视觉是一种非常复杂的接收和解释来自环境的光信号的方法，它允许大脑在一个人的头脑中形成一个形象，在一个人的头脑中。从感光细胞位于眼睛的信号被转换成视觉信息或视线的“有意识的经验。“视觉的所有方面，也许最复杂的为我们理解科学是意识的概念。当提出与光的大脑解释光的视网膜，使我们成为视觉上意识到我们的环境。而从光感受器到视觉皮层的信号转导机制已严重阐明，科学有理解困难的意识和意识的现象，主要是还原论的水平。最近的神经生物学的方法来理解意识的知觉水平，已利用的盲视现象的研究。盲视是一个奇怪的现象，表现为视觉的无意识。这种情况有时会出现在那些已经发生的脑损伤的患者，并有感觉障碍，如皮质盲。在这种情况下，病人出现能够做出基本的感性决策基于视觉刺激尽管声称不知道说的刺激，尽管负责高级视觉功能的大脑区域的情况下，初级视皮层。
Vision is an extremely complex method of receiving and interpreting light signals from the environment which allows the brain to form an image in one's mind of the object being viewed. Signals from photoreceptors which are positioned in the eye are converted into visual information or the "conscious experience of sight." Of all the aspects of vision, perhaps the most complicated for us to understand scientifically is the concept of consciousness. When presented with light the brain interprets light waves striking the retina so that we become visually aware of our environment. While the mechanics of signal transduction from the photoreceptor to the visual cortex has been heavily elucidated, science has difficulty understanding the phenomena of consciousness and awareness, primarily on a reductionist level. Recently neurobiological approaches to understanding consciousness on a perceptual level, has utilised the study of the phenomenon of blindsight. Blindsight is a strange phenomenon presenting as vision without any conscious awareness. This condition is sometimes present in patients who have incurred brain damage and have a sensory impairment such as cortical blindness. In this case the patient appears able to make basic perceptual decisions based upon visual stimuli despite claiming to be unaware of said stimuli and despite the absence of the area of the brain responsible for higher visual functioning, the striate cortex.
“盲视”一词是由桑德斯等人。（1974），谁报道，初级视皮层的任何损害出现阻碍的能力“看”的对象，但找不到明显的看不见的东西的能力。桑德斯等人的报告关注波珀尔等人的研究。（1973），这决定了患者的枪击伤口没有报告的视觉经验，但能够使轻微的眼球运动的视觉刺激。这种现象称为盲2例病人可能意识到刺激但不报告的经验作为一个视觉也有报道（魏斯坎兹1998）。
The term 'blindsight' was coined by Sanders et al. (1974), who reported that any damage to the striate cortex appears to hamper the ability to 'see' objects but not the ability to find apparently unseen objects. Sanders et al.'s report concerned a study by Poppel et al. (1973), which determined that patients with gunshot wounds reported no visual experience and yet were able to make minor eye movements towards a visual stimulus. A phenomenon called blindsight 2 were a patient may be aware of a stimulus but not report the experience as a visual sensation-has also been reported (Weiskrantz 1998).
Psychology Essay 代写： Is The Blindsight Nothing More Than Depredated Vision
In an attempt to better understand the neurobiology of blindsight and the assorted implications for human consciousness, it is essential to understand the roll of the brain in visual perception. The visual cortex is split into 20 individual areas. The main visual cortex (also known as V1 or striate cortex) is the part which, when damaged, leads to blindsight. The optic nerves pass information from photoreceptors in the retina to the dorsal lateral geniculate nucleus. Optic radiations project from the dLGN to the primary visual cortex. The primary visual cortex is made up of six layers, and if spread out flat, would map out, contralaterally, the visual field. The V1 is known to process visual information regarding orientation, spatial frequency, texture, colour and retinal disparity (depth perception) Information then proceeds to the visual association cortex where it is integrated into a visual image (4). It is therefore not surprising, from a neurological point of view, that damage to V1 leads to reports of blindness. Visual processing takes place in the brain in a hierarchical set of stages (with much communication and feedback between areas). As V1 is the first cortical part in this hierarchy, any damage to V1 limits the visual info passing from the retina, via the LGN and then V1, to higher the cortical areas. However, the route from the retina through V1 is not the only pathway into the cortex, though it is the largest; it is thought that the residual performance of a patient exhibiting blindsight is due to preserved routes into the extrastriate cortex that bypass V1. The strange thing is that activity in these extrastriate areas is believed to be insufficient to support visual awareness in the absence of V1. review by Cowey and Stoerig, 1991
Blindsight is commonly tested using perimeter. Perimeter shows small light flashes in the visual field and patient answer 'yes' when they observe the light flash. An area where no flashes are reported is called scotoma. Although suffers of blindsight report nothing, when asked to indicate 'the area they think the light might have been' they point with a good degree of accurately. This test shows that light has been 'detected' and understood by the nervous system and can therefore influence the patients behaviour. This information however is not available to the conscious part of the brain of the patient. Patients not only detect light but can correctly identify shapes, colour, and motion on occasion. In a forced choice experiment, the patient is asked to identify features of a visual nature; the subjects observed in this manner will perform much better than chance would dictate despite the feeling that they are randomly guessing (2).
The first case of blindsight was reported at the beginning of the last century (Holmes 1918; Riddoch 1917). Holmes's patients could identify objects but were not able to notice them within visual range. The patient was also unable to follow a moving object with their eyes. Riddoch noted patients who were apparently blind but who could catch a moving object or describe the direction of movement despite stating that they were unable to see the objects. The reason for this may be due to the fact that the blindness in the patient was not necessarily completed. Damage to the striate cortex can result in areas of complete blindness called scotomas. Blindsight patients can discriminate stimuli in these areas but report being unaware of the stimuli present. The first studies conducted to measure eye movement were by Pöppel Held and Frost in 1973, based upon evidence that the midbrain pathways are implicated in the saccadic control, which can remain after visual cortex removal. Even though the subjects noted that they could not see the stimuli with their field defects, there was a significant, albeit weak correlation between stimulus locus and target eye position, at least out to 20 degrees eccentricity. Probably the most famous case of blindsight is that of a patient called DB (Weiskrantz, 1986). DB required surgery to excise an arterio-venous malformation in his right occipital lobe. The removal of the striate cortex caused a left visual field scotoma in the lower left quadrant of his visual field. Despite the fact DB had no awareness of the objects set in his blind field of vision; he performed well above average on a number of basic perceptual tasks. The teats included indicating if a stick was horizontal or vertical, locating stimuli by pointing, the ability to note the presence or absence of an object and the ability to distinguishing between shapes (such as a cross from a circle or square from a diamond). DB was however unable to distinguish a triangle from a cross or a curved triangle from a normal triangle. Despite these failings and more important was his lack of awareness of any stimuli being presented to him. DB stated that he 'couldn't see anything' when test stimuli was presented to his impaired visual field, a phenomenon that suggests ability to see and awareness of what is seen are possibly not fundamentally linked. DB was also noted as having variable levels of performance depending on the area of the scotoma that the stimuli were presented in. DB was much better at distinguishing a blank stimulus from a grating than at discriminating between a cross and a triangle in one area of the scotoma, but he exhibited the opposite pattern when the stimuli were presented in a different area. Curiously, DB, although not able to 'see' objects when presented to him-even thirty years after his deficit was first studied-appears to be aware of a visual 'after-image' after a stimulus on a monitor is switched off (Weiskrantz et al. 2002). DB could also describe the colour and spatial structure of the stimulus, a phenomenon that is correlated with increased prefrontal cortex activity (Weiskrantz et al. 2003).
Blindsight has extensive implications regarding human consciousness and awareness. Studies have demonstrated that interpreting a visual input is independent of our awareness of the input as a blindsight patient has a feeling or sensation of the presence of the object without really "seeing" it (3). Emotional stimuli can also be discriminated by blindsight subjects, without awareness, when the amygdala is activated by fearful stimuli (DeGelder et al., 2001, 2002; Morris et al., 2001; Pegna et al., 2004)
It is well understood that head trauma or a tumor will often induce the "psychic" blindness of these patients, a model has been developed in monkeys by removing all or part of the primary visual cortex. These monkeys are able to respond to visual inputs. They can be trained to touch illuminated bulbs rather than unlit ones and identify certain colours and patterns in order to obtain food. Monkeys without primary visual cortex can discriminate shapes, demonstrate contrast sensitivity functions over a range of spatial frequencies, and have measurable acuity, although reduced from normal. In certain situations they appear to show a remarkable sensitivity to small and brief visual events, and will fixate them or reach for them; and they are very sensitive to detection of movement. This phenomenon is believed to parallel human blindsight because when trained to respond differently according to whether there is a visual cue or not, these monkeys respond as if there were no cue when a visual input is presented to the blind field (1). It is therefore believed that these animals are able to respond to and identify features of a visual cue even though they do not report seeing it.
Blindsight explanations
A number of hypotheses has sought to find an explanation for blindsight phenomenon. For instance, that perception might be possible due to the remaining depredated normal vision or perhaps because of remained patches of striate cortex. However patient GY who had no remaining striate cortex, still experienced the blindsight phenomenon, what is more no activity in remaining visual cortex is present when scanned while patient reports blindsight perceptual events.
Another exmple suggested by Campion at al, 1983 who claimed that perceptual tasks can be completed successfully, at above chance levels, because stray light reflected by stimuli makes its way from the intact field of vision to the scotoma because it reflects from surfaces outside the eye area-what is called extraocular scatter. However this is unlikely because blindsight is still present in conditions of very high ambient light. Cowey (2004) has suggested that one way for controlling for this light scatter is to mask the blind field from view by placing a half-patch over the viewing eye, but this control is rarely employed. There can also be an intraocular source of light scatter-according to Cowey (2004), visual stimuli always 'smear' the retina. Because stimuli in blindsight studies have been presented very close to the eye, this has allowed the retina to be smeared with the image and stimulate the retina, leading to crude visual perception.
However, the stray light hypothesis appears to be an unlikely explanation, because DB is able to make perceptual decisions in the presence of strong ambient light, which reduces the amount of stray light reflected by stimuli. More to the point, this theory does not explain how DB can still make decisions based on the spatial dimensions of objects.
An alternative hypothesis suggests that the residual perceptual abilities of patients such as DB are attributable to the degrading of normal vision, possibly due to the presence of some residual striatal cortex. There are ten known pathways from the retina to the brain (Stoerig and Cowey, 1997). There appear to be two distinct pathways in the visual system that mediate different aspects of vision. The visual location of objects, for example, is thought to be a function of a system that includes the superior colliculus, the posterior thalamus and areas 20 and 21, whereas the analysis of visual form, pattern or colour is thought to be a function of the geniculo-striate system, which sends projections from the retina to the lateral ganiculate nucleus, then to area 17, 18 and 19, and then to areas 20 and 21. Blindsight could therefore conceivably be due to a disconnection between these two systems. Again, there are arguments against that hypotesis.
Although Blythe et al. (1987), found only five cases of blindsight in a sample of twenty-five patients; and Marzi et al. (1986) found a similar ratio (four patients out of twenty) in their sample would suggest that blindsight following striate removal therefore suggests some restraint in extrapolating from individual cases. However more recently it has become clear that the phenomenon is not rare. Sahraie et al. (2003) have studied a large population of patients with relatively restricted visual cortical damage and residual function was been found in the large majority.
The phenomenon of blindsight raises as many questions as it answers. It is evident that our brain processes visual information which we are not aware of and that this can affect our behavior. What seems intuitively correct, but for which there is no hard evidence, is the hypothesis that what is at work in blindsight is a primitive, early visual system that is not dependent on the striate cortex. While for the moment blindsight remains a somewhat mysterious concept, hopefully further study will help reveal the mechanisms and implications of our own consciousness and awareness.
however. The degree of variability in the appearance of
Is it a real effect?
Blindsight is nonetheless a variable effect as only 20% in two studies reported blindsight phenomenon. Most patients without striate cortex are just 'blind' and without blindsight.
Cowey, A. and Stoerig, P. (1991). The neurobiology of blindsight. Trends in Neuroscience, 29, 65-80.
DeGelder, B., Pourtois, J., Van Raamsdonk, G.M., Vroomen, J., and Weiskrantz, L. (2001). Unseen stimuli modulate conscious visual experience: evidence form inter-hemispheric summation. NeuroReport, 12, 385-391.
DeGelder, B., Pourtois, G., and Weiskrantz, L. (2002). Fear recognition in the voice is modulated by unconsciously recognized facial expressions but not by unconsciously recognized affective pictures. Proc. Natl. Acad. Sci. USA, 2002, 99, 4121-4126.
Morris, J.S., DeGelder, B., Weiskrantz, L., and Dolan, R.J. (2001). Differential extrageniculate and amygdala responses to presentation of emotional faces in a cortically blind field. Brain, 124, 1241-1252.
Pegna, A.J., Khateb, A., Lazeyras, F., and Seghier, M. L. (2004). Discriminating emotional faces without primary visual cortices involves the right amygdala. Nat. Neurosci., 8, 24-25.