Most common:

- Floaters

- Blurred vision

Intermediate uveitis normally only affects one eye. Less common is the presence of pain and photophobia.

Inflammation in the back of the eye is commonly characterized by:

- Floaters

- Blurred vision

- Photopsia or seeing flashing lights

The diagnosis of POHS is based on the clinical triad of multiple white, atrophic choroidal

scars, peripapillary pigment changes (dark spots around optic disc of the eye), and a maculopathy caused by choroidal neovascularization.

Completely distinct from POHS, acute ocular histoplasmosis may rarely occur in immunodeficiency.

The retinal lesion can mimic retinoblastoma in appearance, and mistaken diagnosis of the latter condition can lead to unnecessary "enucleation".

The eye involvement can cause the following inflammatory disorders:

- endophthalmitis

- uveitis

- chorioretinitis

Intermediate uveitis is a form of uveitis localized to the vitreous and peripheral retina. Primary sites of inflammation include the vitreous of which other such entities as pars planitis, posterior cyclitis, and hyalitis are encompassed. Intermediate uveitis may either be an isolated eye disease or associated with the development of a systemic disease such as multiple sclerosis or sarcoidosis. As such, intermediate uveitis may be the first expression of a systemic condition. Infectious causes of intermediate uveitis include Epstein-Barr virus infection, Lyme disease, HTLV-1 virus infection, cat scratch disease, and hepatitis C.

Permanent loss of vision is most commonly seen in patients with chronic cystoid macular edema (CME). Every effort must be made to eradicate CME when present. Other less common causes of visual loss include retinal detachment, glaucoma, band keratopathy, cataract, vitreous hemorrhage, epiretinal membrane and choroidal neovascularization.

This is a partial list of human eye diseases and disorders.

The World Health Organization publishes a classification of known diseases and injuries, the International Statistical Classification of Diseases and Related Health Problems, or ICD-10. This list uses that classification.

Presumed ocular histoplasmosis syndrome (POHS) is a syndrome affecting the eye, which is characterized by peripheral atrophic chorioretinal scars, atrophy or scarring adjacent to the optic disc and maculopathy.

The loss of vision in POHS is caused by choroidal neovascularization.

Clinical signs include redness of the eye, pain, blurring of vision, photophobia and floaters.

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.

In the acute stage of the disease, a catarrhal conjunctivitis is present, with signs of ocular pain, usually blepharospasm, increased lacrimation, and photophobia. Miosis is also usually present. After a few days, this will progress to a keratitis and iridocyclitis. Other ocular problems may also occur, including conjunctival and corneal oedema, and aqueous flare.

After an acute flare-up, no clinical signs of disease may be seen for a prolonged period, which can vary from a few hours to a few years. With frequent acute incidents, though, additional clinical signs may be seen, including anterior and posterior synechiae, poor pupillary responses, cataracts, and a cloudy appearance to the vitreous humour.

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.

Superior limbic keratoconjunctivitis is an ocular disease characterized by episodes of recurrent inflammation of the superior cornea and limbus, as well as of the superior tarsal and bulbar conjunctiva.

Even though the pathophysiology remains unclear, it is thought that mechanical trauma from tight upper lids or loose redundant conjunctiva could lead to the disruption of normal epithelium. This mechanical hypothesis is supported by the increased lid apposition of exophthalmic thyroid patients, who are known to have an increased incidence of superior limbic keratoconjunctivitis.

Patients present with red eye, burning, tearing, foreign body sensation, mild photophobia. Inflammation and thickening of the conjunctiva is observed, especially at the limbus.Lubrication is an effective treatment for this pathology.

Retinal vasculitis presents as painless, decrease of visual acuity (blurry vision), visual floaters, scotomas (dark spot in vision), decreased ability to distinguish colors, and metamorphopsia (distortion of images such as linear images).

The sequence of clinical events in VKH is divided into four phases: prodromal, acute uveitic, convalescent, and chronic recurrent.

The prodromal phase may have no symptoms, or may mimic a non-specific viral infection, marked by flu-like symptoms that typically last for a few days. There may be fever, headache, nausea, meningismus, dysacusia (discomfort caused by loud noises or a distortion in the quality of the sounds being heard), tinnitus, and/or vertigo. Eye symptoms can include orbital pain, photophobia and tearing. The skin and hair may be sensitive to touch. Cranial nerve palsies and optic neuritis are uncommon.

The acute uveitic phase occurs a few days later and typically lasts for several weeks. This phase is heralded by bilateral panuveitis causing blurring of vision. In 70% of VKH, the onset of visual blurring is bilaterally contemporaneous; if initially unilateral, the other eye is involved within several days. The process can include bilateral granulomatous anterior uveitis, variable degree of vitritis, thickening of the posterior choroid with elevation of the peripapillary retinal choroidal layer, optic nerve hyperemia and papillitis, and multiple exudative bullous serous retinal detachments.

The convalescent phase is characterized by gradual tissue depigmentation of skin with vitiligo and poliosis, sometimes with nummular depigmented scars, as well as alopecia and diffuse fundus depigmentation resulting in a classic orange-red discoloration ("sunset glow fundus") and retinal pigment epithelium clumping and/or migration.

The chronic recurrent phase may be marked by repeated bouts of uveitis, but is more commonly a chronic, low-grade, often subclinical, uveitis that may lead to granulomatous anterior inflammation, cataracts, glaucoma and ocular hypertension. Full-blown recurrences are, however, rare after the acute stage is over. Dysacusia may occur in this phase.

The disease is characterised by bilateral diffuse uveitis, with pain, redness and blurring of vision. The eye symptoms may be accompanied by a varying constellation of systemic symptoms, such as auditory (tinnitus, vertigo, and hypoacusis), neurological (meningismus, with malaise, fever, headache, nausea, abdominal pain, stiffness of the neck and back, or a combination of these factors; meningitis, CSF pleocytosis, cranial nerve palsies, hemiparesis, transverse myelitis and ciliary ganglionitis), and cutaneous manifestations, including poliosis, vitiligo, and alopecia. The vitiligo often is found at the sacral region.

Retinal vasculitis is inflammation of the vascular branches of the retinal artery, caused either by primary ocular disease processes, or as a specific presentation of any systemic form of vasculitis such as Behçet's disease, sarcoidosis, multiple sclerosis, or any form of systemic nectrozing vasculitis such as temporal arteritis, polyarteritis nodosa, and granulomatosis with polyangiitis, or due to lupus erythematosus, or rheumatoid arthritis. Eales disease, pars planitis, birdshot retinochoroidopathy (autoimmune bilateral posterior uveitis), and Fuchs heterochromic iridocyclitis (FHI) can also cause retinal vasculitis. Infectious pathogens such as "Mycobacterium tuberculosis", visceral larva migrans ("Toxocara canis" & "Toxocara cati") can also cause retinal vasculitis.

Equine recurrent uveitis (ERU), also known as moon blindness, recurrent iridocyclitis or periodic ophthalmia, is an acute, nongranulomatous inflammation of the uveal tract of the eye, occurring commonly in horses of all breeds, worldwide. The causative factor is not known, but several pathogeneses have been suggested. It is the most common cause of blindness in horses. In some breeds, a genetic factor may be involved.

The following are not classified as diseases of the eye and adnexa (H00-H59) by the World Health Organization:

- (B36.1) Keratomycosis — fungal infection of the cornea

- (E50.6-E50.7) Xerophthalmia — dry eyes, caused by vitamin A deficiency

- (Q13.1) Aniridia — a rare congenital eye condition leading to underdevelopment or even absence of the iris of the eye

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 primary symptom is pupillary distortion (changing of the size or shape of the pupil). Distortion can occur in any segment of the iris. One part of the iris is pulled to a peak, and then returns to normal after the episode. Other symptoms may include blurred vision, abnormal periocular sensations (unusual feelings around the eyes), migraines, and feelings of a chilled face. Some patients who demonstrate tadpole pupil symptoms also experienced Horner’s syndrome or Adie’s tonic pupil

Tadpole pupil symptoms occur in episodes. Episodes are generally brief and less than 5 minutes, however, some episodes have been reported to last anywhere from 3 to 15 minutes. The episodes can occur multiple times a day for days, weeks, or months.

Studies show that a majority of those experiencing tadpole pupil are younger women from an age range of 24 to 48 years old, with no apparent health problems. Although women generally have the tadpole pupil, men are not unaffected by this disease and some have been reported to experience the symptoms.

Those with ocular ischemic syndrome are typically between the ages of 50 and 80 (patients over 65) ; twice as many men as women are affected. More than 90% of those presenting with the condition have vision loss. Patients may report a dull, radiating ache over the eye and eyebrow. Those with ocular ischemic syndrome may also present with a history of other systemic diseases including arterial hypertension, diabetes mellitus, coronary artery disease, previous stroke, and hemodialysis.

The condition presents with visual loss secondary to hypoperfusion of the eye structures. The patient presents with intractable pain or ocular angina. On dilated examination, there may be blot retinal hemorrhages along with dilated and beaded retinal veins. The ocular perfusion pressure is decreased.

The corneal layers show edema and striae. There is mild anterior uveitis. A cherry-red spot may be seen in the macula, along with cotton-wool spots elsewhere, due to retinal nerve fiber layer hemorrhages. The retinal arteries may show spontaneous pulsations.

Ocular causes include:

- Iritis

- Keratitis

- Blepharitis

- Optic disc drusen

- Posterior vitreous detachment

- Closed-angle glaucoma

- Transient elevation of intraocular pressure

- Intraocular hemorrhage

- Coloboma

- Myopia

- Orbital hemangioma

- Orbital osteoma

- Keratoconjunctivitis sicca

Ocular melanosis (OM), also known as ocular melanocytosis or melanosis oculi, is a congenital disease of the eye which affects about 1 in every 5000 people and is a risk factor for uveal melanoma. In dogs is found almost exclusively in the Cairn Terrier, where until recently it was known as pigmentary glaucoma. The disease is caused by an increase of melanocytes in the iris, choroid, and surrounding structures. Overproduction of pigment by these cells can block the trabecular meshwork through which fluid drains from the eye. The increased fluid in the eye leads to increased pressure, which can lead to glaucoma. In humans, this is sometimes known as pigment dispersion syndrome.

According to Mackie's classification, neurotrophic keratitis can be divided into three stages based on severity:

1. "Stage I:" characterized by alterations of the corneal epithelium, which is dry and opaque, with superficial punctate keratopathy and corneal oedema. Long-lasting neurotrophic keratitis may also cause hyperplasia of the epithelium, stromal scarring and neovascularization of the cornea.

2. "Stage II:" characterized by development of epithelial defects, often in the area near the centre of the cornea.

3. "Stage III:" characterized by ulcers of the cornea accompanied by stromal oedema and/or melting that may result in corneal perforation.