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.

There are various causes for the appearance of floaters, of which the most common are described here. Simply stated, any damage to the eye that causes material to enter the vitreous humour can result in floaters.

Floaters can occur when eyes age and in rare cases, floaters may be a sign of retinal detachment or a retinal tear.

Photopsia is the presence of perceived flashes of light. It is most commonly associated with posterior vitreous detachment, migraine with aura, migraine aura without headache, retinal break or detachment, occipital lobe infarction, and sensory deprivation (ophthalmo"pathic" hallucinations). Vitreous shrinkage or liquefaction, which are the most common causes of photopsia, cause a pull in vitreoretinal attachments, irritating the retina and causing it to discharge electrical impulses. These impulses are interpreted by the brain as 'flashes'.

This condition has also been identified as a common initial symptom of Punctate inner choroiditis (PIC), a rare retinal autoimmune disease believed to be caused by the immune system mistakenly attacking and destroying the retina. During pregnancy, new-onset photopsia is concerning for severe preeclampsia.

Photopsia can present as retinal detachment when examined by an optometrist or ophthalmologist. However, it can also be a sign of Uveal melanoma. This condition is extremely rare (5–7 per 1 million people will be affected, typically fair-skinned, blue-eyed northern Europeans). Photopsia should be investigated immediately.

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.

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.

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.

Proposed diagnostic criteria for the "visual snow" syndrome:

- Dynamic, continuous, tiny dots in the entire visual field.

- At least one additional symptom:

- Palinopsia (visual trailing and afterimages)

- Enhanced entoptic phenomena (floaters, photopsia, blue field entoptic phenomenon, self-light of the eye)

- Photophobia

- Tinnitus

- Impaired night vision

- Symptoms are not consistent with typical migraine aura.

- Symptoms are not attributed to another disorder (ophthalmological, drug abuse).

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

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).

Symptoms of this disorder include floaters, blurred vision, photopsia (flashing lights in eyes), loss of color vision and nyctalopia. In an eye examination, light-colored spots on the retina are seen. Complete loss of visual acuity may happenThe name of the condition comes from the small light-colored fundus spots on the retina, scattered in a pattern like birdshot from a shotgun, but these spots might not be present in early stages.

Some neuro-ophthalmologists believe that visual snow is not a medical condition, but a poorly understood symptom. People report seeing "snow", much like the visual noise on a TV screen after transmission ends. These authors hypothesize that what the patients see as "snow" is their own intrinsic visual noise.

Many report more visual snow in low light conditions. This has a natural explanation. "The intrinsic dark noise of primate cones is equivalent to ~4000 absorbed photons per second at mean light levels below this the cone signals are dominated by intrinsic noise".

In addition to visual snow, many of those affected have other types of visual disturbances such as starbursts, increased afterimages, floaters, trails, and many others.

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

- Floaters

- Blurred vision

- Photopsia or seeing flashing lights

Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye. The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.

Moore's lightning streaks are lightning type streaks (photopsia) (seen to the temporal side) due to sudden movement in the dark. They are generally caused by shock waves in the vitreous humor hitting the retina. The implication is that the vitreous is softer than normal, generally this is not a cause for alarm provided they are momentary, occur only in the dark and are due to sudden head movements (acceleration). Professional advice should be sought in cases of doubt, as retinal detachment, a serious condition, also can cause flashes in the eye.

They are named after Robert Foster Moore (1878–1963), a British ophthalmologist.

Most common:

- Floaters

- Blurred vision

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

The initial retinal degenerative symptoms of retinitis pigmentosa are characterized by decreased night vision (nyctalopia) and the loss of the mid-peripheral visual field. The rod photoreceptor cells, which are responsible for low-light vision and are orientated in the retinal periphery, are the retinal processes affected first during non-syndromic forms of this disease. Visual decline progresses relatively quickly to the far peripheral field, eventually extending into the central visual field as tunnel vision increases. Visual acuity and color vision can become compromised due to accompanying abnormalities in the cone photoreceptor cells, which are responsible for color vision, visual acuity, and sight in the central visual field. The progression of disease symptoms occurs in a symmetrical manner, with both the left and right eyes experiencing symptoms at a similar rate.

A variety of indirect symptoms characterize retinitis pigmentosa along with the direct effects of the initial rod photoreceptor degeneration and later cone photoreceptor decline. Phenomena such as photophobia, which describes the event in which light is perceived as an intense glare, and photopsia, the presence of blinking or shimmering lights within the visual field, often manifest during the later stages of RP. Findings related to RP have often been characterized in the fundus of the eye as the "ophthalamic triad". This includes the development of (1) a mottled appearance of the retinal pigment epithelium (RPE) caused by bone spicule formation, (2) a waxy appearance of the optic nerve, and (3) the attentuation of blood vessels in the retina.

Non-syndromic RP usually presents a variety of the following symptoms:

- Night blindness

- Tunnel vision (due to loss of peripheral vision)

- Latticework vision

- Photopsia (blinking/shimmering lights)

- Photophobia (aversion to glare)

- Development of bone spicules in the fundus

- Slow adjustment from dark to light environments and vice versa

- Blurring of vision

- Poor color separation

- Loss of central vision

- Eventual blindness

• 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.

Punctate inner choroiditis (PIC) is an inflammatory choroiditis which occurs mainly in young women. Symptoms include blurred vision and scotomata. Yellow lesions are mainly present in the posterior pole and are between 100 to 300 micrometres in size. PIC is one of the so called White Dot Syndromes. PIC has only been recognised as a distinct condition as recently as 1984 when Watzke identified 10 patients who appeared to make up a distinct group within the White Dot Syndromes.

Birdshot chorioretinopathy now commonly named "Birdshot Uveitis" or ""HLA-A29 Uveitis"" is a rare form of bilateral posterior uveitis affecting the eye. It causes severe, progressive inflammation of both the choroid and retina.

Affected individuals are almost exclusively caucasian and usually diagnosed in the fourth to sixth decade of their lives.

Retinitis pigmentosa (RP) is a genetic disorder of the eyes that causes loss of vision. Symptoms include trouble seeing at night and decreased peripheral vision (side vision). Onset of symptoms is generally gradual. As peripheral vision worsens, people may experience "tunnel vision". Complete blindness is uncommon.

Retinitis pigmentosa is generally inherited from a person's parents. Mutations in one of more than 50 genes is involved. The underlying mechanism involves the progressive loss of rod photoreceptor cells in the back of the eye. This is generally followed by loss of cone photoreceptor cells. Diagnosis is by an examination of the retina finding dark pigment deposits. Other supportive testing may include an electroretinogram, visual field testing, or genetic testing.

There is no cure for retinitis pigmentosa. Efforts to manage the problem may include the use of low vision aids, portable lighting, or a guide dog. Vitamin A palmitate supplements may be useful to slow worsening. A visual prosthesis may be an option in certain people with severe disease. It is estimated to affect 1 in 4,000 people. Onset is often in childhood but some are not affected until adulthood.

Patients present with acute unilateral decreased vision, photopsias and central or paracentral scotoma. An antecedent viral prodrome occurs in approximately one-third of cases. Myopia is commonly seen in patients.

Eye exam during the acute phase of the disease reveals multiple discrete white to orange spots at the level of the RPE or deep retina, typically in a perifoveal location (around the fovea).

Multiple evanescent white dot syndrome (MEWDS) is an uncommon inflammatory condition of the retina that typically affects otherwise healthy young females in the second to fourth decades of life.

The typical patient with MEWDS is a healthy middle aged female age 15-50. There is a gender disparity as women are affected with MEWDS four times more often than men. Roughly 30% of patients have experienced an associated viral prodrome. Patients present with acute, painless, unilateral change in vision.

The onset of ocular symptoms are usually preceded by episode of viral or flu-like symptoms such as fever, cough or sore throat (however this is not always the case). Patients can typically present erythema nodosum, livido reticularus, bilateral uveitis, and sudden onset of marked visual loss associated with the appearance of multiple lesions in the retina. These lesions may be colored from grey-white to cream-shaded yellow.

Other symptoms include scotomata and photopsia. In weeks to a month times the lesions begin to clear and disappear (with prednisone) leaving behind areas of retinal pigment epithelial atrophy and diffuse fine pigmentation (scarring). Rarely choroidal neovascularization occur as a late onset complication.