaware of them. Though there is still much that neuroscientists do not understand about the neural processing underlying blindsight, it can teach us a lot about central visual processing, and about the brain's ability to cope despite severe damage. The brain utilizes several pathways in processing visual information from the retina, which allows for alternative processing methods when the primary visual cortex is damaged. Specifically, it is likely that blindsight is possible because of subcortical structures (like the superior colliculus and thalamic LGN) which project directly to extrastriate areas, and because of residual functioning in "islands" of undamaged striate cortex. Most likely, each of these pathways operates at times in different individuals, and even work together within individuals, to create the broad range of blindsight abilities seen in patients. Whatever the cause, many scientists and philosophers alike have looked to blindsight as a fascinating hint to the mysteries of visual processing and the nature of human consciousness (Ramachandran 2004).
Glossary of Terms
the ability to respond to visual stimuli or engage in residual visual processing despite being cortically blind and unaware of doing so. Usually due to damage of area V1.
- blindness due to damage of visual cortices (as opposed to other visual processing structures, such as the eye itself)
- higher-order visual areas beyond the striate cortex (Kandel 2000).
- an experimental situation in which the researcher "forces" the subject to make a choice in response to a stimulus, though the patient feels he is only guessing and does not really know the answer.
- output cells of the retina; their axons form the optic nerves and project to subcortical regions like the thalamic LGN, superior colliculus, and pretectum.
- one half of the visual field (as perceived by the ipsilateral temporal retina, and contralateral nasal retina).
- having no conscious vision or visual experience of a stimuli, regardless of whether or not visual information is being processed to a degree.
- reflexes of the pupil, such as those which control the diameter of the pupil in response to light intensity.
- when neural signals are spatially organized with respect to the visual stimuli, forming maps of the visual field.
- rapid, jerk-like movements of the eye to focus the fovea on a target.
- blind areas in the visual field
- the primary visual cortex, or area V1; located at the back of the brain in the occipital lobe.
- the mental manifestation of visual information; the image that the brain creates out of visual info. Blindness is the absence of visual perception.
For more information about Blindsight, explore the following links and readings:
This video provides a nice brief and interesting overview of blindsight by discussing a patient with the condition.
This video shows how unconscious visual processing can be studied in healthy patients by simulating blindsight with a technique called visual masking.
This is an easy-to-read discussion of blindsight, written by L. Weiskrantz, who discovered the phenomenon. There is an emphasis on the history and development of blindsight research.
Blindsight: A case study and implications
. Oxford: Oxford University Press, 1986.
Also by Weiskrantz, this book offers a very in-depth study of blindsight. Though it is a bit old now, it still offers a lot of valuable information.
Blindsight and the nature of consciousness
. Toronto: Broadview Press, 2003. ISBN 1-55111-351-1.
For those interested in the implications of blindsight for understanding consciousness, this book offers an interesting philosophical discussion of both.
1.) Which of the following stimulus types can NOT be discriminated by any blindsighted person?
a. line orientations
b. varying wavelengths
c. emotions on faces
d. direction of movement across the blindfield
e. none of the above
2.) After receiving input from the retina, the pretectum projects first to
a. the middle temporal
b. the accessory oculomotor nucleus
d. the ciliary ganglion
3.) Which of the following has been proposed as a possible pathway involved in blindsight?
a. the vestibulospinal tract
b. the anterolateral system
c. the geniculoextrastriate pathways
d. the corticogeniculotectinecerebellar peduncle
4.) A "scotoma" is
a. a blind area in one's visual field
b. the neural map of the visual field created in the superior colliculus
c. a type of photoreceptor in the retina
d. an area of the visual field of which one
True and False
5.) T/F "Blindsight" refers to the phenomenon in which patients have perfect perceptual vision, and yet are completely uncaring and neglectful of everything in one visual field (usually the left).
6.) T/F Forced-choice "guessing" is often needed to identify blindsight behaviors in patients who do not believe they can see anything.
7.) T/F The interlaminar layer of the LGN is thought to have direct projections to the extrastriate cortices.
8.) T/F Approximately 90% of retinal ganglion cells project to the superior colliculus, which then relays the info to V1.
9.) What is one method a researcher might use to identify blindsight behavior in a cortically blind person?
10.) Why is it likely that the neural mechanisms involved in the blindsight phenomenon vary somewhat with each patient?
11.) Explain the theory that "islands" of functioning striate cortex are responsible for blindsight in some patients.
12.) A cortically blind patient with total destruction of the primary visual cortex seems to be exhibiting residual visual processing. When presented with a moving visual stimulus, her eyes tend to perform saccades toward the object. Her pupils constrict and she sometimes blinks in response to lights shined in her eyes. Furthermore, when asked which direction a stimulus is moving, she is able to "guess" correctly by pointing with incredible accuracy. She cannot, however, discriminate between colors. Propose possible neural mechanisms which may be involved in her "blindsight," and explain the pathways that are likely being utilized for her remaining visual processing.
Cowey A. The blindsight saga.
Experimental Brain Research,
200. pp. 3-24, 2009.
De Gelder B. Uncanny sight in the blind.
Scientific American 302
:5, pp. 60-65, 2010.
Kandel ER, Schwartz JH, Jessell TM.
Principles of Neural Science,
New York: McGraw-Hill, 2000.
Radoeva PD, Prasad S, Brainard DH, Aguirre GK. Neural activity within area V1 refelcts unconscious visual performance in a case of blindsight.
Journal of Cognitive Neuroscience 20
:11, pp. 1927-1939, 2008.
A Brief Tour of Human Consciousness: From Impostor Poodles to Purple Numbers
. New York: Pi Press, 2004.
Rees G. The anatomy of blindsight.
131:6. pp.1414-1415, 2008. doi: 10.1093/brain/awn089.
Ro T, Rafal R. Visual restoration in cortical blindness: Insights from natural and TMS-induced blindsight.
16:4. pp. 377-396, 2006. doi: 10.1080/096020105004359.89.
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