The pressure within the eye is maintained by the balance between the fluid that enters the eye through the ciliary body and the fluid that exits the eye through the trabecular meshwork.

Ocular hypertension is the presence of elevated fluid pressure inside the eye (intraocular pressure), usually with no optic nerve damage or visual field loss.

For most individuals, the normal range of introcular pressure is between 10 mmHg and 21 mmHg. Elevated intraocular pressure is an important risk factor for glaucoma. The Ocular Hypertension Treatment Study, a large, multicentered, randomized clinical trial, determined that topical ocular hypotensive medication delays or prevents the onset of Primary Open-Angle Glaucoma. Accordingly, most individuals with consistently elevated intraocular pressures of greater than 21mmHg, particularly if they have other risk factors, are treated in an effort to prevent vision loss from glaucoma.

Many people of East Asian descent are prone to developing angle closure glaucoma due to shallower anterior chamber depths, with the majority of cases of glaucoma in this population consisting of some form of angle closure. Higher rates of glaucoma have also been reported for Inuit populations, compared to white populations, in Canada and Greenland.

No clear evidence indicates vitamin deficiencies cause glaucoma in humans. It follows, then, that oral vitamin supplementation is not a recommended treatment for glaucoma. Caffeine increases intraocular pressure in those with glaucoma, but does not appear to affect normal individuals.

In the United States, the incidence of primary congenital glaucoma is about one in 10,000 live births. Worldwide, the incidence ranges from a low of 1:22,000 in Northern Ireland to a high of 1:2,500 in Saudi Arabia and 1:1,250 in Romania. In about two-thirds of cases, it is bilateral. The distribution between males and females varies with geography. In North America and Europe it is more common in boys, whereas in Japan it is more common in girls.

- Congenital glaucoma

- Incidence: one in every 10000-15000 live births.

- Bilateral in up to 80% of cases.

- Most cases are sporadic (90%). However, in the remaining 10% there appears to be a strong familial component.

Genetic mutations are rare causes of certain retinopathies and are usually X-linked including "NDP" family of genes causing Norrie Disease, FEVR, and Coats disease among others. There is emerging evidence that there may be a genetic predisposition in patients who develop retinopathy of prematurity and diabetic retinopathy. Trauma, especially to the head, and several diseases may cause Purtscher's retinopathy.

The two most common causes of retinopathy include diabetic retinopathy and retinopathy of prematurity. Diabetic retinopathy affects about 5 million people and retinopathy of prematurity affect about 50,000 premature infants each year worldwide. Hypertensive retinopathy is the next most common cause affecting anywhere from 3 to 14% of all non-diabetic adults.

Mydriatic/cycloplegic agents, such as topical homatropine, which is similar in action to atropine, are useful in breaking and preventing the formation of posterior synechia by keeping the iris dilated and away from the crystalline lens. Dilation of the pupil in an eye with the synechia can cause the pupil to take an irregular, non-circular shape (Dyscoria) as shown in the photograph. If the pupil can be fully dilated during the treatment of iritis, the prognosis for recovery from synechia is good. This is a treatable status.

To subdue the inflammation, use topical corticosteroids. If the intra-ocular pressure is elevated then use a PGA such as Travatan Z.

A synechia is an eye condition where the iris adheres to either the cornea (i.e. "anterior synechia") or lens (i.e. "posterior synechia"). Synechiae can be caused by ocular trauma, iritis or iridocyclitis and may lead to certain types of glaucoma. It is sometimes visible on careful examination but usually more easily through an ophthalmoscope or slit-lamp.

Anterior synechia causes closed angle glaucoma, which means that the iris closes the drainage way of aqueous humour which in turn raises the intraocular pressure. Posterior synechia also cause glaucoma, but with a different mechanism. In posterior synechia, the iris adheres to the lens, blocking the flow of aqueous humor from the posterior chamber to the anterior chamber. This blocked drainage raises the intraocular pressure.

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.

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.

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

Two of the more commonly encountered disorders that may be associated with congenital glaucoma are Aniridia and Sturge-Weber syndrome.

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

Pseudomyopia refers to an intermittent and temporary shift in refractive error of the eye towards myopia, in which the focusing of light in front of the retina is due to a transient spasm of the ciliary muscle causing an increase in the refractive power of the eye. It may be either organic, through stimulation of the parasympathetic nervous system, or functional in origin, through eye strain or fatigue of ocular systems. It is common in young adults who have active accommodation, and classically occurs after a change in visual requirements, such as students preparing for an exam, or a change in occupation.

The major symptom is intermittent blurring of distance vision particularly noticeable after prolonged periods of near work, and symptoms of asthenopia. The vision may clear temporarily using concave (minus) lenses. The diagnosis is done by cycloplegic refraction using a strong cycloplegic like atropine or homatropine eye drops. Accommodative amplitude and facility may be reduced as a result of the ciliary muscle spasm.

Treatment is dependent on the underlying aetiology. Organic causes may include systemic or ocular medications, brain stem injury, or active ocular inflammation such as uveitis. Functional pseudomyopia is managed though modification of working conditions, an updated refraction, typically involving a reduction of a myopic prescription to some lower myopic prescription, or through appropriate ocular exercises.

Despite its name, the "presumed" relationship of POHS to "Histoplasma capsulatum" is controversial. The fungus has rarely been isolated from cases with POHS, the condition has also been found in locations where histoplasmosis is rare, and there appears to be a relationship with tobacco smoking.

Severe ipsilateral or bilateral carotid artery stenosis or occlusion is the most common cause of ocular ischemic syndrome. The syndrome has been associated with occlusion of the common carotid artery, internal carotid artery, and less frequently the external carotid artery. Other causes include:

- Takayasu's arteritis

- Giant cell arteritis

- Severe ophthalmic artery occlusion, due to thromboembolism.

- Surgical interruption of anterior ciliary blood vessels supplying the eye, particularly during extensive strabismus surgery on 3 or more rectus muscles, leading to an anterior segment ischemic syndrome.

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.

A recent study estimated that from 2002-2003 there were 27,152 injuries in the United States related to the wearing of eyeglasses. The same study concluded that sports-related injuries due to eyeglasses wear were more common in those under the age of 18 and that fall-related injuries due to eyeglasses wear were more common in those aged 65 or more. Although eyeglasses-related injuries do occur, prescription eyeglasses and non-prescription sunglasses have been found to "offer measurable protection which results in a lower incidence of severe eye injuries to those wearing [them]".

In India study conducted by Dr.Shukla, injuries are found more in n males(81%).This is true for both rural and urban population but in 0-10 age group, the difference between males and females is less.Females account for 28% injuries in this age group.However, in sedentary workers, farmers, labourers and industrial workers the male % is as high as 95%.Chemical injuries are the comments cause of bilateral injuries in the eye .

Risk factors for CRAO include the following: being between 60 and 65 years of age, being over the age of 40, male gender, hypertension, caucasian, smoking and diabetes mellitus. Additional risk factors include endocarditis, atrial myxoma, inflammatory diseases of the blood vessels, and predisposition to forming blood clots.

Smoking does not directly cause high blood pressure. However it is a known risk factor for other serious cardiovascular disease.

Excessive alcohol consumption will increase blood pressure over time. Alcohol also contains a high density of calories and may contribute to obesity.

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.

A link between increased ICP and altered sodium and water retention was suggested by a report in which 77% of IIH patients had evidence of peripheral edema and 80% with orthostatic retention of sodium and water. Impaired saline and water load excretions were noted in the upright position in IIH patients with orthostatic edema compared to lean and obese controls without IIH. However, the precise mechanisms linking orthostatic changes to IIH were not defined, and many IH patients do not have these sodium and water abnormalities. Astronauts are well known to have orthostatic intolerance upon reentry to gravity after long-duration spaceflight, and the dietary sodium on orbit is also known to be in excess of 5 grams per day in some cases. The Majority of the NASA cases did have high dietary sodium during their increment. The ISS program is working to decrease in-flight dietary sodium intake to less than 3 grams per day. Prepackaged foods for the International Space Station were originally high in sodium at 5300 mg/d. This amount has now been substantially reduced to 3000 mg/g as a result of NASA reformulation of over ninety foods as a conscious effort to reduce astronaut sodium intake.

If carotid occlusive disease results in ophthalmic artery occlusion, general ocular ischemia may result in retinal neovascularization, rubeosis iridis, cells and flare, iris necrosis, and cataract. The condition leads to neovascularization in various eye tissues due to the ischemia. The eye pressure may become high due to associated neovascular glaucoma. An ischemic optic neuropathy may eventually occur.