The optokinetic response is a combination of a slow-phase and fast-phase eye movements. It is seen when an individual follows a moving object with their eyes, which then moves out of the field of vision at which point their eye moves back to the position it was in when it first saw the object. The reflex develops at about 6 months of age.

Optokinetic nystagmus (OKN) is nystagmus that occurs in response to a rotation movement. It is present normally. The optokinetic response allows the eye to follow objects in motion when the head remains stationary (e.g., observing individual telephone poles on the side of the road as one travels by them in a car, or observing stationary objects while walking past them).

It may be acquired from:

- Diseases. Some of the diseases that present nystagmus as a pathological sign:

- Aniridia

- Toxic or metabolic reasons could be the result of the following:

- Central nervous system (CNS) disorders, such as with a cerebellar problem, the nystagmus can be in any direction "including" horizontal. Purely vertical nystagmus is usually central in origin, but it is also a frequent adverse effect of high phenytoin toxicity. Causes include:

The cause for pathological nystagmus may be congenital, idiopathic, or secondary to a pre-existing neurological disorder. It also may be induced temporarily by disorientation (such as on roller coaster rides) or by certain drugs (alcohol and other central nervous system depressants, inhalant drugs, stimulants, psychedelic drugs, and dissociative drugs).

If an optokinetic drum is available, rotate the drum in front of the patient. Ask the patient to look at the drum as you rotate it slowly. If an optokinetic drum is not available, move a strip of paper with alternating 2-inch black and white strips across the patient's visual field. Pass it in front of the patient's eye at reading distance while instructing the patient to look at it as it rapidly moves by. With normal vision, a nystagmus develops in both adults and infants. The nystagmus consists of initial slow phases in the direction of the stimulus (smooth pursuits), followed by fast, corrective phases (saccade). Presence of nystagmus indicates an intact visual pathway.

Another effective method is to hold a mirror in front of the patient and slowly rotate the mirror to either side of the patient. The patient with an intact visual pathway will maintain eye contact with herself or himself. This compelling optokinetic stimulus forces reflex slow eye movements.

OKN can be used as a crude assessment of the visual system, particularly in infants. When factitious blindness or malingering is suspected, check for optokinetic nystagmus to determine whether there is an intact visual pathway.

A fit of sneezing while operating a vehicle can cause the operator to lose control of that vehicle, resulting in injury to the person, and damage to the vehicle and/or surroundings. In particular, photic sneezing poses a considerable risk to pilots, due to the frequent presence of bright sunlight and the precise reactions needed to successfully control the aircraft. For the pilot of a fighter aircraft, if an uncontrollable fit of sneezing were to occur during aerial combat, the pilot could be incapacitated when his or her situational awareness needs to be greatest. A plane landing on an aircraft carrier or shoreline also requires precise movements and quick reflexes. The reflection of the sun from surrounding water has a high probability of producing at least one photic sneeze for pilots who have the reflex. Any amount of sneezing while attempting to land could cause the pilot to lose control, potentially resulting in disaster.

Relative afferent pupillary defect (RAPD) or Marcus Gunn pupil is a medical sign observed during the swinging-flashlight test whereupon the patient's pupils constrict less (therefore appearing to dilate) when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced.

The most common cause of Marcus Gunn pupil is a lesion of the optic nerve (between the retina and the optic chiasm) or severe retinal disease. It is named after Scottish ophthalmologist Robert Marcus Gunn.

A second common cause of Marcus Gunn pupil is a contralateral optic tract lesion, due to the different contributions of the intact nasal and temporal hemifields.

Parinaud's Syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye.

Classically, it has been associated with three major groups:

1. Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome.

2. Women in their 20s-30s with multiple sclerosis

3. Older patients following stroke of the upper brainstem

However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome.

Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson's disease, kernicterus, and barbiturate overdose.

The eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported.

Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well.

This remains undetermined at the present time. A recent study by Major et al. reports that:

"Prematurity, family history or secondary ocular history, perinatal or gestational complications, systemic disorders, use of supplemental oxygen as a neonate, use of systemic medications, and male sex were found to be significant risk factors for infantile esotropia."

Further recent evidence indicates that a cause for "infantile strabismus" may lie with the input that is provided to the visual cortex. In particular, neonates who suffer injuries that, directly or indirectly, perturb binocular inputs into the primary visual cortex (V1) have a far higher risk of developing strabismus than other infants.

A paper published by Eltern für Impfaufklärung, a German Anti-Vaccination activist group, cites a study by The Robert Koch Institute (RKI), claiming significant correlation between children who received Vaccinations and the onset of cause of Spine, Face & Eye Asymmetry.

Though there is no clear cause of cerebral polyopia, many cases show associations with occipital or temporal lobe lesions. Most cases of polyopia occur when there are bilateral lesions to occipital or temporal cortex, however some cases are present with unilateral lesions. Thus, polyopia can result from any kind of infarction to the occipital or temporal lobes, though the exact mechanism remains unclear. Some cases have shown that polyopia is experienced when the infarctions were seen to be at the tips and outer surfaces of the occipital lobes. By contrast, some patients experience cerebral polyopia associated with headaches and migraines in the frontotemporal lobe.

The mechanism of infarction differs by patient, but polyopia is experienced most commonly in patients that suffer from epilepsy in the occipital cortex, or in patients who suffer from cerebral strokes. In cases of epilepsy, polyopia is often experienced alongside palinopsia as these two conditions share an epileptic mechanism.

Perhaps the most universal risk of sneezing is the spread of disease. Bacterial infections can spread to susceptible uninfected people via the spread of microscopic organisms suspended in the droplets expelled by a sneeze. Bacteria which commonly spread by sneezing include bacterial meningitis, strep throat, and tuberculosis. Viral infections can also be spread by sneezing. When a virus is expelled by a sneeze, its mucous membrane evaporates, and the virus becomes a droplet nucleus which can be inhaled by another person, thus spreading the virulent infection. Examples of virulent infections that spread by sneezing include measles, mumps, rubella, and influenza.

Cerebral diplopia or polyopia describes seeing two or more images arranged in ordered rows, columns, or diagonals after fixation on a stimulus. The polyopic images occur monocular bilaterally (one eye open on both sides) and binocularly (both eyes open), differentiating it from ocular diplopia or polyopia. The number of duplicated images can range from one to hundreds. Some patients report difficulty in distinguishing the replicated images from the real images, while others report that the false images differ in size, intensity, or color. Cerebral polyopia is sometimes confused with palinopsia (visual trailing), in which multiple images appear while watching an object. However, in cerebral polyopia, the duplicated images are of a stationary object which are perceived even after the object is removed from the visual field. Movement of the original object causes all of the duplicated images to move, or the polyopic images disappear during motion. In palinoptic polyopia, movement causes each polyopic image to leave an image in its wake, creating hundreds of persistent images (entomopia).

Infarctions, tumors, multiple sclerosis, trauma, encephalitis, migraines, and seizures have been reported to cause cerebral polyopia. Cerebral polyopia has been reported in extrastriate visual cortex lesions, which is important for detecting motion, orientation, and direction. Cerebral polyopia often occurs in homonymous field deficits, suggesting deafferentation hyperexcitability could be a possible mechanism, similar to visual release hallucinations (Charles Bonnet syndrome).

Alexanders law refers to spontaneous nystagmus that occurs after an acute unilateral vestibular loss. It was first described in 1912 and has three elements to explain how the vestibulo-ocular reflex responds to an acute vestibular insult. The first element says that spontaneous nystagmus after an acute vestibular impairment has the fast phase directed toward the healthy ear. The direction of the nystagmus, by convention, is named for the fast phase, so the spontaneous nystagmus is directed toward the healthy ear. The second element says nystagmus is greatest when gaze is directed toward the healthy ear, is attentuated at central gaze and may be absent when gaze is directed toward the impaired ear. The third element says that spontaneous nystagmus with central gaze is augmented when vision is denied. This became apparent with the implementation of electrographic testing.

Alexander's law states that in individuals with nystagmus, the amplitude of the nystagmus increases when the eye moves in the direction of the fast phase (saccade).

It is manifested during spontaneous nystagmus in a patient with a vestibular lesion. The nystagmus becomes more intense when the patient looks in the quick-phase than in the slow-phase direction.

The law was named after Gustav Alexander who described it in 1912.

Oscillopsia is a visual disturbance in which objects in the visual field appear to oscillate. The severity of the effect may range from a mild blurring to rapid and periodic jumping. Oscillopsia is an incapacitating condition experienced by many patients with neurological disorders. It may be the result of ocular instability occurring after the oculomotor system is affected, no longer holding images steady on the retina. A change in the magnitude of the vestibulo-ocular reflex due to vestibular disease can also lead to oscillopsia during rapid head movements. Oscillopsia may also be caused by involuntary eye movements such as nystagmus, or impaired coordination in the visual cortex (especially due to toxins) and is one of the symptoms of superior canal dehiscence syndrome. Sufferers may experience dizziness and nausea. Oscillopsia can also be used as a quantitative test to document aminoglycoside toxicity. Permanent oscillopsia can arise from an impairment of the ocular system that serves to maintain ocular stability. Paroxysmal oscillopsia can be due to an abnormal hyperactivity in the peripheral ocular or vestibular system.

Clinically Infantile esotropia must be distinguished from:

1. VIth Cranial nerve or abducens palsy

2. Nystagmus Blockage Syndrome

3. Esotropia arising secondary to central nervous system abnormalities (in cerebral palsy for example)

4. Primary Constant esotropia

5. Duane's Syndrome

The Marcus Gunn pupil is a relative afferent pupillary defect indicating a decreased pupillary response to light in the affected eye.

In the swinging flashlight test, a light is alternately shone into the left and right eyes. A normal response would be equal constriction of both pupils, regardless of which eye the light is directed at. This indicates an intact direct and consensual pupillary light reflex. When the test is performed in an eye with an afferent pupillary defect, light directed in the affected eye will cause only mild constriction of both pupils (due to decreased response to light from the afferent defect), while light in the unaffected eye will cause a normal constriction of both pupils (due to an intact efferent path, and an intact consensual pupillary reflex). Thus, light shone in the affected eye will produce less pupillary constriction than light shone in the unaffected eye.

A Marcus Gunn pupil is distinguished from a total CN II lesion, in which the affected eye perceives "no" light. In that case, shining the light in the affected eye produces no effect.

Anisocoria is absent. A Marcus Gunn pupil is seen, among other conditions, in optic neuritis. It is also common in retrobulbar optic neuritis due to multiple sclerosis but only for 3–4 weeks, until the visual acuity begins to improve in 1–2 weeks and may return to normal.

Iridoplegia is the paralysis of the sphincter of the iris. It can occur in due to direct orbital injury, which may result in short lived blurred vision.

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.

Brain related causes are less commonly associated with isolated vertigo and nystagmus but can still produce signs and symptoms, which mimic peripheral causes. Disequilibrium is often a prominent feature.

- Degenerative: age related decline in balance function

- Infectious: meningitis, encephalitis, epidural abscess, syphilis

- Circulatory: cerebral or cerebellar ischemia or hypoperfusion, stroke, lateral medullary syndrome (Wallenberg's syndrome)

- Autoimmune: Cogan syndrome

- Structural: Arnold-Chiari malformation, hydrocephalus

- Systemic: multiple sclerosis, Parkinson's disease

- Vitamin deficiency: Vitamin B12 deficiency

- CNS or posterior neoplasms, benign or malignant

- Neurological: Vertiginous epilepsy, abasia

- Other – There are a host of other causes of dizziness not related to the ear.

- Mal de debarquement is rare disorder of imbalance caused by being on board a ship. Patients suffering from this condition experience disequilibrium even when they get off the ship. Typically treatments for seasickness are ineffective for this syndrome.

- Motion sickness – a conflict between the input from the various systems involved in balance causes an unpleasant sensation. For this reason, looking out of the window of a moving car is much more pleasant than looking inside the vehicle.

- Migraine-associated vertigo

- Toxins, drugs, medications; it is also a known symptom of carbon monoxide poisoning.

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.

It can be of three types:

1. accommodative iridoplegia- Noncontraction of pupils during accommodation.

2. complete iridoplegia- Iris fails to respond to any stimulation.

3. reflex iridoplegia- The absence of light reflex, with retention of accommodation reflex. Also called Argyll Robertson pupil.

Some causes of blepharospasm have been identified; however, the causes of many cases of blepharospasm remain unknown, although some educated guesses are being made. Some blepharospasm patients have a history of dry eyes and/or light sensitivity, but others report no previous eye problems before onset of initial symptoms.

Some drugs can induce blepharospasm, such as those used to treat Parkinson's disease, as well as sensitivity to hormone treatments, including estrogen-replacement therapy for women going through menopause. Blepharospasm can also be a symptom of acute withdrawal from benzodiazepines. In addition to blepharospasm being a benzodiazepine withdrawal symptom, prolonged use of benzodiazepines can induce blepharospasm and is a known risk factor for the development of blepharospasm.

Blepharospasm may also come from abnormal functioning of the brain basal ganglia. Simultaneous dry eye and dystonias such as Meige's syndrome have been observed. Blepharospasms can be caused by concussions in some rare cases, when a blow to the back of the head damages the basal ganglia.

Multiple sclerosis can cause blepharospasm.

Ocular stability is maintained by three different ocular motor systems

1. The fixation system and its deficit

2. The visuo-vestibular stabilizing systems and their deficits

3. The neural integrator and its deficit

Causes of dizziness related to the ear are often characterized by vertigo (spinning) and nausea. Nystagmus (flickering of the eye, related to the Vestibulo-ocular reflex [VOR]) is often seen in patients with an acute peripheral cause of dizziness.

- Benign Paroxysmal Positional Vertigo (BPPV) – The most common cause of vertigo. It is typically described as a brief, intense sensation of spinning that occurs when there are changes in the position of the head with respect to gravity. An individual may experience BPPV when rolling over to the left or right, upon getting out of bed in the morning, or when looking up for an object on a high shelf. The cause of BPPV is the presence of normal but misplaced calcium crystals called otoconia, which are normally found in the utricle and saccule (the otolith organs) and are used to sense movement. If they fall from the utricle and become loose in the semicircular canals, they can distort the sense of movement and cause a mismatch between actual head movement and the information sent to the brain by the inner ear, causing a spinning sensation.

- Labyrinthitis - An inner ear infection or inflammation causing both dizziness (vertigo) and hearing loss.

- Vestibular neuronitis - an infection of the vestibular nerve, generally viral, causing vertigo

- Cochlear Neuronitis – an infection of the Cochlear nerve, generally viral, causing sudden deafness but no vertigo

- Trauma – Injury to the skull may cause either a fracture or a concussion to the organ of balance. In either case an acute head injury will often result in dizziness and a sudden loss of vestibular function.

- Surgical trauma to the lateral semicircular canal (LSC) is a rare complication which does not always result in cochlear damage. Vestibular symptoms are pronounced. Dizziness and instability usually persist for several months and sometimes for a year or more.

- Ménière's disease - an inner ear fluid balance disorder that causes lasting episodes of vertigo, fluctuating hearing loss, tinnitus (a ringing or roaring in the ears), and the sensation of fullness in the ear. The cause of Ménière's disease is unknown.

- Perilymph fistula – a leakage of inner ear fluid from the inner ear. It can occur after head injury, surgery, physical exertion or without a known cause.

- Superior canal dehiscence syndrome – a balance and hearing disorder caused by a gap in the temporal bone, leading to the dysfunction of the superior canal.

- Bilateral vestibulopathy – a condition involving loss of inner ear balance function in both ears. This may be caused by certain antibiotics, anti-cancer, and other drugs or by chemicals such as solvents, heavy metals, etc., which are ototoxic; or by diseases such as syphilis or autoimmune disease; or other causes. In addition, the function of the semicircular canal can be temporarily affected by a number of medications or combinations of medications.

Leukocoria (also leukokoria or white pupillary reflex) is an abnormal white reflection from the retina of the eye. Leukocoria resembles eyeshine, but leukocoria can occur in humans and other animals that lack eyeshine because their retina lacks a "tapetum lucidum".

Leukocoria is a medical sign for a number of conditions, including Coats disease, congenital cataract, corneal scarring, melanoma of the ciliary body, Norrie disease, ocular toxocariasis, persistence of the tunica vasculosa lentis (PFV/PHPV), retinoblastoma, and retrolental fibroplasia.

Because of the potentially life-threatening nature of retinoblastoma, a cancer, that condition is usually considered in the evaluation of leukocoria. In some rare cases (1%) the leukocoria is caused by Coats' disease (leaking retinal vessels).