Eye floaters and loss of accommodation are among the earliest symptoms. The disease may progress to severe uveitis with pain and photophobia. Commonly the eye remains relatively painless while the inflammatory disease spreads through the uvea, where characteristic focal infiltrates in the choroid named Dalén-Fuchs nodules can be seen. The retina, however, usually remains uninvolved, although perivascular cuffing of the retinal vessels with inflammatory cells may occur. Papilledema, secondary glaucoma, vitiligo, and poliosis of the eyelashes may accompany SO.

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

- Floaters

- Blurred vision

- Photopsia or seeing flashing lights

Most common:

- Floaters

- Blurred vision

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

Sympathetic ophthalmia (SO) or Sympathetic uveitis is a bilateral diffuse granulomatous uveitis (a kind of inflammation) of both eyes following trauma to one eye. It can leave the patient completely blind. Symptoms may develop from days to several years after a penetrating eye injury.

Ophthalmia (also called ophthalmitis) is inflammation of the eye. It is a medical sign which may be indicative of various conditions, including sympathetic ophthalmia (inflammation of both eyes following trauma to one eye), gonococcal ophthalmia, trachoma or "Egyptian" ophthalmia, ophthalmia neonatorum (a conjunctivitis of the newborn due to either of the two previous pathogens), photophthalmia and actinic conjunctivitis (inflammation resulting from prolonged exposure to ultraviolet rays), and others.

In the acute stage of the disease, a catarrhal conjunctivitis is present, with signs of ocular pain, usually blepharospasm, increased lacrimation, and photophobia. Miosis is also usually present. After a few days, this will progress to a keratitis and iridocyclitis. Other ocular problems may also occur, including conjunctival and corneal oedema, and aqueous flare.

After an acute flare-up, no clinical signs of disease may be seen for a prolonged period, which can vary from a few hours to a few years. With frequent acute incidents, though, additional clinical signs may be seen, including anterior and posterior synechiae, poor pupillary responses, cataracts, and a cloudy appearance to the vitreous humour.

The disease is characterised by bilateral diffuse uveitis, with pain, redness and blurring of vision. The eye symptoms may be accompanied by a varying constellation of systemic symptoms, such as auditory (tinnitus, vertigo, and hypoacusis), neurological (meningismus, with malaise, fever, headache, nausea, abdominal pain, stiffness of the neck and back, or a combination of these factors; meningitis, CSF pleocytosis, cranial nerve palsies, hemiparesis, transverse myelitis and ciliary ganglionitis), and cutaneous manifestations, including poliosis, vitiligo, and alopecia. The vitiligo often is found at the sacral region.

The sequence of clinical events in VKH is divided into four phases: prodromal, acute uveitic, convalescent, and chronic recurrent.

The prodromal phase may have no symptoms, or may mimic a non-specific viral infection, marked by flu-like symptoms that typically last for a few days. There may be fever, headache, nausea, meningismus, dysacusia (discomfort caused by loud noises or a distortion in the quality of the sounds being heard), tinnitus, and/or vertigo. Eye symptoms can include orbital pain, photophobia and tearing. The skin and hair may be sensitive to touch. Cranial nerve palsies and optic neuritis are uncommon.

The acute uveitic phase occurs a few days later and typically lasts for several weeks. This phase is heralded by bilateral panuveitis causing blurring of vision. In 70% of VKH, the onset of visual blurring is bilaterally contemporaneous; if initially unilateral, the other eye is involved within several days. The process can include bilateral granulomatous anterior uveitis, variable degree of vitritis, thickening of the posterior choroid with elevation of the peripapillary retinal choroidal layer, optic nerve hyperemia and papillitis, and multiple exudative bullous serous retinal detachments.

The convalescent phase is characterized by gradual tissue depigmentation of skin with vitiligo and poliosis, sometimes with nummular depigmented scars, as well as alopecia and diffuse fundus depigmentation resulting in a classic orange-red discoloration ("sunset glow fundus") and retinal pigment epithelium clumping and/or migration.

The chronic recurrent phase may be marked by repeated bouts of uveitis, but is more commonly a chronic, low-grade, often subclinical, uveitis that may lead to granulomatous anterior inflammation, cataracts, glaucoma and ocular hypertension. Full-blown recurrences are, however, rare after the acute stage is over. Dysacusia may occur in this phase.

Equine recurrent uveitis (ERU), also known as moon blindness, recurrent iridocyclitis or periodic ophthalmia, is an acute, nongranulomatous inflammation of the uveal tract of the eye, occurring commonly in horses of all breeds, worldwide. The causative factor is not known, but several pathogeneses have been suggested. It is the most common cause of blindness in horses. In some breeds, a genetic factor may be involved.

It can present with the following:

- severe burning pain

- lacrimation

- photophobia

- blepharospasm

- swelling of palpebral conjunctiva

- retrotarsal folds

Ophthalmia nodosa is a cutaneous condition characterized by inflammation of the eye due to lodging of (for example) caterpillar hairs in the conjunctiva, cornea, or iris.

Miosis is excessive constriction of the pupil. The term is from Ancient Greek , "mūein", "to close the eyes.

The opposite condition, mydriasis, is the dilation of the pupil. Anisocoria is the condition of one pupil being more dilated than the other.

Depending upon the cause it can be classified into:

- "Neurogenic ptosis" which includes oculomotor nerve palsy, Horner's syndrome, Marcus Gunn jaw winking syndrome, third cranial nerve misdirection.

- "Myogenic ptosis" which includes oculopharyngeal muscular dystrophy, myasthenia gravis, myotonic dystrophy, ocular myopathy, simple congenital ptosis, blepharophimosis syndrome

- "Aponeurotic ptosis" which may be involutional or post-operative

- "Mechanical ptosis" which occurs due to edema or tumors of the upper lid

- "Neurotoxic ptosis" which is a classic symptom of envenomation by elapid snakes such as cobras, kraits, mambas and taipans. Bilateral ptosis is usually accompanied by diplopia, dysphagia and/or progressive muscular paralysis. Regardless, neurotoxic ptosis is a precursor to respiratory failure and eventual suffocation caused by complete paralysis of the thoracic diaphragm. It is therefore a medical emergency and immediate treatment is required. Similarly, ptosis may occur in victims of Botulism (caused by Botulinum toxin) and this is also regarded as a life-threatening symptom

- "Pseudo ptosis" due to:

1. Lack of lid support: empty socket or atrophic globe.

2. Higher lid position on the other side: as in lid retraction

Photophthalmia /pho·toph·thal·mia/ (fōt″of-thal´me-ah) is ophthalmia or inflammation of the eye, especially of the cornea and conjunctiva due to exposure to intense light of short wavelength (as ultraviolet light), as in snow blindness.

It involves occurrence of multiple epithelial erosions due to the effect of ultraviolet rays, especially between 311 and 290 nm. Snow blindness occurs due to reflection of ultraviolet rays from snow surface. Photoretinitis is another form that can occur due to infra-red rays (eclipse burn of retina).

Conjunctivitis eye condition contracted from exposure to actinic rays. Symptoms are redness and swelling.

Myasthenia gravis is a common neurogenic ptosis which could be also classified as neuromuscular ptosis because the site of pathology is at the neuromuscular junction. Studies have shown that up to 70% of myasthenia gravis patients present with ptosis, and 90% of these patients will eventually develop ptosis. In this case, ptosis can be unilateral or bilateral and its severity tends to be oscillating during the day, because of factors such as fatigue or drug effect. This particular type of ptosis is distinguished from the others with the help of a Tensilon challenge test and blood tests. Also, specific to myasthenia gravis is the fact that coldness inhibits the activity of cholinesterase, which makes possible differentiating this type of ptosis by applying ice onto the eyelids. Patients with myasthenic ptosis are very likely to still experience a variation of the drooping of the eyelid at different hours of the day.

The ptosis caused by the oculomotor palsy can be unilateral or bilateral, as the subnucleus to the levator muscle is a shared, midline structure in the brainstem. In cases in which the palsy is caused by the compression of the nerve by a tumor or aneurysm, it is highly likely to result in an abnormal ipsilateral papillary response and a larger pupil. Surgical third nerve palsy is characterized by a sudden onset of unilateral ptosis and an enlarged or sluggish pupil to the light. In this case, imaging tests such as CTs or MRIs should be considered. Medical third nerve palsy, contrary to surgical third nerve palsy, usually does not affect the pupil and it tends to slowly improve in several weeks. Surgery to correct ptosis due to medical third nerve palsy is normally considered only if the improvement of ptosis and ocular motility are unsatisfactory after half a year. Patients with third nerve palsy tend to have diminished or absent function of the levator.

When caused by Horner's syndrome, ptosis is usually accompanied by miosis and anhidrosis. In this case, the ptosis is due to the result of interruption innervations to the sympathetic, autonomic Muller's muscle rather than the somatic levator palpebrae superioris muscle. The lid position and pupil size are typically affected by this condition and the ptosis is generally mild, no more than 2 mm. The pupil might be smaller on the affected side. While 4% cocaine instilled to the eyes can confirm the diagnosis of Horner's syndrome, Hydroxyamphetamine eye drops can differentiate the location of the lesion.

Chronic progressive external ophthalmoplegia is a systemic condition that occurs and which usually affects only the lid position and the external eye movement, without involving the movement of the pupil. This condition accounts for nearly 45% of myogenic ptosis cases. Most patients develop ptosis due to this disease in their adulthood. Characteristic to ptosis caused by this condition is the fact that the protective up rolling of the eyeball when the eyelids are closed is very poor.

Mydriasis () is the dilation of the pupil, usually having a non-physiological cause, or sometimes a physiological pupillary response. Non-physiological causes of mydriasis include disease, trauma, or the use of drugs.

Normally, as part of the pupillary light reflex, the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A "mydriatic" pupil will remain excessively large even in a bright environment. The excitation of the radial fibres of the iris which increases the pupillary aperture is referred to as a mydriasis. More generally, mydriasis also refers to the natural dilation of pupils, for instance in low light conditions or under sympathetic stimulation.

An informal term for mydriasis is blown pupil, and is used by medical providers. It is usually used to refer to a fixed, unilateral mydriasis, which could be a symptom of raised intracranial pressure.

The opposite, constriction of the pupil, is referred to as miosis. Both mydriasis and miosis can be physiological. Anisocoria is the condition of one pupil being more dilated than the other.

Actinic conjunctivitis is an inflammation of the eye contracted from prolonged exposure to actinic (ultraviolet) rays. Symptoms are redness and swelling of the eyes. Most often the condition is caused by prolonged exposure to Klieg lights, therapeutic lamps, or acetylene torches. Other names for the condition include Klieg conjunctivitis, eyeburn, arc-flash, welder's conjunctivitis, flash keratoconjunctivitis, actinic ray ophthalmia, x-ray ophthalmia, and ultraviolet ray ophthalmia.

When detected during childhood, without any other symptoms and when other disorders are discarded through clinical tests, it should be considered a developmental or genetic phenomenon.

Asymmetric pupil or dyscoria, potential causes of anisocoria, refer to an abnormal shape of the pupil which can happens due to developmental and intrauterine anomalies.

The main characteristic that distinguishes physiological anisocoria is an increase of pupil size with lower light or reduced illumination, such that the pupils differ in size between the two eyes. At any given eye examination, up to 41% of healthy patients can show an anisocoria of 0.4 mm or more at one time or another. It can also occur as the difference between both pupils varies from day to day. A normal population survey showed that during poor light or near dark conditions, differences of 1 mm on average between pupils was found.

The presence of physiologic anisocoria has been estimated at 20% of the normal population, so some degree of pupil difference may be expected in at least 1 in 5 clinic patients.

Blast-related ocular trauma comprises a specialized group of penetrating and blunt force injuries to the eye and its structure caused by the detonation of explosive materials. The incidence of ocular trauma due to blast forces has increased dramatically with the introduction of new explosives technology into modern warfare. The availability of these volatile materials, coupled with the tactics of contemporary terrorism, has caused a rise in the number of homemade bombs capable of extreme physical harm.

Untreated cases may develop corneal ulceration, which may perforate resulting in corneal opacification and Staphyloma formation.

Neonatal conjunctivitis by definition presents during the first month of life. It may be infectious or non infectious. In infectious conjunctivitis, the organism is transmitted from the genital tract of an infected mother during birth or by infected hands.

- Pain and tenderness in the eyeball.

- Conjunctival discharge: purulent, mucoid or mucopurulent depending on the cause.

- Conjunctiva shows hyperaemia and chemosis. Eyelids are usually swollen.

- Corneal involvement (rare) may occur in herpes simplex ophthalmia neonatorum.

A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). Phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horner's syndrome.

Light entering the eye strikes three different photoreceptors in the retina: the familiar rods and cones used in image forming and the more newly discovered photosensitive ganglion cells. The ganglion cells give information about ambient light levels, and react sluggishly compared to the rods and cones. Signals from photosensitive ganglion cells have multiple functions including acute suppression of the hormone melatonin, entrainment of the body's circadian rhythms and regulation of the size of the pupil.

The retinal photoceptors convert light stimuli into electric impulses. Nerves involved in the resizing of the pupil connect to the pretectal nucleus of the high midbrain, bypassing the lateral geniculate nucleus and the primary visual cortex. From the pretectal nucleus neurons send axons to neurons of the Edinger-Westphal nucleus whose visceromotor axons run along both the left and right oculomotor nerves. Visceromotor nerve axons (which constitute a portion of cranial nerve III, along with the somatomotor portion derived from the Edinger-Westphal nucleus) synapse on ciliary ganglion neurons, whose parasympathetic axons innervate the iris sphincter muscle, producing miosis. This occurs because sympathetic activity from the ciliary ganglion is "lost" thus parasympathetics are not inhibited.

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