Fixation disparity exists when there is a small misalignment of the eyes when viewing with binocular vision. The misaligment may be vertical, horizontal or both. The misalignment (a few minutes of arc) is much smaller than that of strabismus, which prevents binocular vision, although it may reduce a patient's level of stereopsis. A patient may or may not have fixation disparity and a patient may have a different fixation disparity at distance than near.

Heterophoria is an eye condition in which the directions that the eyes are pointing at rest position, when "not" performing binocular fusion, are not the same as each other, or, "not straight". There can be esophoria, where the eyes tend to cross inward in the absence of fusion; exophoria, in which they diverge; or hyperphoria, in which one eye points up or down relative to the other. Phorias are known as 'latent squint' because the tendency of the eyes to deviate is kept latent by fusion. A person with two normal eyes has single vision (usually) because of the combined use of the sensory and motor systems. The motor system acts to point both eyes at the target of interest; any offset is detected visually (and the motor system corrects it). Heterophoria only occurs during dissociation of the left eye and right eye, when fusion of the eyes is absent. If you cover one eye (e.g. with your hand) you remove the sensory information about the eye's position in the orbit. Without this, there is no stimulus to binocular fusion, and the eye will move to a position of "rest". The difference between this position, and where it would be were the eye uncovered, is the heterophoria. The opposite of heterophoria, where the eyes are straight when relaxed and not fusing, is called orthophoria.

In contrast, fixation disparity is a very small deviation of the pointing directions of the eyes that is present while performing binocular fusion.

Heterophoria is usually asymptomatic. This is when it is said to be "compensated". When fusional reserve is used to compensate for heterophoria, it is known as compensating vergence. In severe cases, when the heterophoria is not overcome by fusional vergence, sign and symptoms appear. This is called decompensated heterophoria.

Heterophoria may lead to squint or also known as strabismus.

When the fusional vergence system can no longer hold back heterophoria, the phoria manifests. In this condition, the eyes deviate from the fixating position.

Retinal image size is determined by many factors. The size and position of the object being viewed affects the characteristics of the light entering the system. Corrective lenses affect these characteristics and are used commonly to correct refractive error. The optics of the eye including its refractive power and axial length also play a major role in retinal image size.

Aniseikonia can occur naturally or be induced by the correction of a refractive error, usually anisometropia (having significantly different refractive errors between each eye) or antimetropia (being myopic (nearsighted) in one eye and hyperopic (farsighted) in the other.) Meridional aniseikonia occurs when these refractive differences only occur in one meridian (see astigmatism). Refractive surgery can cause aniseikonia in much the same way that it is caused by glasses and contacts.

One cause of significant anisometropia and subsequent aniseikonia has been aphakia. Aphakic patients do not have a crystalline lens. The crystalline lens is often removed because of opacities called cataracts. The absence of this lens left the patient highly hyperopic (farsighted) in that eye. For some patients the removal was only performed on one eye, resulting in the anisometropia / aniseikonia. Today, this is rarely a problem because when the lens is removed in cataract surgery, an intraocular lens, or IOL is left in its place.

There are several methods to quantify fixation disparity. The Mallett card, the Bernell lantern slide, the Wesson Card and the Disparometer may be used. A patient's associated phoria is the amount of prism needed to reduce their fixation disparity to zero minutes of arc.

The Mallett Fixation Disparity Unit

Instrument used to measure the associated heterophoria (or compensating prism). It consists of a small central fixation letter X surrounded by two letters O, one on each side of X, the three letters being seen binocularly, and two coloured polarized vertical bars in line with the centre of the X which are seen by each eye separately. The instrument can be swung through 90° to measure any vertical fixation disparity. The associated phoria is indicated by the misalignment of the two polarized bars when the subject fixates the X through cross-polarized filters in front of the eyes. The amount of associated phoria is given by the value of the base-in or base-out prism power necessary to produce alignment and the eye. The unit can also be used to detect suppression. See Disparometer; associated heterophoria; uncompensated heterophoria.

When this magnification difference becomes excessive the effect can cause diplopia, suppression, disorientation, eyestrain, headache, and dizziness and balance disorders.

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.

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.

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).

Controversy has arisen regarding the selection and planning of surgical procedures, the timing of surgery and about what constitutes a favourable outcome.

1. Selection and planning

Some ophthalmologists, notably Ing and Helveston, favour a prescribed approach often involving multiple surgical episodes whereas others prefer to aim for full alignment of the eyes in one procedure and let the number of muscles operated upon during this procedure be determined by the size of the squint.

2. Timing and outcome

This debate relates to the technical anatomical difficulties of operating on the very young versus the possibility of an increased potential for binocularity associated with early surgery. Infants are often operated upon at the age of six to nine months of age and in some cases even earlier at three or four months of age. Some emphasize the importance of intervening early such as to keep the duration of the patient's abnormal visual experience to a minimum. Advocates of early surgery believe that those who have their surgery before the age of one are more likely to be able to use both eyes together post-operatively.

A Dutch study (ELISSS) compared early with late surgery in a prospective, controlled, non-randomized, multicenter trial and reported that:

"Children operated early had better gross stereopsis at age six as compared to children operated late. They had been operated more frequently, however, and a substantial number of children in both [originally-recruited] groups had not been operated at all."

Other studies also report better results with early surgery, notably Birch and Stager and Murray et al. but do not comment on the number of operations undertaken. A recent study on 38 children concluded that surgery for infantile esotropia is most likely to result in measureable stereopsis if patient age at alignment is not more than 16 months.

Another study found that for children with infantile esotropia early surgery decreases the risk of dissociated vertical deviation developing after surgery.

Aside the strabismus itself, there are other aspects or conditions that appear to improve after surgery or botulinum toxin eye alignment. Study outcomes have indicated that after surgery the child catches up in development of fine-motor skills (such as grasping a toy and handling a bottle) and of large-muscle skills (such as sitting, standing, and walking) in case a developmental delay was present before. Evidence also indicates that as of the age of six, strabismic children become less accepted by their peers, leaving them potentially exposed to social exclusion starting at this age unless their eye positioning is corrected by this time ("see also:" Psychosocial effects of strabismus).

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.

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).

Lenticonus (/len·ti·co·nus/ (len″tĭ-ko´nus)) [lens + L. conus, cone] is a rare congenital anomaly of the eye characterized by a conical protrusion on the crystalline lens capsule and the underlying cortex. It can reach a diameter of 2 to 7 mm. The conus may occur anteriorly or posteriorly. If the bulging is spherical, instead of conical, the condition is referred to as "lentiglobus". It produces a decrease in visual acuity and irregular refraction that cannot be corrected by either spectacle or contact lenses.

Biomicroscopically "lenticonus" is characterized by a transparent, localized, sharply demarcated conical projection of the lens capsule and cortex, usually axial in localization. In an early stage, retro-illumination shows an «oil droplet» configuration. Using a narrow slit, the image of a conus is observed. In a more advanced stage associated subcapsular and cortical opacities appear. Retinoscopically the oil droplet produces a pathognomonic scissors movement of the light reflex. This phenomenon is due to the different refraction in the central and the peripheral area of the lens. Ultrasonography also can illustrate the existence of a "lenticonus". A-scan ultrasonography may reveal an increased lens thickness and B- scanultrasonography may show herniated lenticular material, suggestive of a lenticonus. Amblyopia, cataract, strabismus and loss of central fixation may be observed in association with lenticonus posterior. Cataract, flecked retinopathy, posterior polymorphous dystrophy and corneal arcus juvenilis may be encountered in association with lenticonus anterior that occurs as a part of the Alport syndrome.

Exist two distinct types of "lenticonus" based on the face of the lens affected.

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.

Entomopia (from the Greek roots for "insect" and "eye"), is a form of polyopia in which a grid-like pattern of multiple copies of the same visual image is seen.

Entomopia may be due to disease of the occipital lobe, defects in visual integration and fixation or incomplete visual processing due to poor visuospatial localisation in the hemianopic field, although its causes are unknown. Reassurance may be the only treatment.

Palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is the persistent recurrence of a visual image after the stimulus has been removed. Palinopsia is not a diagnosis, it is a diverse group of pathological visual symptoms with a wide variety of causes. Visual perseveration is synonymous with palinopsia.

In 2014, Gersztenkorn and Lee comprehensively reviewed all cases of palinopsia in the literature and subdivided it into two clinically relevant groups: illusory palinopsia and hallucinatory palinopsia. Hallucinatory palinopsia, usually due to seizures or posterior cortical lesions, describes afterimages that are formed, long-lasting, and high resolution. Illusory palinopsia, usually due to migraines, head trauma, prescription drugs, or hallucinogen persisting perception disorder (HPPD), describes afterimages that are affected by ambient light and motion and are unformed, indistinct, or low resolution.

Illusory palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is a subtype of palinopsia, a visual disturbance defined as the persistence or recurrence of a visual image after the stimulus has been removed. Palinopsia is a broad term describing a heterogeneous group of symptoms, which is divided into hallucinatory palinopsia and illusory palinopsia. Illusory palinopsia is likely due to sustained awareness of a stimulus and is similar to a visual illusion: the distorted perception of a real external stimulus.

Illusory palinopsia is caused by migraines, hallucinogen persisting perception disorder (HPPD), prescription drugs, and head trauma, but is also sometimes idiopathic. Illusory palinopsia consists of afterimages that are short-lived or unformed, occur at the same location in the visual field as the original stimulus, and are often exposed or exacerbated based on environmental parameters such as stimulus intensity, background contrast, fixation, and movement. Illusory palinopsia symptoms occur continuously or predictably, based on environmental conditions.

Of the published cases of palinopsia that are idiopathic or attributed to migraines, HPPD, prescription drugs, or head trauma, 94% described illusory palinopsia. Trazodone, nefazodone, mirtazapine, topiramate, clomiphene, oral contraceptives, and risperidone have been reported to cause illusory palinopsia. Clomiphene and oral contraceptives are the only prescription drugs reported to cause permanent symptoms. HPPD is most common after LSD ingestion, but can occur after any hallucinogen use. HPPD is commonly described in psychiatric literature and illusory palinopsia symptoms are sometimes not defined as palinopsia. It is not clear if there is a relationship between HPPD and the quantity and strength of hallucinogen doses taken.

Posterior visual pathway cortical lesions (tumor, abscess, hemorrhage, infarction, arteriovenous malformation, cortical dysplasia, aneurysm) and various seizure causes (hyperglycemia, ion channel mutations, Creutzfeldt–Jakob disease, idiopathic seizures, etc.) cause focal cortical hyperactivity or hyperexcitability, resulting in inappropriate, persistent activation of a visual memory circuit.

Illusory palinopsia is a dysfunction of visual perception, resulting from diffuse, persistent alterations in neuronal excitability that affect physiological mechanisms of light or motion perception. Illusory palinopsia is caused by migraines, HPPD, prescription drugs, head trauma, or may be idiopathic. Trazodone, nefazodone, mirtazepine, topiramate, clomiphene, oral contraceptives, and risperidone have been reported to cause illusory palinopsia. A patient frequently has multiple types of illusory palinopsia, which represent dysfunctions in both light and motion perception. Light and motion are processed via different pathways, suggesting diffuse or global excitability alterations.

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

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.

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.

Multiple evanescent white dot syndrome (MEWDS) is an uncommon inflammatory condition of the retina that typically affects otherwise healthy young females in the second to fourth decades of life.

The typical patient with MEWDS is a healthy middle aged female age 15-50. There is a gender disparity as women are affected with MEWDS four times more often than men. Roughly 30% of patients have experienced an associated viral prodrome. Patients present with acute, painless, unilateral change in vision.

MEWDS is a self limited disease with excellent visual recovery within 2-10 weeks. However residual symptoms including photopsia may persist for months.

The predominant cause of nutritional optic neuropathy is thought to be deficiency of B-complex vitamins, particularly thiamine (vitamin B), cyanocobalamin (vitamin B) and recently copper Deficiency of pyridoxine (vitamin B), niacin (vitamin B), riboflavin (vitamin B), and/or folic acid also seems to play a role. Those individuals who abuse alcohol and tobacco are at greater risk because they tend to be malnourished. Those with pernicious anemia are also at risk due to an impaired ability to absorb vitamin B from the intestinal tract.