Punctate epithelial erosions may be seen with different disorders:

- Rosacea

- Dry-eye syndrome

- Blepharitis

- Acute bacterial conjunctivitis

- Trauma

- Exposure keratopathy from poor eyelide closure

- Ultraviolet or chemical burn

- Contact lens-related disorder such as toxicity or tight lens syndrome

- Trichiasis

- Entropion or ectropion

- Floppy eyelid syndrome

- Chemotherapy i.e. cytosine arabinoside

- Thygeson's Superficial Punctate Keratopathy

The cornea, an avascular tissue, is among the most densely innervated structures of the human body. Corneal nerves are responsible for maintaining the anatomical and functional integrity of the cornea, conveying tactile, temperature and pain sensations, playing a role in the blink reflex, in wound healing and in the production and secretion of tears.

Most corneal nerve fibres are sensory in origin and are derived from the ophthalmic branch of the trigeminal nerve. Congenital or acquired ocular and systemic diseases can determine a lesion at different levels of the trigeminal nerve, which can lead to a reduction (hypoesthesia) or loss (anesthesia) of sensitivity of the cornea.

The most common causes of loss of corneal sensitivity are viral infections (herpes simplex and herpes zoster ophthalmicus), chemical burns, physical injuries, corneal surgery, neurosurgery, chronic use of topical medications, or chronic use of contact lenses.

Possible causes also include systemic diseases such as diabetes, multiple sclerosis or leprosy.

Other, albeit less frequent, potential causes of the disease are: intracranial space-occupying lesions such as neuroma, meningioma and aneurysms, which may compress the trigeminal nerve and reduce corneal sensitivity.

Conversely, congenital conditions that may lead to this disorder are very rare.

A study in Austria found over the course of the testing, a total of 154 cases of "Acanthamoeba" keratitis. The age of the positive tests ranged from 8 to 82 years old and 58% of the people were female. The data showed that 89% of the infected patients were contact lens wearers and 19% required a corneal transplant.

Keratitis–ichthyosis–deafness syndrome (also known as "Erythrokeratodermia progressiva Burns," "Ichthyosiform erythroderma, corneal involvement, and deafness," and "KID syndrome,") presents at birth/infancy and is characterized by pregressive corneal opacification, either mild generalized hyperkeratosis or discrete erythematous plaques, and neurosensory deafness.

It is caused by a mutation in connexin 26.

Several aetiologies are suggested, and any combination of these may be present in any given case.

- Vitamin deficiency (A, B or C)

- Viral infection

- Bacterial infection

- "Leptospira

- "Streptococcus

- "Brucella

- Parasitic infection

- Strongyle

- "Onchocerca cervicalis"

- Autoimmune disease

The disease has been suggested to be primarily autoimmune in nature, being a delayed hypersensitivity reaction to any of the above agents.

Neurotrophic keratitis (NK) is a degenerative disease of the cornea caused by damage of the trigeminal nerve, which results in impairment of corneal sensitivity, spontaneous corneal epithelium breakdown, poor corneal healing and development of corneal ulceration, melting and perforation.

Neurotrophic keratitis is classified as a rare disease, with an estimated prevalence of less than 5 in 10,000 people in Europe. It has been recorded that on average, 6% of herpetic keratitis cases may evolve to this disease, with a peak of 12.8% of cases of keratitis due to herpes zoster virus.

The diagnosis, and particularly the treatment of neurotrophic keratitis are the most complex and challenging aspects of this disease, as a satisfactory therapeutic approach is not yet available.

The Appaloosa has a higher risk of developing ERU than other breeds; this predisposition has a genetic basis. Appaloosas which develop ERU are more likely than other breeds to have ERU in both eyes, and more likely to become blind in one or both eyes.

Dyschromatosis symmetrica hereditaria (also known as "reticulate acropigmentation of Dohi", and "symmetrical dyschromatosis of the extremities") is a rare autosomally inherited dermatosis. It is characterized by progressively pigmented and depigmented macules, often mixed in a reticulate pattern, concentrated on the dorsal extremities. It presents primarily in the Japanese, but has also been found to affect individuals from Europe, India and the Caribbean.

Due to the different underlying causes, proper diagnosis, treatment, and prognosis can only be determined by an eye care professional. Punctate epithelial erosions may be treated with artificial tears. In some disorders, topical antibiotic is added to the treatment. Patients should discontinue contact lens wear until recovery.

This condition can also occur in ruminants suffering from a vitamin B (thiamine) deficiency due to thiamine-related cerebrocortical necrosis (CCN).

The causes of TSPK are currently not yet well known.

However, there seem to be indications that dysfunctioning of the Meibomian gland can cause the condition. Inflammation of the meibomian glands (also known as meibomitis, meibomian gland dysfunction, or posterior blepharitis) causes the glands to be obstructed by thick waxy secretions. Besides leading to dry eyes, the obstructions can be degraded by bacterial lipases, resulting in the formation of free fatty acids, which irritate the eyes and sometimes cause punctate keratopathy.

With respect to embolic and hemodynamic causes, this transient monocular visual loss ultimately occurs due to a temporary reduction in retinal artery, ophthalmic artery, or ciliary artery blood flow, leading to a decrease in retinal circulation which, in turn, causes retinal hypoxia. While, most commonly, emboli causing amaurosis fugax are described as coming from an atherosclerotic carotid artery, any emboli arising from vasculature preceding the retinal artery, ophthalmic artery, or ciliary arteries may cause this transient monocular blindness.

- Atherosclerotic carotid artery: Amaurosis fugax may present as a type of transient ischemic attack (TIA), during which an embolus unilaterally obstructs the lumen of the retinal artery or ophthalmic artery, causing a decrease in blood flow to the ipsilateral retina. The most common source of these athero-emboli is an atherosclerotic carotid artery. However, a severely atherosclerotic carotid artery may also cause amaurosis fugax due to its stenosis of blood flow, leading to ischemia when the retina is exposed to bright light. "Unilateral visual loss in bright light may indicate ipsilateral carotid artery occlusive disease and may reflect the inability of borderline circulation to sustain the increased retinal metabolic activity associated with exposure to bright light."

- Atherosclerotic ophthalmic artery: Will present similarly to an atherosclerotic internal carotid artery.

- Cardiac emboli: Thrombotic emboli arising from the heart may also cause luminal obstruction of the retinal, ophthalmic, and/or ciliary arteries, causing decreased blood flow to the ipsilateral retina; examples being those arising due to (1) atrial fibrillation, (2) valvular abnormalities including post-rheumatic valvular disease, mitral valve prolapse, and a bicuspid aortic valve, and (3) atrial myxomas.

- Temporary vasospasm leading to decreased blood flow can be a cause of amaurosis fugax. Generally, these episodes are brief, lasting no longer than five minutes, and have been associated with exercise. These vasospastic episodes are not restricted to young and healthy individuals. "Observations suggest that a systemic hemodynamic challenge provoke[s] the release of vasospastic substance in the retinal vasculature of one eye."

- Giant cell arteritis: Giant cell arteritis can result in granulomatous inflammation within the central retinal artery and posterior ciliary arteries of eye, resulting in partial or complete occlusion, leading to decreased blood flow manifesting as amaurosis fugax. Commonly, amaurosis fugax caused by giant cell arteritis may be associated with jaw claudication and headache. However, it is also not uncommon for these patients to have no other symptoms. One comprehensive review found a two to nineteen percent incidence of amaurosis fugax among these patients.

- Systemic lupus erythematosus

- Periarteritis nodosa

- Eosinophilic vasculitis

- Hyperviscosity syndrome

- Polycythemia

- Hypercoagulability

- Protein C deficiency

- Antiphospholipid antibodies

- Anticardiolipin antibodies

- Lupus anticoagulant

- Thrombocytosis

- Subclavian steal syndrome

- Malignant hypertension can cause ischemia of the optic nerve head leading to transient monocular visual loss.

- Drug abuse-related intravascular emboli

- Iatrogenic: Amaurosis fugax can present as a complication following carotid endarterectomy, carotid angiography, cardiac catheterization, and cardiac bypass.

CNV causes may be congenital in nature, such as with Aniridia, or acquired. Frequently, inflammatory, infectious, degenerative, traumatic and iatrogenic (from contact lenses) diseases are responsible for acquired CNV.

Some major associated, acquired inflammatory conditions include graft rejection following keratoplasty, graft or host diseases of the new tissue, atopic conjunctivitis, rosacea, ocular pemphigoid, Lyell's syndrome, and Steven's Johnson syndrome.

Infections responsible for CNV range from bacterial (chlamydia, syphilis, pseduomonas), Viral (herpes simplex and herpes zoster viruses), Fungal (candida, asperigillus, fusarium), and parasistic (onchocerca volvolus).

Degenerative diseases such as pterygiums, and terrien's marginal degeneration may be responsible.

Traumas frequently seen with CNV include ulceration, alkali burns, and stem cell deficiency.

One of the most common causes of corneal neovascularization is iastrogenic pathology from contact lens wear. This is especially true of lenses made with older hydrogel materials such as HEMA (2-hydroxyethyl methacrylate) for both daily and extended wear. Such older hydrogel materials have a relatively low oxygen transmissibility so the cornea becomes starved of oxygen leading to the ingress of blood capillaries into the clear cornea to satisfy that oxygen demand. Older estimates have 128,000 to 470,000 cases of lens-induced CNV each year, but this may be decreasing due to the increasing popularity of daily disposable lenses.

The risk for CNV is elevated in certain instances for patients following penetrating keratoplasty without active inflammation or epithelial defects. CNV is more likely to occur in those with active blepharitis, those who receive sutured knots in their host stromas, and those with a large recipient area.

It is currently thought that Cogan's syndrome is an autoimmune disease. The inflammation in the eye and ear are due to the patient's own immune system producing antibodies that attack the inner ear and eye tissue. Autoantibodies can be demonstrated in the blood of some patients, and these antibodies have been shown to attack inner ear tissue in laboratory studies. Infection with the bacteria "Chlamydia pneumoniae" has been demonstrated in some patients prior to the development of Cogan's syndrome, leading some researchers to hypothesize that the autoimmune disease may be initiated by the infection. "C. pneumoniae" is a common cause of mild pneumonia, and the vast majority of patients who are infected with the bacteria do not develop Cogan's syndrome.

This disease is caused by mutation in the double stranded RNA specific adenosine deaminase (ADAR1) gene. This gene is located on the long arm of chromosome 1 (1q21).

Vernal keratoconjunctivitis (VKC) or spring catarrh is a recurrent, bilateral, and self-limiting inflammation of conjunctiva, having a periodic seasonal incidence.

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.

Thygeson's superficial punctate keratopathy (TSPK; also "Thygeson Superficial Punctate Keratitis") is a disease of the eyes. The causes of TSPK are not currently known, but details of the disease were first published in the Journal of the American Medical Association in 1950 by the renowned American Ophthalmologist, Phillips Thygeson (1903–2002) - after whom it is named.

Dyschromatosis universalis hereditaria is a rare genodermatosis characterized by reticulate hyper- and hypo- pigmentated macules in a generalized distribution.

Both autosomal dominant and recessive inheritance have been reported with the disorder.

Those experiencing amaurosis are usually advised to consult a physician immediately as any form of vision loss, even if temporary, is a symptom that may indicate the presence of a serious ocular or systemic problem.

Diffuse lamellar keratitis (DLK) is a sterile inflammation of the cornea which may occur after refractive surgery, such as LASIK. Its incidence has been estimated to be 1 in 500 patients, though this may be as high as 32% in some cases.

Cogan's syndrome is a rare, rheumatic disease characterized by inflammation of the ears and eyes. Cogan's syndrome can lead to vision difficulty, hearing loss and dizziness. The condition may also be associated with blood-vessel inflammation (called vasculitis) in other areas of the body that can cause major organ damage in 15% of those afflicted or, in a small number of cases, even death. It most commonly occurs in a person's 20s or 30s. The cause is not known. However, one theory is that it is an autoimmune disorder in which the body's immune system mistakenly attacks tissue in the eye and ear.

According to the American Optometric Association, the following steps can be taken to prevent "Acanthamoeba" keratitis:

- Always wash and dry your hands before handling contact lenses, ordinary water should never come in contact with your lenses.

- Rub and rinse the surface of the contact lens before storing.

- Use only sterile products recommended by your optometrist to clean and disinfect your lenses. Saline solution and rewetting drops are not designed to disinfect lenses.

- Avoid using tap water to wash or store contact lenses.

- Contact lens solution must be discarded upon opening the case, and fresh solution used each time the lens is placed in the case.

- Replace lenses using your doctor’s prescribed schedule.

- Do not sleep in contact lenses unless prescribed by your doctor and never after swimming.

- Never swap lenses with someone else.

- Never put contact lenses in your mouth.

- See your optometrist regularly for contact lens evaluation.

VKC is thought to be an allergic disorder in which IgE mediated mechanism play a role. Such patients often give family history of other atopic diseases such as hay fever, asthma or eczema, and their peripheral blood shows eosinophilia and increased serum IgE levels.

Prior to 1990, amaurosis fugax could, "clinically, be divided into four identifiable symptom complexes, each with its underlying pathoetiology: embolic, hypoperfusion, angiospasm, and unknown". In 1990, the causes of amaurosis fugax were better refined by the Amaurosis Fugax Study Group, which has defined five distinct classes of transient monocular blindness based on their supposed cause: embolic, hemodynamic, ocular, neurologic, and idiopathic (or "no cause identified") Concerning the pathology underlying these causes (except idiopathic), "some of the more frequent causes include atheromatous disease of the internal carotid or ophthalmic artery, vasospasm, optic neuropathies, giant cell arteritis, angle-closure glaucoma, increased intracranial pressure, orbital compressive disease, a steal phenomenon, and blood hyperviscosity or hypercoagulability."