question: What causes the temporary burn mark left in the eye after looking at a bright light?
comment: Cells in your eye are responsible for reporting light to the brain through changes in pigment. If they receive too much light, they use up all the pigment and need a moment to reset to their natural state. During that time period, they report inaccurate information.
passages: Section::::Signs and symptoms.
  
  Patients with ARN typically present
  
  BULLET::::- floaters
  
  BULLET::::- redness of the eye
  
  BULLET::::- flashes
  
  BULLET::::- decreased sharpness of vision
  
  BULLET::::- photophobia.
   A doctor examining an eye with retinopathy may be able to see no signs at all, or a slight macular edema, which is a sort of blister on or under the macula, an oval colored spot normally visible to an eye doctor on each person's retina.
  
  But while even that edema goes away, within a few days the patient will generally develop a discoloration of the retina at the injured point, often yellow or white, turning red over the next few weeks.
  
  Section::::Treatment.
   Irritant or toxic conjunctivitis is primarily marked by redness. If due to a chemical splash, it is often present in only the lower conjunctival sac. With some chemicals, above all with caustic alkalis such as sodium hydroxide, necrosis of the conjunctiva marked by a deceptively white eye due to vascular closure may occur, followed by sloughing off of the dead epithelium. A slit lamp examination is likely to show evidence of anterior uveitis.
  
  Section::::Signs and symptoms.:Other.
   Ultraviolet radiation of wavelengths shorter than 300 nm (actinic rays) can damage the corneal epithelium. This is most commonly the result of exposure to the sun at high altitude, and in areas where shorter wavelengths are readily reflected from bright surfaces, such as snow, water, and sand. UV generated by a welding arc can similarly cause damage to the cornea, known as "arc eye" or welding flash burn, a form of photokeratitis.
   Infrared lasers are particularly hazardous, since the body's protective glare aversion response, also referred to as the "blink reflex," is triggered only by visible light. For example, some people exposed to high power Nd:YAG laser emitting invisible 1064 nm radiation may not feel pain or notice immediate damage to their eyesight. A pop or click noise emanating from the eyeball may be the only indication that retinal damage has occurred i.e. the retina was heated to over 100 °C resulting in localized explosive boiling accompanied by the immediate creation of a permanent blind spot.
  
  Section::::Laser radiation hazards.:Damage mechanisms.
   Common symptoms include pain, intense tears, eyelid twitching, discomfort from bright light, and constricted pupils.
  
  Section::::Cause.
   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.
   Florida keratopathy appears as multiple cloudy opacities in the stromal layer of the cornea. The spots appear concentrated at the center and become more diffuse at the periphery. They can range in size from one to eight millimeters. There are no other symptoms, and there is no response to treatment with either anti-inflammatory or antimicrobial drugs. Histological analysis of affected corneas has found acid-fast staining organisms, suggesting Florida keratopathy may be caused by a type of mycobacterium. The disease may be induced by repeated stings to the eyes by the little fire ant, "Wasmannia auropunctata".
   BULLET::::- Eye: Ocular manifestations are frequent in patients with ochronosis; most commonly hyperpigmentation of the sclera, primarily observed symmetrically to both sides of the cornea within the palpebral fissure. Furthermore, brown pigment spots in the limbus are generally considered pathognomonic. These ocular signs generally occur early in the development of the disease and can serve as a valuable diagnostic feature of the disease.
   Section::::Injury.:Chemical injury.
  
  The sclera is highly resistant to injury from brief exposure to toxic chemicals. The reflexive production of tears at the onset of chemical exposure tends to quickly wash away such irritants, preventing further harm. Acids with a pH below 2.5 are the source of greatest acidic burn risk, with sulfuric acid, the kind present in car batteries and therefore commonly available, being among the most dangerous in this regard. However, acid burns, even severe ones, seldom result in loss of the eye.
   Section::::Effects by frequency.:Infrared.
  
  Infrared wavelengths longer than 750 nm can produce changes in the lens of the eye. Glassblower's cataract is an example of a heat injury that damages the anterior lens capsule among unprotected glass and iron workers. Cataract-like changes can occur in workers who observe glowing masses of glass or iron without protective eyewear for prolonged periods over many years.
   Symptoms of pterygium include persistent redness, inflammation, foreign body sensation, tearing, dry and itchy eyes. In advanced cases the pterygium can affect vision as it invades the cornea with the potential of obscuring the optical center of the cornea and inducing astigmatism and corneal scarring. Many patients do complain of the cosmetic appearance of the eye either with some of the symptoms above or as their major complaint.
  
  Section::::Cause.
   Section::::Diagnosis.:Classification.:Giant papillary conjunctivitis.
  
  Giant papillary conjunctivitis is not a true ocular allergic reaction and is caused by repeated mechanical irritation of the conjunctiva. Repeated contact with the conjunctival surface caused by the use of contact lenses is associated with GPC.
  
  Section::::Diagnosis.:Classification.:PKC.
  
  Phlyctenular keratoconjunctiviti (PKC) results from a delayed hypersensitivity/inflammatory reaction to antigens expressed by various pathogens. Common agents include Staph. aureus, Mycobacterium tuberculosis, Chlamydia and Candida.
  
  Section::::Management.
   At a later stage, pan-retinal photocoagulation (PRP) with an argon laser appears effective in reducing the neovascular components and their sequelae.
  
  The visual prognosis for ocular ischemic syndrome varies from usually poor to fair, depending on speed and effectiveness of the intervention. However, prompt diagnosis is crucial as the condition may be a presenting sign of serious cerebrovascular and ischemic heart diseases.
   PRK can be associated with glare, halos, and starburst aberrations, which can occur with postoperative corneal haze during the healing process. Night halos are seen more often in revisions with small ablation zone size. With more recent developments in laser technology, this is less common after 6 months though symptoms can persist beyond a year in some cases. A dilute concentration of the chemotherapeutic agent, Mitomycin-C, can be applied briefly at the completion of surgery to reduce risk of hazing, although with increased risk of sicca.
   Section::::Diagnosis.
  
  Although corneal abrasions may be seen with ophthalmoscopes, slit lamp microscopes provide higher magnification which allow for a more thorough evaluation. To aid in viewing, a fluorescein stain that fills in the corneal defect and glows with a cobalt blue-light is generally instilled first.
  
  A careful search should be made for any foreign body, in particular looking under the eyelids. Injury following use of hammers or power-tools should always raise the possibility of a penetrating foreign body into the eye, for which urgent ophthalmology opinion should be sought.
  
  Section::::Diagnosis.:Prevention.
   Section::::Effects.
  
  Severe or chronic photophobia, such as in migraine or seizure disorder, may result in a person not feeling well with eye ache, headache and/or neck ache. These symptoms may persist for days even after the person is no longer exposed to the offensive light source. Further, once the eyes have become sensitized to the offensive light source (which can occur even in short duration exposures), they may become even more photosensitive with extreme pain occurring upon exposure to light.
   Sympathetic ophthalmia is currently thought to be an autoimmune inflammatory response toward ocular antigens, specifically a delayed hypersensitivity to melanin-containing structures from the outer segments of the photoreceptor layer of the retina. The immune system, which normally is not exposed to ocular proteins, is introduced to the contents of the eye following traumatic injury. Once exposed, it senses these antigens as foreign, and begins attacking them. The onset of this process can be from days to years after the inciting traumatic event.
  
  Section::::Diagnosis.
   Vision loss due to solar retinopathy is typically reversible, lasting for as short as one month to over one year. The fundus changes are variable and usually bilateral, mild cases often show no alteration and moderate to severe cases show a foveal yellow spot on the first days after exposure. After a few days it is replaced by a reddish dot often surrounded by pigment.
  
  Section::::Pathophysiology.
   Uveitis
  
  Uveitis is the inflammation of the uvea, the pigmented layer that lies between the inner retina and the outer fibrous layer composed of the sclera and cornea. The uvea consists of the middle layer of pigmented vascular structures of the eye and includes the iris, ciliary body, and choroid. Uveitis is an ophthalmic emergency and requires a thorough examination by an ophthalmologist or optometrist and urgent treatment to control the inflammation. It is often associated with other ocular problems.
  
  Section::::Signs and symptoms.
  
  Section::::Signs and symptoms.:Anterior uveitis.
  
  BULLET::::- Burning of the eye
  
  BULLET::::- Redness of the eye
  
  BULLET::::- Blurred vision
   Blue-light hazard is the potential for photochemically-induced retinal injury resulting from electromagnetic radiation-exposure at wavelengths primarily between 400 and Researchers have not studied the phenomenon in humans, but only ( and inconclusively) in some rodent, primate, and "in vitro" studies. Photochemically-induced retinal injury is caused by the absorption of light by photoreceptors in the eye. Under normal conditions, when light hits a photoreceptor, the cell bleaches and becomes useless until it has recovered through a metabolic process called the visual cycle.
   BULLET::::- Stage 2 Peripheral cells migrate to the center of the cornea, and impair vision; presentation is usually 2 to 3 days after surgery.
  
  BULLET::::- Stage 3 Cells at the central cornea form clumps of dense cell aggregates.
  
  BULLET::::- Stage 4 Otherwise known as central toxic keratopathy, stage 4 characteristically has no inflammatory cells at the anterior chamber or cornea, but there is central stromal necrosis, and the cornea becomes opacified; onset is usually 3 to 9 days after refractive surgery.
  
  Section::::Treatment.
  
  Depending on severity, therapies may range from topical or oral anti-inflammatories to irrigation and surgical repair.
   Some post-LASIK patients see halos and starbursts around bright lights at night. At night, the pupil may dilate to be larger than the flap leading to the edge of the flap or stromal changes causing visual distortion of light that does not occur during the day when the pupil is smaller. The eyes can be examined for large pupils pre-operatively and the risk of this symptom assessed.
   Image burn-in occurs when very bright objects lie in one's field of vision, and should not be confused with closed-eye hallucinations. Visual burn-in from bright lights is visible for a few minutes after closing the eyes, or by blinking repeatedly, but the burn-in effect slowly fades away as the retina recovers, whereas the waking-consciousness CEV noise will not disappear if observed continuously over a period of time.
  
  Section::::What is not a CEV.:Corneal liquid.
   The injury may be prevented by wearing eye protection that blocks most of the ultraviolet radiation, such as welding goggles with the proper filters, a welder's helmet, sunglasses rated for sufficient UV protection, or appropriate snow goggles. The condition is usually managed by removal from the source of ultraviolet radiation, covering the corneas, and administration of pain relief. Photokeratitis is known by a number of different terms including: snow blindness, arc eye, welder's flash, bake eyes, corneal flash burns, sand man's eye, flash burns, niphablepsia, potato eye, or keratoconjunctivitis photoelectrica.
  
  Section::::Signs and symptoms.
  