Blindsight
Blindsight is the ability of people who are cortically blind to respond to visual stimuli that they do not consciously see due to lesions in the primary visual cortex, also known as the striate cortex or Brodmann Area 17.[1] The term was coined by Lawrence Weiskrantz and his colleagues in a paper published in a 1974 issue of Brain.[2] A previous paper studying the discriminatory capacity of a cortically blind patient was published in Nature in 1973.[3] The assumed existence of blindsight is controversial, with some arguing that it is merely degraded conscious vision.[4][5][6]
Type classification
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.[citation needed]
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
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.[10] It is for this reason that the phenomenon has more recently also been called the Riddoch syndrome.[11]
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.[12] 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.[6][5]
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.[13] Since the 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.[5][11][6] 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.
History
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.
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.[19]
Describing blindsight
Patients with blindsight have damage to the system that produces visual perception (the
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,[20] motion[21] and low spatial frequency[22] contribute to, but are not strictly necessary for, an object's salience in blindsight.
Cause
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[23][24] 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.[25] These islands are not large enough to provide conscious perception, but nevertheless enough for some unconscious visual perception.[26]
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
More recently, with the demonstration of a direct input from the LGN to area V5 (MT),[28][29][30][31] which delivers signals from fast moving stimuli at latencies of about 30 ms,[32][33] 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.[11][34][35] 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.[36] The pulvinar nucleus of the thalamus also sends direct, V1 by-passing, signals to V5[37] 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.[38]
Evidence in animals
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.[39]
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.[40]
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
Research
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.[42][page needed] 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).[citation needed]
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.[48]
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.[49] 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.[50]
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.[51] > This failure rate worsened when the stimulus was clearer,[51] indicating that failure was not simply due to unreliability of blindsight.
Case studies
This section's tone or style may not reflect the encyclopedic tone used on Wikipedia. (January 2018) |
Researchers applied the same type of tests that were used to study blindsight in animals to a patient referred to as "DB". The normal techniques used to assess visual acuity in humans involved asking them to verbally describe some visually recognizable aspect of an object or objects. DB was given forced-choice tasks to complete instead. The results of DB's guesses showed that DB was able to determine shape and detect movement at some unconscious level, despite not being visually aware of this. DB themselves chalked up the accuracy of their guesses to be merely coincidental.[52]
The discovery of the condition known as blindsight raised questions about how different types of visual information, even unconscious information, may be affected and sometimes even unaffected by damage to different areas of the visual cortex.[53] Previous studies had already demonstrated that even without conscious awareness of visual stimuli, humans could still determine certain visual features such as presence in the visual field, shape, orientation and movement.[52] But, in a newer study evidence showed that if damage to the visual cortex occurs in areas above the primary visual cortex, the conscious awareness of visual stimuli itself is not damaged.[53] Blindsight shows that even when the primary visual cortex is damaged or removed a person can still perform actions guided by unconscious visual information. Despite damage occurring in the area necessary for conscious awareness of visual information, other functions of the processing of these visual percepts are still available to the individual.[52] The same also goes for damage to other areas of the visual cortex. If an area of the cortex that is responsible for a certain function is damaged, it will only result in the loss of that particular function or aspect, functions that other parts of the visual cortex are responsible for remain intact.[53]
Alexander and Cowey investigated how contrasting stimuli brightness affects blindsight patients' ability to discern movement. Prior studies have already shown that blindsight patients are able to detect motion even though they claim they do not see any visual percepts in their blind fields.[52] The study subjects were two patients who suffered from hemianopsia—blindness in more than half of their visual field. Both subjects had displayed the ability to accurately determine the presence of visual stimuli in their blind hemifields without acknowledging an actual visual percept previously.[54]
To test the effect of brightness on the subject's ability to determine motion they used a white background with a series of colored dots. The contrast of the brightness of the dots compared to the white background was altered in each trial to determine if the participants performed better or worse when there was a larger discrepancy in brightness or not.[54] The subjects focused on the display for two equal length time intervals and where asked whether they thought the dots were moving during the first or the second time interval.[54]
When the contrast in brightness between the background and the dots was higher, both of the subjects could discern motion more accurately than they would have statistically through guesswork. However, one subject was not able to accurately determine whether or not blue dots were moving regardless of the brightness contrast, but he/she was able to do so with every other color dot.[54] When the contrast was highest subjects were able to tell whether or not the dots were moving with very high rates of accuracy. Even when the dots were white, but still of a different brightness from the background, subjects could still determine whether they were moving. But, regardless of the dots' color, subjects could not tell when they were in motion when the white background and the dots were of similar brightness.[54]
Kentridge, Heywood, and Weiskrantz used the phenomenon of blindsight to investigate the connection between visual attention and visual awareness. They wanted to see if their subject—who exhibited blindsight in other studies[54]—could react more quickly when their attention was cued without the ability to be visually aware of it. The researchers aimed to show that being conscious of a stimulus and paying attention to it was not the same thing.[55]
To test the relationship between attention and awareness, they had the participant try to determine where a target was and whether it was oriented horizontally or vertically on a computer screen.[55] The target line would appear at one of two different locations and would be oriented in one of two directions. Before the target would appear an arrow would become visible on the screen, sometimes pointing to the correct position of the target line and less frequently not. This arrow was the cue for the subject. The participant would press a key to indicate whether the line was horizontal or vertical, and could then also indicate to an observer whether or not he/she actually had a feeling that any object was there or not—even if they couldn't see anything. The participant was able to accurately determine the orientation of the line when the target was cued by an arrow before the appearance of the target, even though these visual stimuli did not equal awareness in the subject who had no vision in that area of his/her visual field. The study showed that even without the ability to be visually aware of a stimulus the participant could still focus his/her attention on this object.[55]
In 2003, a patient known as "TN" lost use of his primary visual cortex, area V1. He had two successive
In another case study, a girl brought her grandfather in to see a
Other cases refer to SL, GY and GR.[6]
Brain regions involved
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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[57] in monkeys and behavioral and imaging evidence in humans[11][12][21][58]
To put it in a more complex way, recent physiological findings suggest that
The superior colliculus and prefrontal cortex also have a major role in awareness of a visual stimulus.[46]
Lateral geniculate nucleus
Mosby's Dictionary of Medicine, Nursing & Health Professions defines the LGN as "one of two elevations of the lateral posterior thalamus receiving visual impulses from the retina via the optic nerves and tracts and relaying the impulses to the calcarine (visual) cortex".[60]
What is seen in the left and right visual field is taken in by each eye and brought back to the
Injury to the primary visual cortex, including lesions and other trauma, leads to the loss of visual experience.
Functional magnetic resonance imaging has launched has also been employed to conduct brain scans in normal, healthy human volunteers to attempt to demonstrate that visual motion can bypass V1, through a connection from the LGN to the human middle temporal complex.[11][58] Their findings concluded that there was an indeed a connection of visual motion information that went directly from the LGN to the V5/hMT+ bypassing V1 completely.[58] Evidence also suggests that, following a traumatic injury to V1, there is still a direct pathway from the retina through the LGN to the extrastriate visual areas.[62] The extrastriate visual areas include parts of the occipital lobe that surround V1.[61] In non-human primates, these often include V2, V3, and V4.[61]
In a study conducted in primates, after partial ablation of area V1, areas V2 and V3 were still excited by visual stimulus.[62] Other evidence suggests that "the LGN projections that survive V1 removal are relatively sparse in density, but are nevertheless widespread and probably encompass all extrastriate visual areas," including V2, V4, V5 and the inferotemporal cortex region.[63]
Controversy
The results of some experiments suggest that blindsighted people may be preserving some kind of conscious experience and thus they are not fully blind. The criteria for blindsight has repeatedly changed based on findings that challenge the original definition, which has led some scientists to cast doubt on the existence of blindsight.[4][5][6]
See also
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Further reading
- "Blindsight: How brain sees what you do not see". Medical Press. 14 October 2008. Retrieved 5 February 2018.
- Collins GP. "Blindsight: Seeing without knowing it". Scientific American Blog Network. Retrieved 5 February 2018.
- Danckert J, Rossetti Y (2005). "Blindsight in action: what can the different sub-types of blindsight tell us about the control of visually guided actions?". Neuroscience and Biobehavioral Reviews. 29 (7): 1035–46. S2CID 12833434.
- De Gelder B (May 2010). "Uncanny sight in the blind". Scientific American. 302 (5): 60–5. PMID 20443379.
- Leh SE, Johansen-Berg H, Ptito A (July 2006). "Unconscious vision: new insights into the neuronal correlate of blindsight using diffusion tractography". Brain. 129 (Pt 7): 1822–32. PMID 16714319.
- Leh SE, Mullen KT, Ptito A (November 2006). "Absence of S-cone input in human blindsight following hemispherectomy". The European Journal of Neuroscience. 24 (10): 2954–60. S2CID 14152585.
- McIntosh AR, Rajah MN, Lobaugh NJ (May 1999). "Interactions of prefrontal cortex in relation to awareness in sensory learning". Science. 284 (5419): 1531–3. PMID 10348741.
- Ptito A, Leh SE (October 2007). "Neural substrates of blindsight after hemispherectomy". The Neuroscientist. 13 (5): 506–18. S2CID 23093266.
- Ratey JJ, ISBN 978-0-375-70107-8.
- Beltramo R, Scanziani M (January 2019). "A collicular visual cortex: Neocortical space for an ancient midbrain visual structure". Science. 363 (6422): 64–69. PMID 30606842.