Visual perception is the ability to interpret the surrounding environment through color vision, scotopic vision, and mesopic vision, using light in the visible spectrum reflected by the objects in the environment. This is different from visual acuity, which refers to how clearly a person sees (for example "20/20 vision"). A person can have problems with visual perceptual processing even if they have 20/20 vision.
The resulting perception is also known as vision, sight, or eyesight (respective adjective form: visual, optical, or ocular). The various physiological components involved in vision are referred to collectively as the visual system, and are the focus of much research in linguistics, psychology, cognitive science, neuroscience, and molecular biology, collectively referred to as vision science.
https://en.wikipedia.org/wiki/Visual_perception
The two-streams hypothesis is a model of the neural processing of vision as well as hearing.[1] The hypothesis, given its initial characterisation in a paper by David Milner and Melvyn A. Goodale in 1992, argues that humans possess two distinct visual systems.[2] Recently there seems to be evidence of two distinct auditory systems as well. As visual information exits the occipital lobe, and as sound leaves the phonological network, it follows two main pathways, or "streams". The ventral stream (also known as the "what pathway") leads to the temporal lobe, which is involved with object and visual identification and recognition. The dorsal stream (or, "where pathway") leads to the parietal lobe, which is involved with processing the object's spatial location relative to the viewer and with speech repetition.
https://en.wikipedia.org/wiki/Two-streams_hypothesis
Blindsight is the ability of people who are cortically blind due to lesions in their striate cortex, also known as the primary visual cortex or V1, to respond to visual stimuli that they do not consciously see.[1] The term was coined by Lawrence Weiskrantz and his colleagues in a paper published in Brain[2] in 1974. A similar paper in which the discriminatory capacity of a cortically blind patient had been studied was published in Nature[3] in 1973.
The majority of studies on blindsight are conducted on patients who are hemianopic, that is to say blind in only one half of their visual field. Following the destruction of the 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 do not necessarily 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 were of high contrast and moved 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]
Blindsight, as originally defined, 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 the demonstration that blind patients can experience some visual stimuli consciously, and the consequent redefinition of Blindsight in Type 1 and Type 2, there has been a more nuanced view of it.[11][8][10] It may be thought of as a converse of the form of anosognosia known as Anton–Babinski syndrome, in which there is full cortical blindness along with the confabulation of visual experience.
https://en.wikipedia.org/wiki/Blindsight
Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical condition. Anosognosia results from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere,[1][2][3] and is thus a neuropsychiatric disorder. A deficit of self-awareness, it was first named by the neurologist Joseph Babinski in 1914.[4] Phenomenologically, anosognosia has similarities to denial, which is a psychological defense mechanism; attempts have been made at a unified explanation.[5] Anosognosia is sometimes accompanied by asomatognosia, a form of neglect in which patients deny ownership of body parts such as their limbs. The term is from Ancient Greek ἀ- a-, 'without', νόσος nosos, 'disease' and γνῶσις gnōsis, 'knowledge'. It is also considered a disorder that makes the treatment of the patient more difficult, since it may affect negatively the therapeutic relationship.[6]
https://en.wikipedia.org/wiki/Anosognosia
Anton syndrome, also known as Anton's blindness and visual anosognosia, is a rare symptom of brain damage occurring in the occipital lobe. Those who have it are cortically blind, but affirm, often quite adamantly and in the face of clear evidence of their blindness, that they are capable of seeing. Failing to accept being blind, people with Anton syndrome dismiss evidence of their condition and employ confabulation to fill in the missing sensory input. It is named after the neurologist Gabriel Anton. Only 28 cases have been published.[1]
Although sometimes the two terms are used as synonymous, Anton syndrome must not be confused with Anton–Babinski syndrome[2] which is characterised clinically by contralateral sensory neglect, anosognosia with associated affective indifference toward the condition (anosodiaphoria), construction and dressing apraxia. Anton–Babinski syndrome is the right-hemisphere equivalent of Gerstmann syndrome and it is due to non-dominantinferior parietal lobule damage.
https://en.wikipedia.org/wiki/Anton_syndrome
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