Many people often do not have symptoms until very late in their disease course. Patients often become symptomatic when there is irreversible damage. Symptoms are usually not painful and can include:

- Vitreous hemorrhage

- Floaters, or small objects that drift through the field of vision

- Decreased visual acuity

- "Curtain falling" over eyes

Patients with idiopathic macular telangiectasia type 1 are typically 40 years of age or older. They may have a coincident history of ischemic vascular diseases such as diabetes or hypertension, but these do not appear to be causative factors.

Macular telangiectasia type 2 usually present first between the ages of 50 and 60 years, with a mean age of 55–59 years. They may present with a wide range of visual impact, from totally asymptomatic to substantially impaired; in most cases however, patients retain functional acuity of 20/200 or better. Metamorphopsia may be a subjective complaint. Due to the development of paracentral scotomota (blind spots), reading ability is impaired early in the disease course. It might be even the first symptom of the disease.

The condition may remain stable for extended periods, sometimes interspersed with sudden decreases in vision. Patients’ loss of visual function is disproportionately worse than the impairment of their visual acuity, which is only mildly affected in many cases. In patients with MacTel, as compared with a reference population, there is a significantly higher prevalence of systemic conditions associated with vascular disease, including history of hypertension, history of diabetes, and history of coronary disease. MacTel does not cause total blindness, yet it commonly causes gradual loss of the central vision required for reading and driving.

Acute zonal occult outer retinopathy (AZOOR) is an inflammatory retinopathy in the category of white dot syndromes typified by acute loss of one or more zones of outer retinal function associated with photopsia, minimal funduscopic changes and abnormal electroretinography findings.

Putscher's retinopathy is a disease where part of the eye (retina) is damaged. Usually associated with severe head injuries, it may also occur with other types of trauma, such as long bone fractures, or with several non-traumatic systemic diseases. However, the exact cause of the disease is not well understood. There are no treatments specific for Purtscher's retinopathy, and the prognosis varies. The disease can threaten vision, sometimes causing temporary or permanent blindness.

It is named for the Austrian ophthalmologist, Othmar Purtscher (1852–1927), who detected it in 1910 and described it fully in 1912.

Diabetic retinopathy often has no early warning signs. Even macular edema, which can cause rapid vision loss, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive. In some cases, the vision will get better or worse during the day.

In the first stage which is called non-proliferative diabetic retinopathy (NPDR) there are no symptoms, the signs are not visible to the eye and patients will have 20/20 vision. The only way to detect NPDR is by fundus photography, in which microaneurysms (microscopic blood-filled bulges in the artery walls) can be seen. If there is reduced vision, fluorescein angiography can be done to see the back of the eye. Narrowing or blocked retinal blood vessels can be seen clearly and this is called retinal ischemia (lack of blood flow).

Macular edema in which blood vessels leak their contents into the macular region can occur at any stage of NPDR. The symptoms of macular edema are blurred vision and darkened or distorted images that are not the same in both eyes. Ten percent (10%) of diabetic patients will have vision loss related to macular edema. Optical Coherence Tomography can show the areas of

retinal thickening (due to fluid accumulation) of macular edema.

In the second stage, abnormal new blood vessels (neovascularisation) form at the back of the eye as part of "proliferative diabetic retinopathy" (PDR); these can burst and bleed (vitreous hemorrhage) and blur the vision, because these new blood vessels are fragile. The first time this bleeding occurs, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots floating in a person's visual field, though the spots often go away after a few hours.

These spots are often followed within a few days or weeks by a much greater leakage of blood, which blurs the vision. In extreme cases, a person may only be able to tell light from dark in that eye. It may take the blood anywhere from a few days to months or even years to clear from the inside of the eye, and in some cases the blood will not clear. These types of large hemorrhages tend to happen more than once, often during sleep.

On funduscopic exam, a doctor will see cotton wool spots, flame hemorrhages (similar lesions are also caused by the alpha-toxin of "Clostridium novyi"), and dot-blot hemorrhages.

Retinopathy is any damage to the retina of the eyes, which may cause vision impairment. Retinopathy often refers to retinal vascular disease, or damage to the retina caused by abnormal blood flow. Age-related macular degeneration is technically included under the umbrella term retinopathy but is often discussed as a separate entity. Retinopathy, or retinal vascular disease, can be broadly categorized into proliferative and non-proliferative types. Frequently, retinopathy is an ocular manifestation of systemic disease as seen in diabetes or hypertension. Diabetes is the most common cause of retinopathy in the U.S. as of 2008. Diabetic retinopathy is the leading cause of blindness in working-aged people. It accounts for about 5% of blindness worldwide and is designated a priority eye disease by the World Health Organization.

Purtscher's retinopathy can lead to loss of vision, and recovery of vision may occur very little. However, vision recovery does occur in some cases, and reports have varied on the long-term prognosis.

Diabetic retinopathy, also known as diabetic eye disease, is a medical condition in which damage occurs to the retina due to diabetes and is a leading cause of blindness.

It affects up to 80 percent of people who have had diabetes for 20 years or more. At least 90% of new cases could be reduced if there were proper treatment and monitoring of the eyes. The longer a person has diabetes, the higher his or her chances of developing diabetic retinopathy. Each year in the United States, diabetic retinopathy accounts for 12% of all new cases of blindness. It is also the leading cause of blindness for people aged 20 to 64 years.

Patients with ARN typically present

- floaters

- redness of the eye

- flashes

- decreased sharpness of vision

- photophobia.

Though uncommon, some patients may experience pain. Most patients will only experience this in one eye (unilateral), though possible for the condition to be seen in both (bilateral, BARN). If the first eye is left without treatment, some cases have shown the disease progressing to the other eye in a month's time. Further progressed stages of the disease can cause blindness in the eye experiencing ARN. Though the disease may be present itself, the inflammation of the retina may not been visualized for decades after the initial signs.

Macular telangiectasia type 1 must be differentiated from secondary telangiectasis caused by retinal vascular diseases such as retinal venous occlusions, diabetic retinopathy, radiation retinopathy, sickle cell maculopathy, inflammatory retinopathy/Irvine–Gass syndrome, ocular ischemic syndrome/carotid artery obstruction, hypertensive retinopathy, polycythemia vera retinopathy, and localized retinal capillary hemangioma. In addition, Macular telangiectasia type 1 should be clearly differentiated from dilated perifoveal capillaries with evidence of vitreous cellular infiltration secondary to acquired inflammatory disease or tapetoretinal dystrophy. Less commonly, macular telangiectasis has been described in association with fascioscapulohumeral muscular dystrophy, incontinentia pigmenti, and familial exudative vitreoretinopathy with posterior pole involvement.

Macular telangiectasia type 2 is commonly under-diagnosed. The findings may appear very similar to diabetic retinopathy, and many cases ave been incorrectly ascribed to diabetic retinopathy or age-related macular degeneration. Recognition of this condition can save an affected patient from unnecessarily undergoing extensive medical testing and/or treatment. MacTel should be considered in cases of mild paramacular dot and blot hemorrhages and in cases of macular and paramacular RPE hyperplasia where no other cause can be identified.

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.

The clinical findings in this disease can be divided into acute and end-stage manifestations:

In the acute phase, patients often present with decreased visual acuity, vitritis, papillitis, and crops of gray-white or yellow-white outer retinal lesions. The clustering of the retinal lesions is important because this often helps to localize the causative nematode.

If left untreated, patients ultimately develop late sequel, which may include optic atrophy, retinal arterial narrowing, diffuse retinal pigment epithelial changes, and an abnormal electroretinogram. The late findings of this condition are often misinterpreted as unilateral retinitis pigmentosa.

Most patients with hypertensive retinopathy have no symptoms. However, some may report decreased or blurred vision, and headaches.

Signs of damage to the retina caused by hypertension include:

- Arteriolar changes, such as generalized arteriolar narrowing, focal arteriolar narrowing, arteriovenous nicking, changes in the arteriolar wall (arteriosclerosis) and abnormalities at points where arterioles and venules cross. Manifestations of these changes include "Copper wire arterioles" where the central light reflex occupies most of the width of the arteriole and "Silver wire arterioles" where the central light reflex occupies all of the width of the arteriole, and "arterio-venular (AV) nicking" or "AV nipping", due to venous constriction and banking.

- advanced retinopathy lesions, such as microaneurysms, blot hemorrhages and/or flame hemorrhages, ischemic changes (e.g. "cotton wool spots"), hard exudates and in severe cases swelling of the optic disc (optic disc edema), a ring of exudates around the retina called a "macular star" and visual acuity loss, typically due to macular involvement.

Mild signs of hypertensive retinopathy can be seen quite frequently in normal people (3–14% of adult individuals aged ≥40 years), even without hypertension. Hypertensive retinopathy is commonly considered a diagnostic feature of a hypertensive emergency although it is not invariably present.

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.

Macular edema occurs when fluid and protein deposits collect on or under the macula of the eye (a yellow central area of the retina) and causes it to thicken and swell (edema). The swelling may distort a person's central vision, because the macula holds tightly packed cones that provide sharp, clear, central vision to enable a person to see detail, form, and color that is directly in the centre of the field of view.

Acute Retinal Necrosis (ARN), is a medical inflammatory condition of the eye. The condition presents itself as a necrotizing retinitis. The inflammation onset is due to certain herpes viruses, Varicella Zoster Virus (VZV), Herpes Simplex Virus (HSV-1 and HSV-2) and Epstein-Barr Virus (EBV).

People with the condition usually display redness of the eye, white or off-white colored patches that are patches of retinal necrosis. ARN can progress into other conditions such as uveitis, detachment of the retina, and ultimately can lead to blindness.

The disease was first characterized in 1971, in Japan. Akira Urayama and his colleagues had six patients whose cases showed signs of acute necrotizing retinitis, retinal arertitis, choroiditis, and late-onset retinal detachment. The combination of the conditions was given the name acute retinal necrosis. The first reports of ARN came about in 1971. It is unclear whether it was previously just reported as something else. Urayama and his colleagues reported the disease that they saw in six Japanese patients. Since then the disease has been seen in patient's with AIDS, children, and people who are immunocompromised. In 1978, Young and Bird named the disease when presented in both eyes, Bilateral Acute Retinal Necrosis, otherwise known as BARN.

Progressive retinal atrophy (PRA) is a group of genetic diseases seen in certain breeds of dogs and, more rarely, cats. Similar to retinitis pigmentosa in humans, it is characterized by the bilateral degeneration of the retina, causing progressive vision loss culminating in blindness. The condition in nearly all breeds is inherited as an autosomal recessive trait, with the exception of the Siberian Husky (inherited as an X chromosome linked trait) and the Bullmastiff (inherited as an autosomal dominant trait). There is no treatment.

In general, PRAs are characterised by initial loss of rod photoreceptor cell function followed by that of the cones and for this reason night blindness is the first significant clinical sign for most dogs affected with PRA. As other retinal disorders, PRA can be divided into either dysplastic disease, where the cells develop abnormally, and degenerative, where the cells develop normally but then degenerate during the dog's lifetime.

Generalized PRA is the most common type and causes atrophy of all the neural retinal structures. Central progressive retinal atrophy (CPRA) is a different disease from PRA involving the retinal pigment epithelium (RPE), and is also known as retinal pigment epithelial dystrophy (RPED).

Cystoid macular edema (CME) involves fluid accumulation in the outer plexiform layer secondary to abnormal perifoveal retinal capillary permeability. The edema is termed "cystoid" as it appears cystic; however, lacking an epithelial coating, it is not truly cystic. The cause for CME can be remembered with the mnemonic "DEPRIVEN" (diabetes, epinepherine, pars planitis, retinitis pigmentosa, Irvine-Gass syndrome, venous occlusion, E2-prostaglandin analogues, nicotinic acid/niacin).

Diabetic macular edema (DME) is similarly caused by leaking macular capillaries. DME is the most common cause of visual loss in both proliferative, and non-proliferative diabetic retinopathy.

Central serous retinopathy (CSR), also known as central serous chorioretinopathy (CSC or CSCR), is an eye disease which causes visual impairment, often temporary, usually in one eye. When the disorder is active it is characterized by leakage of fluid under the retina that has a propensity to accumulate under the central macula. This results in blurred or distorted vision (metamorphopsia). A blurred or gray spot in the central visual field is common when the retina is detached. Reduced visual acuity may persist after the fluid has disappeared.

The disease is considered of unknown cause. It mostly affects white males in the age group 20 to 50 and occasionally other groups. The condition is believed to be exacerbated by stress or corticosteroid use.

This type of retinoschisis is very common with a prevalence of up to 7 percent in normal persons. Its cause is unknown. It can easily be confused with retinal detachment by the non-expert observer and in difficult cases even the expert may have difficulty differentiating the two. Such differentiation is important since retinal detachment almost always requires treatment while retinoschisis never itself requires treatment and leads to retinal detachment (and hence to visual loss) only occasionally. Unfortunately one still sees cases of uncomplicated retinoschisis treated by laser retinopexy or cryopexy in an attempt to stop its progression towards the macula. Such treatments are not only ineffective but unnecessarily risk complications. There is no documented case in the literature of degenerative retinoschisis itself (as opposed to the occasional situation of retinal detachment complicating retinoschisis) in which the splitting of the retina has progressed through the fovea. There is no clinical utility in differentiating between typical and reticular retinoschisis. Degenerative retinoschisis is not known to be a genetically inherited condition.

There is always vision loss in the region of the schisis as the sensory retina is separated from the ganglion layer. But like the loss is in the periphery, it goes unnoticed. It is the very rare schisis that encroaches on the macula where retinopexy is then properly used.

A rhegmatogenous retinal detachment is commonly preceded by a posterior vitreous detachment which gives rise to these symptoms:

- flashes of light (photopsia) – very brief in the extreme peripheral (outside of center) part of vision

- a sudden dramatic increase in the number of floaters

- a ring of floaters or hairs just to the temporal (skull) side of the central vision

Although most posterior vitreous detachments do not progress to retinal detachments, those that do produce the following symptoms:

- a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision

- the impression that a veil or curtain was drawn over the field of vision

- straight lines (scale, edge of the wall, road, etc.) that suddenly appear curved (positive Amsler grid test)

- central visual loss

In the event of an appearance of sudden flashes of light or floaters, an eye doctor needs to be consulted immediately. A shower of floaters or any loss of vision, too, is a medical emergency.

Chloroquine retinopathy, also known as Bull's eye maculopathy, is a retinopathy (damage of the retina) caused by the drugs chloroquine or hydroxychloroquine, which are sometimes used in the treatment of autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus. This eye toxicity limits long-term use of the drugs.

Plus disease can be present as a major complicating factor at any stage. It is characterised by:

- Significant level of vascular dilation and tortuosity observed at the posterior retinal arterioles. This reflects the increase of blood flow through the retina.

- Vitreous haze and anterior chamber haze

- Iris vascular engorgement

- Persistent tunica vasculosa lentis or immature blood vessels growing over the lens which also restrict the dilatation of the pupils.