Major symptoms are sudden loss of vision (partial or complete), sudden blurred or "foggy" vision, and pain on movement of the affected eye. Early symptoms that require investigation include symptoms from multiple sclerosis (twitching, lack of coordination, slurred speech, frequent episodes of partial vision loss or blurred vision), episodes of "disturbed/blackened" rather than blurry indicate moderate stage and require immediate medical attention to prevent further loss of vision. Other early symptoms are reduced night vision, photophobia and red eyes. Many patients with optic neuritis may lose some of their color vision in the affected eye (especially red), with colors appearing subtly washed out compared to the other eye. Patients may also experience difficulties judging movement in depth which can be particular troublesome during driving or sport (Pulfrich effect). Likewise transient worsening of vision with increase of body temperature (Uhthoff's phenomenon) and glare disability are a frequent complaint. However, several case studies in children have demonstrated the absence of pain in more than half of cases (approximately 60%) in their pediatric study population, with the most common symptom reported simply as "blurriness." Other remarkable differences between the presentation of adult optic neuritis as compared to pediatric cases include more often unilateral optic neuritis in adults, while children much predominantly present with bilateral involvement.

On medical examination the head of the optic nerve can easily be visualized by a slit lamp with high plus or by using direct ophthalmoscopy; however, frequently there is no abnormal appearance of the nerve head in optic neuritis (in cases of retrobulbar optic neuritis), though it may be swollen in some patients (anterior papillitis or more extensive optic neuritis). In many cases, only one eye is affected and patients may not be aware of the loss of color vision until they are asked to close or cover the healthy eye.

Optic neuritis is a demyelinating inflammation of the optic nerve. It is also known as optic papillitis (when the head of the optic nerve is involved) and retrobulbar neuritis (when the posterior part of the nerve is involved). It is most often associated with multiple sclerosis, and it may lead to complete or partial loss of vision in one or both eyes.

Partial, transient vision loss (lasting less than one hour) can be an indication of early onset multiple sclerosis. Other possible diagnoses include: diabetes mellitus, low phosphorus levels, or hyperkalaemia.

AON was first described in 1982. It presents with visual loss and signs of optic nerve dysfunction, such as loss of color vision, afferent pupil defect, and sometimes abnormalities of the optic disc. The clinical features of AON can be variable and present in several unilateral or bilateral forms:

- Acute anterior or retrobulbar optic neuritis sometimes associated with pain.

- Anterior or retrobulbar ischemic optic neuropathy not associated with pain.

- Chronic progressive vision loss that mimics a compressive lesion.

The main features that differentiate AON from the more common typical demyelinating optic neuritis is the poor recovery of vision and the chronic or recurrent or bilateral course of AON. Furthermore, the workup for multiple sclerosis including MRI, will be negative. Thus, it may be necessary to diagnose AON after a period of observation, noting the problem is not behaving as expected for demyelinative disease.

Optic papillitis is a specific type of optic neuritis. Inflammation of the optic nerve head is called "papillitis" or "intraocular optic neuritis"; inflammation of the orbital portion of the nerve is called "retrobulbar optic neuritis" or "orbital optic neuritis". It is often associated with substantial losses in visual fields, pain on moving the globe, and sensitivity to light pressure on the globe. It is often an early sign of multiple sclerosis.

Papillitis may have the same appearance as papilledema. However, papillitis may be unilateral, whereas papilledema is almost always bilateral. Papillitis can be differentiated from papilledema by an afferent pupillary defect (Marcus Gunn pupil), by its greater effect in decreasing visual acuity and color vision, and by the presence of a central scotoma. Papilledema that is not yet chronic will not have as dramatic an effect on vision. Because increased intracranial pressure can cause both papilledema and a sixth (abducens) nerve palsy, papilledema can be differentiated from papillitis if esotropia and loss of abduction are also present. However, esotropia may also develop secondarily in an eye that has lost vision from papillitis. Retrobulbar neuritis, an inflamed optic nerve, but with a normal-appearing nerve head, is associated with pain and the other findings of papillitis. Pseudopapilledema is a normal variant of the optic disk, in which the disk appears elevated, with indistinct margins and a normal vascular pattern. Pseudopapilledema sometimes occurs in hyperopic individuals.

Workup of the patient with papillitis includes lumbar puncture and cerebrospinal fluid analysis. B henselae infection can be detected by serology. MRI is the preferred imaging study. An abnormal MRI is associated with a worse visual outcome.

Autoimmune optic neuropathy (AON), sometimes called autoimmune optic neuritis, may be a forme fruste of systemic lupus erythematosus (SLE) associated optic neuropathy. AON is more than the presence of any optic neuritis in a patient with an autoimmune process, as it describes a relatively specific clinical syndrome. AON is characterized by chronically progressive or recurrent vision loss associated with serological evidence of autoimmunity. Specifically, this term has been suggested for cases of optic neuritis with serological evidence of vasculitis by positive ANA, despite the lack of meeting criteria for SLE. The clinical manifestations include progressive vision loss that tends to be steroid-responsive and steroid dependent.

Patients with defined SLE that go on to develop optic neuritis should be better identified as lupus optic neuritis.

Tumors, infections, and inflammatory processes can cause lesions within the orbit and, less commonly, the optic canal. These lesions may compress the optic nerve, resulting optic disc swelling and progressive visual loss. Implicated orbital disorders include optic gliomas, meningiomas, hemangiomas, lymphangiomas, dermoid cysts, carcinoma, lymphoma, multiple myeloma, inflammatory orbital pseudotumor, and thyroid ophthalmopathy. Patients often have bulging out of the eye (proptosis) with mild color deficits and almost normal vision with disc swelling.

Optic neuritis is inflammation of the optic nerve, which is associated with swelling and destruction of the myelin sheath covering the optic nerve. Young adults, usually females, are most commonly affected. Symptoms of optic neuritis in the affected eye include pain on eye movement, sudden loss of vision, and decrease in color vision (especially reds). Optic neuritis, when combined with the presence of multiple demyelinating white matter brain lesions on MRI, is suspicious for multiple sclerosis.

Several causes and clinical courses are possible for the optic neuritis. It can be classified in:

- Single isolated optic neuritis (SION)

- relapsing isolated optic neuritis (RION)

- chronic relapsing inflammatory optic neuropathy (CRION)

- the neuromyelitis optica (NMO) spectrum disorder

- multiple sclerosis associated optic neuritis (MSON)

- unclassified optic neuritis (UCON) forms.

Medical examination of the optic nerve with an ophthalmoscope may reveal a swollen optic nerve, but the nerve may also appear normal. Presence of an afferent pupillary defect, decreased color vision, and visual field loss (often central) are suggestive of optic neuritis. Recovery of visual function is expected within 10 weeks. However, attacks may lead to permanent axonal loss and thinning of the retinal nerve fiber layer.

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.

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.

Neuritis () is inflammation of a nerve or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved but may include pain, paresthesia (pins-and-needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes.

Late congenital syphilitic oculopathy is a disease of the eye, a manifestation of late congenital syphilis. It can appear as:

- Interstitial keratitis – this commonly appears between ages 6 and 12. Symptoms include lacrimation and photophobia. Pathological vascularization of the cornea cause it to turn pink or salmon colored. 90% of cases affect both eyes.

- Episcleritis or scleritis – nodules appear in or overlying the sclera (white of eye)

- Iritis or iris papules – vascular infiltration of the iris causes rosy color change and yellow/red nodules.

- Chorioretinitis, papillitis, retinal vasculitis – retinal changes can resemble retinitis pigmentosa.

- Exudative retinal detachment

Congenital syphilis is categorized by the age of the child. Early congenital syphilis occurs in children under 2 years old, and late congenital syphilis in children at or greater than 2 years old. Manifestations of late congenital syphilis are similar to those of secondary syphilis and tertiary syphilis in adults.

The following are not classified as diseases of the eye and adnexa (H00-H59) by the World Health Organization:

- (B36.1) Keratomycosis — fungal infection of the cornea

- (E50.6-E50.7) Xerophthalmia — dry eyes, caused by vitamin A deficiency

- (Q13.1) Aniridia — a rare congenital eye condition leading to underdevelopment or even absence of the iris of the eye

Looking inside the person’s eyes at the time of onset, ophthalmoscope exam reveals no visible changes to the optic nerve head. Weeks after ischemic insult, nerve atrophy originating from the damaged posterior optic nerve progresses to involve the anterior optic nerve head. Four to eight weeks after onset, atrophy of the optic nerve head is observable upon ophthalmoscope exam.

If both eyes are affected by PION, the pupils may look symmetrical. However, if the eyes are asymmetrically affected, i.e. one eye's optic nerve is more damaged than the other, it will produce an important sign called an afferent pupillary defect.

Defective light perception in one eye causes an asymmetrical pupillary constriction reflex called the afferent pupillary defect (APD).

Acutely or at the early sign includes painful, photophobic, red and watery eye. This is due to active corneal inflammation resulting in vascular invasion and stromal necrosis which can be diffuse or localized. This cause the pinkish discoloration of what was a clear transparent normal corneal tissue (called "Salmon patch of Hutchinson").

Chronically or the end result will cause blurring of vision secondary to corneal stromal scarring, presence of ghost vessel and thinning of the cornea especially if it involves the visual axis.

Ocular causes include:

- Iritis

- Keratitis

- Blepharitis

- Optic disc drusen

- Posterior vitreous detachment

- Closed-angle glaucoma

- Transient elevation of intraocular pressure

- Intraocular hemorrhage

- Coloboma

- Myopia

- Orbital hemangioma

- Orbital osteoma

- Keratoconjunctivitis sicca

The main symptoms of Devic's disease are loss of vision and spinal cord function. Optic neuritis may manifest as visual impairment with decreased visual acuity, although visual field defects, or loss of color vision may occur in isolation or prior to formal loss of acuity. Spinal cord dysfunction can lead to muscle weakness, reduced sensation, or loss of bladder and bowel control. The typical patient has an acute and severe spastic weakness of the legs (paraparesis) or all four limbs (quadriparesis) with sensory signs, often accompanied by loss of bladder control.

This is a partial list of human eye diseases and disorders.

The World Health Organization publishes a classification of known diseases and injuries, the International Statistical Classification of Diseases and Related Health Problems, or ICD-10. This list uses that classification.

Neurological causes include:

- Optic neuritis

- Compressive optic neuropathies

- Papilledema: "The underlying mechanism for visual obscurations in all of these patients appear to be transient ischemia of the optic nerve head consequent to increased tissue pressure. Axonal swelling, intraneural masses, and increased influx of interstitial fluid may all contribute to increases in tissue pressure in the optic nerve head. The consequent reduction in perfusion pressure renders the small, low-pressure vessels that supply the optic nerve head vulnerable to compromise. Brief fluctuations in intracranial or systemic blood pressure may then result in transient loss of function in the eyes." Generally, this transient visual loss is also associated with a headache and optic disk swelling.

- Multiple Sclerosis can cause amaurosis fugax due to a unilateral conduction block, which is a result of demyelination and inflammation of the optic nerve, and "...possibly by defects in synaptic transmission and putative circulating blocking factors."

- Migraine

- Pseudotumor cerebri

- Intracranial tumor

- Psychogenic

Neuromyelitis optica (NMO), also known as Devic's disease or Devic's syndrome, is a heterogeneous condition consisting of the simultaneous inflammation and demyelination of the optic nerve (optic neuritis) and the spinal cord (myelitis). It can be monophasic or recurrent.

Currently at least two different causes are proposed based on the presence of autoantibodies against AQP4. AQP4+ NMO is currently considered an autoimmune disease (autoimmune astrocytopathy, or autoimmune astrocytic channelopathy) in which a person's own immune system attacks the astrocytes of the optic nerves and spinal cord. The cause of the AQP4− variants is unknown.

Although inflammation may also affect the brain, the lesions are different from those observed in the related condition, multiple sclerosis. Spinal cord lesions lead to varying degrees of weakness or paralysis in the legs or arms, loss of sensation (including blindness), and/or bladder and bowel dysfunction.

Devic's disease is now studied along a collection of similar diseases called "Neuromyelitis optica spectrum diseases". Some cases of this spectrum resemble multiple sclerosis (MS) in several ways, but require a different course of treatment for optimal results.

In 2004, NMO-IgG (currently known as Anti-AQP IgG) was first described leading to the distinction between positive and negative cases.

In Anti-AQP positive variants, CNS astrocytes, which are the basis for the glymphatic system are the target of the autoimmune attack. NMO-IgG-negative cases are less understood. It seems currently that astrocytes are spared in these IgG negative cases.

Interstitial keratitis (IK) is corneal scarring due to chronic inflammation of the corneal stroma. Interstitial means space between cells i.e. corneal stroma which lies between the epithelium and the endothelium. Keratitis means corneal inflammation.

Distortion of vision refers to straight lines not appearing straight, but instead bent, crooked, or wavy. Usually this is caused by distortion of the retina itself. This distortion can herald a loss of vision in macular degeneration, so anyone with distorted vision should seek medical attention by an ophthalmologist promptly. Other conditions leading to swelling of the retina can cause this distortion, such as macular edema and central serous chorioretinopathy.

An Amsler grid can be supplied by an ophthalmologist so that the vision can be monitored for distortion in people who may be predisposed to this problem.

Tunnel vision implies that the peripheral vision, or side vision, is lost, while the central vision remains. Thus, the vision is like looking through a tunnel, or through a paper towel roll. Some disorders that can cause this include:

Glaucoma - severe glaucoma can result in loss of nearly all of the peripheral vision, with a small island of central vision remaining. Sometimes even this island of vision can be lost as well.

Retinitis pigmentosa - This is usually a hereditary disorder which can be part of numerous syndromes. It is more common in males. The peripheral retina develops pigmentary deposits, and the peripheral vision gradually becomes worse and worse. The central vision can be affected eventually as well. People with this problem may have trouble getting around in the dark. Cataract can be a complication as well. There is no known treatment for this disorder, and supplements of Vitamin A have not been proven to help.

Punctate Inner Choroidopathy - This condition is where vessels gro (( material is missing ))

Stroke - a stroke involving both sides of the visual part of the brain may wipe out nearly all of the peripheral vision. Fortunately, this is a very rare occurrence

Seeing rainbows around lights, especially at night, usually indicates swelling of the cornea. This may occur from a variety of causes which are discussed under Corneal Edema. Cataract can sometimes cause this also.

Colour vision is perceived mainly by the macula, which is the central vision portion of the retina. Thus any disorder affecting the macula may cause a disturbance in color vision. However, about 8% of males and 0.5% of females have some version of "colour blindness" from birth. Usually this is a genetically inherited trait, and is of the "red-green confusion" variety. The reds, browns, olives, and gold may be confused. Purple may be confused with blue, and pastel pinks, oranges, yellows, and greens look similar. Usually both eyes are affected equally.

There are many obscure macular retinal disorders that can lead to a loss of colour vision, and many of these syndromes are inherited as well. There may also be a problem with a generalized loss of vision with these problems as well. Other retinal problems can lead to a temporary disturbance of colour vision, such as Central serous chorioretinopathy, Macular Edema of different causes, and Macular Degeneration.

Certain types of cataract can gradually affect the colour vision, but this is usually not noticed until one cataract is removed. The cataract seems to filter out the colour blue, and everything seems more blue after cataract extraction. Optic nerve disorders such as Optic Neuritis can greatly affect colour vision, with colours seeming washed out during or after an episode.

There are many causes of blurred vision:

- Use of atropine or other anticholinergics

- Presbyopia—Difficulty focusing on objects that are close. Common in the elderly. (Accommodation tends to decrease with age.)

- Cataracts—Cloudiness over the eye's lens, causing poor night-time vision, halos around lights, and sensitivity to glare. Daytime vision is eventually affected. Common in the elderly.

- Glaucoma—Increased pressure in the eye, causing poor night vision, blind spots, and loss of vision to either side. A major cause of blindness. Glaucoma can happen gradually or suddenly—if sudden, it is a medical emergency.

- Diabetes—Poorly controlled blood sugar can lead to temporary swelling of the lens of the eye, resulting in blurred vision. While it resolves if blood sugar control is reestablished, it is believed repeated occurrences promote the formation of cataracts (which are not temporary).

- Diabetic retinopathy—This complication of diabetes can lead to bleeding into the retina. Another common cause of blindness.

- Hypervitaminosis A—Excess consumption of vitamin A can cause blurred vision.

- Macular degeneration—Loss of central vision, blurred vision (especially while reading), distorted vision (like seeing wavy lines), and colors appearing faded. The most common cause of blindness in people over age 60.

- Eye infection, inflammation, or injury.

- Sjögren's syndrome, a chronic autoimmune inflammatory disease that destroys moisture producing glands, including lacrimal (tear)

- Floaters—Tiny particles drifting across the eye. Although often brief and harmless, they may be a sign of retinal detachment.

- Retinal detachment—Symptoms include floaters, flashes of light across your visual field, or a sensation of a shade or curtain hanging on one side of your visual field.

- Optic neuritis—Inflammation of the optic nerve from infection or multiple sclerosis. You may have pain when you move your eye or touch it through the eyelid.

- Stroke or transient ischemic attack

- Brain tumor

- Toxocara—A parasitic roundworm that can cause blurred vision

- Bleeding into the eye

- Temporal arteritis—Inflammation of an artery in the brain that supplies blood to the optic nerve.

- Migraine headaches—Spots of light, halos, or zigzag patterns are common symptoms prior to the start of the headache. A retinal migraine is when you have only visual symptoms without a headache.

- Myopia—Blurred vision may be a systemic sign of local anaesthetic toxicity

- Reduced blinking—Lid closure that occurs too infrequently often leads to irregularities of the tear film due to prolonged evaporation, thus resulting in disruptions in visual perception.

- Carbon monoxide poisoning—Reduced oxygen delivery can effect many areas of the body including vision. Other symptoms caused by CO include vertigo, hallucination and sensitivity to light.

Neuritis is a general term for inflammation of a nerve or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved, but may include pain, paresthesia (pins-and-needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes.

Causes of neuritis include: