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.

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.

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.

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..

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.

Corneal neovascularization (CNV) is the in-growth of new blood vessels from the pericorneal plexus into avascular corneal tissue as a result of oxygen deprivation. Maintaining avascularity of the corneal stroma is an important aspect of corneal pathophysiology as it is required for corneal transparency and optimal vision. A decrease in corneal transparency causes visual acuity deterioration. Corneal tissue is avascular in nature and the presence of vascularization, which can be deep or superficial, is always pathologically related.

Corneal neovascularization is a sight-threatening condition that can be caused by inflammation related to infection, chemical injury, autoimmune conditions, post-corneal transplantation, and traumatic conditions among other ocular pathologies. Common causes of CNV within the cornea include trachoma, corneal ulcers, phylctenular keratoconjunctivitis, rosacea keratitis, interstitial keratitis, sclerosing keratitis, chemical burns, and wearing contact lenses for over-extended periods of time. Superficial presentations of CNV are usually associated with contact lens wear, while deep presentations may be caused by chronic inflammatory and anterior segment ocular diseases.

Corneal neovascularization is becoming increasingly common worldwide with an estimated incidence rate of 1.4 million cases per year, according to a 1998 study by the Massachusetts Eye and Ear Infirmary. The same study found that the tissue from twenty percent of corneas examined during corneal transplantations had some degree of neovascularization, negatively impacting the prognosis for individuals undergoing keratoplasty procedures.

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

Complications are the exception rather than the rule from simple corneal abrasions. It is important that any foreign body be identified and removed, especially if containing iron as rusting will occur.

Occasionally the healed epithelium may be poorly adherent to the underlying basement membrane in which case it may detach at intervals giving rise to recurrent corneal erosions.

Corneal hydrops might be caused by a tear in the recently discovered Dua's layer, a 15 micron thick layer between the corneal stroma and Descemet’s membrane, Harminder Dua suggests that this finding will affect corneal surgery, including penetrating keratoplasty, and understanding of corneal dystrophies and pathologies, such as acute hydrops.

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.

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.

Predisposing factors for Postoperative PVR are preoperative PVR, aphakia, high levels of vitreous proteins, duration of retinal detachment before corrective surgery, the size of the retinal hole or tear, intra-ocular inflammation, vitreous hemorrhage, and trauma to the eye. An equation to calculate the patient's risk for acquiring PVR is:

1 is added if the risk factor is present and 0 if the risk factor is absent. A patient is at a high risk for developing PVR is the PVR score is >6.33.

The incidence and prevalence of PMD are unknown, and no studies have yet investigated its prevalence or incidence. However, it is generally agreed that PMD is a very rare condition. Some uncertainty regarding the incidence of PMD may be attributed to its confusion with keratoconus. PMD is not linked to race or age, although most cases present early in life, between 20 and 40 years of age. While PMD is usually considered to affect men and women equally, some studies suggest that it may affect men more frequently.

Several diseases have been observed in patients with PMD. However, no causal relationships have been established between any of the associated diseases and the pathogenesis of PMD. Such diseases include: chronic open-angle glaucoma, retinitis pigmentosa, retinal lattice degeneration, scleroderma, kerato-conjunctivitis, eczema, and hyperthyroidism.

Previous long-standing eye infection which possibly during childhood time recalled as being treated with antibiotic and/or hospitalized over long period of time.

Recurrence within a few years occurs in all patients following corneal transplantation. Soft contact lenses are effective in decreasing recurrences.

By far the most common cause of IK is syphilitic disease. However, there are two possible causes of the corneal inflammatory response: an infection and/or an immunological response, such as a hypersensitivity type reaction, or (rarely) Cogan syndrome. Infectious causes include syphilis (commonest), followed by other bacterial infections (TB, Leprosy and Lyme disease) and parasitic infections (Acanthamoeba, Onchocerciasis or river blindness, Leishmaniasis, Trypanosoma cruzi or "Chagas disease", Trypanosoma brucei or "African sleeping sickness" and microsporidia)

Corneal hydrops or corneal rupture is an uncommon complication seen in people with advanced keratoconus or other corneal ectatic disorders, and is characterized by stromal edema due to leakage of aqueous humor through a tear in Descemet's membrane. Although a hydrops usually causes increased scarring of the cornea, occasionally it will benefit a patient by creating a flatter cone, aiding the fitting of contact lenses. Corneal transplantation is not usually indicated during corneal hydrops.

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.

Corneal abrasions are generally a result of trauma to the surface of the eye. Common causes include being poked by a finger, walking into a tree branch, and wearing old contact lenses. A foreign body in the eye may also cause a scratch if the eye is rubbed.

Injuries can also be incurred by "hard" or "soft" contact lenses that have been left in too long. Damage may result when the lenses are removed, rather than when the lens is still in contact with the eye. In addition, if the cornea becomes excessively dry, it may become more brittle and easily damaged by movement across the surface. Soft contact lens wear overnight has been extensively linked to gram negative keratitis (infection of the cornea) particularly by a bacterium known as "Pseudomonas aeruginosa" which forms in the eye's biofilm as a result of extended soft contact lens wear. When a corneal abrasion occurs either from the contact lens itself or another source, the injured cornea is much more susceptible to this type of bacterial infection than a non-contact lens user's would be. This is an optical emergency as it is sight (in some cases eye) threatening. Contact lens wearers who present with corneal abrasions should never be pressure patched because it has been shown through clinical studies that patching creates a warm, moist dark environment that can cause the cornea to become infected or cause an existing infection to be greatly accelerated on its destructive path.

Corneal abrasions are also a common and recurrent feature in people who suffer specific types of corneal dystrophy, such as lattice corneal dystrophy. Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma. 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. 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: (1) Alter the cornea's normal curvature, resulting in temporary vision problems; and (2) Expose the nerves that line the cornea, causing severe pain. Even the involuntary act of blinking can be painful.

Boehm Syndrome defines erosion events that occur only during periods of sleep.

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.

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.

Before LASIK surgery, people must be examined for possible risk factors such as keratoconus.

Abnormal corneal topography compromises of keratoconus, pellucid marginal degeneration, or forme fruste keratoconus with an I-S value of 1.4 or more is the most significant risk factor. Low age, low residual stromal bed (RSB) thickness, low preoperative corneal thickness, and high myopia are other important risk factors.

DLK is predominantly associated with Lasik, as the creation of a flap creates a potential space for cells to accumulate. Individuals with atopic conditions with pre-existing allergic conjunctivitis, or ocular rosacea, are more prone to developing the condition after surgery. Some authors have reported that moderate to severe eye allergies and chronic allergic conjunctivitis are an absolute contraindication to the LASIK procedure. This is in distinction to findings of earlier studies. Keratitis can also occur after photorefractive keratectomy (PRK), although because it occurs in the setting of infection, it is distinct from the sterile infiltrates of DLK. DLK can also occur following myopic keratomileusis, in which a disc of corneal tissue is removed, shaped and sutured back into place, although this technique is more historical, having been replaced by Lasik and PRK.

The treatment of corneal perforation depends on the location, severity and the cause of damage

- Tissue adhesive can be used to seal small perforation, but this method cannot be used to treat perforations larger than 1 mm.

- Non infected corneal perforation generally heals when a pressure bandage is used.

- For certain types of corneal perforations, lamellar keratoplasty is used as treatment.

Reis-Bücklers corneal dystrophy is not associated with any systemic conditions.