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Editorial Reviews. Review. `Excellent a book that can be read with benefit by students in Visual Development (Perspectives in Vision Research) Kindle Edition. by Nigel W. Daw (Author).
Table of contents
- Plasticity in the Human Visual Cortex: An Ophthalmology-Based Perspective
- BioMed Research International
It is the ability of the brain to be shaped by experience and, in turn, for this newly rewired brain to facilitate the embracing of new experiences [ 1 ]. Although plastic changes in the brain can occur at any time point in the life cycle, they occur with varying degrees of success [ 5 ]. The explanation for these findings is that there are transient connections that go through a process of Hebbian competition in which stronger input signals are favoured and unused connections are pruned permanently [ 6 ].
Plasticity in the Human Visual Cortex: An Ophthalmology-Based Perspective
In other words, Hebbian competition works during normal early development to tune the connections to visual cortical neurons, eliminating nonefficient inputs and balancing the input from the two eyes [ 6 ]. The connectivity of geniculate-striate and striate-extrastriate networks is reduced, and both feedforward and feedback interactions are affected equally [ 7 ]. This is in apparent agreement with the traditional view in which the visual system is assumed to be hard-wired long before adolescence.
However, it has been shown that visual acuity can be improved in amblyopic adults through practicing a perceptual learning task repeating a demanding visual task, such as contrast detection, to improve performance [ 8 — 11 ]. The improvement of visual function persisted after treatment, showing that the learning was more than a temporary adaptation, thus providing evidence for cortical plasticity in human adults [ 8 — 11 ]. Improvement of visual function after a perceptual learning task was also demonstrated in participants with normal or corrected to normal visual acuity [ 12 ].
Video game playing with the amblyopic eye has also been shown to induce cortical plasticity and improve spatial vision in amblyopic adults [ 14 ], providing further evidence of plasticity in the adult visual system. It is likely that some cortical connections are inhibited rather than pruned and that, for some visual functions, there is visual plasticity in adolescence and adulthood [ 1 ].
These functionally dormant connections appear to provide the substrate for rapid readaptation in adulthood [ 15 ]. Because activity in this area is implicated in visuospatial imagery, the mentioned changes were attributed to the visualization of the movements and ball trajectories involved in juggling.
This study provides evidence for training related structural changes in healthy adult human brain, and, more specifically, in a visual area. Thus, plastic changes have been seen in the adult human cortex not only in association with overt lesions but also in healthy individuals as a function of experience and training [ 17 ].
In conclusion, the majority of studies point to the existence of plasticity in adult human visual cortex in response to visual loss in one or both eyes, and there is also a role for visual cortical plasticity in the absence of visual loss. Functional MRI studies have shown that perceptual learning and voluntary attention can bias visual selection and modulate neuronal response in human adult visual cortex [ 18 ].
- Plasticity in the Human Visual Cortex: An Ophthalmology-Based Perspective.
- Champions #45!
Adaptation is a form of rapid plasticity and leads to strong perceptual effects. By enhancing the visual processing of relevant information and reducing processing of ignored or redundant stimuli, learning, attention, and adaptation shape the landscape of our visual experiences [ 18 ]. A behavioural manifestation of plasticity in humans is the perceptual learning, a process in which practicing a challenging task repeatedly leads to significant and persistent improvements in visual performance over time [ 15 ].
The effects of perceptual learning have been well documented beyond the critical period of development in visually normal adults [ 5 ]. It has been reported that perceptual learning elicits plastic changes in the visual system, as shown by changes in V1 activation during fMRI [ 5 ]. To evaluate this form of plasticity, neural activity has been measured after participants were intensively trained in a visual task, such as texture discrimination and detecting stimuli orientation [ 19 ].
Retinotopic increase in blood oxygenation level-dependent signal BOLD response after learning provides empirical support that learning favours activity in the visual cortex in order to increase the discrimination of trained targets from background flankers [ 20 ]. The improvement that has occurred in adults as well as in juveniles is specific to the trained eye and develops only across multiple days of training [ 15 ].
Training can improve the discrimination of small differences in the offset of two lines Vernier acuity and the ability to discriminate orientation, segregate elements of the visual scene, and detect small differences in the depth of two targets [ 21 ]. The recruitment of larger assemblies of interconnected neurons or sharpening of cell sensitivity to relevant features of the trained stimulus may produce a higher total neural response associated with increased regionally specific BOLD response [ 19 , 22 ].
Perceptual learning in the visual system appears to be mediated primarily by changes in the response strength or the tuning of individual neurons, rather than large-scale spatial reorganization of the cortical network as found in the auditory and somatosensory systems [ 15 ]. More recently, in line with the benefits of perceptual learning, video games have been shown to improve perception, visuomotor coordination, spatial cognition, and attention, illustrating how an action game play can reshape the adult brain [ 2 , 23 ].
These plastic changes have been shown to be long lasting, remaining even 2 years after the end of intervention [ 23 ]. Indeed, it has been shown that complex stimuli are typically not presented at a single retinal location, so their learning is nonspecific to retinal locations and does therefore occur in higher brain areas [ 12 , 24 ].
Top-down projections from the frontal eye field to visual area V4 can enhance stimulus-related activity, which emphasizes the importance of high level mechanisms [ 21 , 25 ]. However, the existence of intrinsic plasticity in V1 is controversial, as revealed by difficulties in identifying low-level processes that are context independent, truly local, and not the indirect result of higher level modulation [ 26 , 27 ]. Additionally, there is increasing evidence for generalization of perceptual learning in conditions previously shown to be specific, such as the training of a different task at a different location allowing the transfer of the feature learning to the second location [ 12 , 28 ].
This suggests that perceptual learning does indeed involve higher nonretinotopic brain areas that enable location transfer [ 12 , 28 ]. Not only the retinotopic early visual cortex, but also the nonretinotopic higher brain areas are involved in visual discrimination [ 29 , 30 ]. Thus, visual perceptual learning seems to involve more than the visual cortex; that is, it involves nonretinotopic higher brain areas, engaged in attention and decision-making [ 12 , 29 , 30 ].
Perceptual learning shows a strong interaction with attention, indicating that it is under top-down control [ 21 ]. Attention is necessary for the consolidation of memory and virtually all other forms of learning. One of the consequences of learning is to release performance from attentional control, leading to an automatization of the task [ 21 , 31 , 32 ].
Therefore, it is important to consider the influence of attention when evaluating manifestations of visual plasticity such as perceptual learning. When processing a visual scene, there are mechanisms for selecting relevant and filtering out irrelevant information [ 33 ]. This function is accomplished by the attentional system. Two basic sources determine attentional processing: Although these top-down influences originate in the frontal lobe, they primarily modulate neural activation in striate and extrastriate visual areas [ 33 ]. Spatial attention seems not only to enhance processing at attended locations but also to suppress processing at nonattended locations [ 35 ].
When more attentional capacity is allocated at central fixation, there is a reduction of cortical activation for task irrelevant peripheral stimuli [ 36 ]. The attentional effect increases from V1 to V4, along the hierarchy of visual areas [ 37 ]. Top-down signals related to spatially directed attention may be generated by a network of areas in frontal and parietal cortices [ 38 ]. Sensory activity in the brain is modulated by attention, memory, and even the intention to act [ 39 ]. As an example, in experiences with monkeys, the baseline firing rate of neurons in lateral intraparietal area increases when the animal is working in a task in which it expects that a relevant visuospatial stimulus will appear [ 39 ].
Likewise, imaging studies have shown that attention modulates visual responsivity in the human brain [ 39 ]. The visual system modifies the retinal image so as to maximize its usefulness to the subject, often originating nonveridical percepts [ 40 ]. The visual system does not provide a copy of the external visual world; in contrast, it optimizes processing resources.
Attention is an example of this perceptual optimization [ 41 ]. Visual attentional load also influences plasticity in the human motor cortex, suggesting that the top-down influence of attention on plasticity is a general feature of the adult human brain [ 42 ]. In sum, attention acts upon sensory signals at many levels to construct a selective representation of visual space [ 39 ]. Looking at a pattern for a short time typically decreases sensitivity to that pattern and results in a bias in the appearance of other patterns [ 43 ].
Ordinary visual adaptation is considered to occur with brief exposures and their consequent aftereffects [ 44 , 45 ]. We will refer to the ordinary adaptation as short-term adaptation. However, a process of long-term adaptation can also be found. In this case, a causal effect may be permanent, and the changes may be given by the structural plasticity following learning processes.
In short-term adaptation, there are changes in sensitivity over short time intervals, ranging from milliseconds to minutes [ 43 ]. A classic example is light adaptation. Changes occur so rapidly that structural plasticity is not able to explain it.
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In long-term adaptation, there are sensitivity adjustments that occur during much longer times, from hours to weeks or even years [ 43 ]. These long-term adjustments have been described for color vision, contrast sensitivity, and perceived distortion blur [ 45 — 47 ]. For example, when the senescent crystalline lens is removed in cataract surgery, the changes in color appearance follow a very long time course and are not entirely normal even months after surgery [ 43 ]. Adaptation has also been shown to occur in natural visual environment, to stimuli that reflect the type of images that observers encounter in everyday viewing [ 43 ].
Many aspects of natural vision are routinely regulated by adaptation. Thus, the way we perceive colors, faces, and scenes is strongly dependent on the specific environments we are adapted to [ 43 ]. Adaptation also occurs when there are changes in the observer, rather than in the environment, because of eye injury, cataract surgery, or simply a new pair of glasses.
For example, adaptation to long-term defocus myopia and hyperopia leads to improvements in visual acuity [ 48 ]. However, the relationship between adaptation and learning is not entirely clear. The visual system has a large variety of adjustments, and it is difficult to define adaptation in a way that it can be clearly distinguished from other forms of plasticity [ 43 ]. Perceptual learning usually produces improvements in discrimination, whereas adaptation is a more immediate loss in sensitivity after exposure to a stimulus [ 49 — 51 ].
Learning can be distinguished from adaptation because it mainly reflects changes in performance rather than in appearance and facilitation instead of suppression. It has a longer time course and changes how the visual system interprets neural signs and not the strength of those signals [ 51 ].
Like adaptation, learning can also change the appearance of patterns, and like learning, adaptation can facilitate some discriminations [ 43 ]. In fact, the process of adaptation itself might contain forms of learning [ 45 ]. With prolonged experience, adaptation is transferred to a long-term memory that can be instantly engaged or disengaged, leaving no aftereffects the existence of an aftereffect is thought to indicate the presence of an adaptation process or a transient recalibration process [ 45 ]. Both short- and long-term adaptation can occur from the blur resulting from the optics of the eye, including low- and high-order aberrations [ 52 ].
In addition, compensatory adjustments of adaptation tend to mask sensitivity losses that appear with disease, so that observers may not be aware of developing visual impairment [ 43 ]. Similarly, compensation for age related losses implies that the process of adaptation remains largely functional in the senescent visual system [ 43 , 53 , 54 ]. Thus, adaptation may be important for matching vision to the optical quality of the eye throughout life. In conclusion, the manifestations of visual plasticity in the human visual cortex include perceptual learning and adaptation, under the influence of attention for resource optimization.
These mechanisms are important not only to improve the treatment of ophthalmic disorders but also to understand the crosstalk between the optical system and the brain. Two types of neuroplasticity can be distinguished, although their frontiers are not well defined: Synaptic plasticity refers to changes in synaptic activity, leading to changes in synaptic efficacy and in behaviour [ 55 ]. Structural plasticity refers to changes in neuronal morphology axons, dendrites, and dendritic spines , suppression and creation of synapses, and genesis of new neurons and neurites.
Repetitive electrical stimulation of animal nerve fibers can induce an immediate and prolonged increase in synaptic transmission. This effect is called long-term potentiation LTP [ 56 , 57 ]. In contrast, low-frequency stimulation typically induces long-term depression LTD. These synaptic mechanisms play a role in many forms of learning and memory as well as neuronal development and circuit reorganization [ 57 ]. Despite the fact that most of the mechanisms referred in the following paragraphs are active during the early phases of visual system development, we have included them in this review since some of them are being increasingly recognized as potential sources of plasticity reinstatement in the adult visual cortex.
The experience-dependent maturation of GABA-mediated inhibition during development establishes the beginning of the critical period for plasticity in the visual system [ 58 ]. After monocular deprivation during early life in transgenic animals lacking one isoform of GABA, no variation of visual cortex responsiveness was observed [ 59 ]. Therefore, a reduction of inhibitory transmission in early life halts the onset of the critical period for visual cortex plasticity [ 58 ].
The limited plasticity in the adult visual cortex can be enhanced by previous visual deprivation, which is associated with a loss of GABA receptors, and reduced by GABAergic modulators [ 60 ]. It has been shown that a brief reduction of GABAergic inhibition in the brains of rats is able to reopen a window of plasticity in the visual system a long time after the normal closure of the critical periods [ 5 ]. The effects caused by early sensory experience in the remodeling of visual cortical circuitries are preserved throughout life by the appearance of molecular factors in the extracellular milieu that restrict plasticity [ 61 ].
The establishment of neuronal connectivity may be, at least in part, under control of structural factors such as myelin-associated proteins NgR, PirB and chondroitin sulphate proteoglycans CSPGs , which all are inhibitory for axonal sprouting [ 62 ].
BioMed Research International
Other important players are the major modulatory systems in the brain, that is, adrenaline, noradrenaline, dopamine, acetylcholine, and serotonin. The adrenergic system has a significant impact on plasticity [ 57 ]. Similarly, a single dose of the serotonin reuptake inhibitor citalopram enhances and prolongs plasticity [ 57 ]. Calcium channel blockade by nimodipine and dopamine receptor blockade by sulpiride or haloperidol diminish a form of plasticity [ 57 ]. Likewise, in the face of compromised cholinergic input to the visual cortex of rats, the ability to perform fine discriminations is impaired, whereas the ability to perform previously learned discrimination remains unaffected, which suggests that acetylcholine facilitates plastic changes in the sensory cortices [ 63 , 64 ].
Functionally, acetylcholine contributes to plasticity in V1 and is involved in the alteration of tuning properties and map organization in other areas of cortex [ 64 ]. Global dopaminergic activation has heterogeneous effects on plasticity. A certain amount of activity of the dopaminergic system is necessary for the induction of plasticity. However, higher dopaminergic activity results in nonlinear effects on plasticity, depending on the dosage, the plasticity induction protocol, and the balance of D1 versus D2 receptor activation [ 57 ]. These mediators regulate complex functions of the central nervous system such as different forms of brain plasticity, cognitive processes, and behavior [ 62 ].
Growing experimental evidence indicates that chromatin structure is highly dynamic within the nervous system and that it is recruited as a target of plasticity-associated signal transduction pathways [ 62 , 65 , 66 ]. These mechanisms seem to be important also in the mature system, as increasing acetylation of histones by treatment with histone deacetylase inhibitors effectively reactivates plasticity in the adult visual system [ 67 , 68 ].
Another mechanism involves CREB a transcription factor activity. CREB activity is induced following monocular deprivation in juveniles and declines with maturation of the visual cortex [ 69 ]. In addition to the function of transcription factors and modifications of chromatin structure, growing experimental evidence supports a critical role for short noncoding RNAs microRNAs which interact with and control translation of mRNA targets, in the regulation of gene expression patterns at the basis of plastic phenomena in the mammalian nervous system [ 70 ].
Experience-dependent brain plasticity is consolidated by sleep. This effect may be mediated through the phosphorylation of protein synthesis regulators and the translation of key plasticity-related mRNAs [ 71 ]. Sleep promotes cortical mRNA translation, and interruption of this process prevents the consolidation of a form of cortical plasticity in vivo [ 71 ]. This way, although experience is required for the transcription of key plasticity-related mRNAs, their translation into protein requires sleep, which may represent a sleep-dependent mechanism that converts labile plastic changes into more permanent forms [ 71 ].
The brain can perceive, detect, discriminate, and recognize consciously only those pieces of information which reach a critical level, which can be at least indirectly related to bioenergetics and neuronal mitochondrial activity [ 72 ]. Representation of various sensory information can become conscious in our minds only if it reaches a threshold level of energy and duration [ 72 ].
Neurotransmitters dopamine and serotonin which regulate different forms of brain plasticity, as explained previously can reversibly control mitochondrial motility and distribution. Dopamine displays a net inhibitory effect on mitochondrial movement, but serotonin has a stimulatory effect [ 72 ]. There is a direct coupling between mitochondrial organization-movement-activity and synaptic activity [ 73 ]. Extension or movement of mitochondria into dendritic axons that are located far from the cell protrusions correlates with the development and morphological plasticity of dendritic spines [ 74 , 75 ].
Molecular manipulations that reduce dendritic mitochondria lead to loss of synapses and dendritic spines [ 75 ]. In contrast, increasing dendritic mitochondrial content or mitochondrial activity enhances the number and plasticity of synapses [ 75 ]. This way, the dendritic distribution of mitochondria can be both essential and limiting for the support of synapses [ 13 , 75 , 76 ]. Moreover, mitochondrial gene upregulation has been observed following synaptic and neuronal activity [ 75 ].
Mitochondrial dysfunction leads to alterations in ATP production and cytoplasmatic calcium concentrations, reactive oxygen species, and nitric oxide production [ 77 ]. Mitochondria dysfunction has been implicated in the defective processes of plasticity occurring in schizophrenia [ 77 ]. Animals under environmental enrichment cages containing toys that are frequently changed develop an increase in brain weight and cortical thickness, including the occipital cortex.
Similarly, grey matter macrostructure changes have been reported in humans after juggling training, aerobic exercise, and intense language studies [ 16 , 79 — 82 ].
Volume and thickness changes are specific to those brain regions that are functionally relevant for the trained task [ 83 ]. Neurochemical changes consisting of an increase in N-acetylaspartate available almost only in neurons were detected with magnetic resonance spectroscopy in adult men after a period of navigation training [ 79 ]. However, the existence of structural plasticity in the human primary visual cortex is controversial. It has been argued that both the location and apparent time course of structural changes vary substantially between studies, despite the similarity of the training paradigms [ 84 ].
Moreover, the reliability of voxel-based morphometry as a method for investigating structural brain changes has been questioned, as well as the biological substrate of the reported structural changes [ 84 , 85 ]. In addition, studies involving cortical plasticity in the context of retinal lesions in humans have important limitations, as it is not possible to exclude spared retinal regions or changing borders in the absence of histological examination [ 85 , 86 ].
It is also possible that V1 responses in the presence of central retinal lesions are due to activation via extrastriate cortex or subcortical structures [ 85 , 87 ]. Despite the absence of large-scale structural remodeling later in life, the reorganization of cortical connections in terms of growth and loss of dendritic spines may be the structural substrate for experience-dependent plasticity [ 62 ]. In conclusion, the biological background of visual plasticity involves several mechanisms which are still incompletely characterized and controversial Figure 1.
Understanding these mechanisms will be important for a better recognition of the occurrence of plasticity and for disease treatment. As stated by Wandell and Smirnakis [ 85 ], it is not worth having a debate as to whether the brain is plastic or not: It is more important to study the conditions under which each system is stable or plastic.
Retinitis pigmentosa RP consists in an inherited progressive degeneration of photoreceptors, starting at the midperipheral rod cells and advancing towards the central retina cone cells , with a subsequent deterioration of the retinal pigment epithelium. Retinal disorders also pose a threat worldwide. Age-related macular degeneration AMD refers to damage to the area of the retina responsible for sharp central vision.
It is the third most common global cause of blindness, accounting for approximately 8. In the United States, there are approximately 1. The risk declines if one stops smoking, to the point that after 20 years of not smoking former smokers have about the same level of risk as nonsmokers. Possible mechanisms of damage linked to smoking include depressed levels of antioxidants, reduced oxygen, and altered blood flow. The effect of diet on AMD risk shares some of the same components as cataract; specifically, low-level antioxidant levels may heighten the chances of developing the disease. Obesity and high blood pressure, fat intake, and cholesterol levels also appear to increase AMD risk, but the specifics are not yet clear.
Family studies imply a genetic link, which is supported by three papers published in the 15 April issue of Science and a fourth published in the 2 May issue of Proceedings of the National Academy of Sciences. The link between those two has been puzzling in the past, and I think there are new studies that suggest that some of the genes that play a role in the development of macular degeneration are genes that may be involved in inflammation and our immune response. In early , the four teams independently associated AMD with a gene coding for complement factor H, an inflammatory component.
I expect that we will find out a great deal more about the so-called molecular pathology of AMD as a result of this discovery. Further, up to six regions within the genome have been implicated as potentially harboring AMD genes, and a second gene was reported in the November Human Molecular Genetics. Retinal damage is also a hallmark of diabetic retinopathy, which blinds about 5 million people worldwide. Centers for Disease Control and Prevention estimates that Duration of diabetes and its control affect risk of diabetic retinopathy, and approximately 5.
With diabetes rates increasing, in part due to increasing obesity, diabetic retinopathy can be expected to become more prevalent. Dietary and genetic factors may also affect its development, as may high blood pressure and high cholesterol. Retinal vein blockages associated with high cholesterol, high triglycerides, and high blood pressure can create capillary-bursting pressure. The tissue then becomes hypoxic, or insufficiently oxygenated. Retinal hypoxia also occurs in diabetes when the capillary network dies through mechanisms that are not completely clear. Hypoxia triggers production of vascular endothelial growth factor, which promotes formation of new blood vessels, but the process is disorganized.
Further, the poorly built new vessels leak, as may existing blood vessels. Ultimately, the retina detaches from the underlying layers, and vision is lost. Distinct from this category, trachoma accounts for an additional 3. Trachoma is the most common infectious cause of vision loss and affects approximately 84 million people, primarily in remote rural areas of Africa, Asia, Central and South America, Australia, and the Middle East.
This disorder arises from repeated infection by Chlamydia trachomatis bacteria that are spread by close contact with an infected person or by flies. After numerous infections, eyelid scarring turns the eyelashes inward, and they rake against the cornea, a condition called trichiasis. The irritation scars the cornea and eventually renders it opaque. Infection typically starts in childhood, although the blinding effects do not occur until well into adulthood. The SAFE strategy utilizes lid surgery S , antibiotics A to treat active infections, facial cleanliness F , and environmental changes E geared toward improving sanitation and access to clean water.
A review of the SAFE strategy published in the June issue of The Lancet Infectious Diseases found strong support for the use of antibiotics and surgery in warding off infection and blindness, although the evidence for face washing and environmental improvements was weaker. Onchocerciasis, also known as river blindness, is caused by Onchocerca volvulus , a parasite transmitted by blackflies in riverside areas.
When a blackfly bites, a juvenile form of the parasite enters the body. Once mature, females release high numbers of larvae that migrate to the skin and eyes. Associated lesions form in all eye tissues except for the lens, and lead to inflammation, bleeding, secondary infections, and eventually blindness. More than 17 million people are infected with the parasite, approximately , people are visually impaired as a result, and another , are blind.
Fear of infection prevents arable riverside land from being used, and local economic growth stagnates. Global efforts at halting river blindness started with effective vector control efforts in , and ongoing community-based treatment with ivermectin, an antiparasite medication, began in The disease has been reduced in most areas and may be eradicated from Latin America by Among children, cornea-clouding vitamin A deficiency is the most common cause of preventable childhood blindness. Poor night vision is the key symptom of the very early stages of the corneal damage preceding blindness.
At this stage, children can retain their vision with repeated doses of vitamin A. In late-stage vitamin A deficiency, the cornea becomes very white and cloudy, and vision loss is irreparable; cornea transplants are impossible because the tissue becomes too damaged. In addition to supplying vitamin A supplements, health organizations also strongly promote vitamin A—rich diets. Breastfeeding provides ample vitamin A to babies, and older children and adults receive the nutrient through garden produce and supplemented foods.
The Right to Sight, a program instituted in by the WHO and the International Agency for the Prevention of Blindness, builds upon previous programs, dovetails with pre-existing efforts of many organizations, identifies remaining regional and national needs, and provides a framework for filling gaps. Through Vision , a coordinated effort is under way to eliminate preventable blindness by by increasing awareness of eye disease, garnering resources for prevention and treatment, controlling major causes of avoidable blindness, training ophthalmologists and other eye care personnel to diagnose and treat the diseases specific to certain regions, and providing these specialists with necessary technology and infrastructure.
Other organizations also have carried out large-scale international programs. For example, Lions Clubs International, a service organization with a long history of combating low vision and blindness, instituted the worldwide SightFirst program with three major goals: On a national level, the U. Healthy Vision is part of Health People , a national program to improve the health of Americans, and seeks to promote regular eye examinations for adults and children, vision screening for preschoolers, and injury prevention.
The National Eye Health Education Program has a more specific focus, encouraging early detection and treatment of glaucoma and diabetic eye disease, and providing education about treatment for low vision. This program provides materials that communities can use to educate the public about eye disease and the importance of early detection and treatment.
A critical gap in eliminating preventable blindness and low vision is delivery of health care. Without access to health care, opportunities are missed to diagnose problems early when treatment is most likely to be successful. Access to health care is a problem in many nations, including the United States.
Stout offers diabetes as an example of the United States falling short in this regard. Cataract, the leading cause of blindness worldwide, arises from a combination of factors including genetics, age, and environmental exposures. Though largely treatable, poor access to health care leaves many around the world to suffer. Top to bottom An acute sudden-onset cortical cataract in a person with type 1 diabetes; a hypermature age-related cataract; a white congenital cataract.
Flies attracted to eye secretions are one way trachoma is transmitted above.