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.

When this occurs there is a characteristic pattern of symptoms:

- Flashes of light (photopsia)

- A sudden dramatic increase in the number of floaters

- A ring of floaters or hairs just to the temporal side of the central vision

As a posterior vitreous detachment proceeds, adherent vitreous membrane may pull on the retina. While there are no pain fibers in the retina, vitreous traction may stimulate the retina, with resultant flashes that can look like a perfect circle.

If a retinal vessel is torn, the leakage of blood into the vitreous cavity is often perceived as a "shower" of floaters. Retinal vessels may tear in association with a retinal tear, or occasionally without the retina being torn.

The risk of retinal detachment is greatest in the first 6 weeks following a vitreous detachment, but can occur over 3 months after the event.

The risk of retinal tears and detachment associated with vitreous detachment is higher in patients with myopic retinal degeneration, lattice degeneration, and a familial or personal history of previous retinal tears/detachment.

Migraine headaches may be preceded by a visual "aura", lasting for 20 to 30 minutes, and then proceeding to the headache. Some people, however, experience the aura but do not have a headache. This visual aura can be very dramatic. Classically, a small blind spot appears in the central vision with a shimmering, zig-zag light inside of it. This enlarges, and moves to one side or the other of the vision, over a 20 to 30 minute period. When it is large, this crescent shaped blind spot containing this brightly flashing light can be difficult to ignore, and some people fear that they are having a stroke. In reality, it is generally a harmless phenomenon, except in people who subsequently get the headache of migraine. Since migraine originates in the brain, the visual effect typically involves the same side of vision in each eye, although it may seem more prominent in one eye or the other.

Some people get different variations of this phenomenon, with the central vision being involved, or with the visual effect similar to "heat rising off of a car". Some people describe a "kaleidoscope" effect, with pieces of the vision being missing. All of these variations are consistent with ophthalmic migraine.

The vitreous is a gel-like fluid which fills most of the eye. As people age, this vitreous becomes more and more liquefied. The vitreous has loose attachments to the retina, and more firm attachments to the optic nerve. At some point in a person's life, the vitreous liquefies enough to shift position in the eye. When this occurs, usually between age 50 and 70, the back edge of the vitreous will pull forward away from the retina, leading to a "vitreous detachment". This is generally a normal process, although it may happen abnormally early in cases of high nearsightedness or trauma. As the vitreous detaches, it tugs on the retina. This is perceived as a flash of light, similar to a lightning flash in the corner of the vision. It may occur especially with eye movement, since the vitreous moves in the eye. Debris pulled off of the optic nerve and retina are then seen as floaters, suspended in the vitreous above the retina. Sometimes this is described as a cobweb, a net, a string, or a fly over the vision.

These symptoms usually resolve over a period of days to weeks, although some people will continue to see the floaters for a longer period of time. The important thing is to determine that the retina is healthy as the vitreous detaches. This requires a careful dilated examination of the retina to look for tears, or other areas which may be at risk for tearing. A retinal tear can then lead to retinal detachment, if not treated. Thus, people experiencing these symptoms should be examined by an ophthalmologist as soon as possible. Only about 1 in 10,000 cases of vitreous detachment lead to retinal detachment, but it still is one of the most common causes of retinal detachment.

A tear in the retina can occur with vitreous detachment, with trauma or eye injury, or in areas at risk for a retinal tear, such as "lattice degeneration". The symptoms of a retinal tear usually are of a flash of light in the peripheral vision followed by floaters. The floaters may be debris, but may also be blood, if the tear extends through a retinal blood vessel. Symptomatic retinal tears should be treated by laser to prevent retinal detachment. Sometimes a retinal tear is discovered incidentally as part of an eye examination. These may or may not need to be treated.

Retinal detachment is a disorder of the eye in which the retina separates from the layer underneath. Symptoms include an increase in the number of floaters, flashes of light, and worsening of the outer part of the visual field. This may be described as a curtain over part of the field of vision. In about 7% of cases both eyes are affected. Without treatment permanent loss of vision may occur.

The mechanism most commonly involves a break in the retina that then allows the fluid in the eye to get behind the retina. A break in the retina can occur from a posterior vitreous detachment, injury to the eye, or inflammation of the eye. Other risk factors include being short sighted and previous cataract surgery. Retinal detachments also rarely occur due to a choroidal tumor. Diagnosis is by either looking at the back of the eye with an ophthalmoscope or by ultrasound.

In those with a retinal tear, efforts to prevent it becoming a detachment include cryotherapy using a cold probe or photocoagulation using a laser. Treatment of retinal detachment should be carried out in a timely manner. This may include scleral buckling where silicone is sutured to the outside of the eye, pneumatic retinopexy where gas is injected into the eye, or vitrectomy where the vitreous is partly removed and replaced with either gas or oil.

Retinal detachments affect between 0.6 and 1.8 people per 10,000 per year. About 0.3% of people are affected at some point in their life. It is most common in people who are in their 60s or 70s. Males are more often affected than females. The long term outcomes depend on the duration of the detachment and whether the macula was detached. If treated before the macula detaches outcomes are generally good.

If the vitreous is firmly attached to the retina when it pulls away, it can tear the retina and create a macular hole. Also, once the vitreous has pulled away from the surface of the retina, some of the fibers can remain on the retinal surface and can contract. This increases tension on the retina and can lead to a macular hole. In either case, the fluid that has replaced the shrunken vitreous can then seep through the hole onto the macula, blurring and distorting central vision.

The most common sign at presentation is leukocoria (abnormal white reflection of the retina). Symptoms typically begin as blurred vision, usually pronounced when one eye is closed (due to the unilateral nature of the disease). Often the unaffected eye will compensate for the loss of vision in the other eye; however, this results in some loss of depth perception and parallax. Deterioration of sight may begin in either the central or peripheral vision. Deterioration is likely to begin in the upper part of the vision field as this corresponds with the bottom of the eye where blood usually pools. Flashes of light, known as photopsia, and floaters are common symptoms. Persistent color patterns may also be perceived in the affected eye. Initially, these may be mistaken for psychological hallucinations, but are actually the result of both retinal detachment and foreign fluids mechanically interacting with the photoreceptors located on the retina.

One early warning sign of Coats' disease is yellow-eye in flash photography. Just as the red-eye effect is caused by a reflection off blood vessels in the back of a normal eye, an eye affected by Coats' will glow yellow in photographs as light reflects off cholesterol deposits. Children with yellow-eye in photographs are typically advised to immediately seek evaluation from an optometrist or ophthalmologist, who will assess and diagnose the condition and refer to a vitreo-retinal specialist.

Coats' disease itself is painless. Pain may occur if fluid is unable to drain from the eye properly, causing the internal pressure to swell, resulting in painful glaucoma.

The eye contains a jelly-like substance called the vitreous. Shrinking of the vitreous usually causes the hole. As a person ages, the vitreous becomes watery and begins to pull away from the retina. If the vitreous is firmly attached to the retina when it pulls away, a hole can result.

Eye floaters are suspended in the vitreous humour, the thick fluid or gel that fills the eye. The vitreous humour, or vitreous body, is a jelly-like, transparent substance that fills a majority of the eye. It lies within the vitreous chamber behind the lens, and is one of the four optical components of the eye. Thus, floaters follow the rapid motions of the eye, while drifting slowly within the fluid. When they are first noticed, the natural reaction is to attempt to look directly at them. However, attempting to shift one's gaze toward them can be difficult as floaters follow the motion of the eye, remaining to the side of the direction of gaze. Floaters are, in fact, visible only because they do not remain perfectly fixed within the eye. Although the blood vessels of the eye also obstruct light, they are invisible under normal circumstances because they are fixed in location relative to the retina, and the brain "tunes out" stabilized images due to neural adaptation. This stabilization is often interrupted by floaters, especially when they tend to remain visible.

Floaters are particularly noticeable when looking at a blank surface or an open monochromatic space, such as blue sky. Despite the name "floaters", many of these specks have a tendency to sink toward the bottom of the eyeball, in whichever way the eyeball is oriented; the supine position (looking up or lying back) tends to concentrate them near the fovea, which is the center of gaze, while the textureless and evenly lit sky forms an ideal background against which to view them. The brightness of the daytime sky also causes the eyes' pupils to contract, reducing the aperture, which makes floaters less blurry and easier to see.

Floaters present at birth usually remain lifelong, while those that appear later may disappear within weeks or months. They are not uncommon, and do not cause serious problems for most persons; they represent one of the most common presentations to hospital eye services. A survey of optometrists in 2002 suggested that an average of 14 patients per month per optometrist presented with symptoms of floaters in the UK. However, floaters are more than a nuisance and a distraction to those with severe cases, especially if the spots seem to constantly drift through the field of vision. The shapes are shadows projected onto the retina by tiny structures of protein or other cell debris discarded over the years and trapped in the vitreous humour. Floaters can even be seen when the eyes are closed on especially bright days, when sufficient light penetrates the eyelids to cast the shadows. It is not, however, only elderly persons who are troubled by floaters; they can also become a problem to younger people, especially if they are myopic. They are also common after cataract operations or after trauma.

Floaters are able to catch and refract light in ways that somewhat blur vision temporarily until the floater moves to a different area. Often they trick persons who are troubled by floaters into thinking they see something out of the corner of their eye that really is not there. Most persons come to terms with the problem, after a time, and learn to ignore their floaters. For persons with severe floaters it is nearly impossible to completely ignore the large masses that constantly stay within almost direct view.

Floaters have been reported in patients as young as 3. Floaters in teenage patients and young adults are usually harder to treat. For persons in this age group, the floater that is seen usually looks like a kind of translucent worm/web/cell. Very little is known about this region, and it only becomes distinct after the vitreous humour detaches from the retina at later stages of life. Due to their microscopic size they cannot be seen by doctors. They only appear as big as they do because of their proximity to the retina. This type of floater is still described occasionally in people in their 30s and very rarely occurs in people in their 40s.

Traction caused by VMA is the underlying pathology of an eye disease called symptomatic VMA. There is evidence that symptomatic VMA can contribute to the development of several well-known eye disorders, such as macular hole and macular pucker, that can cause visual impairment, including blindness. It may also be associated with age-related macular degeneration (AMD), diabetic macular edema (DME), retinal vein occlusion, and diabetic retinopathy (DR).

Sometimes the appearance of floaters has to be attributed to dark specks in the tear film of the eye. Technically, these are not floaters, but they do look the same from the viewpoint of the patient. Persons with blepharitis or a dysfunctional meibomian gland are especially prone to this cause, but ocular allergies can also cause the problem. To differentiate between material in the vitreous humour of the eye and debris in the tear film, one can look at the effect of blinking: debris in the tear film will move quickly with a blink, while floaters are largely unresponsive to it. Tear film debris is diagnosed by eliminating the possibility of true floaters and macular degeneration.

Many times, an optic pit is asymptomatic and is just an incidental finding on examination of the eye by a physician. However, some patients may present with the symptoms of a posterior vitreous detachment or serous retinal detachment. This is because optic pits are associated with these disorders and are even speculated to be the actual cause of these disorders when they arise in patients with optic pits (see "Associated Retinal Changes" below for a more in-depth discussion on this theory). The most common visual field defects include an enlarged blind spot and a scotoma. Visual acuity is typically not affected by the pit but may get worse if serous detachment of the macula occurs. Metamorphopsia (distorted vision) may then result.

Optic pits were first described in 1882 as dark gray depressions in the optic disc. They may, however, appear white or yellowish instead. They can also range greatly in size (e.g. some can be minuscule while others may be large enough as to occupy most of optic disc surface). Optic pits are associated with other abnormalities of the optic nerve including large optic nerve size, large inferior colobomas of the optic disc, and colobomas of the retina. The optic disc originates from the optic cup when the optic vesicle invaginates and forms an embryonic fissure (or groove). Optic pits may develop due to failure of the superior end of the embryonic fissure to close completely.

Signs and symptoms of macular degeneration include:

- Visual symptoms

- Distorted vision in the form of metamorphopsia, in which a grid of straight lines appears wavy and parts of the grid may appear blank: Patients often first notice this when looking at things like miniblinds in their home or telephone poles while driving. There may also be central scotomas, shadows or missing areas of vision

- Slow recovery of visual function after exposure to bright light (photostress test)

- Visual acuity drastically decreasing (two levels or more), e.g.: 20/20 to 20/80

- Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss (often caused by leakage and bleeding of abnormal blood vessels).

- Trouble discerning colors, specifically dark ones from dark ones and light ones from light ones

- A loss in contrast sensitivity

Macular degeneration by itself will not lead to total blindness. For that matter, only a very small number of people with visual impairment are totally blind. In almost all cases, some vision remains, mainly peripheral. Other complicating conditions may possibly lead to such an acute condition (severe stroke or trauma, untreated glaucoma, etc.), but few macular degeneration patients experience total visual loss.

The area of the macula comprises only about 2.1% of the retina, and the remaining 97.9% (the peripheral field) remains unaffected by the disease. Even though the macula provides such a small fraction of the visual field, almost half of the visual cortex is devoted to processing macular information.

The loss of central vision profoundly affects visual functioning. It is quite difficult, for example, to read without central vision. Pictures that attempt to depict the central visual loss of macular degeneration with a black spot do not really do justice to the devastating nature of the visual loss. This can be demonstrated by printing letters six inches high on a piece of paper and attempting to identify them while looking straight ahead and holding the paper slightly to the side. Most people find this difficult to do.

The signs and symptoms of far-sightedness are blurry vision, headaches, and eye strain. The common symptom is eye strain. Difficulty seeing with both eyes (binocular vision) may occur, as well as difficulty with depth perception.

Vitreomacular adhesion (VMA) is a human medical condition where the vitreous gel (or simply vitreous) of the human eye adheres to the retina in an abnormally strong manner. As the eye ages, it is common for the vitreous to separate from the retina. But if this separation is not complete, i.e. there is still an adhesion, this can create pulling forces on the retina that may result in subsequent loss or distortion of vision. The adhesion in of itself is not dangerous, but the resulting pathological vitreomacular traction (VMT) can cause severe ocular damage.

The current standard of care for treating these adhesions is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye. A biological agent for non-invasive treatment of adhesions called ocriplasmin has been approved by the FDA on Oct 17 2012.

Far-sightedness can have rare complications such as strabismus and amblyopia. At a young age, severe far-sightedness can cause the child to have double vision as a result of "over-focusing".

Coats' usually affects only one eye (unilateral) and occurs predominantly in young males 1/100,000, with the onset of symptoms generally appearing in the first decade of life. Peak age of onset is between 6–8 years of age, but onset can range from 5 months to 71 years.

Coats' disease results in a gradual loss of vision. Blood leaks from the abnormal vessels into the back of the eye, leaving behind cholesterol deposits and damaging the retina. Coats' disease normally progresses slowly. At advanced stages, retinal detachment is likely to occur. Glaucoma, atrophy, and cataracts can also develop secondary to Coats' disease. In some cases, removal of the eye may be necessary (enucleation).

"Typical lattice" consists of sharply demarcated, spindle-shaped areas of retinal thinning, usually located between the equator of the retina and the posterior border of the vitreous base. This is more frequently located in the temporal half of the retina and is seen more superiorly than inferiorly.

"Atypical lattice" is characterised by radial lesions which appear continuous with the peripheral blood vessels. This type is typically seen in patients with Stickler syndrome.

Although astigmatism may be asymptomatic, higher degrees of astigmatism may cause symptoms such as blurry vision, squinting, eye strain, fatigue, or headaches. Some research has pointed to the link between astigmatism and higher prevalence of migraine headaches.

Lattice degeneration is a disease of the human eye wherein the peripheral retina becomes atrophic in a lattice pattern and may develop tears, breaks, or holes, which may further progress to retinal detachment. It is an important cause of retinal detachment in young myopic individuals. The cause is unknown, but pathology reveals inadequate blood flow resulting in ischemia and fibrosis.

Lattice degeneration occurs in approximately 6–8% of the general population and in approximately 30% of phakic retinal detachments. Similar lesions are seen in patients with Ehlers-Danlos syndrome, Marfan syndrome, and Stickler syndrome, all of which are associated with an increased risk of retinal detachment. Risk of developing lattice degeneration in one eye is also increased if lattice degeneration is already present in the other eye.

Optic pit, optic nerve pit, or optic disc pit is a congenital excavation (or regional depression) of the optic disc (also optic nerve head), resulting from a malformation during development of the eye. Optic pits are important because they are associated with posterior vitreous detachments (PVD) and even serous retinal detachments.

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.

Common symptoms of vitreous hemorrhage include:

- Blurry vision

- Floaters- faint cobweb-like apparitions floating through the field of vision

- Reddish tint to vision

- Photopsia – brief flashes of light in the peripheral vision

Small vitreous hemorrhage often manifests itself as "floaters". A moderate case will often result in dark streaks in the vision, while dense vitreous hemorrhage can significantly inhibit vision.

Vitreous hemorrhage is diagnosed by identifying symptoms, examining the eye, and performing tests to identify cause. Some common tests include:

- Examination of the eye with a microscope

- Pupil dilation and examination

- An ultrasound examination may be used if the doctor does not have a clear view of the back of the eye

- Blood tests to check for specific causes such as diabetes

- A CT scan to check for injury around the eye

- Referral to a retinal specialist

Retinoschisis is an eye disease characterized by the abnormal splitting of the retina's neurosensory layers, usually in the outer plexiform layer. Most common forms are asymptomatic, some rarer forms result in a loss of vision in the corresponding visual field.