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Chapter-1
Introduction
1.1 Introduction:
Blindness is more feared by the public than any other ailment. Artificial vision for the blind was
once the stuff of science fiction. But now, a limited form of artificial vision is a reality .Now we
are at the beginning of the end of blindness with this type of technology. In an effort to
illuminate the perpetually dark world of the blind, researchers are turning to technology. They
are investigating several electronic-based strategies designed to bypass various defects or
missing links along the brain's image processing pathway and provide some form of artificial
sight.
This paper is about curing blindness. Linking electronics and biotechnology, the scientists has
made the commitment to the development of technology that will provide or restore vision for
the visually impaired around the world. This paper describes the development of artificial vision
system, which cures blindness to some extent. This paper explains the process involved in it and
explains the concepts of artificial silicon retina, cortical implants etc. The roadblocks that are
created are also elucidated clearly. Finally the advancements made in this system and scope of
this in the future is also presented clearly.
Bionic eye, also called a Bio Electronic eye, is the electronic device that replaces functionality of
a part or whole of the eye. It is still at a very early stage in its development, but if successful, it
could restore vision to people who have lost sight during their lifetime. A bionic eye work by
stimulating nerves, which are activated by electrical impulses. In this case the patient has a small
device implanted into the body that can receive radio signals and transmit those signals to nerves.
A bionic eye mimics the function of the retina to restore sight for those with severe vision loss. It
uses a retinal implant connected to a video camera to convert images into electrical impulses that
activate remaining retinal cells which then carry the signal back to the brain.
A video camera fitted to a pair of glasses will capture and process images. These images are sent
wirelessly to a bionic implant at the back of the eye which stimulates dormant optic nerves to
generate points of light (phosphenes) that form the basis of images in the brain.
1.2 Retina:
Artificial-vision researchers take inspiration from another device, the cochlear implant, which
has successfully restored hearing to thousands of deaf people. But the human vision system is far
more complicated than that of hearing. The eye is one of the most amazing organs in the body.
Before we understand how artificial vision is created, it's important to know about the important
role that the retina plays in how we see. Here is a simple explanation of what happens when we
look at an object:
 Scattered light from the object enters through the cornea.
 The light is projected onto the retina.
 The retina sends messages to the brain through the optic nerve.
 The brain interprets what the object is.
The retina is complex in itself. This thin membrane at the back of the eye is a vital part of our
ability to see. Its main function is to receive and transmit images to the brain. These are the three
main types of cells in the eye that help perform this function: Rods, Cones and Ganglion Cells.
The information received by the rods and cones are transmitted to the nearly 1 million ganglion
cells in the retina. These ganglion cells interpret the messages from the rods and cones and send
the information on to the brain by way of the optic nerve. There are a number of retinal diseases
that attack these cells, which can lead to blindness. The most notable of these diseases are
retinitis pigmentosa and age-related macular degeneration. Both of these diseases attack the
retina, rendering the rods and cones inoperative, causing either loss of peripheral vision or total
blindness. However, it's been found that neither of these retinal diseases affects the ganglion
cells or the optic nerve.
The eye collects light from the surrounding world and transduces it into a signal that can be
processed in the brain. Transduction takes place in the photoreceptors found in the retina.
(Nelson 477) In order to get to the photoreceptors, light enters through the cornea, passes
through the anterior chamber, then through the pupil and continues through the lens into the
vitreous humor back onto the retina. The pupil and the lens refract the light in order to form a
clear image on the fovea. (Saladin) The retina consists of several layers, the retinal pigment
epithelium, the receptorlayer, the outer plexiform layer, the inner nuclear layer, the inner
plexiform layer, the retinal ganglion cell layer, and the optic nerve layer. The photoreceptors
consist of Rods and cones. The rods contain rhodopsin, a photopigment that breaks down when
exposed to certain wavelengths of light. They function at low levels of light and are more
sensitive than the cone cells. Rods are found more in the peripheral of the retina. The cones
contain photopigments that are color sensitive. The cone cells are heavily concentrated in the
fovea allowing for high visual acuity. The photoreceptors converge and synapse on bipolar cells,
which then converge and synapse on ganglion cells. The ganglion cells connect the retina to the
brain acting as a direct pathway with their axons forming the optic nerve. The retina is the third
and inner coat of the eye which is a light-sensitive layer of tissue. The optics of the eye create an
image of the visual world on the retina (through the cornea and lens), which serves much the
same function as the film in a camera. Light striking the retina initiates a cascade of chemical
and electrical events that ultimately trigger nerve impulses. These are sent to various visual
centres of the brain through the fibres of the optic nerve.
In vertebrate embryonic development, the retina and the optic nerve originate as outgrowths of
the developing brain, so the retina is considered part of the central nervous system (CNS) and is
actually brain tissue. It is the only part of the CNS that can be visualized non-invasively.
The retina is a layered structure with several layers of neurons interconnected by synapses. The
only neurons that are directly sensitive to light are the photoreceptor cells. These are mainly of
two types: the rods and cones. Rods function mainly in dim light and provide black-and-white
vision, while cones support daytime vision and the perception of colour. A third, much rarer type
of photoreceptor, the intrinsically photosensitive ganglion cell, is important for reflexive
responses to bright daylight.
Neural signals from the rods and cones undergo processing by other neurons of the retina. The
output takes the form of action potentials in retinal ganglion cells whose axons form the optic
nerve. Several important features of visual perception can be traced to the retinal encoding and
processing of light.
1.3 How retina works:
An image is produced by the patterned excitation of the cones and rods in the retina. The
excitation is processed by the neuronal system and various parts of the brain working in parallel
to form a representation of the external environment in the brain.
The cones respond to bright light and mediate high-resolution colour vision during daylight
illumination (also called photopic vision). The rods are saturated at daylight levels and don't
contribute to pattern vision. However, rods do respond to dim light and mediate lower-resolution,
monochromatic vision under very low levels of illumination (called scotopic vision). The
illumination in most office settings falls between these two levels and is called mesopic vision.
At these light levels, both the rods and cones are actively contributing pattern information to that
exiting the eye. What contribution the rod information makes to pattern vision under these
circumstances is unclear.
The response of cones to various wavelengths of light is called their spectral sensitivity. In
normal human vision, the spectral sensitivity of a cone falls into one of three subgroups. These
are often called blue, green, and red cones but more accurately are short, medium, and long
wavelength sensitive cone subgroups. It is a lack of one or more of the cone subtypes that causes
individuals to have deficiencies in colour vision or various kinds of colour blindness. These
individuals are not blind to objects of a particular colour but experience the inability to
distinguish between two groups of colours that can be distinguished by people with normal
vision. Humans have three different types of cones (trichromatic vision) while most other
mammals lack cones with red sensitive pigment and therefore have poorer (dichromatic) colour
vision. However, some animals have four spectral subgroups, e.g. the trout adds an ultraviolet
subgroup to short, medium and long subgroups that are similar to humans. Some fish are
sensitive to the polarization of light as well.
When light falls on a receptor it sends a proportional response synaptically to bipolar cells which
in turn signal the retinal ganglion cells. The receptors are also 'cross-linked' byhorizontal
cells and amacrine cells, which modify the synaptic signal before the ganglion cells. Rod and
cone signals are intermixed and combine, although rods are mostly active in very poorly lit
conditions and saturate in broad daylight, while cones function in brighter lighting because they
are not sensitive enough to work at very low light levels.
Despite the fact that all are nerve cells, only the retinal ganglion cells and few amacrine cells
create action potentials. In the photoreceptors, exposure to light hyperpolarizes the membrane in
a series of graded shifts. The outer cell segment contains a photopigment. Inside the cell the
normal levels of cyclic guanosine monophosphate (cGMP) keep the Na+ channel open and thus
in the resting state the cell is depolarised. The photon causes the retinal bound to the receptor
protein to isomerise to trans-retinal. This causes receptor to activate multiple G-proteins. This in
turn causes the Ga-subunit of the protein to activate a phosphodiesterase (PDE6), which degrades
cGMP, resulting in the closing of Na+ cyclic nucleotide-gated ion channels (CNGs). Thus the
cell is hyperpolarised. The amount of neurotransmitter released is reduced in bright light and
increases as light levels fall. The actual photopigment is bleached away in bright light and only
replaced as a chemical process, so in a transition from bright light to darkness the eye can take
up to thirty minutes to reach full sensitivity .
In the retinal ganglion cells there are two types of response, depending on the receptive field of
the cell. The receptive fields of retinal ganglion cells comprise a central approximately circular
area, where light has one effect on the firing of the cell, and an annular surround, where light has
the opposite effect on the firing of the cell. In ON cells, an increment in light intensity in the
centre of the receptive field causes the firing rate to increase. In OFF cells, it makes it decrease.
In a linear model, this response profile is well described by a Difference of Gaussians and is the
basis for edge detection algorithms. Beyond this simple difference ganglion cells are also
differentiated by chromatic sensitivity and the type of spatial summation. Cells showing linear
spatial summation are termed X cells (also called parvocellular, P, or midget ganglion cells), and
those showing non-linear summation are Y cells (also called magnocellular, M, or parasol retinal
ganglion cells), although the correspondence between X and Y cells (in the cat retina) and P and
M cells (in the primate retina) is not as simple as it once seemed.
In the transfer of visual signals to the brain, the visual pathway, the retina is vertically divided in
two, a temporal (nearer to the temple) half and a nasal (nearer to the nose) half. The axons from
the nasal half cross the brain at the optic chiasma to join with axons from the temporal half of the
other eye before passing into the lateral geniculate body.
Although there are more than 130 million retinal receptors, there are only approximately 1.2
million fibres (axons) in the optic nerve; a large amount of pre-processing is performed within
the retina. The fovea produces the most accurate information. Despite occupying about 0.01% of
the visual field (less than 2° of visual angle), about 10% of axons in the optic nerve are devoted
to the fovea. The resolution limit of the fovea has been determined at around 10,000
points. See visual acuity. The information capacity is estimated at 500,000 bits per second (for
more information on bits, see information theory) without colour or around 600,000 bits per
second including colour.
1.4 What is blindness?
Blindness is defined as the state of being sightless. A blind individual is unable to see. In a strict
sense the word "blindness" denotes the inability of a person to distinguish darkness from bright
light in either eye. The terms blind and blindness have been modified in our society to include a
wide range of visual impairment. Blindness is frequently used today to describe severe visual
decline in one or both eyes with maintenance of some residual vision.
1.5 Causes of Blindness:
i Age-Related Macular Degeneration:
Macular degeneration, often called age-related macular degeneration (AMD), is an eye disorder
associated with aging and results in damaging sharp and central vision. Central vision is needed
for seeing objects clearly and for common daily tasks such as reading and driving. AMD affects
the macula, the central part the retina that allows the eye to see fine details. There are two forms
of AMD—wet and dry.
Wet AMD is when abnormal blood vessel behind the retina start to grow under the macula,
ultimately leading to blood and fluid leakage. Bleeding, leaking, and scarring from these blood
vessels cause damage and lead to rapid central vision loss. An early symptom of wet AMD is
that straight lines appear wavy.
Dry AMD is when the macula thins overtime as part of aging process, gradually blurring central
vision. The dry form is more common and accounts for 70–90% of cases of AMD and it
progresses more slowly than the wet form. Over time, as less of the macula functions, central
vision is gradually lost in the affected eye. Dry AMD generally affects both eyes. One of the
most common early signs of dry AMD is drusen.
Drusen are tiny yellow or white deposits under the retina. They often are found in people aged 60
years and older. The presence of small drusen is normal and does not cause vision loss.
However, the presence of large and more numerous drusen raises the risk of developing
advanced dry AMD or wet AMD.
It is estimated that 1.8 million Americans aged 40 years and older are affected by AMD and an
additional 7.3 million with large drusen are at substantial risk of developing AMD. The number
of people with AMD is estimated to reach 2.95 million in 2020. AMD is the leading cause of
permanent impairment of reading and fine or close-up vision among people aged 65 years and
older.
ii.Cataract:
Cataract is a clouding of the eye’s lens and is the leading cause of blindness worldwide, and the
leading cause of vision loss in the United States. Cataracts can occur at any age because of a
variety of causes, and can be present at birth. Although treatment for the removal of cataract is
widely available, access barriers such as insurance coverage, treatment costs, patient choice, or
lack of awareness prevent many people from receiving the proper treatment.
An estimated 20.5 million (17.2%) Americans aged 40 years and older have cataract in one or
both eyes, and 6.1 million (5.1%) have had their lens removed operatively. The total number of
people who have cataracts is estimated to increase to 30.1 million by 2020.
iii. Diabetic Retinopathy:
Diabetic retinopathy (DR) is a common complication of diabetes. It is the leading cause of
blindness in American adults. It is characterized by progressive damage to the blood vessels of
the retina, the light-sensitive tissue at the back of the eye that is necessary for good vision. DR
progresses through four stages, mild nonproliferative retinopathy (microaneurysms), moderate
nonproliferative retinopathy (blockage in some retinal vessels), severe nonproliferative
retinopathy (more vessels are blocked leading to deprived retina from blood supply leading to
growing new blood vessels), and proliferative retinopathy (most advanced stage). Diabetic
retinopathy usually affects both eyes.
The risks of DR are reduced through disease management that includes good control of blood
sugar, blood pressure, and lipid abnormalities. Early diagnosis of DR and timely treatment
reduce the risk of vision loss; however, as many as 50% of patients are not getting their eyes
examined or are diagnosed too late for treatment to be effective.
It is the leading cause of blindness among U.S. working-aged adults aged 20–74 years. An
estimated 4.1 million and 899,000 Americans are affected by retinopathy and vision-threatening
retinopathy, respectively.
Iv.Glaucoma:
Glaucoma is a group of diseases that can damage the eye's optic nerve and result in vision loss
and blindness. Glaucoma occurs when the normal fluid pressure inside the eyes slowly rises.
However, recent findings now show that glaucoma can occur with normal eye pressure. With
early treatment, you can often protect your eyes against serious vision loss.
There are two major categories “open angle” and “closed angle” glaucoma. Open angle, is a
chronic condition that progress slowly over long period of time without the person noticing
vision loss until the disease is very advanced, that is why it is called “sneak thief of sight." Angle
closure can appear suddenly and is painful. Visual loss can progress quickly; however, the pain
and discomfort lead patients to seek medical attention before permanent damage occurs.
v.Amblyopia:
Amblyopia, also referred to as “lazy eye,” is the most common cause of vision impairment in
children. Amblyopia is the medical term used when the vision in one of the eyes is reduced
because the eye and the brain are not working together properly. The eye itself looks normal, but
it is not being used normally because the brain is favoring the other eye. Conditions leading to
amblyopia include strabismus, an imbalance in the positioning of the two eyes; more
nearsighted, farsighted, or astigmatic in one eye than the other eye, and rarely other eye
conditions such as cataract.
Unless it is successfully treated in early childhood amblyopia usually persists into adulthood, and
is the most common cause of permanent one-eye vision impairment among children and young
and middle-aged adults. An estimated 2%–3% of the population suffer from Amblyopia.
Chapter-2
2.1 How artificial silicon Retina does works:
The ASR contains about 3,500 microscopic solar cells that are able to convert light into electrical
pulses, mimicking the function of cones and rods. To implant this device into the eye, surgeons
make three tiny incisions no larger than the diameter of a needle in the white part of the eye.
Through these incisions, the surgeons introduce a miniature cutting and vacuuming device that
removes the gel in the middle of the eye and replaces it with saline. Next, a pinpoint opening is
made in the retina through which they inject fluid to lift up a portion of the retina from the back
of the eye, which creates a small pocket in the sub retinal space for the device to fit in. The retina
is then resealed over the ASR.
.Figure 5: Here you can see where the ASR is placedbetweenthe outer and innerretinal layers.
For any microchip to work it needs power and the amazing thing about the ASR is that it
receives all of its needed power from the light entering the eye. This means that with the ASR
implant in place behind the retina, it receives all of the light entering the eye. This solar energy
eliminates the need for any wires, batteries or other secondary devices to supply power.
Another microchip device that would restore partial vision is currently in development called the
artificial retina component chip (ARCC), this device is quite similar to the ASR. Both are made
of silicon and both are powered by solar energy. The ARCC is also a very small device
measuring 2 mm square and a thickness of .02 millimeters (.00078 inch). There are significant
differences between the devices, however. According to researchers, the ARCC will give blind
patients the ability to see 10 by 10 pixel images, which is about the size of a single letter on this
page However, researchers have said that they could eventually develop a version of the chip that
would allow 250 by 250 pixel array, which would allow those who were once blind to read a
newspaper.
2.2 Working of artificial vision system:
The main parts of this system are miniature video camera, a signal processor, and the brain
implants. The tiny pinhole camera, mounted on a pair of eyeglasses, captures the scene in front
of the wearer and sends it to a small computer on the patient's belt. The processor translates the
image into a series of signals that the brain can understand, and then sends the information to the
brain implant that is placed in patient’s visual cortex. And, if everything goes according to plan,
the brain will "see" the image.
Figures (6, 7) illustrating the AV SYSTEM.
Light enters the camera, which then sends the image to a wireless wallet-sized computer for
`processing. The computer transmits this information to an infrared LED screen on the goggles.
The goggles reflect an infrared image into the eye and on to the retinal chip, stimulating
photodiodes on the chip. The photodiodes mimic the retinal cells by converting light into
electrical signals, which are then transmitted by cells in the inner retina via nerve pulses to the
brain. The goggles are transparent so if the user still has some vision, they can match that with
the new information - the device would cover about 10° of the wearer’s field of vision.
The patient should wear sunglasses with a tiny pinhole camera mounted on one lensand an
ultrasonic range finder on the other. Both devices communicate with a small computer carried on
his hip, which highlights the edges between light and dark areas in the camera image. It then tells
an adjacent computer to send appropriate signals to an array of small electrodes on the surface of
patient’s brain, through wires entering his skull. The electrodes stimulate certain brain cells,
making the person perceive the specks of light. The shifting patterns as scans across a scene tells
him where light areas meet dark ones, letting him find the black cap on the white wall, for
example. The device provides a sort of tunnelvision, reading an area about the size of a card 2
inches wide and 8 inches tall, held at arm's length
Chapter-3
3.1 Advancements in creating Artificial Vision:
Ceramic optical detectors based on the photo-ferroelectrics effect are being developed for direct
implantation into the eyes of patients with retinal dystrophies. In retinal dystrophies where the
optic nerve and retinal ganglia are intact (such as Retinitis Pigmentosa), direct retinal implant of
an optical detector to stimulate retinal ganglia could allow patients to regain some sight. In such
cases additional wiring to the brain cortex is not required, and for biologically inert detectors,
surgical implantation can be quite direct. The detector currently being developed for this
application is a thin film ferroelectric detector, which under optical illumination can generate a
local photocurrent and photo voltage. The local electric current generated by this miniature
detector excites the retinal neural circuit resulting in a signal at the optic nerve that may be
translated by the cortex of the brain as "seeing light". Detectors based on PbLaZrTiO3(PLZT)
and BiVMnO3 (BVMO) films exhibit a strong photo response in visible range overlapping eye
response from 380 nm to 650 nm. The thin film detector heterostructures have been implanted
into the eyes of rabbits for biocompatibility test, and have shown no biologicalincompatibilities.
The bionic devices tested so far include both those attached to the back of the eye itself
and those implanted directly in the brain. Patients with both types of implants describe seeing
multiple points of light and, in some cases, crude outlines of objects. Placing electrodes in the
eye has proved easier. During the past decade, work on these retinal implants has attracted
growing government funding and commercial interest. Such implants zap electrical signals to
nerves on the back of the eye, which then carry them to the brain. However, since these devices
take advantage of surviving parts of the eye they will help only the subset of blind people whose
blindness is due to retinal disease, by some estimates about 30% of the blind. Moreover,
scientists don't believe any implant could help those blind since birth, because their brains never
have learned to recognize vision.
3.2 What blind patients would not be able to use this device?
We believe the device will be applicable to virtually all patients who are blind or who have very
low vision. The only ones contraindicated would be a few blinded by serious brain damage, or
who have chronic infections, etc. that preclude surgical implants. Patients who have a small
amount of vision are not contraindicated. Visual cortex stimulation seems to work the same in
both sighted and blind patients.
3.3 Bottlenecks raised by this technology:
1. The first and foremost thing is the cost .The miniaturization of equipment and more powerful
computers have made this artificial vision possible, but it's not cheap: The operation, equipment
and necessary training cost $70,000 per patient. And also may be much higher depending upon
the context and severity.
2. It may not work for people blinded as children or as infants, because the visual cortex do not
develop normally. But it will work for the vast majority of the blind -- 98 to 99 percent.
3. Researchers caution, however, that artificial vision devices are still highly experimental and
practical systems are many years away. Even after they are refined, the first wave will most
likely provide only crude images, such as the outline of a kitchen doorway. It does not function
as well as the real eye, and does not have crystal-clear vision (as it is only a camera).The device
is a very limited navigational aid, and it's a far cry from the visual experience normal people
enjoy.
3.4 Other reasons causing blindness and their remedies:
The main aim of Artificial Vision is to restore some degree of sight to the profoundly blind.
Since blindness can result from defects at many different points along the visual pathway, there
are accordingly a wide variety of proposed models for an "Artificial Eye".
The earliest stage of visual processing is the transudation of light into electrical signals by the
photoreceptors. If this is the only process that is interrupted in a blind individual, he or she may
benefit from a Sub-Retinal Prosthesis, a device that is designed to replace only the
photoreceptors in the retina. However, if the Optic Nerve itself is damaged, the only possibility
for restoring sight is to directly stimulate the visual cortex. Cortical prosthesis is designed
specifically for this task. Although the categories presented account for most of the research in
Artificial Vision, there are a few more exotic techniques being developed. One of these is the
BioHybrid Implant a device that incorporates living cells with man-made elements. Regardless
of the specific design, all of these devices are working towards the same goal-- a permanent
replacement for part of the human visual system.
3.5 conclusion:
The electronic eye is the latest in high-tech gadgets aimed at helping millions of blind and
visually impaired people. Although the images produced by the artificial eye were far from
perfect, they could be clear enough to allow someone who is otherwise blind to recognize faces.
The first useful artificial eye is now helping a blind man walk safely around and read large
letters. Several efforts are now underway to create vision in otherwise blind eyes. While
technically exciting, much more work in this area needs to be completed before anything is
available to the majority of patients. Research is ongoing in two areas: cortical implants and
retinal implants. There is still an enormous amount of work to be done in developing artificial
retinas. In recent years, progress is being made towards sensory distribution devices for the
blind. In the long run, there could be the possibility of brain implants. A brain implant or cortical
implant provides visual input from a camera directly to the brain via electrodes in contact with
the visual cortex at the backside of the head.

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Mounika seminar doc

  • 1. Chapter-1 Introduction 1.1 Introduction: Blindness is more feared by the public than any other ailment. Artificial vision for the blind was once the stuff of science fiction. But now, a limited form of artificial vision is a reality .Now we are at the beginning of the end of blindness with this type of technology. In an effort to illuminate the perpetually dark world of the blind, researchers are turning to technology. They are investigating several electronic-based strategies designed to bypass various defects or missing links along the brain's image processing pathway and provide some form of artificial sight. This paper is about curing blindness. Linking electronics and biotechnology, the scientists has made the commitment to the development of technology that will provide or restore vision for the visually impaired around the world. This paper describes the development of artificial vision system, which cures blindness to some extent. This paper explains the process involved in it and explains the concepts of artificial silicon retina, cortical implants etc. The roadblocks that are created are also elucidated clearly. Finally the advancements made in this system and scope of this in the future is also presented clearly. Bionic eye, also called a Bio Electronic eye, is the electronic device that replaces functionality of a part or whole of the eye. It is still at a very early stage in its development, but if successful, it could restore vision to people who have lost sight during their lifetime. A bionic eye work by stimulating nerves, which are activated by electrical impulses. In this case the patient has a small device implanted into the body that can receive radio signals and transmit those signals to nerves. A bionic eye mimics the function of the retina to restore sight for those with severe vision loss. It uses a retinal implant connected to a video camera to convert images into electrical impulses that activate remaining retinal cells which then carry the signal back to the brain. A video camera fitted to a pair of glasses will capture and process images. These images are sent wirelessly to a bionic implant at the back of the eye which stimulates dormant optic nerves to generate points of light (phosphenes) that form the basis of images in the brain.
  • 2. 1.2 Retina: Artificial-vision researchers take inspiration from another device, the cochlear implant, which has successfully restored hearing to thousands of deaf people. But the human vision system is far more complicated than that of hearing. The eye is one of the most amazing organs in the body. Before we understand how artificial vision is created, it's important to know about the important role that the retina plays in how we see. Here is a simple explanation of what happens when we look at an object:  Scattered light from the object enters through the cornea.  The light is projected onto the retina.  The retina sends messages to the brain through the optic nerve.  The brain interprets what the object is. The retina is complex in itself. This thin membrane at the back of the eye is a vital part of our ability to see. Its main function is to receive and transmit images to the brain. These are the three main types of cells in the eye that help perform this function: Rods, Cones and Ganglion Cells. The information received by the rods and cones are transmitted to the nearly 1 million ganglion cells in the retina. These ganglion cells interpret the messages from the rods and cones and send the information on to the brain by way of the optic nerve. There are a number of retinal diseases that attack these cells, which can lead to blindness. The most notable of these diseases are
  • 3. retinitis pigmentosa and age-related macular degeneration. Both of these diseases attack the retina, rendering the rods and cones inoperative, causing either loss of peripheral vision or total blindness. However, it's been found that neither of these retinal diseases affects the ganglion cells or the optic nerve. The eye collects light from the surrounding world and transduces it into a signal that can be processed in the brain. Transduction takes place in the photoreceptors found in the retina. (Nelson 477) In order to get to the photoreceptors, light enters through the cornea, passes through the anterior chamber, then through the pupil and continues through the lens into the vitreous humor back onto the retina. The pupil and the lens refract the light in order to form a clear image on the fovea. (Saladin) The retina consists of several layers, the retinal pigment epithelium, the receptorlayer, the outer plexiform layer, the inner nuclear layer, the inner plexiform layer, the retinal ganglion cell layer, and the optic nerve layer. The photoreceptors consist of Rods and cones. The rods contain rhodopsin, a photopigment that breaks down when exposed to certain wavelengths of light. They function at low levels of light and are more sensitive than the cone cells. Rods are found more in the peripheral of the retina. The cones contain photopigments that are color sensitive. The cone cells are heavily concentrated in the fovea allowing for high visual acuity. The photoreceptors converge and synapse on bipolar cells, which then converge and synapse on ganglion cells. The ganglion cells connect the retina to the brain acting as a direct pathway with their axons forming the optic nerve. The retina is the third and inner coat of the eye which is a light-sensitive layer of tissue. The optics of the eye create an image of the visual world on the retina (through the cornea and lens), which serves much the same function as the film in a camera. Light striking the retina initiates a cascade of chemical and electrical events that ultimately trigger nerve impulses. These are sent to various visual centres of the brain through the fibres of the optic nerve.
  • 4. In vertebrate embryonic development, the retina and the optic nerve originate as outgrowths of the developing brain, so the retina is considered part of the central nervous system (CNS) and is actually brain tissue. It is the only part of the CNS that can be visualized non-invasively. The retina is a layered structure with several layers of neurons interconnected by synapses. The only neurons that are directly sensitive to light are the photoreceptor cells. These are mainly of two types: the rods and cones. Rods function mainly in dim light and provide black-and-white vision, while cones support daytime vision and the perception of colour. A third, much rarer type of photoreceptor, the intrinsically photosensitive ganglion cell, is important for reflexive responses to bright daylight. Neural signals from the rods and cones undergo processing by other neurons of the retina. The output takes the form of action potentials in retinal ganglion cells whose axons form the optic nerve. Several important features of visual perception can be traced to the retinal encoding and processing of light. 1.3 How retina works:
  • 5. An image is produced by the patterned excitation of the cones and rods in the retina. The excitation is processed by the neuronal system and various parts of the brain working in parallel to form a representation of the external environment in the brain. The cones respond to bright light and mediate high-resolution colour vision during daylight illumination (also called photopic vision). The rods are saturated at daylight levels and don't contribute to pattern vision. However, rods do respond to dim light and mediate lower-resolution, monochromatic vision under very low levels of illumination (called scotopic vision). The illumination in most office settings falls between these two levels and is called mesopic vision. At these light levels, both the rods and cones are actively contributing pattern information to that exiting the eye. What contribution the rod information makes to pattern vision under these circumstances is unclear. The response of cones to various wavelengths of light is called their spectral sensitivity. In normal human vision, the spectral sensitivity of a cone falls into one of three subgroups. These are often called blue, green, and red cones but more accurately are short, medium, and long wavelength sensitive cone subgroups. It is a lack of one or more of the cone subtypes that causes individuals to have deficiencies in colour vision or various kinds of colour blindness. These individuals are not blind to objects of a particular colour but experience the inability to distinguish between two groups of colours that can be distinguished by people with normal vision. Humans have three different types of cones (trichromatic vision) while most other mammals lack cones with red sensitive pigment and therefore have poorer (dichromatic) colour vision. However, some animals have four spectral subgroups, e.g. the trout adds an ultraviolet subgroup to short, medium and long subgroups that are similar to humans. Some fish are sensitive to the polarization of light as well. When light falls on a receptor it sends a proportional response synaptically to bipolar cells which in turn signal the retinal ganglion cells. The receptors are also 'cross-linked' byhorizontal cells and amacrine cells, which modify the synaptic signal before the ganglion cells. Rod and cone signals are intermixed and combine, although rods are mostly active in very poorly lit conditions and saturate in broad daylight, while cones function in brighter lighting because they are not sensitive enough to work at very low light levels. Despite the fact that all are nerve cells, only the retinal ganglion cells and few amacrine cells create action potentials. In the photoreceptors, exposure to light hyperpolarizes the membrane in a series of graded shifts. The outer cell segment contains a photopigment. Inside the cell the normal levels of cyclic guanosine monophosphate (cGMP) keep the Na+ channel open and thus in the resting state the cell is depolarised. The photon causes the retinal bound to the receptor protein to isomerise to trans-retinal. This causes receptor to activate multiple G-proteins. This in turn causes the Ga-subunit of the protein to activate a phosphodiesterase (PDE6), which degrades cGMP, resulting in the closing of Na+ cyclic nucleotide-gated ion channels (CNGs). Thus the cell is hyperpolarised. The amount of neurotransmitter released is reduced in bright light and increases as light levels fall. The actual photopigment is bleached away in bright light and only
  • 6. replaced as a chemical process, so in a transition from bright light to darkness the eye can take up to thirty minutes to reach full sensitivity . In the retinal ganglion cells there are two types of response, depending on the receptive field of the cell. The receptive fields of retinal ganglion cells comprise a central approximately circular area, where light has one effect on the firing of the cell, and an annular surround, where light has the opposite effect on the firing of the cell. In ON cells, an increment in light intensity in the centre of the receptive field causes the firing rate to increase. In OFF cells, it makes it decrease. In a linear model, this response profile is well described by a Difference of Gaussians and is the basis for edge detection algorithms. Beyond this simple difference ganglion cells are also differentiated by chromatic sensitivity and the type of spatial summation. Cells showing linear spatial summation are termed X cells (also called parvocellular, P, or midget ganglion cells), and those showing non-linear summation are Y cells (also called magnocellular, M, or parasol retinal ganglion cells), although the correspondence between X and Y cells (in the cat retina) and P and M cells (in the primate retina) is not as simple as it once seemed. In the transfer of visual signals to the brain, the visual pathway, the retina is vertically divided in two, a temporal (nearer to the temple) half and a nasal (nearer to the nose) half. The axons from the nasal half cross the brain at the optic chiasma to join with axons from the temporal half of the other eye before passing into the lateral geniculate body. Although there are more than 130 million retinal receptors, there are only approximately 1.2 million fibres (axons) in the optic nerve; a large amount of pre-processing is performed within the retina. The fovea produces the most accurate information. Despite occupying about 0.01% of the visual field (less than 2° of visual angle), about 10% of axons in the optic nerve are devoted to the fovea. The resolution limit of the fovea has been determined at around 10,000 points. See visual acuity. The information capacity is estimated at 500,000 bits per second (for more information on bits, see information theory) without colour or around 600,000 bits per second including colour. 1.4 What is blindness? Blindness is defined as the state of being sightless. A blind individual is unable to see. In a strict sense the word "blindness" denotes the inability of a person to distinguish darkness from bright light in either eye. The terms blind and blindness have been modified in our society to include a wide range of visual impairment. Blindness is frequently used today to describe severe visual decline in one or both eyes with maintenance of some residual vision. 1.5 Causes of Blindness: i Age-Related Macular Degeneration: Macular degeneration, often called age-related macular degeneration (AMD), is an eye disorder associated with aging and results in damaging sharp and central vision. Central vision is needed for seeing objects clearly and for common daily tasks such as reading and driving. AMD affects
  • 7. the macula, the central part the retina that allows the eye to see fine details. There are two forms of AMD—wet and dry. Wet AMD is when abnormal blood vessel behind the retina start to grow under the macula, ultimately leading to blood and fluid leakage. Bleeding, leaking, and scarring from these blood vessels cause damage and lead to rapid central vision loss. An early symptom of wet AMD is that straight lines appear wavy. Dry AMD is when the macula thins overtime as part of aging process, gradually blurring central vision. The dry form is more common and accounts for 70–90% of cases of AMD and it progresses more slowly than the wet form. Over time, as less of the macula functions, central vision is gradually lost in the affected eye. Dry AMD generally affects both eyes. One of the most common early signs of dry AMD is drusen. Drusen are tiny yellow or white deposits under the retina. They often are found in people aged 60 years and older. The presence of small drusen is normal and does not cause vision loss. However, the presence of large and more numerous drusen raises the risk of developing advanced dry AMD or wet AMD. It is estimated that 1.8 million Americans aged 40 years and older are affected by AMD and an additional 7.3 million with large drusen are at substantial risk of developing AMD. The number of people with AMD is estimated to reach 2.95 million in 2020. AMD is the leading cause of permanent impairment of reading and fine or close-up vision among people aged 65 years and older. ii.Cataract: Cataract is a clouding of the eye’s lens and is the leading cause of blindness worldwide, and the leading cause of vision loss in the United States. Cataracts can occur at any age because of a variety of causes, and can be present at birth. Although treatment for the removal of cataract is widely available, access barriers such as insurance coverage, treatment costs, patient choice, or lack of awareness prevent many people from receiving the proper treatment. An estimated 20.5 million (17.2%) Americans aged 40 years and older have cataract in one or both eyes, and 6.1 million (5.1%) have had their lens removed operatively. The total number of people who have cataracts is estimated to increase to 30.1 million by 2020. iii. Diabetic Retinopathy: Diabetic retinopathy (DR) is a common complication of diabetes. It is the leading cause of blindness in American adults. It is characterized by progressive damage to the blood vessels of the retina, the light-sensitive tissue at the back of the eye that is necessary for good vision. DR
  • 8. progresses through four stages, mild nonproliferative retinopathy (microaneurysms), moderate nonproliferative retinopathy (blockage in some retinal vessels), severe nonproliferative retinopathy (more vessels are blocked leading to deprived retina from blood supply leading to growing new blood vessels), and proliferative retinopathy (most advanced stage). Diabetic retinopathy usually affects both eyes. The risks of DR are reduced through disease management that includes good control of blood sugar, blood pressure, and lipid abnormalities. Early diagnosis of DR and timely treatment reduce the risk of vision loss; however, as many as 50% of patients are not getting their eyes examined or are diagnosed too late for treatment to be effective. It is the leading cause of blindness among U.S. working-aged adults aged 20–74 years. An estimated 4.1 million and 899,000 Americans are affected by retinopathy and vision-threatening retinopathy, respectively. Iv.Glaucoma: Glaucoma is a group of diseases that can damage the eye's optic nerve and result in vision loss and blindness. Glaucoma occurs when the normal fluid pressure inside the eyes slowly rises. However, recent findings now show that glaucoma can occur with normal eye pressure. With early treatment, you can often protect your eyes against serious vision loss. There are two major categories “open angle” and “closed angle” glaucoma. Open angle, is a chronic condition that progress slowly over long period of time without the person noticing vision loss until the disease is very advanced, that is why it is called “sneak thief of sight." Angle closure can appear suddenly and is painful. Visual loss can progress quickly; however, the pain and discomfort lead patients to seek medical attention before permanent damage occurs. v.Amblyopia: Amblyopia, also referred to as “lazy eye,” is the most common cause of vision impairment in children. Amblyopia is the medical term used when the vision in one of the eyes is reduced because the eye and the brain are not working together properly. The eye itself looks normal, but it is not being used normally because the brain is favoring the other eye. Conditions leading to amblyopia include strabismus, an imbalance in the positioning of the two eyes; more nearsighted, farsighted, or astigmatic in one eye than the other eye, and rarely other eye conditions such as cataract. Unless it is successfully treated in early childhood amblyopia usually persists into adulthood, and is the most common cause of permanent one-eye vision impairment among children and young and middle-aged adults. An estimated 2%–3% of the population suffer from Amblyopia.
  • 9. Chapter-2 2.1 How artificial silicon Retina does works: The ASR contains about 3,500 microscopic solar cells that are able to convert light into electrical pulses, mimicking the function of cones and rods. To implant this device into the eye, surgeons make three tiny incisions no larger than the diameter of a needle in the white part of the eye. Through these incisions, the surgeons introduce a miniature cutting and vacuuming device that removes the gel in the middle of the eye and replaces it with saline. Next, a pinpoint opening is made in the retina through which they inject fluid to lift up a portion of the retina from the back of the eye, which creates a small pocket in the sub retinal space for the device to fit in. The retina is then resealed over the ASR. .Figure 5: Here you can see where the ASR is placedbetweenthe outer and innerretinal layers. For any microchip to work it needs power and the amazing thing about the ASR is that it receives all of its needed power from the light entering the eye. This means that with the ASR implant in place behind the retina, it receives all of the light entering the eye. This solar energy eliminates the need for any wires, batteries or other secondary devices to supply power. Another microchip device that would restore partial vision is currently in development called the artificial retina component chip (ARCC), this device is quite similar to the ASR. Both are made of silicon and both are powered by solar energy. The ARCC is also a very small device measuring 2 mm square and a thickness of .02 millimeters (.00078 inch). There are significant differences between the devices, however. According to researchers, the ARCC will give blind
  • 10. patients the ability to see 10 by 10 pixel images, which is about the size of a single letter on this page However, researchers have said that they could eventually develop a version of the chip that would allow 250 by 250 pixel array, which would allow those who were once blind to read a newspaper. 2.2 Working of artificial vision system: The main parts of this system are miniature video camera, a signal processor, and the brain implants. The tiny pinhole camera, mounted on a pair of eyeglasses, captures the scene in front of the wearer and sends it to a small computer on the patient's belt. The processor translates the image into a series of signals that the brain can understand, and then sends the information to the brain implant that is placed in patient’s visual cortex. And, if everything goes according to plan, the brain will "see" the image. Figures (6, 7) illustrating the AV SYSTEM. Light enters the camera, which then sends the image to a wireless wallet-sized computer for `processing. The computer transmits this information to an infrared LED screen on the goggles. The goggles reflect an infrared image into the eye and on to the retinal chip, stimulating photodiodes on the chip. The photodiodes mimic the retinal cells by converting light into electrical signals, which are then transmitted by cells in the inner retina via nerve pulses to the brain. The goggles are transparent so if the user still has some vision, they can match that with the new information - the device would cover about 10° of the wearer’s field of vision. The patient should wear sunglasses with a tiny pinhole camera mounted on one lensand an ultrasonic range finder on the other. Both devices communicate with a small computer carried on his hip, which highlights the edges between light and dark areas in the camera image. It then tells an adjacent computer to send appropriate signals to an array of small electrodes on the surface of patient’s brain, through wires entering his skull. The electrodes stimulate certain brain cells, making the person perceive the specks of light. The shifting patterns as scans across a scene tells him where light areas meet dark ones, letting him find the black cap on the white wall, for example. The device provides a sort of tunnelvision, reading an area about the size of a card 2 inches wide and 8 inches tall, held at arm's length
  • 11. Chapter-3 3.1 Advancements in creating Artificial Vision: Ceramic optical detectors based on the photo-ferroelectrics effect are being developed for direct implantation into the eyes of patients with retinal dystrophies. In retinal dystrophies where the optic nerve and retinal ganglia are intact (such as Retinitis Pigmentosa), direct retinal implant of an optical detector to stimulate retinal ganglia could allow patients to regain some sight. In such cases additional wiring to the brain cortex is not required, and for biologically inert detectors, surgical implantation can be quite direct. The detector currently being developed for this application is a thin film ferroelectric detector, which under optical illumination can generate a local photocurrent and photo voltage. The local electric current generated by this miniature detector excites the retinal neural circuit resulting in a signal at the optic nerve that may be translated by the cortex of the brain as "seeing light". Detectors based on PbLaZrTiO3(PLZT) and BiVMnO3 (BVMO) films exhibit a strong photo response in visible range overlapping eye response from 380 nm to 650 nm. The thin film detector heterostructures have been implanted into the eyes of rabbits for biocompatibility test, and have shown no biologicalincompatibilities. The bionic devices tested so far include both those attached to the back of the eye itself and those implanted directly in the brain. Patients with both types of implants describe seeing multiple points of light and, in some cases, crude outlines of objects. Placing electrodes in the eye has proved easier. During the past decade, work on these retinal implants has attracted growing government funding and commercial interest. Such implants zap electrical signals to nerves on the back of the eye, which then carry them to the brain. However, since these devices take advantage of surviving parts of the eye they will help only the subset of blind people whose blindness is due to retinal disease, by some estimates about 30% of the blind. Moreover, scientists don't believe any implant could help those blind since birth, because their brains never have learned to recognize vision. 3.2 What blind patients would not be able to use this device? We believe the device will be applicable to virtually all patients who are blind or who have very low vision. The only ones contraindicated would be a few blinded by serious brain damage, or who have chronic infections, etc. that preclude surgical implants. Patients who have a small amount of vision are not contraindicated. Visual cortex stimulation seems to work the same in both sighted and blind patients.
  • 12. 3.3 Bottlenecks raised by this technology: 1. The first and foremost thing is the cost .The miniaturization of equipment and more powerful computers have made this artificial vision possible, but it's not cheap: The operation, equipment and necessary training cost $70,000 per patient. And also may be much higher depending upon the context and severity. 2. It may not work for people blinded as children or as infants, because the visual cortex do not develop normally. But it will work for the vast majority of the blind -- 98 to 99 percent. 3. Researchers caution, however, that artificial vision devices are still highly experimental and practical systems are many years away. Even after they are refined, the first wave will most likely provide only crude images, such as the outline of a kitchen doorway. It does not function as well as the real eye, and does not have crystal-clear vision (as it is only a camera).The device is a very limited navigational aid, and it's a far cry from the visual experience normal people enjoy. 3.4 Other reasons causing blindness and their remedies: The main aim of Artificial Vision is to restore some degree of sight to the profoundly blind. Since blindness can result from defects at many different points along the visual pathway, there are accordingly a wide variety of proposed models for an "Artificial Eye". The earliest stage of visual processing is the transudation of light into electrical signals by the photoreceptors. If this is the only process that is interrupted in a blind individual, he or she may benefit from a Sub-Retinal Prosthesis, a device that is designed to replace only the photoreceptors in the retina. However, if the Optic Nerve itself is damaged, the only possibility for restoring sight is to directly stimulate the visual cortex. Cortical prosthesis is designed specifically for this task. Although the categories presented account for most of the research in Artificial Vision, there are a few more exotic techniques being developed. One of these is the BioHybrid Implant a device that incorporates living cells with man-made elements. Regardless of the specific design, all of these devices are working towards the same goal-- a permanent replacement for part of the human visual system.
  • 13. 3.5 conclusion: The electronic eye is the latest in high-tech gadgets aimed at helping millions of blind and visually impaired people. Although the images produced by the artificial eye were far from perfect, they could be clear enough to allow someone who is otherwise blind to recognize faces. The first useful artificial eye is now helping a blind man walk safely around and read large letters. Several efforts are now underway to create vision in otherwise blind eyes. While technically exciting, much more work in this area needs to be completed before anything is available to the majority of patients. Research is ongoing in two areas: cortical implants and retinal implants. There is still an enormous amount of work to be done in developing artificial retinas. In recent years, progress is being made towards sensory distribution devices for the blind. In the long run, there could be the possibility of brain implants. A brain implant or cortical implant provides visual input from a camera directly to the brain via electrodes in contact with the visual cortex at the backside of the head.