question: Why do you see a coloured spot for a short period of time after looking directly into a bright light?
comment: In your eye there's a bit in the back with special cells that process light that enters your eye. If you look too long, those cells get used up or tired, and they can't process light very well for a while. That spot you see is basically that spot in the back of your eye projected onto your visual field.
passages: Field-size metameric failure or field-size metamerism occurs because the relative proportions of the three cone types in the retina vary from the center of the visual field to the periphery, so that colors that match when viewed as very small, centrally fixated areas may appear different when presented as large color areas. In many industrial applications, large-field color matches are used to define color tolerances.
   Paradiso and Nakayama (1991) performed an experiment to verify this hypothesis. They presented a large disk of uniform brightness on a black background. The stimulus was briefly flashed and, after a variable stimulus offset asynchrony, a masking stimulus was presented. The mask consisted of a circle on a black background with the masking contours positioned within the boundaries of the large uniform disk. This experiment is grounded on the assumption that filling-in consists of a spreading of neural activity from the boundaries of luminance and through the surfaces, that is stopped when another luminance-contrast border is reached (this is proposed by many models of brightness perception, see for example Walls 1954, Gerrits and Vendrik 1970, Cohen and Grossberg 1984), and that the process takes some time to be completed.
   At certain combinations of spacing and timing of the two images, a viewer will report a sensation of motion in the space between the two dots. The first spot will begin to appear to be moving, and will then "change color abruptly in the middle of its illusory path". 
  
  Section::::Philosophical significance.
   If after looking at the effect for 5 minutes or so, one moves one's eyes elsewhere (e.g., to another point on the figure or to a blank sheet of white paper), one will see a stationary ring of 12 green discs that will fade after a short time. These green discs are the afterimages of the 12 lilac discs.
   These effects combine to yield the remarkable sight of a green spot running around in a circle on a grey background when only stationary, flashing grey spots have been presented.
  
  Section::::Psychophysics.
   Patients who suffer from nutritional optic neuropathy may notice that colors are not as vivid or bright as before and that the color red is washed out. This normally occurs in both eyes at the same time and is not associated with any eye pain. They might initially notice a blur or fog, followed by a drop in vision. While vision loss may be rapid, progression to blindness is unusual. These patients tend to have blind spots in the center of their vision with preserved peripheral vision. In most cases, the pupils continue to respond normally to light.
   Sensitivity to a prolonged stimulation tends to decline over time, leading to neural adaptation. An interesting effect occurs when staring at a particular color for a minute or so. Such action leads to an exhaustion of the cone cells that respond to that color – resulting in the afterimage. This vivid color aftereffect can last for a minute or more.
  
  Section::::Clinical significance.
   When this occurs there is a characteristic pattern of symptoms:
  
  BULLET::::- Flashes of light (photopsia)
  
  BULLET::::- A sudden dramatic increase in the number of floaters
  
  BULLET::::- 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.
   Nuclear sclerosis is the most common type of cataract, and involves the central or 'nuclear' part of the lens. This eventually becomes hard, or 'sclerotic', due to condensation on the lens nucleus and the deposition of brown pigment within the lens. In its advanced stages it is called a brunescent cataract. In early stages, an increase in sclerosis cause an increase in refractive index of the lens. This causes a myopic shift (lenticular shift) that decreases hyperopia and enables presbyopic patients to see at near without reading glasses. This is only tempororary and is called second sight.
   Section::::Nature of white dots.:Suspected etiology.
  
  One cause of the White Dot Syndromes as suggested by Gass involves viral or infectious agents. Specifically pertaining to the ‘AZOOR complex,’ Gass has postulated that a virus may enter the retina at the optic head and the infection may spread from one photoreceptor to another. Some unexplained features include the development of more than one disease in the same patient and the majority of cases occurring in females.
   Occasionally, uveitis is not associated with a systemic condition: the inflammation is confined to the eye and has unknown cause. In some of these cases, the presentation in the eye is characteristic of a described syndrome, which are called white dot syndromes, and include the following diagnoses:
  
  BULLET::::- acute posterior multifocal placoid pigment epitheliopathy
  
  BULLET::::- birdshot chorioretinopathy
  
  BULLET::::- multifocal choroiditis and panuveitis
  
  BULLET::::- multiple evanescent white dot syndrome
  
  BULLET::::- punctate inner choroiditis
  
  BULLET::::- serpiginous choroiditis
  
  BULLET::::- acute zonal occult outer retinopathy
  
  Section::::Causes.:Masquerade syndromes.
   BULLET::::- Blue field entoptic phenomenon has the appearance of tiny bright dots moving rapidly along squiggly lines in the visual field. It is much more noticeable when viewed against a field of pure blue light and is caused by white blood cells moving in the capillaries in front of the retina. The white cells are larger than the red cells and must deform to fit. As they go through a capillary, a space opens up in front of them and red blood cells pile up behind. This makes the dots of light appear slightly elongated with dark tails.
   Diagnosis of PIC can be difficult because the appearance may be similar to other conditions and types of posterior uveitis, especially other forms of the so-called white dot syndromes. The diagnosis is made by eliminating all the other possibilities by careful examination by an experienced ophthalmologist, aided with visual field testing and Fluorescein angiography (an intravenous dye used to show the blood vessels at the back of the eye).
  
  It is important that the correct diagnosis is made because treatment may be quite different for apparently similar conditions.
  
  Section::::Diagnosis.:Natural course of the condition.
   BULLET::::- Purkinje's blue arcs are associated with the activity of the nerves sending signals from where a spot of light is focussed on the retina near the fovea to the optic disk. Look at the right edge of a small red light in a dark room with your right eye (left eye closed) after dark-accommodating your eye for about 30 seconds and you should see two faint blue arcs starting at the light and heading towards the blind spot. Look at the left edge and you will see a faint blue spike going from the light to the right.
   The exact causes of the neon color spreading illusion are not known. It seems to occur most often when black lines are substituted with colored lines on a white background. One theory as to why this happens is that the simultaneous stimulation between the visual processing of lines and the color receptors in the eyes are not congruent. For this reasoning to work neon effects would only be possible if all black lines and colored lines were in contact, however there are illusions where this is not the case.
   According to the isomorphic filling-in theory, colour is represented by the activity of cells whose receptive fields point at the surface, but it is assumed that these cells receive additional activation through horizontal connections that keeps their activity level high despite mechanisms of lateral inhibition tending to suppress surface activity and despite the transient nature of the afferent signals. The lateral activation comes from receptive fields at contrast borders. These signals are strong because receptive fields are exposed to contrast, and reliable because the border produces continuous light modulation even during fixation, due to small residual eye movements. In the alternative symbolic hypothesis, there is no spreading of activity, but all the information would be carried by the relevant features, that would be tagged with information on contrast polarity, colour and lightness of the surfaces they enclose. Despite the many attempts to verify the two different models by psychophysical and physiological experiments, the mechanisms of colour and lightness filling-in are still debated.
   Section::::Diagnosis.
  
  Optic pits should be diagnosed by an eye care professional who can perform a thorough exam of the back of the eye using an ophthalmoscope.
  
  More recently, the development of a special technology called optical coherence tomography (OCT) has allowed better visualization of the retinal layers. It has been used to demonstrate a marked reduction in the thickness of the retinal nerve fiber layer in the quadrant corresponding to the optic pit. This is not yet in standard use for diagnosis of an optic pit, but may be helpful in supporting a diagnosis.
  
  Section::::Treatment.
   In the visual system, retinal, technically called "retinene" or "retinaldehyde", is a light-sensitive molecule found in the rods and cones of the retina. Retinal is the fundamental structure involved in the transduction of light into visual signals, i.e. nerve impulses in the ocular system of the central nervous system. In the presence of light, the retinal molecule changes configuration and as a result a nerve impulse is generated.
  
  Section::::Structure.:Optic nerve.
   Scotopic vision
  
  Scotopic vision is the vision of the eye under low-light levels. The term comes from Greek "skotos", meaning "darkness", and "-opia", meaning "a condition of sight". In the human eye, cone cells are nonfunctional in low visible light. Scotopic vision is produced exclusively through rod cells, which are most sensitive to wavelengths of around 498 nm (green–blue) and are insensitive to wavelengths longer than about 640 nm (reddish orange). This condition is called the Purkinje effect.
  
  Section::::Amacrine cells.
   • 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:
  
  BULLET::::1. Blurring of vision
  
  BULLET::::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.
  
  BULLET::::3. Seeing flashing lights. This is known as photopsia.
   The effect is specific to the region of the retina that is exposed to the induction stimuli. This has been shown by inducing opposite effects in adjacent regions of the retina (i.e., from one region of the retina verticals appear pink and horizontals appear greenish; from an adjacent region of the retina, verticals appear greenish and horizontals appear pink). Nevertheless, if a small region of the retina is exposed to the induction stimuli, and the test contours run through this region, the effect spreads along those test contours. Of course, if the induced area is in the fovea (central vision) and the eyes are allowed to move, then the effect will appear everywhere in the visual scene visited by the fovea.
   Section::::Isomorphic filling-in.:Recordings from striate cortex of cat.
  
  An isomorphic filling-in theory calls for the existence of surface responsive neurons in early retinotopic visual areas. The activity of such neurons would be raised by elements capable of responding to the luminance of the surface also in the absence of edges; and would be strongly modulated by spreading of activity from the luminance borders enclosing the surface.
  
  Electro-physiological recordings in retinal ganglion cells, LGN and primary visual cortex showed that neurons of these areas responded to luminance modulation within the receptive field even in the absence of contrast borders.
   BULLET::::- very brief flashes of light (photopsia) in the extreme peripheral (outside of center) part of vision
  
  BULLET::::- a sudden dramatic increase in the number of floaters
  
  BULLET::::- 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:
  
  BULLET::::- a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision
  
  BULLET::::- the impression that a veil or curtain was drawn over the field of vision
   The dots will not appear at the very center of the visual field, because there are no blood vessels in the foveal avascular zone.
  
  Section::::Blue field entoptoscopy.
  
  In a technique known as blue field entoptoscopy, the effect is used to estimate the blood flow in the retinal capillaries. The patient is alternatingly shown blue light and a computer generated picture of moving dots; by adjusting the speed and density of these dots, the patient tries to match the computer generated picture to the perceived entoptic dots.
  
  Section::::Difference from other entoptic phenomena.
   The behaviour of primary visual cortex neurons seems to be in agreement with the one hypothesized by an isomorphic filling-in theory in that they both respond to luminance of the surfaces also in the absence of borders, and their activity is modulated by that of edges far outside the receptive field. Moreover, when the temporal frequency of luminance modulation in the surrounding patches exceeded a threshold value, the induced response disappeared, suggesting that it was the result of a spreading of activity, taking a finite time to happen, likely explainable in the context of isomorphic filling-in.
  
  Section::::Symbolic filling-in.
  