Treatment options include contact lenses and intrastromal corneal ring segments for correcting refractive errors caused by irregular corneal surface, corneal collagen cross-linking to strengthen a weak and ectatic cornea, or corneal transplant for advanced cases.

Corneal dystrophy may not significantly affect vision in the early stages. However, it does require proper evaluation and treatment for restoration of optimal vision. Corneal dystrophies usually manifest themselves during the first or second decade but sometimes later. It appears as grayish white lines, circles, or clouding of the cornea. Corneal dystrophy can also have a crystalline appearance.

There are over 20 corneal dystrophies that affect all parts of the cornea. These diseases share many traits:

- They are usually inherited.

- They affect the right and left eyes equally.

- They are not caused by outside factors, such as injury or diet.

- Most progress gradually.

- Most usually begin in one of the five corneal layers and may later spread to nearby layers.

- Most do not affect other parts of the body, nor are they related to diseases affecting other parts of the eye or body.

- Most can occur in otherwise totally healthy people, male or female.

Corneal dystrophies affect vision in widely differing ways. Some cause severe visual impairment, while a few cause no vision problems and are diagnosed during a specialized eye examination by an ophthalmologist. Other dystrophies may cause repeated episodes of pain without leading to permanent loss of vision.

Patients with Reis-Bücklers dystrophy develop a reticular pattern of cloudiness in the cornea. This cloudiness, or opacity, usually appears in both eyes (bilaterally) in the upper cornea by 4 or 5 years of age. The opacity elevates the corneal epithelium, eventually leading to corneal erosions that prompt attacks of ocular hyperemia, pain, and photophobia. These recurrent painful corneal epithelial erosions often begin as early as 1 year of age.

With time, the corneal changes progress into opacities in Bowman's membrane, which gradually becomes more irregular and more dense. Significant vision loss may occur. However, vascularization of the cornea is not present.

Corneal ectatic disorders or corneal ectasia are a group of uncommon, noninflammatory, eye disorders characterised by bilateral thinning of the central, paracentral, or peripheral cornea.

- Keratoconus, a progressive, noninflammatory, bilateral, asymmetric disease, characterized by paraxial stromal thinning and weakening that leads to corneal surface distortion.

- Keratoglobus, a rare noninflammatory corneal thinning disorder, characterised by generalised thinning and globular protrusion of the cornea.

- Pellucid marginal degeneration, a bilateral, noninflammatory disorder, characterized by a peripheral band of thinning of the inferior cornea.

- Posterior keratoconus, a rare condition, usually congenital, which causes a nonprogressive thinning of the inner surface of the cornea, while the curvature of the anterior surface remains normal. Usually only a single eye is affected.

- Post-LASIK ectasia, a complication of LASIK eye surgery.

- Terrien's marginal degeneration, a painless, noninflammatory, unilateral or asymmetrically bilateral, slowly progressive thinning of the peripheral corneal stroma.

Reis-Bücklers corneal dystrophy, also known as corneal dystrophy of Bowman layer, type I, is a rare, corneal dystrophy of unknown cause, in which the Bowman's layer of the cornea undergoes disintegration. The disorder is inherited in an autosomal dominant fashion, and is associated with mutations in the gene TGFB1.

Reis-Bücklers dystrophy causes a cloudiness in the corneas of both eyes, which may occur as early as 1 year of age, but usually develops by 4 to 5 years of age. It is usually evident within the first decade of life. This cloudiness, or opacity, causes the corneal epithelium to become elevated, which leads to corneal opacities. The corneal erosions may prompt attacks of redness and swelling in the eye (ocular hyperemia), eye pain, and photophobia. Significant vision loss may occur.

Reis-Bücklers dystrophy is diagnosed by clinical history physical examination of the eye. Labs and imaging studies are not necessary. Treatment may include a complete or partial corneal transplant, or photorefractive keratectomy.

Symptoms include recurring attacks of severe acute ocular pain, foreign-body sensation, photophobia (i.e. sensitivity to bright lights), and tearing often at the time of awakening or during sleep when the eyelids are rubbed or opened. Signs of the condition include corneal abrasion or localized roughening of the corneal epithelium, sometimes with map-like lines, epithelial dots or microcysts, or fingerprint patterns. An epithelial defect may be present, usually in the inferior interpalpebral zone.

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

The main pathological features in this dystrophy are mulberry-shaped gelatinous masses beneath the corneal epithelium. Patients suffer from photophobia, foreign body sensation in the cornea. The loss of vision is severe. The amyloid nodules have been found to contain lactoferrin, but the gene encoding lactoferrin is unaffected.

This form of corneal amyloidosis appears to be more frequent in Japan.

FED may be discovered as an incidental finding at a routine visit to an optometrist. or by an ophthalmologist during assessment for cataract surgery. As a result of irregularities on the inner surface of the cornea, affected individuals may simply notice a reduction in the quality of vision or glare or haloes particularly when driving at night. Individuals with symptomatic Fuchs' dystrophy typically awaken with blurred vision which improves during the day. This occurs because the cornea is normally more swollen in the morning due to nocturnal fluid retention in the absence of normal evaporation due to the lids being closed. During waking hours this fluid evaporates once the eyes are open. As the disease worsens vision remains blurred despite evaporation due to endothelial pump failure and fluid retention. As Fuchs' dystrophy typically occurs in older individuals there may also be cataract of the lens, which also reduces vision.

Researchers are finding that Fuchs' is a genetically heterogeneous disease, and many different genes and loci have been associated as contributing to a small percentage of overall Fuchs' cases. Certain genetic lesions have been correlated with more severe disease and earlier onset. Therefore, some individuals may experience symptoms of the disease at a much earlier age, while others may not experience symptoms until late in life.

Lattice corneal dystrophy type, also known as Biber-Haab-Dimmer dystrophy, is a rare form of corneal dystrophy. It has no systemic manifestations, unlike the other type of the dystrophy, Lattice corneal dystrophy type II. Lattice corneal dystrophy was first described by Swiss ophthalmologist Hugo Biber in 1890.

Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma.

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".

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..

Filamentous opacities appear in the cornea with intertwining delicate branching processes. During an eye examination, the doctor sees these deposits in the stroma as clear, comma-shaped overlapping dots and branching filaments, creating a lattice effect. Over time, the lattice lines will grow opaque and involve more of the stroma. They will also gradually converge, giving the cornea a cloudiness that may also reduce vision. The disease is bilateral, usually noted before the end of the first decade of life. Although lattice dystrophy can occur at any time in life, the condition usually arises in children between the ages of two and seven.

In some people, these abnormal protein fibers can accumulate under the cornea's outer layer—the epithelium. This can cause erosion of the epithelium. This condition is known as recurrent epithelial erosion. These erosions alter the cornea's normal curvature, resulting in temporary vision problems, and expose the nerves that line the cornea, causing severe pain. Even the involuntary act of blinking can be painful.

In systemic cases, kidney failure, heart failure and neuropathy such as facial nerve palsy, laxity of the skin may be noted.

Onset occurs in the first decade, usually between ages 5 and 9. The disorder is progressive. Minute, gray, punctate opacities develop. Corneal sensitivity is usually reduced. Painful attacks with photophobia, foreign body sensations, and recurrent erosions occur in most patients. Macular corneal dystrophy is very common in Iceland and accounts for almost one-third of all corneal grafts performed there.

People with early keratoconus typically notice a minor blurring of their vision and come to their clinician seeking corrective lenses for reading or driving. At early stages, the symptoms of keratoconus may be no different from those of any other refractive defect of the eye. As the disease progresses, vision deteriorates, sometimes rapidly. Visual acuity becomes impaired at all distances, and night vision is often poor. Some individuals have vision in one eye that is markedly worse than that in the other. The disease is often bilateral, though asymmetrical. Some develop photophobia (sensitivity to bright light), eye strain from squinting in order to read, or itching in the eye, but there is normally little or no sensation of pain. It may cause luminous objects to appear as cylindrical pipes with the same intensity at all points.

The classic symptom of keratoconus is the perception of multiple "ghost" images, known as monocular polyopia. This effect is most clearly seen with a high contrast field, such as a point of light on a dark background. Instead of seeing just one point, a person with keratoconus sees many images of the point, spread out in a chaotic pattern. This pattern does not typically change from day to day, but over time, it often takes on new forms. People also commonly notice streaking and flaring distortion around light sources. Some even notice the images moving relative to one another in time with their heart beat.

The predominant optical aberration of the eye in keratoconus is coma. The visual distortion experienced by the person comes from two sources, one being the irregular deformation of the surface of the cornea, and the other being scarring that occurs on its exposed highpoints. These factors act to form regions on the cornea that map an image to different locations on the retina. The effect can worsen in low light conditions, as the dark-adapted pupil dilates to expose more of the irregular surface of the cornea.

This condition is usually unilateral, and its symptoms vary from none to mild blurring and discomfort. Signs include diffuse iris atrophy and small white keratic precipitates (deposits on the inner surface of the cornea), cells presenting in the anterior chamber as well as the anterior vitreous. Glaucoma and cataract occur frequently.

Pain is not typically present in pellucid marginal degeneration, and aside from vision loss, no symptoms accompany the condition. However, in rare cases, PMD may present with sudden onset vision loss and excruciating eye pain, which occurs if the thinning of the cornea leads to perforation. While PMD usually affects both eyes, some unilateral cases have been reported.

PMD is characterized by bilateral thinning (ectasia) in the inferior and peripheral region of the cornea. The distribution of the degeneration is crescent or arcuate shaped. The cornea just above the region of thinning is of normal thickness, and may protrude anteriorly, which creates an irregular astigmatism. This is described as a "beer belly" appearance since the greatest protrusion occurs below the horizontal midline (unlike keratoconus). Normally, PMD does not present with vascularization of the cornea, scarring, or any deposits of lipid.

Posterior Polymorphous Corneal Dystrophy (PPCD; sometimes also "Schlichting dystrophy") is a type of corneal dystrophy, characterised by changes in Descemet's membrane and endothelial layer. Symptoms mainly consist of decreased vision due to corneal edema. In some cases they are present from birth, other patients are asymptomatic. Histopathological analysis shows that the cells of endothelium have some characteristics of epithelial cells and have become multilayered. The disease was first described in 1916 by Koeppe as "keratitis bullosa interna".

PPCD type 2 is linked to the mutations in COL8A2, and PPCD type 3 mutations in ZEB1 gene, but the underlying genetic disturbance in PPCD type 1 is unknown.

Signs and symptoms of corneal abrasion include pain, trouble with bright lights, a foreign-body sensation, excessive squinting, and reflex production of tears. Signs include epithelial defects and edema, and often redness of the eye. The vision may be blurred, both from any swelling of the cornea and from excess tears. Crusty buildup from excess tears may also be present.

Gelatinous drop-like corneal dystrophy, also known as amyloid corneal dystrophy, is a rare form of corneal dystrophy. The disease was described by Nakaizumi as early as 1914.

Epithelial basement membrane dystrophy (EBMD), also known as map-dot-fingerprint dystrophy and Cogans's microcystic dystrophy, is a disorder of the eye that can cause pain and dryness.

It is sometimes included in the group of corneal dystrophies. It diverges from the formal definition of corneal dystrophy in being in most cases non-familial. It also has a fluctuating course, while for a typical corneal dystrophy the course is progressive. When it is considered part of this group, it is the most common type of corneal dystrophy.

Corneal perforation is an anomaly in the cornea resulting from damage to the corneal surface. A corneal perforation means that the cornea has been penetrated, thus leaving the cornea damaged.

The cornea is a clear part of the eye which controls and focuses the entry of light into the eye. Damage to the cornea due to corneal perforation can cause decreased visual acuity.

A reduction in visual acuity in a 'red eye' is indicative of serious ocular disease, such as keratitis, iridocyclitis, and glaucoma, and never occurs in simple conjunctivitis without accompanying corneal involvement.

Many cases are asymptomatic, however patients many have decreased vision, glare, monocular diplopia or polyopia, and noticeable iris changes [2,6]. On exam patients have normal to decreased visual acuity, and a “beaten metal appearance” of the corneal endothelium, corneal edema, increased intraocular pressure, peripheral anterior synechiae, and iris changes [1,2,6].

Patients may complain of severe problems with dry eyes, or with visual obscurations. It can also be asymptomatic, and only discovered because of subtle lines and marks seen during an eye exam.

EBMD is a bilateral anterior corneal dystrophy characterized by grayish epithelial fingerprint lines, geographic map-like lines, and dots (or microcysts) on slit-lamp examination. Findings are variable and can change with time. While the disorder is usually asymptomatic, up to 10% of patients may have recurrent corneal erosions, usually beginning after age 30; conversely, 50% of patients presenting with idiopathic recurrent erosions have evidence of this dystrophy.