Artificial Eye
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01-03-2009, 01:31 PM


Artificial Eye

The retina is a thin layer of neural tissue that lines the back wall inside the eye. Some of these cells act to receive light, while others interpret the information and send messages to the brain through the optic nerve. This is part of the process that enables us to see. In damaged or dysfunctional retina, the photoreceptors stop working, causing blindness. By some estimates, there are more than 10 million people worldwide affected by retinal diseases that lead to loss of vision.

The absence of effective therapeutic remedies for retinitis pigmentosa (RP) and age-related macular degeneration (AMD) has motivated the development of experimental strategies to restore some degree of visual function to affected patients. Because the remaining retinal layers are anatomically spared, several approaches have been designed to artificially activate this residual retina and thereby the visual system.

At present, two general strategies have been pursued. The "Epiretinal" approach involves a semiconductor-based device placed above the retina, close to or in contact with the nerve fiber layer retinal ganglion cells. The information in this approach must be captured by a camera system before transmitting data and energy to the implant. The "Sub retinal" approach involves the electrical stimulation of the inner retina from the sub retinal space by implantation of a semiconductor-based micro photodiode array (MPA) into this location. The concept of the sub retinal approach is that electrical charge generated by the MPA in response to a light stimulus may be used to artificially alter the membrane potential of neurons in the remaining retinal layers in a manner to produce formed images.
Some researchers have developed an implant system where a video camera captures images, a chip processes the images, and an electrode array transmits the images to the brain. It's called Cortical Implants.



The Visual System
The human visual system is remarkable instrument. It features two mobile acquisition units each has formidable preprocessing circuitry placed at a remote location from the central processing system (brain). Its primary task include transmitting images with a viewing angle of at least 140deg and resolution of 1 arc min over a limited capacity carrier, the million or so fibers in each optic nerve through these fibers the signals are passed to the so called higher visual cortex of the brain

The nerve system can achieve this type of high volume data transfer by confining such capability to just part of the retina surface, whereas the center of the retina has a 1:1 ration between the photoreceptors and the transmitting elements, the far periphery has a ratio of 300:1. This results in gradual shift in resolution and other system parameters.
At the brain's highest level the visual cortex an impressive array of feature extraction mechanisms can rapidly adjust the eye's position to sudden movements in the peripherals filed of objects too small to se when stationary. The visual system can resolve spatial depth differences by combining signals from both eyes with a precision less than one tenth the size of a single photoreceptor.
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thanks ..for this report[/color][/size][/font]
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The Artificial Eye
We hope this information will help answer any questions you may have regarding artificial eyes. Please feel free to ask any further questions when you see Mr Cheung when you attend the hospital next time. This information sheet is for your general information only and is not intended to be a substitute for a proper consultation by a trained medical professional.
Introduction
This handout is intended to be of use for patients about to undergo or have undergone artificial eye surgery (Evisceration/Enucleation). It refers to the removal of the natural eye (the eye with which you were born) and rehabilitation of the socketto make it look cosmetically pleasing. We understand that the removal of an eye can be emotionally and psychologicallychallenging for a patient. Our aim is help the patient and his or her family come to grips with this difficult stage in their life.For this reason, we have a team professionals who are ready to answer any questions and offer guidance. Please feelfree to contact us to discuss any questions or queries you may have about artificial eye surgery.Note: This handout does NOT refer to the experimental vision systems which are being researched to allow blind orpartially sighted patient to see. It is envisaged that it will be many years before these will be available for generalised use.IndicationsThere are three main reasons why one!s natural eye needs to be removed.1. If the natural eye becomes blind and painful. Its removal can give the patient welcome comfort and relief. This is usually only done when most other treatments have failed2. If the natural eye becomes blind and looks cosmetically poor. For example the natural eye may look very scarred,start to shrink in size and the cornea (clear window at the front of the eye) may turn white.3. If the natural eye becomes dangerous e.g. for cancer of the eye- Is comfortable- Shows good movement- Looks normal to the observer- Is easy to look after
The operationThere are essentially two types of operation for removalof the eye: Evisceration and Enucleation.Evisceration involves removal of the clear window atthe front of the eye (cornea) & the core of the eye.Enucleation- involves removal of the entire eyeball.In both types of operation, the outer coverings of theeyeball are then sutured together, usually to cover anorbital implant, so that the cavity of the socket isshallower and lined with the pink membrane(conjunctiva). Most patients nowadays undergo anevisceration since it is quicker, thought to offer bettermotility and has a lower rate of long term problems.However enucleations are still performed in certain casese.g. for melanoma of the eye, a type of cancer where oneneeds to be sure of complete removal of the entire eye.Although both operations are usually performed undergeneral anaesthesia (patient asleep and ventilated), if theanaesthetist considers that general anaesthesia is toodangerous e.g. if the patient has severe lung or heartdisease, surgery can be performed quite comfortablyunder local anaesthesia, often with a mild sedative torelax the patient
.Early period after surgery
A pressure dressing is applied to the socket for the firstweek to try to reduce the postoperative swelling. Contraryto belief, usually the patient is very comfortableimmediately after surgery. A course of antibiotic tablets isusually prescribed with anti-inflammatory medication(ibruprofen or diclofenac). The patent is then reviewedusually one week after surgery and the dressing isremoved. A clear plastic disc called a conformer is ofteninserted into the cavity of the socket at the time of surgeryto help the socket attain the correct shape.At 6 weeks to 8 weeks, the patient is then usually seenby an ocular prosthetist (sometimes called an ocularist).This is someone who is trained in making artificial eyes.A mould of the cavity of the socket is made so that a newcustom made artificial eye known to match the patient!sother eye can be manufactured. The manufacture of anew cosmetic shell can take a couple of months and aAfter 3 monthsThe patient is advised on how to look after the artificialeye and socket by the ocular prosthetist. It is usuallyadvisable to remove the artificial eye from time to timee.g. at night or weekly and to clean it. Your ocularprosthetist will be able to advise you about this. Somepatients who are uncomfortable with handling thecosmetic shell, may leave the shell in all the time
.Potential complications and problems
The risk of things going wrong with artificial eye surgery isextremely low but as with any type of surgerycomplications and problems can occur.InfectionWith artificial eye surgery, the most serious complicationwhich can happen early on following surgery is infection.This usually responds very well to antibiotics.Implant extrusion/exposureAs stated above an orbital implant is usually implanteddeep into the socket at the time of removing the eye. Themain role of the orbital implant is compensate for the lossin volume from removing the natural eye therefore fillingout the socket so that the cavity of the socket isshallower. This means the artificial eye can be thinnerand lighter, thus allowing better movement and bettercomfort for the patient. Very, very rarely, the orbitalimplant may start become exposed and may even workits way out. This may require further surgery to rectify.Imperfect appearance/comfortThe vast majority of patients are very very happy with theappearance, movement & comfort of their artificial eye.However, a tiny proportion of patients request improvedmotility, a better appearance or greater comfort. This canoften be easily achieved but may require additionalsurgery.Long term changesAfter many, many years of wearing an artificial eye, thepatient!s socket may start to alter slightly sometimesresulting in an imperfect appearance, comfort ormovement of the artificial eye. For example, the artificialeye may start to look sunken, the upper lid may start todroop or the lower lid may start to sag. If the patientwishes, further procedures may be performed to improvematters.

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INTRODUCTION
The retina is a thin layer of neural tissue that lines the back wall inside the eye. Some of these cells act to receive light, while others interpret the information and send messages to the brain through the optic nerve. This is part of the process that enables us to see. In damaged or dysfunctional retina, the photoreceptors stop working, causing blindness. By some estimates, there are more than 10 million people worldwide affected by retinal diseases that lead to loss of vision.
The absence of effective therapeutic remedies for retinitis pigmentosa (RP) and age-related macular degeneration (AMD) has motivated the development of experimental strategies to restore some degree of visual function to affected patients. Because the remaining retinal layers are anatomically spared, several approaches have been designed to artificially activate this residual retina and thereby the visual system.
At present, two general strategies have been pursued. The “Epiretinal” approach involves a semiconductor-based device placed above the retina, close to or in contact with the nerve fiber layer retinal ganglion cells. The information in this approach must be captured by a camera system before transmitting data and energy to the implant. The “Sub retinal” approach involves the electrical stimulation of the inner retina from the sub retinal space by implantation of a semiconductor-based micro photodiode array (MPA) into this location. The concept of the subretinal approach is that electrical charge generated by the MPA in response to a light stimulus may be used to artificially alter the membrane potential of neurons in the remaining retinal layers in a manner to produce formed images.
Some researchers have developed an implant system where a video camera captures images, a chip processes the images, and an electrode array transmits the images to the brain. It’s called Cortical Implants.
VISUAL SYSTEM
The human visual system is remarkable instrument. It features two mobile acquisition units each has formidable preprocessing circuitry placed at a remote location from the central processing system (brain). Its primary task include transmitting images with a viewing angle of at least 140deg and resolution of 1 arc min over a limited capacity carrier, the million or so fibers in each optic nerve through these fibers the signals are passed to the so called higher visual cortex of the brain.
The nerve system can achieve this type of high volume data transfer byconfining such capability to just part of the retina surface, whereas the center of the retina has a 1:1 ration between the photoreceptors and the transmitting elements, the far periphery has aratio of 300:1. This results in gradual shift in resolution and other system parameters.
At the brain’s highest level the visual cortex an impressive array of feature extraction mechanisms can rapidly adjust the eye’s position to sudden movements in the peripherals filed of objects too small to se when stationary. The visual system can resolve spatial depth ifferences by combining signals from both eyes with a precision less than one tenth the size of a single photoreceptor
THE EYE :
The main part in our visual system is the eye. Our ability to see is the result of a process very similar to that of a camera. A camera needs a lens and a film to produce an image. In the same way, the eyeball needs a lens (cornea, crystalline lens, vitreous) to refract, or focus the light and a film (retina) on which to focus the rays. The retina represents the film in our camera. It captures the image and sends it to the brain to be developed.
The macula is the highly sensitive area of the retina. The macula is responsible for our critical focusing vision. It is the part of the retina most used. We use our macula to read or to stare intently at an object. About 130 million photoreceptors in the outermost layer (as seen from the center of the eye) of the transparent retina transform local intensity and color patterns into chemical and electrical signals which trigger activity of the many different retinal
cells: horizontal cells, bipolar cells, amacrine cells, and ganglion cells.
The information is processed by astonishing amounts of serial and parallel pathways by in parts still unknown mechanisms. The information of these 130 million photoreceptors is compressed to the level of 1 million highly specialized GC-fibers. These 1 million fibers in the retina then form the optic nerve and transmit visual information to the visual cortex and its various areas in the back of the brain.
The area of the retina that receives and processes the detailed images—and then sends them via the optic nerve to the brain—is referred to as the macula. The macula is of significant importance in that this area provides the highest resolution for the images we see. The macula is comprised of multiple layers of cells which process the initial “analog” light energy entering the eye into “digital” electro-chemical impulses. The retina is the innermost layer of the wall of the eyeball. Millions of light-sensitive cells there absorb light rays and convert them to electrical signals. The signals are sent through the optic nerve to the brain, where they are interpreted as vision.
RETINA :
Light first enters the optic (or nerve) fiber layer and the ganglion cell layer, under which most of the nourishing blood vessels of the retina are located. This is where the nerves begin, picking up the impulses from the retina and transmitting them to the brain.
The light is received by photoreceptor cells called rods (responsible for peripheral and dim light vision) and cones (providing central, bright light, fine detail, and color vision). The photoreceptors convert light into nerve impulses, which are then processed by the retina and sent through nerve fibers to the brain. The nerve fibers exit the eyeball at the optic disk and reach the brain through the optic nerve. Directly beneath the photoreceptor cells is a single layer of retinal pigment epithelium (RPE) cells, which nourish the photoreceptors. These cells are fed by the blood vessels in the choroids.
RETINAL DISEASES :
There are two important types of retinal degenerative disease:
 Retinitis pigmentosa (RP), and
 Age-related macular degeneration (AMD)
They are detailed below.
Retinitis Pigmentosa (RP) is a general term for a number of diseases that predominately affect the photoreceptor layer or “light sensing” cells of the retina. These diseases are usually hereditary and affect individuals earlier in life. Injury to the photoreceptor cell layer, in particular, reduces the retina’s ability to sense an initial light signal. Despite this damage, however, the remainder of the retinal processing cells in other layers usually continues to function.RP affects the mid-peripheral vision first and sometimes progresses to affect the far-periphery and the central areas of vision. The narrowing of the field of vision into “tunnel vision” can sometimes result in complete blindness.
Age-Related Macular Degeneration (AMD) refers to a degenerative condition that occurs most frequently in the elderly.AMD is a disease that progressively decreases the function of specific cellular layers of the retina’s macula. The affected areas within the macula are the outer retina and inner retina photoreceptor layer.
Patients with macular degeneration experience a loss of their central vision, which affects their ability to read and perform visually demanding tasks. Although macular degeneration is associated with aging, the exact cause is still unknown.Together, AMD and RP affect at least 30 million people in the world. They are the most common causes of untreatable blindness in developed countries and, currently, there is no effective means of restoring vision.
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INTRODUCTION
A visual prosthetic or bionic eye is a form of neural prosthesis intended to partially restore lost vision or amplify existing vision. It usually takes the form of an externally-worn camera that is attached to a stimulator on the retina, optic nerve, or in the visual cortex, in order to produce perceptions in the visual cortex.
Visual percepts are the final product of a rich interplay of stimulus processing that occurs without the intervention of one's consciousness. While this is a fascinating issue to consider, especially as it pertains to the philosophical and practical definitions of ideas like the "self," the converse is equally interesting to me. In this modern era of exploding technological ingenuity, the sum of which is a product of the conscious brain, increasingly more opportunities exist for the brain to design the input it receives. One method by which this occurs is observable in the treatment of visual pathologies. A development of particular interest to me is the use of visual prosthetic devices in the treatment of some forms of progressive blindness. Research in this area raises numerous conflicts within the realm of bioengineering, but promises, at least, to challenge the boundaries of current microtechnology and instigate further integration of the rapidly expanding fields of electronics and medicine.
In 1988, a multidisciplinary research team called the "Retinal Implant Project," spanning the knowledge bases of Harvard Medical School, the Massachusetts Eye and Ear Infirmary, and the Massachusetts Institute of Technology's Department of Electrical Engineering and Computer Science, was formed with the explicit goal of creating an intraocular retinal prosthetic device to combat the effects of certain types of progressive blindness. The prostheses are intended to stimulate retinal ganglion cells whose associated photoreceptor cells have fallen victim to degradation by macular degeneration or retinitis pigmentosa, two currently incurable but widespread conditions. Their most recent work has been to orchestrate short-term clinical trials in which blind volunteers receive a temporary intraocular prosthetic implant and undergo a series of tests to determine the quality of visual percepts experienced over a two- to three-hour period . The leaders of the Retinal Implant Project, while enthusiastic about their progress, do not anticipate the realization of a workable prosthetic within the next five years.
The goal of retinal prosthetic proposed by the collaborators is to bypass degenerate photoreceptors by providing electrical stimulation directly to the underlying ganglion cells. The ganglion cell axons compose the optic nerve, which travels from the eye and terminates in various regions of the brain, where the combined input is processed along multiple routes and ultimately results in the experience of sight . Ganglion cell excitation will be accomplished by attaching a two-silicon-microchip system onto the surface of the retina, which will be powered by a specially designed laser mounted on a pair of glasses worn by the patient . This laser will also be receiving visual data input from a small, charge-coupled camera, whose output will dictate the pattern intensity of the laser beam . The laser's emitted radiation will be collected by the first microchip within the eye on an array of photodiodes and transferred to the second chip, which will be responsible for electrically stimulating a set of retinal ganglion cells via fine microelectrodes . Because the ganglion cells in a healthy retina are stimulated by photoreceptors, this activation process is designed to mimic the electrical activity within a retinal ganglion cell corresponding to a visual stimulus, with the hope that some measure of sight can be restored to individuals with faulty photoreceptors.
The team selected the retina as the site of artificial stimulation after careful consideration of the effects of the target diseases and the successes and limitations of electrical excitation at various regions along the visual pathway. Dr. T. Hambrecht of the National Institutes of Health and Dr. R. Normann of the University of Utah are two neurobiologists examining the effects of microelectrode stimulation of various regions of the visual cortex, a portion of the brain believed to be involved in visual perception. Upon administration of electrical stimuli to subsurface regions of the visual cortex of a blind patient, the patient identified spots of light, called phosphenes, which varied in color and depth, depending on the location of the stimulus. While this is exciting in its implications for elucidating the physical arrangement of the neuronal cells involved in the visual pathway, it fails to replicate the experience of sight because the stimuli are independent of external factors. Also, the visual percept is the product of neuronal activity in more than one brain region, a fact that renders the proposition that artificial stimulation in any single cortical area (or small collection of cortical areas) could recreate the elaborate perception of vision rather dubious.
The researchers involved with the Retinal Implant Project hypothesize that higher quality visual perceptions will be experienced with retinal than with intracortical stimulation. Joseph Wyatt and John Rizzo, III, the co-heads of the Retinal Implant Project write, ". . . in principle, the earlier the electronic input is fed into the nerves along the visual pathway, the better, inasmuch as neural signals farther down the pathway are processed and modified in ways not entirely well understood". This hypothesis is validated by the observation that photoreceptors are the sole neurons decimated by macular degeneration and retinitis pigmentosa, leaving the remaining cells involved in the visual process unharmed. Therefore, with the proper artificial input, it is reasonable to expect that those with prosthetic photoreceptive apparatuses will experience some returned vision.
While this proposal is exciting in its scope and purpose, it is not without drawbacks and complications. While the prosthetic's design offsets many potential biological problems by having most of its functional parts external to the body, this fails to solve every obstacle attendant upon the insertion of an inorganic and electrically active device into a living eye. Rizzo and Wyatt explain, "Biocompatibility, which encompasses biological, material, mechanical, and electrochemical issues, is the most significant obstacle to the development of a visual prosthesis".
Specifically, the electrical components of the prosthesis must be sequestered from all intraocular fluids, which could corrode the thin metal of the diodes and ruin the chips' ability to transmit electrical impulses from the laser to the retinal ganglion cells. Likewise, the by-products of electrical impulse transmission through metallic electrodes are toxic to living cells, and must be diminished in order to insure minimal chemical devastation of the retina. The electrodes themselves must also be anchored to the retina with sufficient strength to accommodate physical agitation due to daily activity. This promises to be a trying procedure. The retina is a slim 0.25 millimeters thick, a dauntingly thin fabric onto which to stitch a complex, albeit tiny, piece of machinery. As in all retinal surgical procedures, the implantation of a prosthetic poses a risk of retinal detachment and infection of the associated membranes, both of which would exacerbate, rather than prevent, vision loss. These concerns have not been seriously addressed in this stage of the research, because no long-term clinical trials of the prosthesis have been undertaken.
A final barrier to the project and implimentation, and perhaps the most complex to troubleshoot, is determining whether the engineered apparatus will be effective in restoring sight with chronic implantation. Although short-term tests of the photodiode array have been undertaken, their success was only measured in the ability of the diodes to generate output once inserted into the eye. While this was a necessary experimental step to prove the short-term mechanical soundness of the diode apparatus to fluids of the inner eye, the diodes have never been attached to the retinal tissue, and therefore, their viability as conduits of visual information has not been examined. The data the researchers cite in their preliminary investigations and those of their colleagues report that the single visual percept accomplished by artificial stimulation to date is phosphene recognition. This, however, is not equivalent to true sight, and certainly falls short of the lofty goal claimed by its spearheads: to "improve quality of life by providing gross perception with some geometric detail that would increase independence by making it easier for a blind person to walk down the street, for instance".
THE BIONIC EYE SYSTEM
In the past 20 years, biotechnology has become the fastest-growing area of scientific research, with new devices going into clinical trials at a breakneck pace. A bionic arm allows amputees to control movements of the prosthesis with their thoughts. A training system called BrainPort is letting people with visual and balance disorders bypass their damaged sensory organs and instead send information to their brain through the tongue. Now, a company called Second Sight has received FDA approval to begin U.S. trials of a retinal implant system that gives blind people a limited degree of vision.
The Argus II Retinal Prosthesis System can provide sight -- the detection of light -- to people who have gone blind from degenerative eye diseases like macular degeneration and retinitis pigmentosa. Ten percent of people over the age of 55 suffer from various stages of macular degeneration. Retinitis pigmentosa is an inherited disease that affects about 1.5 million people around the globe. Both diseases damage the eyes' photoreceptors, the cells at the back of the retina that perceive light patterns and pass them on to the brain in the form of nerve impulses, where the impulse patterns are then interpreted as images. The Argus II system takes the place of these photoreceptors.
The second incarnation of Second Sight's retinal prosthesis consists of five main parts:
• A digital camera that's built into a pair of glasses. It captures images in real time and sends images to a microchip.
• A video-processing microchip that's built into a handheld unit. It processes images into electrical pulses representing patterns of light and dark and sends the pulses to a radio transmitter in the glasses.
• A radio transmitter that wirelessly transmits pulses to a receiver implanted above the ear or under the eye
• A radio receiver that sends pulses to the retinal implant by a hair-thin implanted wire
• A retinal implant with an array of 60 electrodes on a chip measuring 1 mm by 1 mm
The entire system runs on a battery pack that's housed with the video processing unit. When the camera captures an image -- of, say, a tree -- the image is in the form of light and dark pixels. It sends this image to the video processor, which converts the tree-shaped pattern of pixels into a series of electrical pulses that represent "light" and "dark." The processor sends these pulses to a radio transmitter on the glasses, which then transmits the pulses in radio form to a receiver implanted underneath the subject's skin. The receiver is directly connected via a wire to the electrode array implanted at the back of the eye, and it sends the pulses down the wire.
When the pulses reach the retinal implant, they excite the electrode array. The array acts as the artificial equivalent of the retina's photoreceptors. The electrodes are stimulated in accordance with the encoded pattern of light and dark that represents the tree, as the retina's photoreceptors would be if they were working (except that the pattern wouldn't be digitally encoded). The electrical signals generated by the stimulated electrodes then travel as neural signals to the visual center of the brain by way of the normal pathways used by healthy eyes -- the optic nerves. In macular degeneration and retinitis pigmentosa, the optical neural pathways aren't damaged. The brain, in turn, interprets these signals as a tree and tells the subject, "You're seeing a tree."
It takes some training for subjects to actually see a tree. At first, they see mostly light and dark spots. But after a while, they learn to interpret what the brain is showing them, and they eventually perceive that pattern of light and dark as a tree. The first version of the system had 16 electrodes on the implant and is still in clinical trials at the University of California in Los Angeles. Doctors implanted the retinal chip in six subjects, all of whom regained some degree of sight. They are now able to perceive shapes (such as the shaded outline of a tree) and detect movement to varying degrees. The newest version of the system should offer greater image resolution because it has far more electrodes. If the upcoming clinical trials, in which doctors will implant the second-generation device into 75 subjects, are successful, the retinal prosthesis could be commercially available by 2010. The estimated cost is $30,000.
Researchers are already planning a third version that has a thousand electrodes on the retinal implant, which they believe could allow for facial-recognition capabilities
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INTRODUCTION
A visual prosthetic or bionic eye is a form of neural prosthesis intended to partially restore lost vision or amplify existing vision. It usually takes the form of an externally-worn camera that is attached to a stimulator on the retina, optic nerve, or in the visual cortex, in order to produce perceptions in the visual cortex.
Visual percepts are the final product of a rich interplay of stimulus processing that occurs without the intervention of one's consciousness. While this is a fascinating issue to consider, especially as it pertains to the philosophical and practical definitions of ideas like the "self," the converse is equally interesting to me. In this modern era of exploding technological ingenuity, the sum of which is a product of the conscious brain, increasingly more opportunities exist for the brain to design the input it receives. One method by which this occurs is observable in the treatment of visual pathologies. A development of particular interest to me is the use of visual prosthetic devices in the treatment of some forms of progressive blindness. Research in this area raises numerous conflicts within the realm of bioengineering, but promises, at least, to challenge the boundaries of current microtechnology and instigate further integration of the rapidly expanding fields of electronics and medicine.
In 1988, a multidisciplinary research team called the "Retinal Implant Project," spanning the knowledge bases of Harvard Medical School, the Massachusetts Eye and Ear Infirmary, and the Massachusetts Institute of Technology's Department of Electrical Engineering and Computer Science, was formed with the explicit goal of creating an intraocular retinal prosthetic device to combat the effects of certain types of progressive blindness. The prostheses are intended to stimulate retinal ganglion cells whose associated photoreceptor cells have fallen victim to degradation by macular degeneration or retinitis pigmentosa, two currently incurable but widespread conditions. Their most recent work has been to orchestrate short-term clinical trials in which blind volunteers receive a temporary intraocular prosthetic implant and undergo a series of tests to determine the quality of visual percepts experienced over a two- to three-hour period . The leaders of the Retinal Implant Project, while enthusiastic about their progress, do not anticipate the realization of a workable prosthetic within the next five years.
The goal of retinal prosthetic proposed by the collaborators is to bypass degenerate photoreceptors by providing electrical stimulation directly to the underlying ganglion cells. The ganglion cell axons compose the optic nerve, which travels from the eye and terminates in various regions of the brain, where the combined input is processed along multiple routes and ultimately results in the experience of sight . Ganglion cell excitation will be accomplished by attaching a two-silicon-microchip system onto the surface of the retina, which will be powered by a specially designed laser mounted on a pair of glasses worn by the patient . This laser will also be receiving visual data input from a small, charge-coupled camera, whose output will dictate the pattern intensity of the laser beam . The laser's emitted radiation will be collected by the first microchip within the eye on an array of photodiodes and transferred to the second chip, which will be responsible for electrically stimulating a set of retinal ganglion cells via fine microelectrodes . Because the ganglion cells in a healthy retina are stimulated by photoreceptors, this activation process is designed to mimic the electrical activity within a retinal ganglion cell corresponding to a visual stimulus, with the hope that some measure of sight can be restored to individuals with faulty photoreceptors.
The team selected the retina as the site of artificial stimulation after careful consideration of the effects of the target diseases and the successes and limitations of electrical excitation at various regions along the visual pathway. Dr. T. Hambrecht of the National Institutes of Health and Dr. R. Normann of the University of Utah are two neurobiologists examining the effects of microelectrode stimulation of various regions of the visual cortex, a portion of the brain believed to be involved in visual perception. Upon administration of electrical stimuli to subsurface regions of the visual cortex of a blind patient, the patient identified spots of light, called phosphenes, which varied in color and depth, depending on the location of the stimulus. While this is exciting in its implications for elucidating the physical arrangement of the neuronal cells involved in the visual pathway, it fails to replicate the experience of sight because the stimuli are independent of external factors. Also, the visual percept is the product of neuronal activity in more than one brain region, a fact that renders the proposition that artificial stimulation in any single cortical area (or small collection of cortical areas) could recreate the elaborate perception of vision rather dubious.
The researchers involved with the Retinal Implant Project hypothesize that higher quality visual perceptions will be experienced with retinal than with intracortical stimulation. Joseph Wyatt and John Rizzo, III, the co-heads of the Retinal Implant Project write, ". . . in principle, the earlier the electronic input is fed into the nerves along the visual pathway, the better, inasmuch as neural signals farther down the pathway are processed and modified in ways not entirely well understood". This hypothesis is validated by the observation that photoreceptors are the sole neurons decimated by macular degeneration and retinitis pigmentosa, leaving the remaining cells involved in the visual process unharmed. Therefore, with the proper artificial input, it is reasonable to expect that those with prosthetic photoreceptive apparatuses will experience some returned vision.
While this proposal is exciting in its scope and purpose, it is not without drawbacks and complications. While the prosthetic's design offsets many potential biological problems by having most of its functional parts external to the body, this fails to solve every obstacle attendant upon the insertion of an inorganic and electrically active device into a living eye. Rizzo and Wyatt explain, "Biocompatibility, which encompasses biological, material, mechanical, and electrochemical issues, is the most significant obstacle to the development of a visual prosthesis".
Specifically, the electrical components of the prosthesis must be sequestered from all intraocular fluids, which could corrode the thin metal of the diodes and ruin the chips' ability to transmit electrical impulses from the laser to the retinal ganglion cells. Likewise, the by-products of electrical impulse transmission through metallic electrodes are toxic to living cells, and must be diminished in order to insure minimal chemical devastation of the retina. The electrodes themselves must also be anchored to the retina with sufficient strength to accommodate physical agitation due to daily activity. This promises to be a trying procedure. The retina is a slim 0.25 millimeters thick, a dauntingly thin fabric onto which to stitch a complex, albeit tiny, piece of machinery. As in all retinal surgical procedures, the implantation of a prosthetic poses a risk of retinal detachment and infection of the associated membranes, both of which would exacerbate, rather than prevent, vision loss. These concerns have not been seriously addressed in this stage of the research, because no long-term clinical trials of the prosthesis have been undertaken.
A final barrier to the project and implimentation, and perhaps the most complex to troubleshoot, is determining whether the engineered apparatus will be effective in restoring sight with chronic implantation. Although short-term tests of the photodiode array have been undertaken, their success was only measured in the ability of the diodes to generate output once inserted into the eye. While this was a necessary experimental step to prove the short-term mechanical soundness of the diode apparatus to fluids of the inner eye, the diodes have never been attached to the retinal tissue, and therefore, their viability as conduits of visual information has not been examined. The data the researchers cite in their preliminary investigations and those of their colleagues report that the single visual percept accomplished by artificial stimulation to date is phosphene recognition. This, however, is not equivalent to true sight, and certainly falls short of the lofty goal claimed by its spearheads: to "improve quality of life by providing gross perception with some geometric detail that would increase independence by making it easier for a blind person to walk down the street, for instance".
THE BIONIC EYE SYSTEM
In the past 20 years, biotechnology has become the fastest-growing area of scientific research, with new devices going into clinical trials at a breakneck pace. A bionic arm allows amputees to control movements of the prosthesis with their thoughts. A training system called BrainPort is letting people with visual and balance disorders bypass their damaged sensory organs and instead send information to their brain through the tongue. Now, a company called Second Sight has received FDA approval to begin U.S. trials of a retinal implant system that gives blind people a limited degree of vision.
The Argus II Retinal Prosthesis System can provide sight -- the detection of light -- to people who have gone blind from degenerative eye diseases like macular degeneration and retinitis pigmentosa. Ten percent of people over the age of 55 suffer from various stages of macular degeneration. Retinitis pigmentosa is an inherited disease that affects about 1.5 million people around the globe. Both diseases damage the eyes' photoreceptors, the cells at the back of the retina that perceive light patterns and pass them on to the brain in the form of nerve impulses, where the impulse patterns are then interpreted as images. The Argus II system takes the place of these photoreceptors.
The second incarnation of Second Sight's retinal prosthesis consists of five main parts:
• A digital camera that's built into a pair of glasses. It captures images in real time and sends images to a microchip.
• A video-processing microchip that's built into a handheld unit. It processes images into electrical pulses representing patterns of light and dark and sends the pulses to a radio transmitter in the glasses.
• A radio transmitter that wirelessly transmits pulses to a receiver implanted above the ear or under the eye
• A radio receiver that sends pulses to the retinal implant by a hair-thin implanted wire
• A retinal implant with an array of 60 electrodes on a chip measuring 1 mm by 1 mm
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linhely
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22-06-2011, 12:20 PM

The risk of things going wrong with artificial eye surgery isextremely low but as with any type of surgerycomplications and problems can occur.InfectionWith artificial eye surgery, the most serious complicationwhich can happen early on following surgery is infection.This usually responds very well to antibiotics.
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Implant extrusion/exposureAs stated above an orbital implant is usually implanteddeep into the socket at the time of removing the eye. Themain role of the orbital implant is compensate for the lossin volume from removing the natural eye therefore fillingout the socket so that the cavity of the socket isshallower. This means the artificial eye can be thinnerand lighter,

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01-02-2012, 11:13 AM

to get information about the topic artificial eye full report ppt, and related topics refer the link bellow

topicideashow-to-artificial-eye--1999

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06-02-2012, 04:05 PM

Artificial Eye


.ppt   artificial_eyes.ppt (Size: 7.02 MB / Downloads: 55)
The Camera Obscura Hockney’s thesis


.Around 1430, painters began employing a concave mirror to project and implimentation brightly-lit subjects onto a canvas, thus allowing them to render subjects with unprecedented naturalism

.Towards the end of the sixteenth century, painters began to use refractive lenses instead of concave mirrors to project and implimentation their images, producing images in which left and right were reversed.

History of the camera obscura
4th century BCE: Aristotle -- during solar eclipse, circles of light on ground beneath a plane tree turn to thin crescents

10th century: Ibn-al-Haitham: images of sun could be project and implimentationed onto wall of room

1550: Cardano -- addition of lens in aperture (Hockney “late” device)

1558: Della Porta, concave mirror camera obscura (Hockney “early” device)

1585: Benedetti: Lens and oblique plane mirror

1589: Della Porta, revised edition, concave mirror with convex lens

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