Patients who have malignant gliomas of the optic nerve have rapidly progressive, painful visual loss accompanied by signs of an optic neuropathy. Initial visual loss may be unilateral or bilateral (chiasmal involvement), but rapid progression to bilateral blindness and death are constant features. Depending on the initial location of the tumor, visual loss may be accompanied by exophthalmos, extraocular motility

Optic nerve melanocytoma does not usually produce symptoms or grow. If they slowly grow, optic nerve melanocytoma can produce afferent pupillary defects (30%), subretinal fluid (10%), and an enlarged blind spot (75%).

On fundoscopic exam, the optic disc may be swollen, atrophic, or even normal. Central retinal vein occlusion may occur.

If the tumor is next to the optic nerve, growth can compress the nerve and cause gradual loss of vision and unilateral proptosis. Dyschromatopsia may occur. Growth can also cause compressive vascular problems like central retinal vein occlusion. Lastly, growth also causes the tumor to exceed its blood supply. In these cases, necrotic areas form inside the tumor. Necrosis can (in turn) cause intraocular and rarely orbital inflammation.

There are several signs and symptoms of the eye that can indicate the growth of a tumor, which include:

- White or reddening pupil

- Eye enlargement or bulging

- Redness or irritation

- Visual disturbances

- Vision loss or changes

- Drooping eyelid.

The most common and obvious sign of retinoblastoma is an abnormal appearance of the retina as viewed through the pupil, the medical term for which is leukocoria, also known as amaurotic cat's eye reflex. Other signs and symptoms include deterioration of vision, a red and irritated eye with glaucoma, and faltering growth or delayed development. Some children with retinoblastoma can develop a squint, commonly referred to as "cross-eyed" or "wall-eyed" (strabismus). Retinoblastoma presents with advanced disease in developing countries and eye enlargement is a common finding.

Depending on the position of the tumors, they may be visible during a simple eye exam using an ophthalmoscope to look through the pupil. A positive diagnosis is usually made only with an examination under anesthetic (). A white eye reflection is not always a positive indication of retinoblastoma and can be caused by light being reflected badly or by other conditions such as Coats' disease.

The presence of the photographic fault red eye in only one eye and not in the other may be a sign of retinoblastoma. A clearer sign is "white eye" or "cat's eye" (leukocoria).

Most optic nerve tumors (65 percent) are gliomas that occur somewhere along the anterior visual pathway.

The typical infant who has congenital glaucoma usually is initially referred to an ophthalmologist because of apparent corneal edema. The commonly described triad of epiphora (excessive tearing), blepharospasm and photophobia may be missed until the corneal edema becomes apparent.

Persistent tunica vasculosa lentis is a congenital ocular anomaly. It is a form of persistent hyperplastic primary vitreous (PHPV).

It is a developmental disorder of the vitreous. It is usually unilateral and first noticed in the neonatal period. It may be associated with micropthalmos, cataracts, and increased intraocular pressure. Elongated ciliary processes are visible through the dilated pupil. A USG B-scan confirms diagnosis in the presence of a cataract.

Buphthalmos in itself is merely a clinical sign and does not generate symptoms. Patients with glaucoma often initially have no symptoms; later, they can exhibit excessive tearing (lacrimation) and extreme sensitivity to light (photophobia). On ophthalmologic exam, one can detect increased intraocular pressure, distortion of the optic disc, and corneal edema, which manifests as haziness.

Other symptoms include a prominent eyeball, Haab's striae in the Descemet's membrane of the cornea, an enlarged cornea, and myopia.

The diagnosis is clinical. The intraocular pressure (IOP) can be measured in the office in a conscious swaddled infant using a Tonopen or hand-held Goldmann tonometer. Usually, the IOP in normal infants is in the range of 11-14 mmHg. Buphthalmos and Haab's striae can often be seen in case of congenital glaucoma.

Intraocular Schwannoma, also termed uveal schwannoma, is a type of schwannoma found in the eye. These tumors are almost always benign in nature and while malignant forms have been documented in other areas of the body, this has not been reported in the uveal region. Composed of Schwann cells, these masses are generally slow growing and can be found in the peripheral nerve tract, often around the head and neck.

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].

The most common sign of CEA is the presence of an area of undeveloped choroid (appearing as a pale spot) lateral to the optic disc. The choroid is a collection of blood vessels supplying the retina. CEA can also cause retinal or scleral coloboma, coloboma of the optic disc, retinal detachment, or intraocular hemorrhage. It can be diagnosed by fundoscopy by the age of six or seven weeks. Severe cases may be blind.

Infantile glaucoma, which often produces the clinical sign of buphthalmos, can be caused when an abnormally narrow angle between the cornea and iris blocks the outflow of aqueous humor; this causes increased intraocular pressure and eventual enlargement of the globe (eyeball). Angle closure can be caused by developmental abnormalities of the eye as well as the presence of abnormal structures within the vitreous.

There are two forms of the disease, a heritable form and non-heritable form (all cancers are considered genetic in that mutations of the genome are required for their development, but this does not imply that they are heritable, or transmitted to offspring). Approximately 55% of children with retinoblastoma have the non-heritable form. If there is no history of the disease within the family, the disease is labeled "sporadic", but this does not necessarily indicate that it is the non-heritable form. Bilateral retinoblastomas are commonly heritable, while unilateral retinoblastomas are commonly non-heritable.

In about two-thirds of cases, only one eye is affected (unilateral retinoblastoma); in the other third, tumors develop in both eyes (bilateral retinoblastoma). The number and size of tumours on each eye may vary. In certain cases, the pineal gland or the suprasellar or parasellar region (or in very rare cases other midline intracranial locations) is also affected (trilateral retinoblastoma). The position, size and quantity of tumours are considered when choosing the type of treatment for the disease.

Open-angle glaucoma is painless and does not have acute attacks, thus the lack of clear symptoms make screening via regular eye check-ups important. The only signs are gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination).

About 10% of people with closed angles present with acute angle closure characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure (>30 mmHg), nausea and vomiting, suddenly decreased vision, and a fixed, mid-dilated pupil. It is also associated with an oval pupil in some cases. Acute angle closure is an emergency.

Opaque specks may occur in the lens in glaucoma, known as glaukomflecken.

Collie eye anomaly (CEA) is a congenital, inherited, bilateral eye disease of dogs, which affects the retina, choroid, and sclera. It can be a mild disease or cause blindness. CEA is caused by a simple autosomal recessive gene defect. There is no treatment.

Intraocular lymphoma is a rare malignant form of eye cancer. Intraocular lymphoma may affect the eye secondarily from a metastasis from a non-ocular tumor or may arise within the eye primarily (primary intraocular lymphoma, PIOL). PIOL is a subset of primary central nervous system lymphoma (PCNSL). PCNSL (and PIOL) are most commonly a diffuse large B-cell immunohistologic subtype of non-Hodgkin's lymphoma according to the World Health Organization (WHO) classification of lymphomas. The most common symptoms of PIOL include blurred or decreased vision due to tumor cells in the vitreous. Most cases of PIOL eventuate to central nervous system involvement (PCNSL) while only 20% of PCNSL lead to intraocular (PIOL) involvement. PIOL and PCNSL remain enigmas because both structures are immunologically privileged sites (the brain sits behind the blood–brain barrier and the retina sits behind the blood-retinal barrier) and so do not normally have immune cells trafficking through these structures. What is more, while the vast majority of PCNSL in patients with acquired immune deficiency syndrome (AIDS) is related to the Epstein-Barr virus (EBV), the development of PCNSL and PIOL in immunocompetent patients is unknown and shows no general relation to infectious DNAs.

In immunocompetent patients, PIOL most commonly affects patients in their fifties and sixties. AIDS patients typically develop the disease earlier in their lives.

PIOL affects the sub-retinal pigment epithelium (RPE), can invade into the retina, the vitreous, and the optic nerve. Ophthalmoscopy frequently reveals creamy yellow-to-orange colored subretinal infiltrates. Fluorescein angiography may reveal "leopard spot" patterns due to sub-RPE infiltrates that stain early and progressively or mottling of the RPE due to hyper- and hypofluorescent window defects.

PIOL is known as a masquerade syndrome because it frequently simulates the signs and symptoms of uveitis. As such, PIOL is frequently treated with corticosteroids. Occasionally, PIOL has mimicked a retinitis and has been treated with antiviral medication. It is not until the supposed uveitis fails to respond to treatment, becomes recalcitrant to treatment, or shows worsening with discontinuation of corticosteroid treatment that another cause is sought out. If PIOL is suspected, it is important to first obtain a magnetic resonance image (MRI) of the brain to rule out cerebral involvement (PCNSL). If MRI is negative, lumbar puncture with cerebrospinal fluid (CSF) cytology should be performed to further rule out CNS disease. Histopathologic identification of atypical lymphocytes is considered the gold standard for diagnosing PCNSL/PIOL. If CSF cytology is negative or inconclusive and PIOL is suspected, a vitrectomy is often performed with cytologic analysis. Furthermore, adjunctive testing including polymerase chain reaction (PCR) amplification to identify monoclonal rearrangements of the immunoglobulin heavy chain (IgH) gene (for B-cell lymphomas) or T-cell receptor (TCR, for the very rare T-cell lymphomas) can be performed.

Previously, radiation therapy was the mainstay treatment for PCNSL/PIOL, but methotrexate has now become first-line.

• Typically affects short sighted (myopic) women. (90% of cases are female).

• The average age of patients with PIC is 27 years with a range of 16–40 years.

• Patients are otherwise healthy and there is usually no illness, which triggers the condition or precedes it.

• The inflammation is confined to the back of the eye (posterior). There is no inflammation in the front of the eye (anterior chamber) or vitreous (the clear jelly inside the eye). This is an important distinguishing feature of PIC.

• It usually affects both eyes.

• The appearance of gray-white or yellow punctate (punched out) areas (lesions) at the level of the inner choroid. These lesions are typically located centrally at the back of the eye (posterior pole).

Symptoms typically include:

1. Blurring of vision

2. Partial ‘blind spots’ or scotoma. These areas of diminished or lost areas of the visual field are typically near the centre of vision but occasionally can be peripheral. These may be temporary or permanent.

3. Seeing flashing lights. This is known as photopsia.

The PIC lesions, which form scars deep in the choroid layer of the eye, may result in new blood vessels forming. These can be seen as the body’s attempts at repair, but these new blood vessels (neovascularisation) are weak, can spread to form a membrane and can threaten the vision. It is

suspected that at least 40% of patients with PIC develop CNV (choroidal neovascularization). This is a complication, which can occur in other white dot syndromes and other eye conditions such as macular degeneration but occurs rarely in other forms of uveitis.

CNV is a sight threatening complication and so must be picked up early and always treated. It may occur whether the uveitis is active or not. CNV, if not treated, may lead to subretinal fibrosis (scarring), a further complication, which is more difficult to treat, and which leads to poor vision.

Good monitoring for patients with PIC is therefore very important.

Some discrepancy exists as to whether acute zonal occult outer retinopathy (AZOOR) is actually considered a white dot syndrome. However, AZOOR may definitely be related to other diseases included in the white dot syndrome group. AZOOR occurs in young to middle age adults and may eventually progress to retinal cell death. Symptoms include acute visual field loss and photopsias. Suspected causes for AZOOR include autoimmune, viral, and fungal.

Optic disc drusen (ODD) or optic nerve head drusen (ONHD) are globules of mucoproteins and mucopolysaccharides that progressively calcify in the optic disc. They are thought to be the remnants of the axonal transport system of degenerated retinal ganglion cells.

ODD have also been referred to as congenitally elevated or anomalous discs, pseudopapilledema, pseudoneuritis, buried disc drusen, and disc hyaline bodies. They may be associated with vision loss of varying degree occasionally resulting in blindness.

Multifocal Choroiditis (MPC) occurs mainly in myopic females. The fundus presents with yellow or gray lesions (white dots) at the level of the choroid and RPE. The size of the white dots are between 50 and 500 micrometres and localized in the macula. MPC is characterized by vitritis and anterior chamber inflammation. Decreased vision due to vitreous inflammation may occur. Unlike MEWDS, MPC is a chronic disorder and macular scarring contributes to severe visual loss. Theories regarding the cause include an exogenous pathogen sensitizing an individual to antigens within photoreceptors, RPE, or choroid.

Secondary glaucoma (H40.3-H40.6)

- Inflammatory glaucoma

- Phacogenic glaucoma

- Glaucoma secondary to intraocular hemorrhage

- Traumatic glaucoma

- Neovascular glaucoma (see below for more details)

- Drug-induced glaucoma

- Glaucoma of miscellaneous origin

Neovascular glaucoma, an uncommon type of glaucoma, is difficult or nearly impossible to treat, and is often caused by proliferative diabetic retinopathy (PDR) or central retinal vein occlusion (CRVO). It may also be triggered by other conditions that result in ischemia of the retina or ciliary body. Individuals with poor blood flow to the eye are highly at risk for this condition.

Neovascular glaucoma results when new, abnormal vessels begin developing in the angle of the eye that begin blocking the drainage. Patients with such condition begin to rapidly lose their eyesight. Sometimes, the disease appears very rapidly, especially after cataract surgery procedures. A new treatment for this disease, as first reported by Kahook and colleagues, involves the use of a novel group of medications known as anti-VEGF agents. These injectable medications can lead to a dramatic decrease in new vessel formation and, if injected early enough in the disease process, may lead to normalization of intraocular pressure. Currently, there are no high-quality controlled trials demonstrating a beneficial effect of anti-VEGF treatments in lowering IOP in people with neovascular glaucoma.

Toxic glaucoma is open angle glaucoma with an unexplained significant rise of intraocular pressure following unknown pathogenesis. Intraocular pressure can sometimes reach . It characteristically manifests as ciliary body inflammation and massive trabecular oedema that sometimes extends to Schlemm's canal. This condition is differentiated from malignant glaucoma by the presence of a deep and clear anterior chamber and a lack of aqueous misdirection. Also, the corneal appearance is not as hazy. A reduction in visual acuity can occur followed neuroretinal breakdown.

Associated factors include inflammation, drugs, trauma and intraocular surgery, including cataract surgery and vitrectomy procedures. Gede Pardianto (2005) reported on four patients who had toxic glaucoma. One of them underwent phacoemulsification with small particle nucleus drops. Some cases can be resolved with some medication, vitrectomy procedures or trabeculectomy. Valving procedures can give some relief, but further research is required.

Epiretinal membrane is a disease of the eye in response to changes in the vitreous humor or more rarely, diabetes. It is also called macular pucker. Sometimes, as a result of immune system response to protect the retina, cells converge in the macular area as the vitreous ages and pulls away in posterior vitreous detachment (PVD). PVD can create minor damage to the retina, stimulating exudate, inflammation, and leucocyte response. These cells can form a transparent layer gradually and, like all scar tissue, tighten to create tension on the retina which may bulge and pucker (e.g., macular pucker), or even cause swelling or macular edema. Often this results in distortions of vision that are clearly visible as bowing ←→ when looking at lines on chart paper (or an Amsler grid) within the macular area, or central 1.0 degree of visual arc. Usually it occurs in one eye first, and may cause binocular diplopia or double vision if the image from one eye is too different from the image of the other eye. The distortions can make objects look different in size (usually larger = macropsia), especially in the central portion of the visual field, creating a localized or field dependent aniseikonia that cannot be fully corrected optically with glasses. Partial correction often improves the binocular vision considerably though. In the young (under 50 years of age), these cells occasionally pull free and disintegrate on their own; but in the majority of sufferers (over 60 years of age) the condition is permanent. The underlying photoreceptor cells, rod cells and cone cells, are usually not damaged unless the membrane becomes quite thick and hard; so usually there is no macular degeneration.

With anterior lens luxation, the lens pushes into the iris or actually enters the anterior chamber of the eye. This can cause glaucoma, uveitis, or damage to the cornea. Uveitis (inflammation of the eye) causes the pupil to constrict (miosis) and trap the lens in the anterior chamber, leading to an obstruction of outflow of aqueous humour and subsequent increase in ocular pressure (glaucoma). Better prognosis is valued in lens replacement surgery (retained vision and normal intraocular pressure) when it is performed before the onset of secondary glaucoma. Glaucoma secondary to anterior lens luxation is less common in cats than dogs due to their naturally deeper anterior chamber and the liquification of the vitreous humour secondary to chronic inflammation. Anterior lens luxation is considered to be an ophthalmological emergency.

Uveal melanomas, often referred to by the media and in the general population as ocular melanomas, may arise from any of the three parts of the uvea, and are sometimes referred to by their location, as choroidal melanoma, ciliary body melanoma, or iris melanoma. Large tumors often encompass multiple parts of the uvea and can be named accordingly. True iris melanomas, originating from within the iris as opposed to originating elsewhere and invading the iris, are distinct in their etiology and prognosis, such that the other tumors are often referred to collectively as Posterior uveal melanomas.

Uveal melanoma was first described in the literature in 1809-1812 by two Scottish surgeons, Allan Burns and James Wardrop.