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What do you see if you look at your own retina with the same eye? (optical feedback)


When you record a video while pointing the viewfinder towards the screen showing a live preview you create optical feedback: video example. An anoalogous effect occurs when you turn your microphone towards the speaker.

Once you look at your own retina with the same eye, does our brain create a similar effect as recorded in the video? Or could it be something different all together?

Obviously the best way to find out is to 'just go ahead' and see for myself, but it seems as if I don't have the proper conditions to test this at home: The pupil gets too small in the mirror and thus the retina is plain dark. Such an experiment would require eye drops to force widen the pupil and allow for more light onto the retina.


There was an answer posted here and deleted again - which I think has found the error my question. Please undelete it :)

What the eye observes once it glances at the retina is a physically constant image of the retina.

In order for the optical feedback loop to work however, the retina image 'in' the mirror would need to be affected by what is projected onto the retina of the observing eye. Since the retina image in the mirror is constant (there is no link of any kind between whe mirrored retina an the observing retina) the projected image onto the retina of the observing eye is constant as well.

The loop is broken and there is no optical feedback.


You would see your retina and that's all. There would have no "mise-en-abyme".

In order to experience this feedback loop you describe, you need to see something which includes the total picture of what you see. For example: You might see a woman holding a frame of the totality of what you see.

When you look at your retina, you can't see something which includes the total picture of what you see, you just see your retina! It would probably work if the retina was a mirror (or any output device)

This question might not really a good fit for Biology.SE. You might have a chance to make a good fit by asking a question on the mechanistic nature of the process called mise-en-abyme on Phylosophy.SE. And ask wether one can live this same process with any of their sense (perception). You can ask whether the Larsen effect (audio feedback) is a similar process to the one we experience when looking at this picture and in what terms they are similar and in what terms they differ. If you ask such question, I welcome you to add the link on this post (except if the post get closed)!


Feedback means that the output from a device is fed back to it as new input. You can feed input to a retina, but cannot take its output.

You will get no feedback if the microphone is not linked to a speaker, or cannot hear the speaker.

You will get no feedback if the video camera is not pointing to the display.

Your eye consumes input, but this input is only used to change the state of your brain in mysterious ways. No output is produced. There is no "Kodak" organ in the human body which reproduces with fidelity the image seen by the retina*. Without output, there is nothing to feed back - same as how you can't get feedback when a camera is not linked to a display. A display, with human beings, would be analogous to a magic machine that reads your mind.

If you looked at your retina, you'd see your retina. Just like a camera pointed at a mirror would see a camera.

The closest thing you can do is imagine yourself, imagining yourself, imagining yourself… Although you would probably need to take mind-altering substances to experience this fully.


*: I say no organ exists, but it is possible for humans to reproduce an image they've seen. It's called "painting". Some famous painters apparently have included an image of themselves in their picture, depicted while painting the picture.

This isn't really a classical painting, but to give an example:

The trouble is that actually painting a picture takes a long time, so the feedback is very slow - each iteration may take days.


Color Optical Illusions

A combination of color, our perception and the structure of our eyes can result in some interesting optical illusions. Here are some examples.

After Image

Stare at the red dot.
What do you see when the image disappears?

When the screen goes white, most people will see an after image of the US flag. When we stare at a bright object for some time, there is a fatigue of the retinal process. Because of this fatigue, when the image disappears, we see the complimentary color. The complimentary color may linger for some time until the retinal process dies out.

Color Perception Optical Illusion

How many colors are there in this picture, not including white?

If you answered two, you're correct. A close inspection will show that the "new" colors in the middle are actually not new. They are perceived to be different because the two colors are placed next to each other.

The darker colors that seem to appear are caused by a dithering effect. Dithering occurs when colors are so close together that your eye mixes them to create a new color.

Color Dot Optical Illusion

Which circle is largest? Which is smallest?

All of the color dots are the same size. Color sensation is due to changes in the frequency of light that is detected by our eyes. Here's a link to a site discussing information about color, and it's potential to affect health.

Flag Color Optical Illusion

What is the difference between the two shades of green?

There is no difference. It is the same shade of green. If you don't believe it, cover up the other colors and you'll see that they are the same.

Our perception of color is affected by the contrast with the nearby colors. Here the other colors strongly affect the green to make it appear different.

Color Reading Optical Illusion

Read through this list of colors. But instead of reading the word, speak the color of each word.

If you are like most people, you found this exercise to be hard. This is known as the Stroop Effect. There is a conflict between what we read and what we perceive. Orange should not be blue. Indigo should not be gray. It is also possible that this task is difficult because it requires both hemispheres of our brain to work together.

Blue and Yellow Spinning Wheel Optical Illusion

What do you see when you stare at this high speed animation?

Do you see any other colors besides blue and yellow?

Because of different types of computers and monitors, this illusion may be more or less pronounced. If this illusion is drawn on a piece of paper and spun around, there can be some interesting color effects.

The color effects seem to be related to how fast color can be sensed in the cones of our eyes. Blue seems to be detected the fastest, while green seems to be detected the slowest. Red is in the middle. These effects can even be seen if the two colors are black and white.

Block Contrast Optical Illusion

Which block is larger?

They are the same size. The perceived size of an object is affected by the color surrounding it. Also, in this illusion, the framed object grabs more attention, making it seem larger.

Circle Contrast Optical Illusion

Which of these two dots is larger?

Both dots are the same size. This optical illusion shows how different colors can make a circle look different.


The hidden math behind your DMV’s eye test

At least once in your life, you must have squinted at the eye chart at the doctor’s office or DMV, trying to make out the blurry bottom line. The test seems simple enough, right? Read a random string of consonants and vowels on one line, then repeat the process with the line below until you can’t make out the letters anymore.

Turns out, there’s some very precise math that determines the size and arrangement of those block letters in order to test your ability to see details — known as your “visual acuity.” First developed in 1862 by Dutch ophthalmologist Herman Snellen, the prototypes of this eye chart began with abstract shapes. Eventually, the chart included those familiar block letters.

One of Snellen’s big accomplishments was standardizing the eye chart so that others could use the same principles to develop their own tests. So we decided to give it a try. In the video above, we trace the eye chart back to its origins and take a close look at the biology of visual acuity and the math that goes into testing its limits. Then, we go to ridiculous lengths to test my own eyesight. Spoiler alert: it’s awesome.


Diagnosis and Tests

How do you diagnose retinal vein occlusions?

    (OCT): This is a high definition image of the retina taken by a scanning ophthalmoscope with a resolution of 5 microns. These images can determine the presence of swelling and edema by measuring the thickness of your retina. The doctor will use OCT images to objectively document the progress of the disease throughout the course of your treatment.
  • Ophthalmoscopy: The changes caused by RVO may be seen by examination of the retina with an instrument called an ophthalmoscope.
  • Fluorescein angiography: This is a test procedure in which a dye that is injected into a vein in the arm travels to the retinal blood vessels. Special photographs allow the physician to see the vessels.

How Do Our Photoreceptors Work?

Click on these eyes to see photoreceptors

We have two main types of photoreceptors called rods and cones. They are called rods and cones because of their shapes. These cells are located in a layer at the back of the eye called the retina. Rods are used to see in very dim light and only show the world to us in black and white.

This is why you see only black and white when you are outside in the evening or in a dimly lit room. The other type of photoreceptors, the cones, allow us to see colors. They are not as sensitive as the rods so they only work in bright light. There are three types of cones, one for each of the three main colors we see, red, green and blue. (click on the eyes above to learn more)

Some people have a genetic defect that makes one or more of the cones fail. This condition is known as color deficiency. You may have heard it called color blindness. Color blindness is fairly common, affecting about nine percent of all humans. It is much more common in men than in women. To test for color blindness a special picture called an Ishihara test is used. If you jump to our color test page you will be able to test yourself and also experience another interesting phenomenon of our color vision.

What about other animals? What kind of colors do they see? Most animals see fewer colors than we do, but some see more! We know this by looking at how many kinds of cone photoreceptors they have. Another good indication of what an animal can see is by looking at their own colors. The colors of their prey are also an indication of an animal's ability to see color. We have made a table of some common animals and what colors they see.


Simple Anatomy of the Retina by Helga Kolb

When an ophthalmologist uses an ophthalmoscope to look into your eye he sees the following view of the retina (Fig. 1).

In the center of the retina is the optic nerve, a circular to oval white area measuring about 2 x 1.5 mm across. From the center of the optic nerve radiates the major blood vessels of the retina. Approximately 17 degrees (4.5-5 mm), or two and half disc diameters to the left of the disc, can be seen the slightly oval-shaped, blood vessel-free reddish spot, the fovea, which is at the center of the area known as the macula by ophthalmologists.

Fig. 1. Retina as seen through an opthalmoscope
CLICK HERE to see an animation (from the iris to the retina) (Quicktime movie)

A circular field of approximately 6 mm around the fovea is considered the central retina while beyond this is peripheral retina stretching to the ora serrata, 21 mm from the center of the retina (fovea). The total retina is a circular disc of between 30 and 40 mm in diameter (Polyak, 1941 Van Buren, 1963 Kolb, 1991).

Fig. 1.1. A schematic section through the human eye with a schematic enlargement of the retina

The retina is approximately 0.5 mm thick and lines the back of the eye. The optic nerve contains the ganglion cell axons running to the brain and, additionally, incoming blood vessels that open into the retina to vascularize the retinal layers and neurons (Fig. 1.1). A radial section of a portion of the retina reveals that the ganglion cells (the output neurons of the retina) lie innermost in the retina closest to the lens and front of the eye, and the photosensors (the rods and cones) lie outermost in the retina against the pigment epithelium and choroid. Light must, therefore, travel through the thickness of the retina before striking and activating the rods and cones (Fig. 1.1). Subsequently the absorbtion of photons by the visual pigment of the photoreceptors is translated into first a biochemical message and then an electrical message that can stimulate all the succeeding neurons of the retina. The retinal message concerning the photic input and some preliminary organization of the visual image into several forms of sensation are transmitted to the brain from the spiking discharge pattern of the ganglion cells.

A simplistic wiring diagram of the retina emphasizes only the sensory photoreceptors and the ganglion cells with a few interneurons connecting the two cell types such as seen in Figure 2.

When an anatomist takes a vertical section of the retina and processes it for microscopic examination it becomes obvious that the retina is much more complex and contains many more nerve cell types than the simplistic scheme (above) had indicated. It is immediately obvious that there are many interneurons packed into the central part of the section of retina intervening between the photoreceptors and the ganglion cells (Fig 3).

All vertebrate retinas are composed of three layers of nerve cell bodies and two layers of synapses (Fig. 4). The outer nuclear layer contains cell bodies of the rods and cones, the inner nuclear layer contains cell bodies of the bipolar, horizontal and amacrine cells and the ganglion cell layer contains cell bodies of ganglion cells and displaced amacrine cells. Dividing these nerve cell layers are two neuropils where synaptic contacts occur (Fig. 4).

The first area of neuropil is the outer plexiform layer (OPL) where connections between rod and cones, and vertically running bipolar cells and horizontally oriented horizontal cells occur (Figs. 5 and 6).

Fig. 5. 3-D block of retina with OPL highlighted
Fig. 6. Light micrograph of a vertical section through the OPL

The second neuropil of the retina, is the inner plexiform layer (IPL), and it functions as a relay station for the vertical-information-carrying nerve cells, the bipolar cells, to connect to ganglion cells (Figs. 7 and 8). In addition, different varieties of horizontally- and vertically-directed amacrine cells, somehow interact in further networks to influence and integrate the ganglion cell signals. It is at the culmination of all this neural processing in the inner plexiform layer that the message concerning the visual image is transmitted to the brain along the optic nerve.

Fig. 7. 3-D block of retina with IPL highlighted
Fig. 8. Light micrograph of a vertical section through the IPL

2. Central and peripheral retina compared.

Central retina close to the fovea is considerably thicker than peripheral retina (compare Figs. 9 and 10). This is due to the increased packing density of photoreceptors, particularly the cones, and their associated bipolar and ganglion cells in central retina compared with peripheral retina.

Fig. 9. Light micrograph of a vertical section through human central retina
Fig. 10. Light micrograph of a vertical section through human peripheral retina
  • Central retina is cone-dominated retina whereas peripheral retina is rod-dominated. Thus in central retina the cones are closely spaced and the rods fewer in number between the cones (Figs. 9 and 10).
  • The outer nuclear layer (ONL), composed of the cell bodies of the rods and cones is about the same thickness in central and peripheral retina. However in the peripheral the rod cell bodies outnumber the cone cell bodies while the reverse is true for central retina. In central retina, the cones have oblique axons displacing their cell bodies from their synaptic pedicles in the outer plexiform layer (OPL). These oblique axons with accompanying Muller cell processes form a pale-staining fibrous-looking area known as the Henle fibre layer. The latter layer is absent in peripheral retina.
  • The inner nuclear layer (INL) is thicker in the central area of the retina compared with peripheral retina, due to a greater density of cone-connecting second-order neurons (cone bipolar cells) and smaller-field and more closely-spaced horizontal cells and amacrine cells concerned with the cone pathways (Fig. 9). As we shall see later, cone-connected circuits of neurons are less convergent in that fewer cones impinge on second order neurons, than rods do in rod-connected pathways.
  • A remarkable difference between central and peripheral retina can be seen in the relative thicknesses of the inner plexiform layers (IPL), ganglion cell layers (GCL) and nerve fibre layer (NFL) (Figs. 9 and 10). This is again due to the greater numbers and increased packing-density of ganglion cells needed for the cone pathways in the cone-dominant foveal retina as compared the rod-dominant peripheral retina. The greater number of ganglion cells means more synaptic interaction in a thicker IPL and greater numbers of ganglion cell axons coursing to the optic nerve in the nerve fibre layer (Fig. 9).

3. Muller glial cells.

Fig. 11. Vertical view of Golgi stained Muller glial cells

Muller cells are the radial glial cells of the retina (Fig. 11). The outer limiting membrane (OLM) of the retina is formed from adherens junctions between Muller cells and photoreceptor cell inner segments. The inner limiting membrane (ILM) of the retina is likewise composed of laterally contacting Muller cell end feet and associated basement membrane constituents.

The OLM forms a barrier between the subretinal space, into which the inner and outer segments of the photoreceptors project to be in close association with the pigment epithelial layer behind the retina, and the neural retina proper. The ILM is the inner surface of the retina bordering the vitreous humor and thereby forming a diffusion barrier between neural retina and vitreous humor (Fig. 11).

Throughout the retina the major blood vessels of the retinal vasculature supply the capillaries that run into the neural tissue. Capillaries are found running through all parts of the retina from the nerve fibre layer to the outer plexiform layer and even occasionally as high as in the outer nuclear layer. Nutrients from the vasculature of the choriocapillaris (cc) behind the pigment epithelium layer supply the delicate photoreceptor layer.

4. Foveal structure.

The center of the fovea is known as the foveal pit (Polyak, 1941) and is a highly specialized region of the retina different again from central and peripheral retina we have considered so far. Radial sections of this small circular region of retina measuring less than a quarter of a millimeter (200 microns) across is shown below for human (Fig. 12a) and for monkey (Fig.12b).

Fig. 12a. Vertical section of the human fovea from Yamada (1969)
Fig. 12b. Vertical section of the monkey fovea from Hageman and Johnson (1991)

The fovea lies in the middle of the macula area of the retina to the temporal side of the optic nerve head (Fig. 13a, A, B). It is an area where cone photoreceptors are concentrated at maximum density, with exclusion of the rods, and arranged at their most efficient packing density which is in a hexagonal mosaic. This is more clearly seen in a tangential section through the foveal cone inner segments (Fig. 13b).

Fig. 13. Tangential section through the human fovea

Below this central 200 micron diameter central foveal pit, the other layers of the retina are displaced concentrically leaving only the thinnest sheet of retina consisting of the cone cells and some of their cell bodies (right and left sides of Figs. 12a and 12b). This is particularly well seen in optical coherence tomography (OCT) images of the living eye and retina (Fig. 13a, B). Radially distorted but complete layering of the retina then appears gradually along the foveal slope until the rim of the fovea is made up of the displaced second- and third-order neurons related to the central cones. Here the ganglion cells are piled into six layers so making this area, called the foveal rim or parafovea (Polyak, 1941), the thickest portion of the entire retina.

5. Macula lutea.

The whole foveal area including foveal pit, foveal slope, parafovea and perifovea is considered the macula of the human eye. Familiar to ophthalmologists is a yellow pigmentation to the macular area known as the macula lutea (Fig. 14).

This pigmentation is the reflection from yellow screening pigments, the xanthophyll carotenoids zeaxanthin and lutein (Balashov and Bernstein, 1998), present in the cone axons of the Henle fibre layer. The macula lutea is thought to act as a short wavelength filter, additional to that provided by the lens (Rodieck, 1973). As the fovea is the most essential part of the retina for human vision, protective mechanisms for avoiding bright light and especially ultraviolet irradiation damage are essential. For, if the delicate cones of our fovea are destroyed we become blind.

Fig. 14. Ophthalmoscopic appearance of the retina to show macula lutea
Fig. 15. Vertical section through the monkey fovea to show the distribution of the macula lutea. From Snodderly et al., 1984

The yellow pigment that forms the macula lutea in the fovea can be clearly demonstrated by viewing a section of the fovea in the microscope with blue light (Fig. 15). The dark pattern in the foveal pit extending out to the edge of the foveal slope is caused by the macular pigment distribution (Snodderly et al., 1984).

If one were to visualize the foveal photoreceptor mosaic as though the visual pigments in the individual cones were not bleached, one would see the picture shown in Figure 16 (lower frame) (picture from Lall and Cone, 1996). The short-wavelength sensitive cones on the foveal slope look pale yellow green, the middle wavelength cones, pink and the long wavelength sensitive cones, purple. If we now add the effect of the yellow screening pigment of the macula lutea we see the appearance of the cone mosaic in Figure 16 (upper frame). The macula lutea helps enhance achromatic resolution of the foveal cones and blocks out harmful UV light irradiation (Fig. 16 from Abner Lall and Richard Cone, unpublished data).

6. Ganglion cell fiber layer.

The ganglion cell axons run in the nerve fiber layer above the inner limiting membrane towards the optic nerve head in a arcuate form (Fig. 00, streaming pink fibers). The fovea is, of course, free of a nerve fiber layer as the inner retina and ganglion cells are pushed away to the foveal slope. The central ganglion cell fibers run around the foveal slope and sweep in the direction of the optic nerve. Peripheral ganglion cell axons continue this arcing course to the optic nerve with a dorso/ventral split along the horizontal meridian (Fig. 00). Retinal topography is maintained in the optic nerve, through the lateral geniculate to the visual cortex.

7. Blood supply to the retina.

There are two sources of blood supply to the mammalian retina: the central retinal artery and the choroidal blood vessels. The choroid receives the greatest blood flow (65-85%) (Henkind et al., 1979) and is vital for the maintainance of the outer retina (particularly the photoreceptors) and the remaining 20-30% flows to the retina through the central retinal artery from the optic nerve head to nourish the inner retinal layers. The central retinal artery has 4 main branches in the human retina (Fig. 17).

Fig. 17. Fundus photograph showing flourescein imaging of the major arteries and veins in a normal human right eye retina. The vessels emerge from the optic nerve head and run in a radial fashion curving towards and around the fovea (asterisk in photograph) (Image courtesy of Isabel Pinilla, Spain)

The arterial intraretinal branches then supply three layers of capillary networks i.e. 1) the radial peripapillary capillaries (RPCs) and 2) an inner and 3) an outer layer of capillaries (Fig. 18a). The precapillary venules drain into venules and through the corresponding venous system to the central retinal vein (Fig. 18b).

Fig. 18a. Flatmount view of a rat retina stained with NADPH-diaphorase at the level of focus of a major artery and arterioles. (Courtesy of Toby Holmes, Moran Eye Center)
Fig. 18b. Flatmount view of a rat retina stained with NADPH-diaphorase at the level of focus of a major vein and venules. (Courtesy of Toby Holmes, Moran Eye Center)

The radial peripapillary capillaries (RPCs) are the most superfical layer of capillaries lying in the inner part of the nerve fiber layer, and run along the paths of the major superotemporal and inferotemporal vessels 4-5 mm from the optic disk (Zhang, 1994). The RPCs anatomose with each other and the deeper capillaries. The inner capillaries lie in the ganglion cell layers under and parallel to the RPCs. The outer capillary network runs from the inner plexiform layer to the outer plexiform layer thought the inner nuclear layer (Zhang, 1974).

As will be noticed from the flourescein angiography of Figure 17, there as a ring of blood vessels in the macular area around a blood vessel- and capillary-free zone 450-600 um in diameter, denoting the fovea. The macular vessels arise from branches of the superior temporal and inferotemporal arteries. At the border of the avascular zone the capillaries become two layered and finally join as a single layered ring. The collecting venules are more deep (posterior) to the arterioles and drain blood flow back into the main veins (Fig. 19, from Zhang, 1974). In the rhesus monkey this perimacular ring and blood vessel free fovea is clearly seen in the beautiful drawings made by Max Snodderly’s group (Fig. 20, Sodderly et al., 1992.)

Fig. 19. The macular vessels of the monkey eye form a ring around the avascular fovea (star)(From Zhang, 1994)
Fig. 20. Diagram of the retinal vasculature around the fovea in the rhesus monkey derived from more than 80 microscope fields. (From Snodderly et al., 1992)

The choroidal arteries arise from long and short posterior ciliary arteries and branches of Zinn’s circle (around the optic disc). Each of the posterior ciliary arteries break up into fan-shaped lobules of capillaries that supply localized regions of the choroid (Hayreh, 1975). The macular area of the choroidal vessels are not specialized like the retinal blood supply is (Zhang, 1994). The arteries pierce the sclera around the optic nerve and fan out to form the three vascular layers in the choroid: outer (most scleral), medial and inner (nearest Bruchs membrane of the pigment epithelium) layers of blood vessels. This is clearly shown in the corrosion cast of a cut face of the human choroid in Figure 21a (Zhang, 1974). The corresponding venous lobules drain into the venules and veins that run anterior towards the equator of the eyeball to enter the vortex veins (Fig. 21b). One or two vortex veins drain each of the 4 quadrants of the eyeball. The vortex veins penetrate the sclera and merge into the ophthalmic vein as shown in the corrosion cast of Figure 21b (Zhang. 1994).

Fig. 21a. The three vascular layers in the choroid: outer arteries and veins(red/blue arrow), medial arterioles and venules(red arrow) and inner capillary bed (yellow star. Corrosion cast of a cut face of the human choroid (From Zhang, 1994)
Fig. 21b. Corrosion cast of the upper back of the human eye with the sclera removed. The vortex veins collect the blood from the equator of the eye and merge with the ophthalmic vein. (From Zhang, 1994).

8. Degenerative diseases of the human retina.

The human retina is a delicate organization of neurons, glia and nourishing blood vessels. In some eye diseases, the retina becomes damaged or compromised, and degenerative changes set in that eventally lead to serious damage to the nerve cells that carry the vital mesages about the visual image to the brain. We indicate four different conditions where the retina is diseased and blindness may be the end result. Much more information concerning pathology of the whole eye and retina can be found in a website made by eye pathologist Dr. Nick Mamalis, Moran Eye Center.

Fig. 22. A view of the fundus of the eye and of the retina in a patient who has age-related macular degeneration.
Fig. 23. A view of the fundus of the eye and of the retina in a patient who has advanced glaucoma.

Age related macular degeneration is a common retinal problem of the aging eye and a leading cause of blindness in the world. The macular area and fovea become compromised due to the pigment epithelium behind the retina degenerating and forming drusen (white spots, Fig. 22) and allowing leakage of fluid behind the fovea. The cones of the fovea die causing central visual loss so we cannot read or see fine detail.

Glaucoma (Fig. 23) is also a common problem in aging, where the pressure within the eye becomes elevated. The pressure rises because the anterior chamber of the eye cannot exchange fluid properly by the normal aqueous outflow methods. The pressure within the vitreous chamber rises and compromises the blood vessels of the optic nerve head and eventually the axons of the ganglion cells so that these vital cells die. Treatment to reduce the intraocular pressure is essential in glaucoma.

Fig. 24. A view of the fundus of the eye and of the retina in a patient who has retinitis pigmentosa
Fig. 25. A view of the fundus of the eye and of the retina in a patient who has advanced diabetic retinopathy

Retinits pigmentosa (Fig. 24) is a nasty hereditary disease of the retina for which there is no cure at present. It comes in many forms and consists of large numbers of genetic mutations presently being analysed. Most of the faulty genes that have been discoverd concern the rod photoreceptors. The rods of the peripheral retina begin to degenerate in early stages of the disease. Patients become night blind gradually as more and more of the peripheral retina (where the rods reside) becomes damaged. Eventally patients are reduced to tunnel vision with only the fovea spared the disease process. Characteristic pathology is the occurence of black pigment in the peripheral retina and thinned blood vessels at the optic nerve head (Fig. 24).

Diabetic retinopathy is a side effect of diabetes that affects the retina and can cause blindness (Fig. 25). The vital nourishing blood vessels of the eye become compromised, distorted and multiply in uncontrollable ways. Laser treatment for stopping blood vessel proliferation and leakage of fluid into the retina, is the commonest treatment at present.

9. References.

Balashov NA, Bernstein PS. Purification and identification of the components of the human macular carotenoid metabolism pathways. Invest Ophthal Vis Sci.199839:s38.

Hageman GS, Johnson LV. The photoreceptor-retinal pigmented epithelium interface. In: Heckenlively JR, Arden GB, editors. Principles and practice of clinical electrophysiology of vision. St. Louis: Mosby Year Book 1991. p. 53-68.

Harrington, D.O. and Drake, M.V. (1990) The Visual Fields, 6th ed. Mosby. St. Louis.

Hayreh SS. Segmental nature of the choroidal vasculature. Br J Ophthal. 197559:631–648. [PubMed] [Free Full text in PMC]

Henkind P, Hansen RI, Szalay J. Ocular circulation. In: Records RE, editor. Physiology of the human eye and visual system. New York: Harper & Row 1979. p. 98-155.

Kolb H. The neural organization of the human retina. In: Heckenlively JR, Arden GB, editors. Principles and practices of clinical electrophysiology of vision. St. Louis: Mosby Year Book Inc. 1991. p. 25-52.

Polyak SL. The retina. Chicago: University of Chicago Press 1941.

Rodieck RW. The vertebrate retina: principles of structure and function. San Francisco: W.H. Freeman and Company 1973.

Snodderly DM, Auran JD, Delori FC. The macular pigment. II. Spatial distribution in primate retina. Invest Ophthal Vis Sci. 198425:674–685. [PubMed]

Snodderly DM, Weinhaus RS, Choi JC. Neural-vascular relationships in central retina of Macaque monkeys (Macaca fascicularis). J Neurosci. 199212:1169–1193.[PubMed]

Van Buren JM. The retinal ganglion cell layer. Springfield (IL): Charles C. Thomas 1963.

Yamada E. Some structural features of the fovea centralis in the human retina. Arch Ophthal. 196982:151–159. [PubMed]

Zhang HR. Scanning electron-microscopic study of corrosion casts on retinal and choroidal angioarchitecture in man and animals. Prog Ret Eye Res. 199413:243–270.


World's first spherical artificial eye has 3D retina

An international team led by scientists at the Hong Kong University of Science and Technology (HKUST) has recently developed the world's first 3D artificial eye with capabilities better than existing bionic eyes and in some cases, even exceed those of the human eyes, bringing vision to humanoid robots and new hope to patients with visual impairment.

Scientists have spent decades trying to replicate the structure and clarity of a biological eye, but vision provided by existing prosthetic eyes -- largely in the form of spectacles attached with external cables, are still in poor resolution with 2D flat image sensors. The Electrochemical Eye (EC-Eye) developed at HKUST, however, not only replicates the structure of a natural eye for the first time, but may actually offer sharper vision than a human eye in the future, with extra functions such as the ability to detect infrared radiation in darkness.

The key feature allowing such breakthroughs is a 3D artificial retina -- made of an array of nanowire light sensors which mimic the photoreceptors in human retinas. Developed by Prof. FAN Zhiyong and Dr. GU Leilei from the Department of Electronic and Computer Engineering at HKUST, the team connected the nanowire light sensors to a bundle of liquid-metal wires serving as nerves behind the human-made hemispherical retina during the experiment, and successfully replicated the visual signal transmission to reflect what the eye sees onto the computer screen.

In the future, those nanowire light sensors could be directly connected to the nerves of the visually impaired patients. Unlike in a human eye where bundles of optic nerve fibers (for signal transmission) need to route through the retina via a pore -- from the front side of the retina to the backside (thus creating a blind spot in human vision) before reaching the brain the light sensors that now scatters across the entire human-made retina could each feed signals through its own liquid-metal wire at the back, thereby eliminating the blind spot issue as they do not have to route through a single spot.

Apart from that, as nanowires have even higher density than photoreceptors in human retina, the artificial retina can thus receive more light signals and potentially attain a higher image resolution than human retina -- if the back contacts to individual nanowires are made in the future. With different materials used to boost the sensors' sensitivity and spectral range, the artificial eye may also achieve other functions such as night vision.

"I have always been a big fan of science fiction, and I believe many technologies featured in stories such as those of intergalactic travel, will one day become reality. However, regardless of image resolution, angle of views or user-friendliness, the current bionic eyes are still of no match to their natural human counterpart. A new technology to address these problems is in urgent need, and it gives me a strong motivation to start this unconventional project," said Prof. Fan, whose team has spent nine years to complete the current study from idea inception.

The team collaborated with the University of California, Berkeley on this project and their findings were recently published in the journal Nature.

"In the next step, we plan to further improve the performance, stability and biocompatibility of our device. For prosthesis application, we look forward to collaborating with medical research experts who have the relevant expertise on optometry and ocular prosthesis," Prof. Fan added.

The working principle of the artificial eye involves an electrochemical process which is adopted from a type of solar cell. In principle, each photo sensor on the artificial retina can serve as a nanoscale solar cell. With further modification, the EC-Eye can be a self-powered image sensor, so there is no need for external power source nor circuitry when used for ocular prosthesis, which will be much more user-friendly as compared with the current technology.


Other tests carried out in the ophthalmology department [12]

Other tests that are routinely performed in specialist units include:

  • Visual field assessment - using static and kinetic perimeters. Perimetry or campimetry systematically tests the visual field through the detection of the presence of test targets on a defined background. Perimetry maps and quantifies the visual field, especially at the extreme periphery. Automated perimeters are used widely.
  • Ultrasound - to visualise the structures of lens, vitreous and retina.
  • Exophthalmometer - to assess proptosis (eg, thyroid eye disease). There are several types of exophthalmometers, some of which measure the distance of the corneal apex from the level of the lateral orbital rim while others measure the relative difference between each eye
  • Keratometry - this is the measurement of the corneal curvature, which determines the power of the cornea. Differences in power across the cornea result in astigmatism. Keratometry can be done manually or using automated devices. Keratometry allows visualisation of the pre-corneal tear film and a dynamic view of the surface of the cornea and of the tear film. You can recognise areas of corneal surface irregularity or compromise. If the tear film is oily or disrupted, or the cornea has subtle dystrophy or degeneration, it will be reflected in the quality of the measurements.
  • Hess chart - this maps extraocular muscle movement and assesses diplopia. In the Hess test the patient's left and right eyes see two similar grids superimposed by angled mirrors. They are then asked to point out the grid's intersection points with a marker. In a normal patient, the results would be centred on each chart. Distortion in caused by unco-ordinated movements of the eye muscles.
  • Fluorescein angiography - this allows the assessor to visualise and map retinal and choroidal vessels and to identify abnormalities.
  • Optical coherence tomography (OCT) - uses light waves to take detailed cross-section images of the retina. Imaging of retinal layers helps with diagnosis and provides treatment guidance for glaucoma and retinal disease, such as age-related macular degeneration and diabetic retinopathy. The OCT machine scans the eye without touching it, through a dilated pupil. Scanning takes about 5-10 minutes.
  • Visually evoked potential (VEP), also called visually evoked response (VER) and visually evoked cortical potential (VECP) - this measures electrical potentials, initiated by brief visual stimuli, recorded from the scalp overlying the visual cortex. VEPs are used primarily to measure the functional integrity of the visual pathways from retina via the optic nerves to the visual cortex. Any abnormality that affects the visual pathways or visual cortex can affect the VEP - eg, cortical blindness due to meningitis or anoxia, optic neuritis as a consequence of demyelination, optic atrophy, stroke and compression of the optic pathways. Myelin plaques (found in multiple sclerosis) tend to slow the speed of VEP wave peaks. Compression of the optic pathways reduces amplitude of wave peaks.

Further reading and references

Red eye NICE CKS, October 2016 (UK access only)

Glaucoma NICE CKS, November 2020 (UK access only)

Conjunctivitis - infective NICE CKS, April 2018 (UK access only)

Biousse V, Bruce BB, Newman NJ Ophthalmoscopy in the 21st century: The 2017 H. Houston Merritt Lecture. Neurology. 2018 Jan 2390(4):167-175. doi: 10.1212/WNL.0000000000004868. Epub 2017 Dec 22.

Takusewanya M How to take a complete eye history. Community Eye Health. 201932(107):44-45. Epub 2019 Dec 17.

Bell FC The External Eye Examination

Romanchuk KG Seidel's test using 10% fluorescein. Can J Ophthalmol. 1979 Oct14(4):253-6.

Kennedy SA, Noble J, Wong AM Examining the pupils. CMAJ. 2013 Jun 11185(9):E424. doi: 10.1503/cmaj.120306. Epub 2013 Feb 11.

Bowman R, Foster A Testing the red reflex. Community Eye Health. 201831(101):23.

Schneiderman H The Funduscopic Examination

Anstice NS, Thompson B The measurement of visual acuity in children: an evidence-based update. Clin Exp Optom. 2014 Jan97(1):3-11. doi: 10.1111/cxo.12086. Epub 2013 Jul 31.

Crumbie L Cranial nerves examination: Optic nerve, 2020.

Yadav S, Tandon R Comprehensive eye examination: what does it mean? Community Eye Health. 201932(107):S1-S4. Epub 2019 Dec 17.

Sanders RD Cranial Nerves III, IV, and VI: Oculomotor Function. Psychiatry (Edgmont). 2009 Nov6(11):34-9.


Try These 3 Fun Tests To Find Your Visual Blind Spot

When we talk of `blind spots’, we always think of driving with an area of the road not visible through the rear-view or side-view mirrors. But there is another kind of `blind spot’ that all humans have in each eye. These blind spots are natural, and we are not even aware of them because the brain fills in the gaps in our vision, based on whatever information it has about what our eyes are looking at.

If you’re interested in the science behind this phenomenon, it is this:

Light enters the eye by passing through the pupil and hitting the retina at the back. The retina is encased in light-sensing proteins, which transmit what they sense to the optic nerve. The optic nerve, in turn, relays that message to the brain. The blind spots occur because the optic nerve ends in the field of the retina itself. Whatever shortfall there is about visual information, the brain fills in by looking at the surrounding picture, and as a result, we are never conscious of the existence of blind spots as we go about our day-to-day lives.

But they’re there alright, and you can test your own blind spot by looking at the images below:

  • Look at the image above with the plus sign and the circle.
  • Look straight at the image, with your nose positioned somewhere between the plus and the circle.
  • Close your left eye, and focus your eyes on the plus sign with your right eye. Do not look deliberately at the circle.
  • Now move closer to the image, slowly. Don’t take your focus off the plus sign while you are doing this.
  • At some point between 10”-14”, the circle will disappear from your peripheral vision. And the brain will read the surrounding white color to fill up the empty space.
  • This exact spot is your blind spot.

Now let’s try the same exercise with the new image above.

  • Position your head to look straight at the image.
  • Cover your left eye, and look at the plus in the middle of the green background with your right eye.
  • Move closer to the screen as before. When you hit your blind spot, the circle will disappear and the brain will fill the gap with the surrounding yellow color.

The brain’s habit of using surrounding visual information to make up for a missing piece in the picture is even more apparent with this third image.

  • Cover the left eye and look at the plus sign with your right eye.
  • When you the hit the blind spot, the yellow circle will disappear and the brain will fill the gap with another red circle – information it picked up by assessing all the red circles that make up the surrounding area.

To take a deeper dive into your vision, schedule a free consultation with the specialists at LASIK of Nevada today!
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Exercise and Posterior Vitreous Detachment

How Long Before Resuming Normal Exercise After a Retinal Detachment?

Strenuous exercise should be avoided for six weeks after the onset of a posterior vitreous detachment. This is the time when the retina is most at risk for detachment. Avoid activities that are jarring such as running, aerobics, and basketball. Also avoid heavy lifting. After the diagnosis of a posterior vitreous detachment is made, typically you will be seen at a six to eight week interval following the initial visit. Your eye care provider will be able to determine if the vitreous is completely detached and the tension on the retina is gone. Wait for the all clear from your doctor to resume your regular activities.


Watch the video: What You See First Reveals Unexpected Truth About You (November 2021).