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.

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.

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

Sympathetic ophthalmia is rare, affecting 0.2% to 0.5% of non-surgical eye wounds, and less than 0.01% of surgical penetrating eye wounds. There are no gender or racial differences in incidence of SO.

Few studies have examined the prevalence of FCED on a large scale. First assessed in a clinical setting, Fuchs himself estimated the occurrence of dystrophia epithelialis corneae to be one in every 2000 patients; a rate that is likely reflective of those who progress to advanced disease. Cross-sectional studies suggest a relatively higher prevalence of disease in European countries relative to other areas of the world. Fuchs' dystrophy rarely affects individuals under 50 years of age.

According to recent research not a single theory is able to explain the cause fully. However current plausible theories include infection with "Toxoplasma gondii", Herpes simplex virus, Rubella, neurogenic causes, and autoimmune pathology.

Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Neovascularisation (growth of new abnormal vessels) is possible and any eye surgery, such as cataract surgery, can cause bleeding from the fragile vessels in the atrophic iris causing accumulation of blood in anterior chamber of the eye, also known as hyphema.

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.

Fuchs' dystrophy, also referred to as Fuchs' corneal endothelial dystrophy (FCED) and Fuchs' endothelial dystrophy (FED), is a slowly progressing corneal dystrophy that usually affects both eyes and is slightly more common in women than in men. Although early signs of Fuchs' dystrophy are sometimes seen in people in their 30s and 40s, the disease rarely affects vision until people reach their 50s and 60s.

The condition was first described by Austrian ophthalmologist Ernst Fuchs (1851–1930), after whom it is named. In 1910, Fuchs first reported 13 cases of central corneal clouding, loss of corneal sensation and the formation of epithelial bullae, or blisters, which he labeled 'dystrophia epithelialis corneae'. It was characterized by late onset, slow progression, decreased visual acuity in the morning, lack of inflammation, diffuse corneal opacity, intense centrally, and roughened epithelium with vesicle-like features.

A shift to the understanding of FCED as primarily a disease of the corneal endothelium resulted after a number of observations in the 1920s. Crystal-like features of the endothelium were noted by Kraupa in 1920, who suggested that the epithelial changes were dependent on the endothelium. Using a slit lamp, Vogt described the excrescences associated with FCD as drop-like in appearance in 1921. In 1924, Graves then provided an extremely detailed explanation of the endothelial elevations visible with slit-lamp biomicroscopy. A patient with unilateral epithelial dystrophy and bilateral endothelial changes was described by the Friedenwalds in 1925; subsequent involvement of the second eye led them to emphasize that endothelial changes preceded epithelial changes. As only a subset of patients with endothelial changes proceeded to epithelial involvement, Graves stated on 19 October 1925 to the New York Academy of Medicine that "Fuchs' epithelial dystrophy may be a very late sequel to severer cases of the deeper affection".

Entoptic images have a physical basis in the image cast upon the retina. Hence, they are different from optical illusions, which are perceptual effects that arise from interpretations of the image by the brain. Because entoptic images are caused by phenomena within the observer's own eye, they share one feature with optical illusions and hallucinations: the observer cannot share a direct and specific view of the phenomenon with others.

Helmholtz comments on phenomena which could be seen easily by some observers, but could not be seen at all by others. This variance is not surprising because the specific aspects of the eye that produce these images are unique to each individual. Because of the variation between individuals, and the inability for two observers to share a nearly identical stimulus, these phenomena are unlike most visual sensations. They are also unlike most optical illusions which are produced by viewing a common stimulus. Yet, there is enough commonality between the main entoptic phenomena that their physical origin is now well understood.

Keratopathy is common in older people. Keratopathy occurs after cataract surgery, its incidence has decreased since the advent of intraoperative viscoelastic agents that protect the endothelium.

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"."

Berlin's edema (commotio retinae) is a common condition caused by blunt injury to the eye. It is characterized by decreased vision in the injured eye a few hours after the injury. Under examination the retina appears opaque and white in colour in the periphery but the blood vessels are normally seen along with "cherry red spot" in the foveal reigion.This whitening is indicative of cell damage, which occurs in the retinal pigment epithelium and outer segment layer of photoreceptors. Damage to the outer segment often results in photoreceptor death through uncertain mechanisms. Usually there is no leakage of fluid and therefore it is not considered a true edema. The choroidal fluorescence in fluorescent angiography is absent. Visual acuity ranges from 20/20 to 20/400.

The prognosis is excellent except in case of complications of choroidal rupture, hemorrhage or pigment epithelial damage, but damage to the macula will result in poorer recovery. The outcome can be worsened in the case of retinal detachment, atrophy or hyperplasia. Visual field defects can occur. In late cases cystoid macular edema sometimes develops which can further lead to macular destruction.

Commotio retinae is usually self limiting and there is no treatment as such. It usually resolves in 3–4 weeks without any complications and sequelae.

Sympathetic ophthalmia (SO) or Sympathetic uveitis is a bilateral diffuse granulomatous uveitis (a kind of inflammation) of both eyes following trauma to one eye. It can leave the patient completely blind. Symptoms may develop from days to several years after a penetrating eye injury.

Given that episodes tend to occur on awakening and managed by use of good 'wetting agents', approaches to be taken to help prevent episodes include:

- Environmental:

- ensuring that the air is humidified rather than dry, not overheated and without excessive airflow over the face. Also avoiding irritants such as cigarette smoke.

- use of protective glasses especially when gardening or playing with children.

- General personal measures:

- maintaining general hydration levels with adequate fluid intake.

- not sleeping-in late as the cornea tends to dry out the longer the eyelids are closed.

- Pre-bed routine:

- routine use of long-lasting eye ointments applied before going to bed.

- occasional use of the anti-inflammatory eyedrop FML (prescribed by an ophthalmologist or optometrist) before going to bed if the affected eye feels inflamed, dry or gritty

- use of a hyperosmotic (hypertonic) ointment before bed reduces the amount of water in the epithelium, strengthening its structure

- use the pressure patch as mentioned above.

- use surgical tape to keep the eye closed (if Nocturnal Lagophthalmos is a factor)

- Waking options:

- learn to wake with eyes closed and still and keeping artificial tear drops within reach so that they may be squirted under the inner corner of the eyelids if the eyes feel uncomfortable upon waking.

- It has also been suggested that the eyelids should be rubbed gently, or pulled slowly open with your fingers, before trying to open them, or keeping the affected eye closed while "looking" left and right to help spread lubricating tears. If the patient's eyelids feel stuck to the cornea on waking and no intense pain is present, use a fingertip to press firmly on the eyelid to push the eye's natural lubricants onto the affected area. This procedure frees the eyelid from the cornea and prevents tearing of the cornea.

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.

Corneal dystrophy is a group of rare hereditary disorders characterised by bilateral abnormal deposition of substances in the transparent front part of the eye called the cornea.

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.

A corneal dystrophy can be caused by an accumulation of extraneous material in the cornea, including lipids and cholesterol crystals.

Disease begins with vesicles that coalesce. There is severe progressing edema and rupture may occur in 24 hours or less.

Most cases of recurrent corneal erosion are acquired. There is often a history of recent corneal injury (corneal abrasion or ulcer), but also may be due to corneal dystrophy or corneal disease. In other words, one may suffer from corneal erosions as a result of another disorder, such as map-dot fingerprint dystrophy. Familial corneal erosions occur in dominantly inherited recurrent corneal erosion dystrophy (ERED) in which COL17A1 gene is mutated..

As it is associated with excessive sun or wind exposure, wearing protective sunglasses with side shields and/or wide brimmed hats and using artificial tears throughout the day may help prevent their formation or stop further growth. Surfers and other water-sport athletes should wear eye protection that blocks 100% of the UV rays from the water, as is often used by snow-sport athletes. Many of those who are at greatest risk of pterygium from work or play sun exposure do not understand the importance of protection.

A scotoma (Greek σκότος/"skótos", "darkness"; plural: "scotomas" or "scotomata") is an area of partial alteration in the field of vision consisting of a partially diminished or entirely degenerated visual acuity that is surrounded by a field of normal – or relatively well-preserved – vision.

Every normal mammal eye has a scotoma in its field of vision, usually termed its blind spot. This is a location with no photoreceptor cells, where the retinal ganglion cell axons that compose the optic nerve exit the retina. This location is called the optic disc. There is no direct conscious awareness of visual scotomas. They are simply regions of reduced information within the visual field. Rather than recognizing an incomplete image, patients with scotomas report that things "disappear" on them.

The presence of the blind spot scotoma can be demonstrated subjectively by covering one eye, carefully holding fixation with the open eye, and placing an object (such as one's thumb) in the lateral and horizontal visual field, about 15 degrees from fixation (see the blind spot article). The size of the monocular scotoma is 5×7 degrees of visual angle.

A scotoma can be a symptom of damage to any part of the visual system, such as retinal damage from exposure to high-powered lasers, macular degeneration and brain damage.

The term "scotoma" is also used metaphorically in several fields. The common theme of all the figurative senses is of a gap not in visual function but in the mind's perception, cognition, or world view.

Symptom-producing, or pathological, scotomata may be due to a wide range of disease processes, affecting any part of the visual system, including the retina (in particular its most sensitive portion, the macula), the optic nerve and even the visual cortex. A pathological scotoma may involve any part of the visual field and may be of any shape or size. A scotoma may include and enlarge the normal blind spot. Even a small scotoma that happens to affect central or macular vision will produce a severe visual disability, whereas a large scotoma in the more peripheral part of a visual field may go unnoticed by the bearer because of the normal reduced optical resolution in the peripheral visual field.

Amniotic membrane transplantation is an effective and safe procedure for pterygium removal. Amniotic membrane transplantation offers practical alternative to conjunctival auto graft transplantation for extensive pterygium removal. Amniotic membrane transplantation is tissue that is acquired from the innermost layer of the human placenta and has been used to replace and heal damaged mucosal surfaces including successful reconstruction of the ocular surface. It has been used as a surgical material since the 1940s, and has been shown to have a strong anti-adhesive effect.

Using an amniotic graft facilitates epithelialization, and has anti-inflammatory as well as surface rejuvenation properties. Amniotic membrane transplantation can also be fixated to the sclera using sutures, or glue adhesive. Amniotic membrane by itself does not provide an acceptable recurrence rate.