Blindsight

The majority of studies on blindsight are conducted on patients who are hemianopic, i.e. blind in one half of their visual field. Following the destruction of the left or right striate cortex, patients are asked to detect, localize, and discriminate amongst visual stimuli that are presented to their blind side, often in a forced-response or guessing situation, even though they may not consciously recognize the visual stimulus. Research shows that such blind patients may achieve a higher accuracy than would be expected from chance alone. Type 1 blindsight is the term given to this ability to guess—at levels significantly above chance—aspects of a visual stimulus (such as location or type of movement) without any conscious awareness of any stimuli. Type 2 blindsight occurs when patients claim to have a feeling that there has been a change within their blind area—e.g. movement—but that it was not a visual percept.[4] The re-classification of blindsight into Type 1 and Type 2 was made after it was shown that the most celebrated blindsight patient, "GY", was in fact usually conscious of stimuli presented to his blind field if the stimuli had certain specific characteristics, namely being of high contrast and moving fast (at speeds in excess of 20 degrees per second).[5][6] In fact, in the aftermath of the First World War, a neurologist, George Riddoch, had described patients who had been blinded by gunshot wounds to V1, who could not see stationary objects but who were, as he reported, "conscious" of seeing moving objects in their blind field.[7] It is for this reason that the phenomenon has more recently also been called the Riddoch syndrome.[8] Since then it has become apparent that such subjects can also become aware of visual stimuli belonging to other visual domains, such as color and luminance, when presented to their blind fields.[9] The ability of such hemianopic subjects to become consciously aware of stimuli presented to their blind field is also commonly referred to as "residual" or "degraded" vision.[10][11]

As originally defined, blindsight challenged the common belief that perceptions must enter consciousness to affect our behavior, by showing that our behavior can be guided by sensory information of which we have no conscious awareness.[12] Since demonstration that blind patients can experience some visual stimuli consciously, and the consequent redefinition of blindsight into Type 1 and Type 2, a more nuanced view of the phenomenon has developed.[11][8][10] Blindsight may be thought of as a converse of the form of anosognosia known as Anton syndrome, in which there is full cortical blindness along with the confabulation of visual experience.

Much of our current understanding of blindsight can be attributed to early experiments on monkeys. One monkey, named Helen, could be considered the "star monkey in visual research" because she was the original blindsight subject. Helen was a macaque monkey that had been decorticated; specifically, her primary visual cortex (V1) was completely removed, blinding her. Nevertheless, under certain specific situations, Helen exhibited sighted behavior. Her pupils would dilate and she would blink at stimuli that threatened her eyes. Furthermore, under certain experimental conditions, she could detect a variety of visual stimuli, such as the presence and location of objects, as well as shape, pattern, orientation, motion, and color.[13][14][15] In many cases she was able to navigate her environment and interact with objects as if she were sighted.[16]

A similar phenomenon was also discovered in humans. Subjects who had suffered damage to their visual cortices due to accidents or strokes reported partial or total blindness. Despite this, when prompted they could "guess" the presence and details of objects with above-average accuracy and, much like animal subjects, could catch objects tossed at them. The subjects never developed any kind of confidence in their abilities. Even when told of their successes, they would not begin to spontaneously make "guesses" about objects, but instead still required prompting. Furthermore, blindsight subjects rarely express the amazement about their abilities that sighted people would expect them to express.[17]

Patients with blindsight have damage to the system that produces visual perception (the visual cortex of the brain and some of the nerve fibers that bring information to it from the eyes) rather than to the underlying brain system controlling eye movements.[12] The phenomenon was originally thought to show how, after the more complex perception system is damaged, people can use the underlying control system to guide hand movements towards an object even though they cannot see what they are reaching for.[12] Hence, visual information can control behavior without producing a conscious sensation. This ability of those with blindsight to act as if able to see objects that they are unconscious of suggested that consciousness is not a general property of all parts of the brain, but is produced by specialised parts of it.[12]

Blindsight patients show awareness of single visual features, such as edges and motion, but cannot gain a holistic visual percept. This suggests that perceptual awareness is modular and that—in sighted individuals—there is a "binding process that unifies all information into a whole percept", which is interrupted in patients with such conditions as blindsight and visual agnosia.[1] Therefore, object identification and object recognition are thought to be separate processes and occur in different areas of the brain, working independently from one another. The modular theory of object perception and integration would account for the "hidden perception" experienced in blindsight patients. Research has shown that visual stimuli with the single visual features of sharp borders, sharp onset/offset times,[18] motion[19] and low spatial frequency[20] contribute to, but are not strictly necessary for, an object's salience in blindsight.

There are three theories for the explanation of blindsight. The first states that after damage to area V1, other branches of the optic nerve deliver visual information to the superior colliculus, pulvinar[21][22] and several other areas, including parts of the cerebral cortex. In turn, these areas might then control the blindsight responses.

Another explanation for the phenomenon of blindsight is that even though the majority of a person's visual cortex may be damaged, tiny islands of functioning tissue remain.[23] These islands are not large enough to provide conscious perception, but nevertheless enough for some unconscious visual perception.[24]

A third theory is that the information required to determine the distance to and velocity of an object in object space is determined by the lateral geniculate nucleus (LGN) before the information is projected to the visual cortex. In a normal subject, these signals are used to merge the information from the eyes into a three-dimensional representation (which includes the position and velocity of individual objects relative to the organism), extract a vergence signal to benefit the precision (previously auxiliary) optical system, and extract a focus control signal for the lenses of the eyes. The stereoscopic information is attached to the object information passed to the visual cortex.[25]

More recently, with the demonstration of a direct input from the LGN to area V5 (MT),[26][27][28][29] which delivers signals from fast moving stimuli at latencies of about 30 ms,[30][31] another explanation has emerged. This one proposes that the delivery of these signals is sufficient to arouse a conscious experience of fast visual motion, without implying that it is V5 alone that is responsible, since once signals reach V5, they may be propagated to other areas of the brain.[8][32][33] The latter account would seem to exclude the possibility that signals are "pre-processed" by V1 or "post-processed" by it (through return connections from V5 back to V1), as has been suggested.[34] The pulvinar nucleus of the thalamus also sends direct, V1 by-passing, signals to V5[35] but their precise role in generating a conscious visual experience of motion has not yet been determined.

Evidence of blindsight can be indirectly observed in children as young as two months, although there is difficulty in determining the type in a patient who is not old enough to answer questions.[36]

In a 1995 experiment, researchers attempted to show that monkeys with lesions in or even wholly removed striate cortexes also experienced blindsight. To study this, they had the monkeys complete tasks similar to those commonly used for human subjects. The monkeys were placed in front of a monitor and taught to indicate whether a stationary object or nothing was present in their visual field when a tone was played. Then the monkeys performed the same task except the stationary objects were presented outside of their visual field. The monkeys performed very similar to human participants and were unable to perceive the presence of stationary objects outside of their visual field.[37]

Another 1995 study by the same group sought to prove that monkeys could also be conscious of movement in their deficit visual field despite not being consciously aware of the presence of an object there. To do this, researchers used another standard test for humans which was similar to the previous study except moving objects were presented in the deficit visual field. Starting from the center of the deficit visual field, the object would either move up, down, or to the right. The monkeys performed identically to humans on the test, getting them right almost every time. This showed that the monkey's ability to detect movement is separate from their ability to consciously detect an object in their deficit visual field, and gave further evidence for the claim that damage to the striate cortex plays a large role in causing the disorder.[38]

Several years later, another study compared and contrasted the data collected from monkeys and that of a specific human patient with blindsight, GY. GY's striate cortical region was damaged through trauma at the age of eight, though for the most part he retained full functionality, GY was not consciously aware of anything in his right visual field. In the monkeys, the striate cortex of the left hemisphere was surgically removed. By comparing the test results of both GY and the monkeys, the researchers concluded that similar patterns of responses to stimuli in the "blind" visual field can be found in both species.[39]

Lawrence Weiskrantz and colleagues showed in the early 1970s that if forced to guess about whether a stimulus is present in their blind field, some observers do better than chance.[40] This ability to detect stimuli that the observer is not conscious of can extend to discrimination of the type of stimulus (for example, whether an 'X' or 'O' has been presented in the blind field).

Electrophysiological evidence from the late 1970s has shown that there is no direct retinal input from S-cones to the superior colliculus, implying that the perception of color information should be impaired.[41][42][43] However, more recent evidence point to a pathway from S-cones to the superior colliculus, opposing previous research and supporting the idea that some chromatic processing mechanisms are intact in blindsight.[44][45]

Patients shown images on their blind side of people expressing emotions correctly guessed the emotion most of the time. The movement of facial muscles used in smiling and frowning were measured and reacted in ways that matched the kind of emotion in the unseen image. Therefore, the emotions were recognized without involving conscious sight.[46]

A 2011 study found that a young woman with a unilateral lesion of area V1 could scale her grasping movement as she reached out to pick up objects of different sizes placed in her blind field, even though she could not report the sizes of the objects.[47] Similarly, another patient with unilateral lesion of area V1 could avoid obstacles placed in his blind field when he reached toward a target that was visible in his intact visual field. Even though he avoided the obstacles, he never reported seeing them.[48]

A study reported in 2008 asked patient GY to misstate where in his visual field a distinctive stimulus was presented. If the stimulus was in the upper part of his visual field, he was to say it was in the lower part, and vice versa. He was able to misstate, as requested, in his left visual field (with normal conscious vision); but he tended to fail in the task—to state the location correctly—when the stimulus was in his blindsight (right) visual field.[49] > This failure rate worsened when the stimulus was clearer,[49] indicating that failure was not simply due to unreliability of blindsight.

Visual processing in the brain goes through a series of stages. Destruction of the primary visual cortex leads to blindness in the part of the visual field that corresponds to the damaged cortical representation. The area of blindness – known as a scotoma – is in the visual field opposite the damaged hemisphere and can vary from a small area up to the entire hemifield. Visual processing occurs in the brain in a hierarchical series of stages (with much crosstalk and feedback between areas). The route from the retina through V1 is not the only visual pathway into the cortex, though it is by far the largest; it is commonly thought that the residual performance of people exhibiting blindsight is due to preserved pathways into the extrastriate cortex that bypass V1. However both physiological evidence[55] in monkeys and behavioral and imaging evidence in humans[8][9][19][56] shows that activity in these extrastriate areas, and especially in V5, is apparently sufficient to support visual awareness in the absence of V1.

To put it in a more complex way, recent physiological findings suggest that visual processing takes place along several independent, parallel pathways. One system processes information about shape, one about color, and one about movement, location and spatial organization. This information moves through an area of the brain called the lateral geniculate nucleus, located in the thalamus, and on to be processed in the primary visual cortex, area V1 (also known as the striate cortex because of its striped appearance). People with damage to V1 report no conscious vision, no visual imagery, and no visual images in their dreams. However, some of these people still experience the blindsight phenomenon,[24] though this too is controversial, with some studies showing a limited amount of consciousness without V1 or projections relating to it.[57]

The superior colliculus and prefrontal cortex also have a major role in awareness of a visual stimulus.[44]

• Visual agnosia
• Riddoch syndrome

• Blind man navigates maze
• Blind man avoids obstacles when reaching