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Blind Spot on the Eye - Essay Example

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From the paper "Blind Spot on the Eye" it is clear that the filling in the phenomenon, responsible for completing missing information across the artificial and natural scotomata as well as the physiological blind spot, occurs generally under a selection of conditions…
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Blind Spot on the Eye
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Blind Spot Blind Spot Blood vessels and the optic nerve exit the eye at a location known as the optic disk on the retina, a light-sensitive layer of membrane at the inner back of the eye. Since this location has neither rods nor cones, collectively referred to as photoreceptors, a small gap occurs in the field of view because the area is not able to respond to stimulations of light (von der Heydt & Friedman, 2003). Cones are responsible for color vision whereas rods facilitate vision in conditions of dim light. The blood vessels and optic nerve converge into the optic nerve head in front of the retina, which results in a hole in the retina. This natural arrangement of the eye’s structure results in what is known as a blind spot or scotoma. There is also an artificial blind spot that can occur due to a prolonged fixation of light, producing several seconds of loss of vision or local blindness, also called the Troxler Effect. However, this phenomenon is only present in the eyes of vertebrates. Cephalopod eyes, although similar superficially, do not have blind spots. This is because the optic nerve in them approaches the photoreceptors and converges from behind the retina and, therefore, creating no breaks in the visual field. An example of such an eye is that of the octopus. Apart from the naturally occurring blind spots, there are also instances where they are associated with various optical or ocular diseases, significantly reducing the level and extent to which sensory information are derived (von der Heydt & Friedman, 2003). The significance of this observation is that growing degrees of the visual field’s obscuration need to be examined for potential diseases that may lead to total blindness. The diseases that affect the retina are both acquired and inherited and they include macular degeneration, retinitis pigmentosa, cone-rod dystrophy, retinal separation, posterior vitreous detachment, hypertension and retinoblastoma, which is a cancer affecting the retina. In the case of macular degeneration, the part of the retina known as macula, which is also one of the nervous system’s highly specialized parts, is affected and deteriorated by various pathologic by common conditions, affecting central vision (García-Fernández, Castro-Navarro & Bajo-Fuente, 2013). Since the retina’s central portion is the macula, it is, therefore, responsible for the details of vision such as color, reading and functions like face recognition. Macular degeneration usually affect people aged above 55 and occurs in two types; dry or atrophic and wet or exudative. The dry form is caused by the breakdown of the macula’s cells, which leads to the central vision getting gradually blurred. It is characterized by small and round whitish-yellowish spots, either single or multiple, on the outer retina. In the wet form, abnormal blood vessels that are newly created grow under the retina’s central part (Kolb, 2003). The cause of destruction or distortion of vision in this type is the bleeding and leaking of the abnormal blood vessels, often scarring the retina. The distortion of vision may initially be in one eye only, but will eventually affect the other as the problem develops. The wet type differs from the dry one mainly because vision distortion is much faster in wet form than it occurs in the dry form, and it affects about only 15 percent of persons with age-related muscular degeneration (García-Fernández, Castro-Navarro & Bajo-Fuente, 2013). Macular degeneration has several causes and risk factors. Around 10 percent of patients aged 66 to 74 years will exhibit macular degeneration, with the prevalence increasing to 30 percent among patients between 75 and 85 years old. Family history also determines the lifetime risk of the disease’s late-stage development, which is at 50 percent for persons with relatives who have suffered from macular degeneration. People with relatives with the disease only have a 12 percent chance of developing it. Other risk factors are presented by fat intake, obesity, cholesterol, hypertension, deficiency of vitamin D, race and smoking. Another disorder, retinal detachment, is caused by the retina’s movement away from the eyeball’s outer, pigmented wall, which results in a sudden vision defect. It is a likely occurrence among people suffering from diabetes. Other conditions that may result in retinal detachment include cataract surgery, shrinkage or scarring the vitreous, bleeding behind the retina and physical injury which can knock the retina out of place (Kolb, 2003). Retinitis pigmentosa, which is an inherited and degenerative disease of the eye, also causes severe impairment of vision as well as blindness due to the loss of photoreceptor cells. Because of the inconsistency of its progress, some people may exhibit the symptoms as early as infancy while others only notice them later in adulthood. One of its traits is that the later its onset, the faster the patient suffers sight deterioration. It denies persons suffering from it a peripheral vision of 90 degrees, unlike those free from it who achieve the 90 degrees vision. Those suffering from the disease will have symptoms that include night blindness, blurred vision, poor separation of color and peripheral vision (or lack of central vision) (Sudhakar, Natarajan & Parikumar, 2013). In posterior vitreous detachment, the posterior segment of the vitreous body separates from the retina’s internal membrane. The main cause of this is the shrinking of the vitreous. This is, in turn, occasioned by old age, diabetes, trauma and inflammatory conditions. In such conditions, the vitreous often liquefies, causing floaters in the eye, which becomes a cause of visual black spots. Common symptoms include photopsia and flashes. Apart from diseases, another unique factor is aging. Persons above 50 years are associated with various health hazards, and the blind spots in their eyes are usually bits of the eyeball’s inner fluid floating into view. Medically, they are called floaters. With the aging process, the eyeball also shrinks, separating the fluid in it into a stringy residue and a clear fluid. The strings float behind the lens and, being opaque, throw a shade on the retina, making old age in itself a causal factor for visual blind spots (Sudhakar, Natarajan & Parikumar, 2013). Studies have shown that the human eye does not see direct representations of external realities in spite of popular misconception but rather, what they see is a translation that the eyes and the mind form. However, the blind spot is not noticed in everyday life, partly because of the eyes’ looking around constantly and getting varied and wide ranges of view (Shepherd, 2004). It is also partly because the brain gets information from both eyes and uses it to create a single mental view, therefore, what is missed by one eye is picked up by the other. The blind spots in humans are more glaring because of their eyes’ placement in the head and they cannot see naturally behind them, directly below at their feet or on top of their heads. Other animals have their eyes placed on the sides of their heads, for example a horse or a robin, giving them better view on the sides but much worse view directly ahead of them. The lives of such animals depend on their ability to detect predators from the back and sides (Shepherd, 2004). When they hunt for worms, robins, or birds in general, turn their heads to get a better view of what is in front of them. An animal like a wolf has eyes that are best suited to see directly ahead, hence its ability to stealthily stalk its prey. A different eye arrangement is that of a crocodile, which are placed above its head. This adaptation enables it a different view as well as allowing it to see above water as the rest of its body remains submerged below the water. The human vision is described as binocular, which means that the single image perceived by the mind is constructed from the two different views of each eye. It is, therefore, evident that when blind spots and the associated optical diseases are not attended to, they threaten the very survival of animals, both the hunters and the hunted. Among all land mammals, the equine eye, like that of the horse, is the largest. The visual abilities of animals with equine vision are related directly to their behavior and more so for the non-domestic horse, mainly because it is a flight animal (Shepherd, 2004). For the domestic horse, many of them tend to have near-sightedness or myopia. The horse’s eyeball is not a perfect sphere but is instead flattened from forward towards the back, with its wall consisting of three layers. The retina, or nervous tunic, consists of cells that are the brain’s extension coming from the optic nerve. The cells are light-sensitive receptors that include rods and cones. Since light can only be received by about 66 percent of the eye, the receptor cells only line the part between the pupil and the optic disk, not necessarily the eye’s entire interior. The second layer is the uvea or vascular tunic and is made up of the iris, ciliary body and choroid. In-between the lens and the cornea is the iris, which allows light to pass in varying amounts through the pupil, which is the center hole. The iris also gives the eye its color. The choroid is made up of blood vessels and has a considerable amount of pigment. The third layer, fibrous tunic, is made up of cornea and sclera and provides the eye with protection. The ciliary suspensory ligament holds the eye’s lens behind the iris. The suspended arrangement allows for accommodation. Accommodation is the change of focus which is achieved by changing the lens’ shape to adjust to far or near objects into a sharper view (Riegal & Hakola, 2000). The placement of the horse’s eyes in the head allows it to have a binocular focus when it holds its head vertical, even though the eyes are on the sides of the head. As a survival adaptation, it can have a range of upto 350 degrees of monocular vision, 65 degrees of which are binocular vision. Its widest monocular range of vision has two blind spots. One is directly in front of its face and the other behind its head extending to the tail when it faces straight ahead. The direct front view makes a cone-shape with its shape at about four feet ahead of the horse’s head. This implies that when it jumps an obstacle, it disappears briefly from sight immediately before the animal jumps. To increase it binocular vision range, it will have to lower or raise its head. Clinical signs of disease or injury are abnormal discharge, redness and swelling. Untreated injuries, even seemingly minor ones, can result in serious complication leading to blindness. The common diseases and injuries include habronema, corneal abrasion, keratitis, corneal ulcer, conjunctivitis, keratoconjunctivitis sicca and uveitis. In Darwinian days, the existence of an organ like the eye with extreme perfection was considered as evidence of God (Miller, 2000). It was the only explanation for the substructure and intricate organs of the eye having come together in the correct way to facilitate vision. But the eye was later faulted as being imperfect because it evolutionary ancestry which leads to retinal tears when people age. The imperfection, or defect, are observed because blood vessels and nerve cells evolved to place themselves in front of the retina, thereby interfering with its capacity to form sharp images. This is synonymous to taking pictures through foggy glasses. This was the Darwinian explanation of blind spots, which is also attributed to natural selection. It was further claimed that evolution has to start with what is already there, modifying it but not really redesigning it. Therefore, even the eye bears clues of the fact that, even with its optical perfections, it has its origins in the process of blindness through natural selection (Miller, 2000). However, studies conducted many years after the Darwinian era have shown that natural black spots take care of themselves in the sense that they are not noticeable when a person uses both eyes. Even when an observer only uses one eye, they rarely detect the blind spot because it is filled in by the brain, which speculates what the missing information may be. One of the significant functions of the brain is integrating disparate sensory information and creating the perception of a logical whole from them. When the brain faces incomplete information, it compiles the available data and establishes, in a manner similar to making the best guess, what is missing. When applied to the phenomenon of the blind spot, this concept of making the best guess is known as filling in. For example, when an observer views a vertical line with one eye in a manner that part of it falls on his eye’s blind spot, the line will still seem to be continuous. In a more interesting experiment, even if the line actually had a gap in it and it falls on the blind spot, the brain would fill in the line’s non-existent segment, making it appear continuous. The filling in phenomenon, responsible for completing missing information across the artificial and natural scotomata as well as the physiological blind spot, occurs generally under a selection of conditions (Pessoa & Weerd, 2003). When objects pass through the blind spot, filling in occurs as a result of perceptual constructions that are achieved synonymously to the amodally and modally perceived completion of objects that are not in the blind spot. Evidence exists for similar completion mechanisms in visual analysis. A tested demonstration of perceptual filling-in entails stabilized images on the retina by using special lenses. It can also be under prescribed circumstances of steady fixation. Two theories, the symbolic filling-in and isomorphic filling-in have been proposed to explain the concept of filling-in completion (Pessoa & Weerd, 2003). In the isomorphic filling-in theory, it is assumed that perception is based on the representation of an image which is held in a two-dimensional arrangement of neurons. The neurons are arranged retinotopically, which implies that signals of color disperse in every direction apart from across the boarders that are formed via contour activity. This process is also assumed to be synonymous to physical diffusion, where the act as barriers of diffusion to the brightness and color of the signals. The alternative theory, symbolic filling-theory, states that the information of an image is transformed into an oriented aspect depiction at the cortical level. Color and form are drawn from a later stage (Pessoa & Weerd, 2003). This does not occur as an isomorphic filling-in process’ result but rather, a proto-object’s or object’s result. As per the isomorphic filling-in theory, the activity of cells with receptive fields pointing at the surface represent color. Symbolic filling-in presents perceptual filling-in as basically filling-in information that is not provided directly to the input. This information that is not provided is extrapolated or inferred from visual data obtained another area of the visual field. Apart from filling-in theories, there are various instruments for the diagnosis and treatment of disorders and diseases that affect the retina (Bainbridge, Smith & Viswanathan, 2008). The retina is examined by the use of fundus photography and ophthalmoscopy. More recently, the use of adaptive optics has been employed to image individual cones and rods in the human retina. A non-invasive measure known as electroretinogram is used to measure the electrical activity of the retina. Another relatively new technology, known as optical coherence tomography, is also a non-invasive technique which enables one to get a three-dimension high resolution or volumetric cross-sectional tomogram of the fine structure of the retina with histologic quality. References Bainbridge, J., Smith, A., & Viswanathan, A. (2008). Effect of gene therapy on visual function in Lebers congenital amaurosis. The New England Journal of Medicine 358(21), 2231–2239. García-Fernández, M., Castro-Navarro, J., & Bajo-Fuente, A. (2013). Unilateral recurrent macular hole in a patient with retinitis pigmentosa: a case report. Journal Of Medical Case Reports 7(1), 1-4. Kolb, H. 2003. How the retina works. American Scientist, 91(2), 28-35. Miller, K. (2000). Finding Darwins God. New York: Cliff Street Books. Pessoa, L., & Weerd, P. (2003). Filling-In: form perceptual completion to cortical recognition. Oxford: OUP Riegal, R., & Hakola, S. (2000). Illustrated Atlas of Clinical Equine Anatomy and Common Disorders of the Horse. Ohio: Equistar Publication. Shepherd, G. (2004). The synaptic organization of the brain. New York: OUP. Sudhakar, J., Natarajan, S., & Parikumar, P. (2013). Choice of cell source in cell based therapies for retinal damage due to age related macular degeneration: A review. Indian Journal of Ophthalmology 39(4), 449-539. von der Heydt, R., & Friedman, H. (2003). From perceptual completion to cortical reorganization. Oxford: OUP. Read More
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