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:

Early onset nystagmus occurs more frequently than acquired nystagmus. It can be insular or accompany other disorders (such as micro-ophthalmic anomalies or Down Syndrome). Early-onset nystagmus itself is usually mild and non-progressive. The affected persons are not normally aware of their spontaneous eye movements, but vision can be impaired depending on the severity of the movements.

Types of early-onset nystagmus include the following:

- Infantile:

- Albinism

- Aniridia

- Bilateral congenital cataract

- Bilateral optic nerve hypoplasia

- Idiopathic

- Leber's congenital amaurosis

- Optic nerve or macular disease

- Persistent tunica vasculosa lentis

- Rod monochromatism

- Visual-motor syndrome of functional monophthalmus

- Latent nystagmus

- Noonan syndrome

- Nystagmus blockage syndrome

X-linked infantile nystagmus is associated with mutations of the gene FRMD7, which is located on the X chromosome.

Infantile nystagmus is also associated with two X-linked eye diseases known as complete congenital stationary night blindness (CSNB) and incomplete CSNB (iCSNB or CSNB-2), which are caused by mutations of one of two genes located on the X chromosome. In CSNB, mutations are found in NYX (nyctalopin). CSNB-2 involves mutations of CACNA1F, a voltage-gated calcium channel that, when mutated, does not conduct ions.

Dissociation refers to the situation where the innervation of one eye causes it to move involuntarily and independently of the other eye. Usually both eyes work together as described by Hering's and Sherrington's laws of innervation. A DVD is a slow upward and sometimes temporal movement of one eye, with cortical suppression of the vision in that eye while it is deviated. On returning downward and possibly inward to take up fixation, the DVD slow movement will be reversed.

The dissociative movement seen 'objectively' should not be confused with the dissociation that occurs 'subjectively' - as when the brain begins to not visualise both images simultaneously (by ignoring or suppressing vision in that eye).

DVD typically becomes apparent between 18 months and three years of age, however, the difficulties of achieving the prolonged occlusion required for accurate detection in the very young, make it possible that onset is generally earlier than these figures suggest.

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.

"Congenital esotropia," or "infantile esotropia," is a specific sub-type of primary concomitant esotropia. It is a constant esotropia of large and consistent size with onset between birth and six months of age. It is not associated with hyperopia, so the exertion of accommodative effort will not significantly affect the angle of deviation. It is, however, associated with other ocular dysfunctions including oblique muscle over-actions, Dissociated Vertical Deviation (DVD,) Manifest Latent Nystagmus, and defective abduction, which develops as a consequence of the tendency of those with infantile esotropia to 'cross fixate.' Cross fixation involves the use of the right eye to look to the left and the left eye to look to the right; a visual pattern that will be 'natural' for the person with the large angle esotropia whose eye is already deviated towards the opposing side.

The origin of the condition is unknown, and its early onset means that the affected individual's potential for developing binocular vision is limited. The appropriate treatment approach remains a matter of some debate. Some ophthalmologists favour an early surgical approach as offering the best prospect of binocularity whilst others remain unconvinced that the prospects of achieving this result are good enough to justify the increased complexity and risk associated with operating on those under the age of one year.

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).

Esotropia is a form of strabismus in which one or both eyes turns inward. The condition can be constantly present, or occur intermittently, and can give the affected individual a "cross-eyed" appearance. It is the opposite of exotropia and usually involves more severe axis deviation than esophoria. Esotropia is sometimes erroneously called "lazy eye", which describes the condition of amblyopia—a reduction in vision of one or both eyes that is not the result of any pathology of the eye and cannot be resolved by the use of corrective lenses. Amblyopia can, however, arise as a result of esotropia occurring in childhood: In order to relieve symptoms of diplopia or double vision, the child's brain will ignore or "suppress" the image from the esotropic eye, which when allowed to continue untreated will lead to the development of amblyopia. Treatment options for esotropia include glasses to correct refractive errors (see accommodative esotropia below), the use of prisms and/or orthoptic exercises and/or eye muscle surgery. The term is from Greek "eso" meaning "inward" and "trope" meaning "a turning".

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

Pseudomyopia refers to an intermittent and temporary shift in refractive error of the eye towards myopia, in which the focusing of light in front of the retina is due to a transient spasm of the ciliary muscle causing an increase in the refractive power of the eye. It may be either organic, through stimulation of the parasympathetic nervous system, or functional in origin, through eye strain or fatigue of ocular systems. It is common in young adults who have active accommodation, and classically occurs after a change in visual requirements, such as students preparing for an exam, or a change in occupation.

The major symptom is intermittent blurring of distance vision particularly noticeable after prolonged periods of near work, and symptoms of asthenopia. The vision may clear temporarily using concave (minus) lenses. The diagnosis is done by cycloplegic refraction using a strong cycloplegic like atropine or homatropine eye drops. Accommodative amplitude and facility may be reduced as a result of the ciliary muscle spasm.

Treatment is dependent on the underlying aetiology. Organic causes may include systemic or ocular medications, brain stem injury, or active ocular inflammation such as uveitis. Functional pseudomyopia is managed though modification of working conditions, an updated refraction, typically involving a reduction of a myopic prescription to some lower myopic prescription, or through appropriate ocular exercises.

There have been cases of improvement in extra-ocular movement with botulinum toxin injection.

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.

Amaurotic nystagmus is defined as the nystagmus associated with blindness or the central vision defects. It is characterized by the pendular or jerky movements of the eyes in the patients who have visual impairement for a long period of time.

Pendular nystagmus is a sinusoidal oscillation, which refers to the waveform of involuntary eye movements that may occur in any direction. It is characterized by the multidimensional slow eye movements of the eyes (1 Hz frequency) with an equal velocity in each direction that resembles the trajectory of a pendulum. These pattern of these movements may differ between the two eyes. Depending upon the pattern of movements, pendular nystagmus has been divided into different subtypes such as congenital nystagmus, acquired pendular nystagmus, and amaurotic nystagmus.

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.

Since this condition is usually coupled with other neurological disorders or deficits, there is no known cure for cerebral polyopia. However, measures can be taken to reduce the effects of associated disorders, which have proven to reduce the effects of polyopia. In a case of occipital lobe epilepsy, the patient experienced polyopia. Following administration of valproate sodium to reduce headaches, the patient’s polyopia was reduced to palinopsia. Further, after administering the anticonvulsant drug Gabapentin in addition to valproate sodium, the effects of palinopsia were decreased, as visual perseveration is suppressed by this anticonvulsant drug. Thus, in cases of epilepsy, anticonvulsant drugs may prove to reduce the effects of polyopia and palinopsia, a topic of which should be further studied.

In other cases of polyopia, it is necessary to determine all other present visual disturbances before attempting treatment. Neurological imaging can be performed to determine if there are present occipital or temporal lobe infarctions that may be causing the polyopia. CT scans are relatively insensitive to the presence of cerebral lesions, so other neurological imaging such as PET and MRI may be performed. The presence of seizures and epilepsy may also be assessed through EEG. In addition, motor visual function should be assessed through examination of pupillary reactions, ocular motility, optokinetic nystagmus, slit-lamp examination, visual field examination, visual acuity, stereo vision, bimicroscopic examination, and funduscopic examination. Once the performance of such functions have been assessed, a plan for treatment can follow accordingly. Further research should be conducted to determine if the treatment of associated neurological disturbances can reduce the effects of polyopia.

The number of cases is around 0.5 to 0.7 per 10,000 births, making it a relatively rare condition.

The pressure within the eye is maintained by the balance between the fluid that enters the eye through the ciliary body and the fluid that exits the eye through the trabecular meshwork.

Because the nerve emerges near the bottom of the brain, it is often the first nerve compressed when there is any rise in intracranial pressure. Different presentations of the condition, or associations with other conditions, can help to localize the site of the lesion along the VIth cranial nerve pathway.

The most common causes of VIth nerve palsy in adults are:

- More common: Vasculopathic (diabetes, hypertension, atherosclerosis), trauma, idiopathic.

- Less common: Increased intracranial pressure, giant cell arteritis, cavernous sinus mass (e.g. meningioma, Brain stem Glioblastoma aneurysm, metastasis), multiple sclerosis, sarcoidosis/vasculitis, postmyelography, lumbar puncture, stroke (usually not isolated), Chiari Malformation, hydrocephalus, intracranial hypertension, tuberculosis meningitis.

In children, Harley reports typical causes as traumatic, neoplastic (most commonly brainstem glioma), as well as idiopathic. Sixth nerve palsy causes the eyes to deviate inward (see: Pathophysiology of strabismus). Vallee et al. report that benign and rapidly recovering isolated VIth nerve palsy can occur in childhood, sometimes precipitated by ear, nose and throat infections.

Diagnosing CVI is difficult. A diagnosis is usually made when visual performance is poor but it is not possible to explain this from an eye examination. Before CVI was widely known among professionals, some would conclude that the patient was faking their problems or had for some reason engaged in self-deception. However, there are now testing techniques that do not depend on the patient's words and actions, such as fMRI scanning, or the use of electrodes to detect responses to stimuli in both the retina and the brain. These can be used to verify that the problem is indeed due to a malfunction of the visual cortex and/or the posterior visual pathway.

Cortical visual impairment (CVI) is a form of visual impairment that is caused by a brain problem rather than an eye problem. (The latter is sometimes termed "ocular visual impairment" when discussed in contrast to cortical visual impairment.) Some people have both CVI and a form of ocular visual impairment.

CVI is also sometimes known as cortical blindness, although most people with CVI are not totally blind. The term neurological visual impairment (NVI) covers both CVI and total cortical blindness. Delayed visual maturation, another form of NVI, is similar to CVI, except the child's visual difficulties resolve in a few months. Though the vision of a person with CVI may change, it rarely if ever becomes totally normal.

The major causes of CVI are as follows: asphyxia, hypoxia (a lack of sufficient oxygen in the body’s blood cells), or ischemia (not enough blood supply to the brain), all of which may occur during the birth process; developmental brain defects; head injury; hydrocephalus (when the cerebrospinal fluid does not circulate properly around the brain, and collects in the head, putting pressure on the brain); a stroke involving the occipital lobe; and infections of the central nervous system, such as meningitis and encephalitis.

Colobomas can be associated with a mutation in the "PAX2" gene.

Eye abnormalities have been shown to occur in over 90% of children with fetal alcohol syndrome.

The syndrome usually results from single unilateral lesion of the paramedian pontine reticular formation and the ipsilateral medial longitudinal fasciculus. An alternative anatomical cause is a lesion of the abducens nucleus (VI) on one side (resulting in a failure of abduction of the ipsilateral eye and adduction of the contralateral eye = conjugate gaze palsy towards affected side), with interruption of the ipsilateral medial longitudinal fasciculus after it has crossed the midline from its site of origin in the contralateral abducens (VI) nucleus (resulting in a failure of adduction of the ipsilateral eye).

The nerve dysfunction induces esotropia, a convergent squint on distance fixation. On near fixation the affected individual may have only a latent deviation and be able to maintain binocularity or have an esotropia of a smaller size. Patients sometimes adopt a face turned towards the side of the affected eye, moving the eye away from the field of action of the affected lateral rectus muscle, with the aim of controlling diplopia and maintaining binocular vision.

Diplopia is typically experienced by adults with VI nerve palsies, but children with the condition may not experience diplopia due to suppression. The neuroplasticity present in childhood allows the child to 'switch off' the information coming from one eye, thus relieving any diplopic symptoms. Whilst this is a positive adaptation in the short term, in the long term it can lead to a lack of appropriate development of the visual cortex giving rise to permanent visual loss in the suppressed eye; a condition known as amblyopia.

Ocular hypertension is the presence of elevated fluid pressure inside the eye (intraocular pressure), usually with no optic nerve damage or visual field loss.

For most individuals, the normal range of introcular pressure is between 10 mmHg and 21 mmHg. Elevated intraocular pressure is an important risk factor for glaucoma. The Ocular Hypertension Treatment Study, a large, multicentered, randomized clinical trial, determined that topical ocular hypotensive medication delays or prevents the onset of Primary Open-Angle Glaucoma. Accordingly, most individuals with consistently elevated intraocular pressures of greater than 21mmHg, particularly if they have other risk factors, are treated in an effort to prevent vision loss from glaucoma.