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.

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

In one study, heredity was an important factor associated with juvenile myopia, with smaller contributions from more near work, higher school achievement, and less time in sports activity.

Long hours of exposure to daylight appears to be a protective factor. Lack of outdoor play could be linked to myopia.

Other personal characteristics, such as value systems, school achievements, time spent in reading for pleasure, language abilities, and time spent in sport activities all correlated to the occurrence of myopia in studies.

Some suggest that more time spent outdoors during childhood is effective for prevention.

Various methods have been employed in an attempt to decrease the progression of myopia, although studies show mixed results. Many myopia treatment studies have a number of design drawbacks: small numbers, lack of adequate control group, and failure to mask examiners from knowledge of treatments used.

Far-sightedness, also known as hyperopia, is a condition of the eye in which light is focused behind, instead of on, the retina. This results in close objects appearing blurry, while far objects may appear normal. As the condition worsens, objects at all distances may be blurry. Other symptoms may include headaches and eye strain. People may also experience accommodative dysfunction, binocular dysfunction, amblyopia, and strabismus.

The cause is an imperfection of the eyes. Often it occurs when the eyeball is too short, or the lens or cornea is misshapen. Risk factors include a family history of the condition, diabetes, certain medications, and tumors around the eye. It is a type of refractive error. Diagnosis is based on an eye exam.

Management can occur with eyeglasses, contact lenses, or surgery. Glasses are easiest while contact lenses can provide a wider field of vision. Surgery works by changing the shape of the cornea. Far-sightedness primarily affects young children, with rates of 8% at 6 years and 1% at 15 years. It then becomes more common again after the age of 40, affecting about half of people.

Many people with near-sightedness can read comfortably without eyeglasses or contact lenses even after age forty. However, their myopia does not disappear and the long-distance visual challenges remain. Myopes considering refractive surgery are advised that surgically correcting their nearsightedness may be a disadvantage after age forty, when the eyes become presbyopic and lose their ability to accommodate or change focus, because they will then need to use glasses for reading. Myopes with astigmatism find near vision better, though not perfect, without glasses or contact lenses when presbyopia sets in, but the more astigmatism, the poorer the uncorrected near vision.

A surgical technique offered is to create a "reading eye" and a "distance vision eye," a technique commonly used in contact lens practice, known as monovision. Monovision can be created with contact lenses, so candidates for this procedure can determine if they are prepared to have their corneas reshaped by surgery to cause this effect permanently.

As hyperopia is the result of the visual image being focused behind the retina, it has two main causes:

- Low converging power of eye lens because of weak action of ciliary muscles

- Abnormal shape of the cornea

Far-sightedness is often present from birth, but children have a very flexible eye lens, which helps to compensate. In rare instances hyperopia can be due to diabetes, and problems with the blood vessels in the retina.

In the visual system, images captured by the eye are translated into electric signals that are transmitted to the brain where they are interpreted. As such, in order to overcome presbyopia, two main components of the visual system can be addressed: the optical system of the eye and the visual processing of the brain.

1. Image capturing in the eye – Solutions for presbyopia have advanced significantly in recent years, thanks to widened availability of optometry care as well as over-the-counter vision correction.

2. Image processing in the brain – Scientific solutions for overcoming the symptoms of presbyopia were developed in recent years and tested successfully in multiple studies. These solutions are available thanks to significant progress in the understanding of human brain plasticity and the field of perceptual learning.

Aphakia is the absence of the lens of the eye, due to surgical removal, a perforating wound or ulcer, or congenital anomaly. It causes a loss of accommodation, far sightedness (hyperopia), and a deep anterior chamber. Complications include detachment of the vitreous or retina, and glaucoma.

Babies are rarely born with aphakia. Occurrence most often results from surgery to remove congenital cataract (clouding of the eye's lens, which can block light from entering the eye and focusing clearly). Congenital cataracts usually develop as a result of infection of the fetus or genetic reasons. It is often difficult to identify the exact cause of these cataracts, especially if only one eye is affected.

People with aphakia have relatively small pupils and their pupils dilate to a lesser degree.

Eyeglass users experience tunnel vision to varying degrees due to the corrective lens only providing a small area of proper focus, with the rest of the field of view beyond the lenses being unfocused and blurry. Where a naturally sighted person only needs to move their eyes to see an object far to the side or far down, the eyeglass wearer may need to move their whole head to point the eyeglasses towards the target object.

The eyeglass frame also blocks the view of the world with a thin opaque boundary separating the lens area from the rest of the field of view. The eyeglass frame is capable of obscuring small objects and details in the peripheral field.

Activities which require a protective mask, safety goggles, or fully enclosing protective helmet can also result in an experience approximating tunnel vision. Underwater diving masks using a single flat transparent lens usually have the lens surface several centimeters from the eyes. The lens is typically enclosed with an opaque black rubber sealing shell to keep out water. For this type of mask the peripheral field of the diver is extremely limited. Generally, the peripheral field of a diving mask is improved if the lenses are as close to the eye as possible, or if the lenses are large, multi-window, or is a curved wrap-around design.

Protective helmets such as a welding helmet restrict vision to an extremely small slot or hole, with no peripheral perception at all. This is done out of necessity so that ultraviolet radiation emitted from the welding arc does not damage the welder's eyes due to reflections off of shiny objects in the peripheral field.

Without the focusing power of the lens, the eye becomes very farsighted. This can be corrected by wearing glasses, contact lenses, or by implant of an artificial lens. Artificial lenses are described as "pseudophakic." Also, since the lens is responsible for adjusting the focus of vision to different lengths, patients with aphakia have a total loss of accommodation.

Some individuals have said that they perceive ultraviolet light, invisible to those with a lens, as whitish blue or whitish-violet.

Telecanthus (from the Greek word "tele" (τῆλε) meaning far, and the Latin word canthus, meaning either corner of the eye, where the eyelids meet) refers to increased distance between the medial canthi of the eyes, while the inter-pupillary distance is normal. This is in contrast to hypertelorism, where the inter-pupillary distance is increased.

The distance between the inner corner of the left eye and the inner corner of the right eye, is called intercanthal distance. In most people, the intercanthal distance is equal to the distance between the inner corner and the outer corner of each eye, that is, the width of the eye. The average interpupillary distance is 60–62 millimeters (mm), which corresponds to an intercanthal distance of approximately 30–31 mm. The situation, where intercanthal distance is intensely bigger than the width of the eye, is called telecanthus (tele= Greek τηλε = far, and Greek ακανθα = thorn). This can be an ethnic index or an indication for hypertelorism or hypotelorism, if it is combined with abnormal relation to the interpupillary distance (A D STEAS).

"Traumatic Telecanthus" refers to telcanthus resulting from traumatic injury to the nasal-orbital-ethmoid (NOE) complex. The diagnosis of traumatic telecanthus requires a measurement in excess of those normative values. The pathology can be either unilateral or bilateral, with the former more difficult to measure.

Telecanthus is often associated with many congenital disorders. Congenital disorders such as Down syndrome, fetal alcohol syndrome, Cri du Chat syndrome, Klinefelter syndrome, Turner syndrome, Ehlers-Danlos syndrome, Waardenburg syndrome often present with prominent epicanthal fold and if these folds are nasal (most commonly are) they will cause telecanthus.

Fig of the used terms

Epicanthic folds appear in East Asians, Southeast Asians, Central Asians, North Asians, some South Asians, Polynesians, Micronesians, Indigenous Americans (as well as Mestizos), the Khoisan, Malagasy, occasionally Europeans (e.g., Scandinavians, Hungarians, Samis, Irish and Poles) and among Nilotes.

Anthropologist Carleton S. Coon states that the "median fold" occurs in Finnic and Slavic populations, while the "true inner or mongoloid fold" appears in populations of the east and the far north.

Knobloch syndrome is a rare genetic disorder presenting severe eyesight problems and often a defect in the skull. It was named after W.H. Knobloch, who first described the syndrome in 1971. A usual occurrence is a degeneration of the vitreous humour and the retina, two components of the eye. This breakdown often results in the separation of the retina (the light-sensitive tissue at the back of the eye) from the eye, called retinal detachment, which can be recurrent. Extreme myopia (near-sightedness) is a common feature. The limited evidence available from electroretinography suggests a cone-rod pattern of dysfunction is also a feature.

Knobloch syndrome is caused by mutations in an autosomal recessive inherited gene. These mutations have been found in the COL18A1 gene that instructs for the formation of a protein that builds collagen XVIII. This type of collagen is found in the basement membranes of various body tissues. Its deficiency in the eye is thought to be responsible for affecting normal eye development. There are two types of Knobloch syndrome and the case has been made for a third.

When caused by mutations in the COL18A1 gene it is called Knobloch syndrome type 1. The genes causing types II and III have yet to be identified.

Knobloch syndrome is also characterised by cataracts, dislocated lens with skull defects such as occipital encephalocele and occipital aplasia. Encephalocele is a neural tube defect where the skull has not completely closed and sac-like protrusions of the brain can push through the skull; (it can also result from other causes).

In Knobloch’s syndrome this is usually seen in the occipital region, and aplasia is the underdevelopment of tissue again in this reference in the occipital area.

Many fetuses lose their epicanthic folds after three to six months of gestation.

Micro syndrome also known as WARBM, and Warburg–Sjo–Fledelius syndrome, is a rare autosomal recessive genetic disorder characterized by microcephaly, microcornea, congenital cataract, intellectual or developmental disability, optic atrophy, and hypogenitalism.

The rare cases that have been examined are often within families, or the people that have cases of micro syndrome have a mutation in their genes.

It can be associated with "RAB3GAP".

PEHO syndrome is a progressive encephalopathy with edema, hypsarrhythmia and optic atrophy. It is a very rare disease, one of the Finnish heritage diseases, although approximately half of the cases reported so far are not-Finnish and have been described worldwide .

It has been suggested that it may also be present in Australian and American populations.

A recent article in 2015 reported a persistent notochord in a fetus at 23 weeks of gestation. The fetus had an abnormal spine, shortened long bones and a left clubfoot. After running postmortem tests and ultrasound, the researchers believed that the fetus suffered from hypochondrogenesis. Hypochondrogenesis is caused when type II collagen is abnormally formed due to a mutation in the COL2A1 gene. Normally, the cartilaginous notochord develops into the bony vertebrae in a human body. The COL2A1 gene results in malformed type II collagen, which is essential in the transition from collagen to bone. This is the first time that researchers found a persistent notochord in a human body due to a COL2A1 mutation.

A supernumerary nipple (also known as a third nipple, triple nipple, accessory nipple, polythelia or the related condition: polymastia) is an additional nipple occurring in mammals, including humans. Often mistaken for moles, supernumerary nipples are diagnosed in humans at a rate of approximately 1 in 18 people.

The nipples appear along the two vertical "milk lines," which start in the armpit on each side, run down through the typical nipples and end at the groin. They are classified into eight levels of completeness from a simple patch of hair to a milk-bearing breast in miniature.

"Polythelia" refers to the presence of an additional nipple alone while "polymastia" denotes the much rarer presence of additional mammary glands.

Although usually presenting on the milk line, pseudomamma can appear as far away as the foot.

A possible relationship with mitral valve prolapse has been proposed.

A mutation in the ZNHIT3 gene - a nuclear zinc finger protein involved in transcriptional regulation and in small nucleolar ribonucleoprotein particle assembly has been shown to be the cause of the Finnish-type of PEHO syndrome. However, the syndrome appear to be genetically heterogeneous and it might reflect an underlying genetic tubulinopathy, with biallelic mutations in the gene PRUNE1 also identified in non-Finnish patients with PEHO syndrome.

Circumvallate placenta is a placental morphological abnormalitiy, a subtype of placenta extrachorialis in which the fetal membranes (chorion and amnion) "double back" on the fetal side around the edge of the placenta. After delivery, a circumvallate placenta has a thick ring of membranes on its fetal surface.

The fetal surface is divided into a central depressed zone surrounded by a thickened white ring which is incomplete the ring is situated at varying distance from the margin of the placenta. The ring is composed of a double fold of amnion and chorion with degenerated decidua vera and fibrin in between. Vessels radiate from the cord insertion as far as the ring and then disappear from the view.

Complete circumvallate placenta occurs in approximately 1% of pregnancies. It is diagnosed prenatally by medical ultrasonography, although one 1997 study of prenatal ultrasounds found that "of the normal placentas, 35% were graded as probably or definitely circumvallate by at least one sonologist," and "all sonologists misgraded the case of complete circumvallation as normal." The condition is associated with perinatal complications such as placental abruption, oligohydramnios, abnormal cardiotocography, preterm birth, and miscarriage.

Kniest Dysplasia is an autosomal dominant condition. This means that the person only needs to have one copy of the mutated gene in order to have the condition. People with a family history are at a higher risk of having the disease than people with no family history. A random mutation in the gene can cause a person with no family history to also have the condition.