Concomitant esotropia – that is, an inward squint that does not vary with the direction of gaze – mostly sets in before 12 months of age (this constitutes 40% of all strabismus cases) or at the age of three or four. Most patients with "early-onset" concomitant esotropia are emmetropic, whereas most of the "later-onset" patients are hyperopic. It is the most frequent type of natural strabismus not only in humans, but also in monkeys.

Concomitant esotropia can itself be subdivided into esotropias that are ether "constant," or "intermittent."

- Constant esotropia

- Intermittent esotropia

A patient can have a constant esotropia for reading, but an intermittent esotropia for distance (but rarely vice versa).

The earliest sign of exotropia is usually a noticeable outward deviation of the eye. This sign may at first be intermittent, occurring when a child is daydreaming, not feeling well, or tired. It may also be more noticeable when the child looks at something in the distance. Squinting or frequent rubbing of the eyes is also common with exotropia. The child probably will not mention seeing double, i.e., double vision. However, he or she may close one eye to compensate for the problem.

Generally, exotropia progresses in frequency and duration. As the disorder progresses, the eyes will start to turn out when looking at close objects as well as those in the distance. If left untreated, the eye may turn out continually, causing a loss of binocular vision.

In young children with any form of strabismus, the brain may learn to ignore the misaligned eye's image and see only the image from the best-seeing eye. This is called amblyopia, or lazy eye, and results in a loss of binocular vision, impairing depth perception. In adults who develop strabismus, double vision sometimes occurs because the brain has already been trained to receive images from both eyes and cannot ignore the image from the turned eye.

Additionally in adults who have had exotropia since childhood, the brain may adapt to using a "blind-spot" whereby it receives images from both eyes, but no full image from the deviating eye, thus avoiding double vision and in fact increasing peripheral vision on the side of the deviating eye.

When observing a person with strabismus, the misalignment of the eyes may be quite apparent. A patient with a constant eye turn of significant magnitude is very easy to notice. However, a small magnitude or intermittent strabismus can easily be missed upon casual observation. In any case, an eye care professional can conduct various tests, such as cover testing, to determine the full extent of the strabismus.

Symptoms of strabismus include double vision and/or eye strain. To avoid double vision, the brain may adapt by ignoring one eye. In this case, often no noticeable symptoms are seen other than a minor loss of depth perception. This deficit may not be noticeable in someone who has had strabismus since birth or early childhood, as they have likely learned to judge depth and distances using monocular cues. However, a constant unilateral strabismus causing constant suppression is a risk for amblyopia in children. Small-angle and intermittent strabismus are more likely to cause disruptive visual symptoms. In addition to headaches and eye strain, symptoms may include an inability to read comfortably, fatigue when reading, and unstable or "jittery" vision.

Strabismus may also be classified based on time of onset, either congenital, acquired, or secondary to another pathological process. Many infants are born with their eyes slightly misaligned, and this is typically outgrown by six to 12 months of age. Acquired and secondary strabismus develop later. The onset of accommodative esotropia, an overconvergence of the eyes due to the effort of accommodation, is mostly in early childhood. Acquired non-accommodative strabismus and secondary strabismus are developed after normal binocular vision has developed. In adults with previously normal alignment, the onset of strabismus usually results in double vision.

Any disease that causes vision loss may also cause strabismus, but it can also result from any severe and/or traumatic injury to the affected eye. Sensory strabismus is strabismus due to vision loss or impairment, leading to horizontal, vertical or torsional misalignment or to a combination thereof, with the eye with poorer vision drifting slightly over time. Most often, the outcome is horizontal misalignment. Its direction depends on the patient age at which the damage occurs: patients whose vision is lost or impaired at birth are more likely to develop esotropia, whereas patients with acquired vision loss or impairment mostly develop exotropia. In the extreme, complete blindness in one eye generally leads to the blind eye reverting to an anatomical position of rest.

Although many possible causes of strabismus are known, among them severe and/or traumatic injuries to the afflicted eye, in many cases no specific cause can be identified. This last is typically the case when strabismus is present since early childhood.

Results of a U.S. cohort study indicate that the incidence of adult-onset strabismus increases with age, especially after the sixth decade of life, and peaks in the eighth decade of life, and that the lifetime risk of being diagnosed with adult-onset strabismus is approximately 4%.

Concomitant esotropias can arise as an initial problem, in which case they are designated as 'Primary,' as a consequence of loss or impairment of vision, in which case they are designated as 'Secondary,' or following overcorrection of an initial Exotropia in which case they are described as being 'Consecutive'. The vast majority of esotropias are primary.

Refractive amblyopia may result from anisometropia (unequal refractive error between the two eyes). Anisometropia exists when there is a difference in the power between the two eyes. The eye which provides the brain with a clearer image typically becomes the dominant eye. The image in the other eye is blurred, which results in abnormal development of one half of the visual system. Refractive amblyopia is usually less severe than strabismic amblyopia and is commonly missed by primary care physicians because of its less dramatic appearance and lack of obvious physical manifestation, such as with strabismus. Given that the refractive correction of anisometropia by means of spectacles typically leads to different image magnification for the two eyes, which may in turn prevent binocular vision, a refractive correction using contact lenses is to be considered. Also pediatric refractive surgery is a treatment option, in particular if conventional approaches have failed due to aniseikonia or lack of compliance or both.

Frequently, amblyopia is associated with a combination of anisometropia and strabismus. In some cases, the vision between the eyes can differ to the point where one eye has twice average vision while the other eye is completely blind.

Many people with amblyopia, especially those who only have a mild form, are not aware they have the condition until tested at older ages, since the vision in their stronger eye is normal. People typically have poor stereo vision, however, since it requires both eyes. Those with amblyopia further may have, on the affected eye, poor pattern recognition, poor visual acuity, and low sensitivity to contrast and motion.

Amblyopia is characterized by several functional abnormalities in spatial vision, including reductions in visual acuity, contrast sensitivity function, and vernier acuity, as well as spatial distortion, abnormal spatial interactions, and impaired contour detection. In addition, individuals with amblyopia suffer from binocular abnormalities such as impaired stereoacuity (stereoscopic acuity) and abnormal binocular summation. Also, a crowding phenomenon is present.

These deficits are usually specific to the amblyopic eye. However, subclinical deficits of the "better" eye have also been demonstrated.

People with amblyopia also have problems of binocular vision such as limited stereoscopic depth perception and usually have difficulty seeing the three-dimensional images in hidden stereoscopic displays such as autostereograms. Perception of depth, however, from monocular cues such as size, perspective, and motion parallax remains normal.

Exotropia is a form of strabismus where the eyes are deviated outward. It is the opposite of esotropia and usually involves more severe axis deviation than exophoria. People with exotropia often experience crossed diplopia. Intermittent exotropia is a fairly common condition. "Sensory exotropia" occurs in the presence of poor vision. Infantile exotropia (sometimes called "congenital exotropia") is seen during the first year of life, and is less common than "essential exotropia" which usually becomes apparent several years later.

The brain's ability to see three-dimensional objects depends on proper alignment of the eyes. When both eyes are properly aligned and aimed at the same target, the visual portion of the brain fuses the forms into a single image. When one eye turns inward, outward, upward, or downward, two different pictures are sent to the brain. This causes loss of depth perception and binocular vision. There have also been some reports of people that can "control" their afflicted eye. The term is from Greek "exo" meaning "outward" and "trope" meaning "a turning".

Diplopia can also occur when viewing with only one eye; this is called monocular diplopia, or, where the patient perceives more than two images, monocular polyopia. While there rarely may be serious causes behind monocular diplopia symptoms, this is much less often the case than with binocular diplopia. The differential diagnosis of multiple image perception includes the consideration of such conditions as corneal surface keratoconus, subluxation of the lens, a structural defect within the eye, a lesion in the anterior visual cortex or non-organic conditions, however diffraction-based (rather than geometrical) optical models have shown that common optical conditions, especially astigmatism, can also produce this symptom.

Temporary binocular diplopia can be caused by alcohol intoxication or head injuries, such as concussion (if temporary double vision does not resolve quickly, one should see an optometrist or ophthalmologist immediately). It can also be a side effect of benzodiazepines or opioids, particularly if used in larger doses for recreation, the anti-epileptic drugs Phenytoin and Zonisamide, and the anti-convulsant drug Lamotrigine, as well as the hypnotic drug Zolpidem and the dissociative drugs Ketamine and Dextromethorphan. Temporary diplopia can also be caused by tired and/or strained eye muscles or voluntarily. If diplopia appears with other symptoms such as fatigue and acute or chronic pain, the patient should see an ophthalmologist immediately.

"Cross-fixation congenital esotropia", also called "Cianci's syndrome" is a particular type of large-angle infantile esotropia associated with tight medius rectus muscles. With the tight muscles, which hinder adduction, there is a constant inward eye turn. The patient cross-fixates, that is, to fixate objects on the left, the patient looks across the nose with the right eye, and vice versa. The patient tends to adopt a head turn, turning the head to the right to better see objects in the left visual field and turning the head to the left to see those in the right visual field. Binasal occlusion can be used to discourage cross-fixation. However, the management of cross-fixation congenital esotropia usually involves surgery.

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

Anisometropia is the condition in which the two eyes have unequal refractive power. Each eye can be nearsighted (myopia), farsighted (hyperopia) or a combination of both, which is called antimetropia. Generally a difference in power of two diopters or more is the accepted threshold to label the condition anisometropia.

In certain types of anisometropia, the visual cortex of the brain will not use both eyes together (binocular vision), and will instead suppress the central vision of one of the eyes. If this occurs often enough during the first 10 years of life while the visual cortex is developing, it can result in amblyopia, a condition where even when correcting the refractive error properly, the person's vision in the affected eye is still not correctable to 20/20.

The name is from four Greek components: "an-" "not," "iso-" "same," "metr-" "measure," "ops" "eye."

An estimated 6% of subjects aged 6 to 18 have anisometropia.

People with early keratoconus typically notice a minor blurring of their vision and come to their clinician seeking corrective lenses for reading or driving. At early stages, the symptoms of keratoconus may be no different from those of any other refractive defect of the eye. As the disease progresses, vision deteriorates, sometimes rapidly. Visual acuity becomes impaired at all distances, and night vision is often poor. Some individuals have vision in one eye that is markedly worse than that in the other. The disease is often bilateral, though asymmetrical. Some develop photophobia (sensitivity to bright light), eye strain from squinting in order to read, or itching in the eye, but there is normally little or no sensation of pain. It may cause luminous objects to appear as cylindrical pipes with the same intensity at all points.

The classic symptom of keratoconus is the perception of multiple "ghost" images, known as monocular polyopia. This effect is most clearly seen with a high contrast field, such as a point of light on a dark background. Instead of seeing just one point, a person with keratoconus sees many images of the point, spread out in a chaotic pattern. This pattern does not typically change from day to day, but over time, it often takes on new forms. People also commonly notice streaking and flaring distortion around light sources. Some even notice the images moving relative to one another in time with their heart beat.

The predominant optical aberration of the eye in keratoconus is coma. The visual distortion experienced by the person comes from two sources, one being the irregular deformation of the surface of the cornea, and the other being scarring that occurs on its exposed highpoints. These factors act to form regions on the cornea that map an image to different locations on the retina. The effect can worsen in low light conditions, as the dark-adapted pupil dilates to expose more of the irregular surface of the cornea.

The eye, like any other optical system, suffers from a number of specific optical aberrations. The optical quality of the eye is limited by optical aberrations, diffraction and scatter. Correction of spherocylindrical refractive errors has been possible for nearly two centuries following Airy's development of methods to measure and correct ocular astigmatism. It has only recently become possible to measure the aberrations of the eye and with the advent of refractive surgery it might be possible to correct certain types of irregular astigmatism.

The appearance of visual complaints such as halos, glare and monocular diplopia after corneal refractive surgery has long been correlated with the induction of optical aberrations. Several mechanisms may explain the increase in the amount of higher-order aberrations with conventional eximer laser refractive procedures: a change in corneal shape toward oblateness or prolateness (after myopic and hyperopic ablations respectively), insufficient optical zone size and imperfect centration. These adverse effects are particularly noticeable when the pupil is large.

Exophoria can be caused by several factors, which include:

- Refractive errors - distance and near deviation approximately equal.

- Divergence excess - exodeviation is more than 15 dioptres greater for distance than near deviation.

- Convergence insufficiency - near exodeviation greater than distance deviation.

These can be due to nerve, muscle, or congenital problems, or due to mechanical anomalies. Unlike exotropia, fusion is possible in this condition, causing diplopia to be uncommon.

Keratoconus (KC) is a disorder of the eye which results in progressive thinning of the cornea. This may result in blurry vision, double vision, nearsightedness, astigmatism, and light sensitivity. Usually both eyes are affected. In more severe cases a scarring or a circle may be seen within the cornea.

While the cause is unknown, it is believed to occur due to a combination of genetic, environmental, and hormonal factors. About seven percent of those affected have a family history of the condition. Proposed environmental factors include rubbing the eyes and allergies. The underlying mechanism involves changes of the cornea to a cone shape. Diagnosis is by examination with a slit lamp.

Initially the condition can typically be corrected with glasses or soft contact lenses. As the disease worsens special contact lenses may be required. In most people the disease stabilizes after a few years without severe vision problems. In a small number of people scarring of the cornea occurs and a corneal transplantation is required.

Keratoconus affects about 1 in 2000 people. It occurs most commonly in late childhood to early adulthood. While it occurs in all populations it may be more frequent in certain ethnic groups such as those of Asian descent. The word is from the Greek "kéras" meaning cornea and the Latin "cōnus" meaning cone.

Symptom-producing, or pathological, scotomata may be due to a wide range of disease processes, affecting any part of the visual system, including the retina (in particular its most sensitive portion, the macula), the optic nerve and even the visual cortex. A pathological scotoma may involve any part of the visual field and may be of any shape or size. A scotoma may include and enlarge the normal blind spot. Even a small scotoma that happens to affect central or macular vision will produce a severe visual disability, whereas a large scotoma in the more peripheral part of a visual field may go unnoticed by the bearer because of the normal reduced optical resolution in the peripheral visual field.

Low order aberrations include Myopia (positive defocus), hyperopia (negative defocus), and regular astigmatism. Other lower-order aberrations are non- visually significant aberrations known as first order aberrations, such as prisms and zero-order aberrations (piston). Low order aberrations account for approximately 90% of the overall wave aberration in the eye.

Exophoria is particularly common in infancy and childhood, and increases with age.

Common causes of scotomata include demyelinating disease such as multiple sclerosis (retrobulbar neuritis), damage to nerve fiber layer in the retina (seen as cotton wool spots) due to hypertension, toxic substances such as methyl alcohol, ethambutol and quinine, nutritional deficiencies, vascular blockages either in the retina or in the optic nerve, stroke or other brain injury, and macular degeneration, often associated with aging. Scintillating scotoma is a common visual aura in migraine. Less common, but important because they are sometimes reversible or curable by surgery, are scotomata due to tumors such as those arising from the pituitary gland, which may compress the optic nerve or interfere with its blood supply.

Rarely, scotomata are . One important variety of bilateral scotoma may occur when a pituitary tumour begins to compress the optic chiasm (as distinct from a single optic nerve) and produces a bitemporal paracentral scotoma, and later, when the tumor enlarges, the scotomas extend out to the periphery to cause the characteristic bitemporal hemianopsia. This type of visual-field defect tends to be obvious to the person experiencing it but often evades early objective diagnosis, as it is more difficult to detect by cursory clinical examination than the classical or textbook bitemporal peripheral hemianopia and may even elude sophisticated electronic modes of visual-field assessment.

In a pregnant woman, scotomata can present as a symptom of severe preeclampsia, a form of pregnancy-induced hypertension. Similarly, scotomata may develop as a result of the increased intracranial pressure that occurs in malignant hypertension.

The scotoma is also caused by the aminoglycoside antibiotics mainly by Streptomycin.

A determination of the prevalence of anisometropia has several difficulties. First of all, the measurement of refractive error may vary from one measurement to the next. Secondly, different criteria have been employed to define anisometropia, and the boundary between anisometropia and isometropia depend on their definition.

Several studies have found that anisometropia occurs more frequently and tends to be more severe for persons with high ametropia, and that this is particularly true for myopes. Anisometropia follows a U-shape distribution according to age: it is frequent in infants aged only a few weeks, is more rare in young children, comparatively more frequent in teenagers and young adults, and more prevalent after presbyopia sets in, progressively increasing into old age.

One study estimated that 6% of those between the ages of 6 and 18 have anisometropia.

Notwithstanding research performed on the biomechanical, structural and optical characteristics of anisometropic eyes, the underlying reasons for anisometropia are still poorly understood.

Anisometropic persons who have strabismus are mostly far-sighted, and almost all of these have (or have had) esotropia. However, there are indications that anisometropia influences the long-term outcome of a surgical correction of an inward squint, and vice versa. More specifically, for patients with esotropia who undergo strabismus surgery, anisometropia may be one of the risk factors for developing consecutive exotropia and poor binocular function may be a risk factor for anisometropia to develop or increase.

Cerebral polyopia is most often associated with occipital or temporal lobe lesions, as well as occipital lobe epilepsy. This condition is relatively uncommon, thus further research regarding its causes and mechanism has not been performed. Polyopia can be experienced as partial second or multiple images to either side (or in any eccentricity) of an object at fixation. Polyopia occurs when both eyes are open, or when one eye is open, during fixation on a stimulus. Known cases of polyopia provide evidence that, in relation to the stimulus at fixation, multiple images can appear at a constant distance in any direction; gaps in portions of an object at fixation can exist; multiple images can be overlaid vertically, horizontally, or diagonally on top of the stimulus; and the multiple images can appear different sizes, alignments, and complexities. The complexity of the stimulus does not appear to affect the clarity of the multiple images. The physical distance of the stimulus from the patient (near or far) also does not seem to affect the presence of multiple images. However, if the stimulus is swung or moved, multiple images of that object can either be extinguished or transformed into different objects, depending on the severity of the condition.

The onset of polyopia is not immediate upon perception of visual stimuli; rather, it occurs within milliseconds to seconds of fixation upon a stimulus. Polyopia has been described by patients as images “suddenly multiplying.” These multiple images can drift, fade, and disappear, depending on the severity of the condition. These episodes of polyopia can last from seconds to hours. In one specific case, a patient described difficulties reading due to letters “run[ning] together” and momentarily disappearing.

Most cases of polyopia are accompanied by another neurological condition. Polyopia is often accompanied by visual field defects (such as the presence of a scotoma) or transient visual hallucinations. Polyopic images often form in the direction and position of such visual field defects. Current research shows that when stimuli are close to the patient’s scotoma, the latency of polyopic images is much shorter than if the stimuli was far from the scotoma, and there is a higher probability that polyopic images will result.

Aside from a complete inability to see color, individuals with complete achromatopsia have a number of other ophthalmologic aberrations. Included among these aberrations are greatly decreased visual acuity (<0.1 or 20/200) in daylight, Hemeralopia, nystagmus, and severe photophobia. The fundus of the eye appears completely normal. Also see Pingelap.

The syndrome is frequently noticed first in children around six months of age by their photophobic activity and/or their nystagmus. The nystagmus becomes less noticeable with age but the other symptoms of the syndrome become more relevant as school age approaches. Visual acuity and stability of the eye motions generally improve during the first 6–7 years of life (but remain near 20/200).

The congenital forms of the condition are considered stationary and do not worsen with age.

The five symptoms associated with achromatopsia/dyschromatopsia are:

- Achromatopsia

- Amblyopia (reduced visual acuity)

- Hemeralopia (with the subject exhibiting photophobia)

- Nystagmus

- Iris operating abnormalities

The syndrome of achromatopsia/dyschromatopsia is poorly described in current medical and neuro-ophthalmological texts. It became a common term following the popular book by the neuroscientist Oliver Sacks, ""The Island of the Colorblind"" in 1997. Up to that time most color-blind subjects were described as achromats or achromatopes. Those with a lesser degree of color perception abnormality were described as either protanopes, deuteranopes or tetartanopes (historically tritanopes).

Achromatopsia has also been called rod monochromacy and total congenital color blindness. Individuals with the congenital form of this condition show complete absence of cone cell activity via electroretinography at high light levels. There are at least four genetic causes of congenital ACHM, two of which involve cyclic nucleotide-gated ion channels (ACHM2/ACHM3), a third involves the cone photoreceptor transducin ("GNAT2", ACHM4), and the last remains unknown.