Слепое зрение: феномен и классификация.

Visual response in some blind people
the neurological phenomenon
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. The term was coined by Lawrence Weiskrantz and his colleagues in a paper published in a 1974 issue of Brain. A previous paper studying the discriminatory capacity of a cortically blind patient was published in Nature in 1973. The assumed existence of blindsight is controversial, with some arguing that it is merely degraded conscious vision.

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. 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 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). 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. It is for this reason that the phenomenon has more recently also been called the Riddoch syndrome. 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. 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. 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. 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. In many cases she was able to navigate her environment and interact with objects as if she were sighted. 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.

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. motion and low spatial frequency 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 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. These islands are not large enough to provide conscious perception, but nevertheless enough for some unconscious visual perception. 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. More recently, with the demonstration of a direct input from the LGN to area V5 (MT), which delivers signals from fast moving stimuli at latencies of about 30 ms, 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. 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. The pulvinar nucleus of the thalamus also sends direct, V1 by passing, signals to V5 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.

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. 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. 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.

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". What is seen in the left and right visual field is taken in by each eye and brought back to the optic disc via the nerve fibres of the retina. From the optic disc, visual information travels through the optic nerve and into the optic chiasm. Visual information then enters the optic tract and travels to four different areas of the brain including the superior colliculus, pretectum of the mid brain, the suprachiasmatic nucleus of the hypothalamus, and the lateral geniculate nucleus (LGN). Most axons from the LGN will then travel to the primary visual cortex. Furthermore, once the LGN was inactivated, virtually all of the extrastriate areas of the brain no longer showed a response on the fMRI. 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. The extrastriate visual areas include parts of the occipital lobe that surround V1.

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.