In studies of the genetic predisposition of refractive error, there is a correlation between environmental factors and the risk of developing myopia. Myopia has been observed in individuals with visually intensive occupations. Reading has also been found to be a predictor of myopia in children. It has been reported that children with myopia spent significantly more time reading than non-myopic children who spent more time playing outdoors. Socioeconomic status and higher levels of education have also been reported to be a risk factor for myopia.

Blindness can occur in combination with such conditions as intellectual disability, autism spectrum disorders, cerebral palsy, hearing impairments, and epilepsy. Blindness in combination with hearing loss is known as deafblindness.

It has been estimated that over half of completely blind people have non-24-hour sleep–wake disorder, a condition in which a person's circadian rhythm, normally slightly longer than 24 hours, is not entrained (synchronized) to the light/dark cycle.

Of these, cataract is responsible for >65%, or more than 22 million cases of blindness, and glaucoma is responsible for 6 million cases.

Cataracts: is the congenital and pediatric pathology that describes the greying or opacity of the crystalline lens, which is most commonly caused by intrauterine infections, metabolic disorders, and genetically transmitted syndromes. Cataracts are the leading cause of child and adult blindness that doubles in prevalence with every ten years after the age of 40. Consequently, today cataracts are more common among adults than in children. That is, people face higher chances of developing cataracts as they age. Nonetheless, cataracts tend to have a greater financial and emotional toll upon children as they must undergo expensive diagnosis, long term rehabilitation, and visual assistance. Also, according to the Saudi Journal for Health Sciences, sometimes patients experience irreversible amblyopia after pediatric cataract surgery because the cataracts prevented the normal maturation of vision prior to operation. Despite the great progress in treatment, cataracts remain a global problem in both economically developed and developing countries. At present, with the variant outcomes as well as the unequal access to cataract surgery, the best way to reduce the risk of developing cataracts is to avoid smoking and extensive exposure to sun light (i.e. UV-B rays).

The yearly cost of correcting refractive errors is estimated at 3.9 to 7.2 billion dollars in the United States.

Other causes of color blindness include brain or retinal damage caused by shaken baby syndrome, accidents and other trauma which produce swelling of the brain in the occipital lobe, and damage to the retina caused by exposure to ultraviolet light (10–300 nm). Damage often presents itself later on in life.

Color blindness may also present itself in the spectrum of degenerative diseases of the eye, such as age-related macular degeneration, and as part of the retinal damage caused by diabetes. Another factor that may affect color blindness includes a deficiency in Vitamin A.

Some subtle forms of colorblindness may be associated with chronic solvent-induced encephalopathy (CSE), caused by longtime exposure to solvent vapors.

Red–green color blindness can be caused by ethambutol, a drug used in the treatment of tuberculosis.

Vitamin A supplementation plays an important role, specifically vitamin A deficiency is a top causes of preventable childhood blindness. Though in measles cases, the administration of the vitamin to offset visual impairment has not been proven effective, as of yet.

Color blindness is typically inherited. It is most commonly inherited from mutations on the X chromosome but the mapping of the human genome has shown there are many causative mutations—mutations capable of causing color blindness originate from at least 19 different chromosomes and 56 different genes (as shown online at the Online Mendelian Inheritance in Man (OMIM)).

Two of the most common inherited forms of color blindness are protanomaly (and, more rarely, protanopia – the two together often known as "protans") and deuteranomaly (or, more rarely, deuteranopia – the two together often referred to as "deutans").

Both "protans" and "deutans" (of which the deutans are by far the most common) are known as "red–green color-blind" which is present in about 8 percent of human males and 0.6 percent of females of Northern European ancestry.

Some of the inherited diseases known to cause color blindness are:

- cone dystrophy

- cone-rod dystrophy

- achromatopsia (a.k.a. rod monochromatism, stationary cone dystrophy or cone dysfunction syndrome)

- blue cone monochromatism (a.k.a. blue cone monochromacy or X-linked achromatopsia)

- Leber's congenital amaurosis

- retinitis pigmentosa (initially affects rods but can later progress to cones and therefore color blindness).

Inherited color blindness can be congenital (from birth), or it can commence in childhood or adulthood. Depending on the mutation, it can be stationary, that is, remain the same throughout a person's lifetime, or progressive. As progressive phenotypes involve deterioration of the retina and other parts of the eye, certain forms of color blindness can progress to legal blindness, i.e., an acuity of 6/60 (20/200) or worse, and often leave a person with complete blindness.

Color blindness always pertains to the cone photoreceptors in retinas, as the cones are capable of detecting the color frequencies of light.

About 8 percent of males, and 0.6 percent of females, are red-green color blind in some way or another, whether it is one color, a color combination, or another mutation. The reason males are at a greater risk of inheriting an X linked mutation is that males only have one X chromosome (XY, with the Y chromosome carrying altogether different genes than the X chromosome), and females have two (XX); if a woman inherits a normal X chromosome in addition to the one that carries the mutation, she will not display the mutation. Men do not have a second X chromosome to override the chromosome that carries the mutation. If 8% of variants of a given gene are defective, the probability of a single copy being defective is 8%, but the probability that two copies are both defective is 0.08 × 0.08 = 0.0064, or just 0.64%.

is a program launched by the International Agency for the Prevention of Blindness (IAPB) and is supported by the WHO in 1999 that has made controlling blindness in children a high priority.

Optic pits occur equally between men and women. They are seen in roughly 1 in 10,000 eyes, and approximately 85% of optic pits are found to be unilateral (i.e. in only one eye of any affected individual). About 70% are found on the temporal side (or lateral one-half) of the optic disc. Another 20% are found centrally, while the remaining pits are located either superiorly (in the upper one-half), inferiorly (in the lower one-half), or nasally (in the medial one-half towards the nose).

No particular risk factors have been conclusively identified; however, there have been a few reports that demonstrate an autosomal dominant pattern of inheritance in some families. Therefore, a family history of optic pits may be a possible risk factor.

Distortion of vision refers to straight lines not appearing straight, but instead bent, crooked, or wavy. Usually this is caused by distortion of the retina itself. This distortion can herald a loss of vision in macular degeneration, so anyone with distorted vision should seek medical attention by an ophthalmologist promptly. Other conditions leading to swelling of the retina can cause this distortion, such as macular edema and central serous chorioretinopathy.

An Amsler grid can be supplied by an ophthalmologist so that the vision can be monitored for distortion in people who may be predisposed to this problem.

Tunnel vision implies that the peripheral vision, or side vision, is lost, while the central vision remains. Thus, the vision is like looking through a tunnel, or through a paper towel roll. Some disorders that can cause this include:

Glaucoma - severe glaucoma can result in loss of nearly all of the peripheral vision, with a small island of central vision remaining. Sometimes even this island of vision can be lost as well.

Retinitis pigmentosa - This is usually a hereditary disorder which can be part of numerous syndromes. It is more common in males. The peripheral retina develops pigmentary deposits, and the peripheral vision gradually becomes worse and worse. The central vision can be affected eventually as well. People with this problem may have trouble getting around in the dark. Cataract can be a complication as well. There is no known treatment for this disorder, and supplements of Vitamin A have not been proven to help.

Punctate Inner Choroidopathy - This condition is where vessels gro (( material is missing ))

Stroke - a stroke involving both sides of the visual part of the brain may wipe out nearly all of the peripheral vision. Fortunately, this is a very rare occurrence

Seeing rainbows around lights, especially at night, usually indicates swelling of the cornea. This may occur from a variety of causes which are discussed under Corneal Edema. Cataract can sometimes cause this also.

Colour vision is perceived mainly by the macula, which is the central vision portion of the retina. Thus any disorder affecting the macula may cause a disturbance in color vision. However, about 8% of males and 0.5% of females have some version of "colour blindness" from birth. Usually this is a genetically inherited trait, and is of the "red-green confusion" variety. The reds, browns, olives, and gold may be confused. Purple may be confused with blue, and pastel pinks, oranges, yellows, and greens look similar. Usually both eyes are affected equally.

There are many obscure macular retinal disorders that can lead to a loss of colour vision, and many of these syndromes are inherited as well. There may also be a problem with a generalized loss of vision with these problems as well. Other retinal problems can lead to a temporary disturbance of colour vision, such as Central serous chorioretinopathy, Macular Edema of different causes, and Macular Degeneration.

Certain types of cataract can gradually affect the colour vision, but this is usually not noticed until one cataract is removed. The cataract seems to filter out the colour blue, and everything seems more blue after cataract extraction. Optic nerve disorders such as Optic Neuritis can greatly affect colour vision, with colours seeming washed out during or after an episode.

A blind spot, scotoma, is an obscuration of the visual field. A particular blind spot known as the "physiological blind spot", "blind point", or "punctum caecum" in medical literature, is the place in the visual field that corresponds to the lack of light-detecting photoreceptor cells on the optic disc of the retina where the optic nerve passes through the optic disc. Because there are no cells to detect light on the optic disc, the corresponding part of the field of vision is invisible. Some process in our brains interpolates the blind spot based on surrounding detail and information from the other eye, so we do not normally perceive the blind spot.

Although all vertebrates have this blind spot, cephalopod eyes, which are only superficially similar, do not. In them, the optic nerve approaches the receptors from behind, so it does not create a break in the retina.

The first documented observation of the phenomenon was in the 1660s by Edme Mariotte in France. At the time it was generally thought that the point at which the optic nerve entered the eye should actually be the most sensitive portion of the retina; however, Mariotte's discovery disproved this theory.

The blind spot is located about 12–15° temporally and 1.5° below the horizontal and is roughly 7.5° high and 5.5° wide.

It is known to occur in Scotch Collies (smooth and rough collies), Shetland Sheepdogs, Australian Shepherds, Border Collies, Lancashire Heelers, and Nova Scotia Duck Tolling Retrievers. Frequency is high in Collies and Shetland Sheepdogs, and low in Border Collies and NSDTRs. In the United States, incidence in the genotype of collies has been estimated to be as high as 95 percent, with a phenotypic incidence of 80 to 85 percent.

The Fuchs spot or sometimes Forster-Fuchs' retinal spot is a degeneration of the macula in case of high myopia. It is named after the two persons who first described it: Ernst Fuchs, who described a pigmented lesion in 1901, and Forster, who described subretinal neovascularisation in 1862. The size of the spots are proportionate to the severity of the pathological myopia.

Entoptic phenomena (from Greek ἐντός "within" and ὀπτικός "visual") are visual effects whose source is within the eye itself. (Occasionally, these are called entopic phenomena, which is probably a typographical mistake.)

In Helmholtz's words; "Under suitable conditions light falling on the eye may render visible certain objects within the eye itself. These perceptions are called "entoptical"."

Although it is frequently claimed that the retina is burned by looking at the sun, retinal damage appears to occur primarily due to photochemical injury rather than thermal injury. The temperature rise from looking at the sun with a 3-mm pupil only causes a 4 °C increase in temperature, insufficient to photocoagulate. The energy is still phototoxic: since light promotes oxidation, chemical reactions occur in the exposed tissues with unbonded oxygen molecules. It also appears that central serous retinopathy can be a result of a depression in a treated solar damaged eye.

The duration of exposure necessary to cause injury varies with the intensity of light, and also affects the possibility and length of recovery

Controversies exist around eliminating this disorder from breeding Collies. Some veterinarians advocate only breeding dogs with no evidence of disease, but this would eliminate a large portion of potential breeding stock. Because of this, others recommend only breeding mildly affected dogs, but this would never completely eradicate the condition. Also, mild cases of choroidal hypoplasia may become pigmented and therefore undiagnosable by the age of three to seven months. If puppies are not checked for CEA before this happens, they may be mistaken for normal and bred as such. Checking for CEA by seven weeks of age can eliminate this possibility. Diagnosis is also difficult in dogs with coats of dilute color because lack of pigment in the choroid of these animals can be confused with choroidal hypoplasia. Also, because of the lack of choroidal pigment, mild choroidal hypoplasia is difficult to see, and therefore cases of CEA may be missed.

Until recently, the only way to know if a dog was a carrier was for it to produce an affected puppy. However, a genetic test for CEA became available at the beginning of 2005, developed by the Baker Institute for Animal Health, Cornell University, and administered through OptiGen. The test can determine whether a dog is affected, a carrier, or clear, and is therefore a useful tool in determining a particular dog's suitability for breeding.

Some examples of entoptical effects include:

- Floaters or "muscae volitantes" are slowly drifting blobs of varying size, shape, and transparency, which are particularly noticeable when viewing a bright, featureless background (such as the sky) or a point source of diffuse light very close to the eye. They are all shadow images of objects suspended just above the retina. Some may be individual red blood cells swollen due to osmotic pressure or chains of these cells stuck together and diffraction patterns can be seen around these. They may also be "coagula of the proteins of the vitreous gel, to embryonic remnants, or the condensation round the walls of Cloquet's canal". Floaters may collect over the fovea (the center of vision) and therefore be more visible when lying on your back looking upwards.

- Blue field entoptic phenomenon has the appearance of tiny bright dots moving rapidly along squiggly lines in the visual field. It is much more noticeable when viewed against a field of pure blue light and is caused by white blood cells moving in the capillaries in front of the retina. The white cells are larger than the red cells and must deform to fit. As they go through a capillary, a space opens up in front of them and red blood cells pile up behind. This makes the dots of light appear slightly elongated with dark tails.

- Haidinger's brush is a very subtle bowtie or hourglass shaped pattern that is seen when viewing a field with a component of blue light that is plane or circularly polarized and rotating with respect to the observer's eye. If the light is all blue, it will appear as a dark shadow, if the light is full spectrum, it will appear yellow. It is due to the preferential absorption of blue polarized light by pigment molecules in the fovea.

- Purkinje images are the reflections from the anterior and posterior surfaces of the cornea and the anterior and posterior surfaces of the lens. While these first four reflections are not entoptic, Becker described how light can reflect from the posterior surface of the lens and then again from the anterior surface of the cornea to focus a second image on the retina, this one much fainter and inverted. Tscherning referred to this as the sixth image (the fifth image being formed by reflections from the anterior surfaces of the lens and cornea to form an image too far in front of the retina to be visible) and noted it was much fainter and best seen with a relaxed emmetropic eye. In a dark room, with one eye closed and looking ahead with the other eye, move a light back and forth under your gaze – you should see a dimmer image moving in the opposite direction.

- The Purkinje tree is an image of the retinal blood vessels in one's own eye, first described by Purkyně in 1823. It can be seen by shining the beam of a small bright light penlight through the pupil from the periphery of a subject's vision. This results in an image of the light being focused on the periphery of the retina. Light from this spot then casts shadows of the blood vessels (which lie on top of the retina) onto unadapted portions of the retina. Normally the image of the retinal blood vessels is invisible because of adaptation. Unless the light moves, the image disappears within a second or so. If the light is moved at about 1 Hz, adaptation is defeated, and a clear image can be seen indefinitely. The vascular figure is often seen by patients during an ophthalmic examination when the doctor is using an ophthalmoscope. Another way in which the shadows of blood vessels may be seen is by holding a bright light against the eyelid at the corner of the eye. The light penetrates the eye and casts a shadow on the blood vessels as described previously. The light must be jiggled to defeat adaptation. Viewing in both cases is improved in a dark room while looking at a featureless background. This topic is discussed in more detail by Helmholtz.

- Purkinje's blue arcs are associated with the activity of the nerves sending signals from where a spot of light is focussed on the retina near the fovea to the optic disk. Look at the right edge of a small red light in a dark room with your right eye (left eye closed) after dark-accommodating your eye for about 30 seconds and you should see two faint blue arcs starting at the light and heading towards the blind spot. Look at the left edge and you will see a faint blue spike going from the light to the right.

- A phosphene is the perception of light without light actually entering the eye, for instance caused by pressure applied to the closed eyes.

A phenomenon that could be entoptical if the eyelashes are considered to be part of the eye is seeing light diffracted through the eyelashes. The phenomenon appears as one or more light disks crossed by dark blurry lines (the shadows of the lashes), each having fringes of spectral colour. The disk shape is given by the circular aperture of the pupil.

First signs of a Fuchs spot are distorted sight of straight lines near the fovea, which some days later turn to the typical well-circumscribed patches after absorption of haemorrhage, and a pigmented scar remains. As in macular degeneration, central sight is affected. Atrophy leads to the loss of two or more lines of the Snellen chart.

Vision loss due to solar retinopathy is typically reversible, lasting for as short as one month to over one year. The fundus changes are variable and usually bilateral, mild cases often show no alteration and moderate to severe cases show a foveal yellow spot on the first days after exposure. After a few days it is replaced by a reddish dot often surrounded by pigment.

Permanent holes and lesions are possible; prognosis worsens with dilated pupils or prolonged exposure.

CSR is a fluid detachment of macula layers from their supporting tissue. This allows choroidal fluid to leak beneath the retina. The buildup of fluid seems to occur because of small breaks in the retinal pigment epithelium.

CSR is sometimes called "idiopathic CSR" which means that its cause is unknown. Nevertheless, stress appears to play an important role. An oft-cited but potentially inaccurate conclusion is that persons in stressful occupations, such as airplane pilots, have a higher incidence of CSR.

CSR has also been associated with cortisol and corticosteroids. Persons with CSR have higher levels of cortisol. Cortisol is a hormone secreted by the adrenal cortex which allows the body to deal with stress, which may explain the CSR-stress association. There is extensive evidence to the effect that corticosteroids (e.g. cortisone), commonly used to treat inflammations, allergies, skin conditions and even certain eye conditions, can trigger CSR, aggravate it and cause relapses. In a study documented by Indian Journal of Pharmacology, a young male was using Prednisolone and began to display subretinal fluid indicative of CSR. With the discontinuation of the steroid drop the subretinal fluid resolved and did not show any sign of recurrence. Thus indicating the steroid was the probable cause of the CSR. A study of 60 persons with Cushing's syndrome found CSR in 3 (5%). Cushing's syndrome is characterized by very high cortisol levels. Certain sympathomimetic drugs have also been associated with causing the disease.

Evidence has also implicated helicobacter pylori (see gastritis) as playing a role. It would appear that the presence of the bacteria is well correlated with visual acuity and other retinal findings following an attack.

Evidence also shows that sufferers of MPGN type II kidney disease can develop retinal abnormalities including CSR caused by deposits of the same material that originally damaged the glomerular basement membrane in the kidneys.

An ectopic cilia is a special type of distichia. It is usually found in younger dogs. Commonly affected breeds include Poodles, Golden Retrievers, and Shih Tzus. The eyelash exits through the conjunctiva of the eyelid facing toward the eye, usually at the middle of the upper eyelid. It can cause intense pain and corneal ulcers. Treatment is surgery or cryotherapy.

It is estimated that this much less common form of retinoschisis affects one in 5,000 to 25,000 individuals, primarily young males. "Schisis" is derived from the Greek word meaning "splitting", describing the splitting of the retinal layers from each other. However, "schisis" is a word fragment, and the term "retinoschisis" should be used, as should the term "iridoschisis" when describing splitting of the iris. If the retinoschisis involves the macula, then the high-resolution central area of vision used to view detail is lost, and this one form of macular disease. Although it might be described by some as a "degeneration", the term "macular degeneration" should be reserved for the specific disease "age-related macular degeneration".

Retinoschisis can be caused by an X-linked genetic defect, affecting the vision of men who inherit the disease from their unaffected carrier mothers. The genetic form of this disease usually starts during childhood and is called X-linked Juvenile Retinoschisis (XLRS) or Congenital Retinoschisis. Affected males are usually identified in grade school, but occasionally are identified as young infants.

Very few affected individuals go completely blind from retinoschisis, but some sufferers have very limited reading vision and are "legally blind". Visual acuity can be reduced to less than 20/200 in both eyes. Individuals affected by XLRS are at an increased risk for retinal detachment and eye hemorrhage, among other potential complications.

Retinoschisis causes acuity loss in the center of the visual field through the formation of tiny cysts in the retina, often forming a "spoke-wheel" pattern that can be very subtle. The cysts are usually only detectable by a trained clinician. In some cases vision cannot be improved by glasses, as the nerve tissue itself is damaged by these cysts.

The National Eye Institute (NEI) of the National Institutes of Health (NIH) is currently conducting clinical and genetic studies of X-Linked Juvenile Retinoschisis. This study is currently recruiting patients. A better understanding of why and how XLRS develops might lead to improved treatments. Males diagnosed with X-linked juvenile retinoschisis and females who are suspected carriers may be eligible to participate. In addition to giving a medical history and submitting medical records, participants submit a blood sample and the NEI will perform a genetic analysis. There is no cost to participate in this study.

This type of retinoschisis is very common with a prevalence of up to 7 percent in normal persons. Its cause is unknown. It can easily be confused with retinal detachment by the non-expert observer and in difficult cases even the expert may have difficulty differentiating the two. Such differentiation is important since retinal detachment almost always requires treatment while retinoschisis never itself requires treatment and leads to retinal detachment (and hence to visual loss) only occasionally. Unfortunately one still sees cases of uncomplicated retinoschisis treated by laser retinopexy or cryopexy in an attempt to stop its progression towards the macula. Such treatments are not only ineffective but unnecessarily risk complications. There is no documented case in the literature of degenerative retinoschisis itself (as opposed to the occasional situation of retinal detachment complicating retinoschisis) in which the splitting of the retina has progressed through the fovea. There is no clinical utility in differentiating between typical and reticular retinoschisis. Degenerative retinoschisis is not known to be a genetically inherited condition.

There is always vision loss in the region of the schisis as the sensory retina is separated from the ganglion layer. But like the loss is in the periphery, it goes unnoticed. It is the very rare schisis that encroaches on the macula where retinopexy is then properly used.