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.

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%.

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.

Accommodative esotropia (also called "refractive esotropia") is an inward turning of the eyes due to efforts of accommodation. It is often seen in patients with moderate amounts of hyperopia. The person with hyperopia, in an attempt to "accommodate" or focus the eyes, converges the eyes as well, as convergence is associated with activation of the accommodation reflex. The over-convergence associated with the extra accommodation required to overcome a hyperopic refractive error can precipitate a loss of binocular control and lead to the development of esotropia.

The chances of an esotropia developing in a hyperopic child will depend to some degree on the amount of hyperopia present. Where the degree of error is small, the child will typically be able to maintain control because the amount of over-accommodation required to produce clear vision is also small. Where the degree of hyperopia is large, the child may not be able to produce clear vision no matter how much extra-accommodation is exerted and thus no incentive exists for the over-accommodation and convergence that can give rise to the onset of esotropia. However, where the degree of error is small enough to allow the child to generate clear vision by over-accommodation, but large enough to disrupt their binocular control, esotropia will result.

Only about 20% of children with hyperopia greater than +3.5 diopters develop strabismus.

Where the esotropia is solely a consequence of uncorrected hyperopic refractive error, providing the child with the correct glasses and ensuring that these are worn all the time, is often enough to control the deviation. In such cases, known as 'fully accommodative esotropias,' the esotropia will only be seen when the child removes their glasses. Many adults with childhood esotropias of this type make use of contact lenses to control their 'squint.' Some undergo refractive surgery for this purpose.

A second type of accommodative esotropia also exists, known as 'convergence excess esotropia.' In this condition the child exerts excessive accommodative convergence relative to their accommodation. Thus, in such cases, even when all underlying hyperopic refractive errors have been corrected, the child will continue to squint when looking at very small objects or reading small print. Even though they are exerting a normal amount of accommodative or 'focusing' effort, the amount of convergence associated with this effort is excessive, thus giving rise to esotropia. In such cases an additional hyperopic correction is often prescribed in the form of bifocal lenses, to reduce the degree of accommodation, and hence convergence, being exerted. Many children will gradually learn to control their esotropias, sometimes with the help of orthoptic exercises. However, others will eventually require extra-ocular muscle surgery to resolve their problems.

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.

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.

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.

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.

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

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.

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.

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.

Though present from birth, symptoms of congenital fourth cranial nerve palsy may start as subtle and increase with age. Hence, diagnosis by a healthcare practitioner may not be made until later childhood or adulthood. Young children adopt a compensatory head position in order to compensate for the underacting superior oblique muscle. The characteristic head tilt is usually away from the affected side to reduce eye strain and prevent double vision (diplopia). Old photographs may reveal the presence of a consistent head tilt (ocular torticollis) from an early age. Most patients with congenital CN IV palsy have facial asymmetry due to the chronic head tilt. Other compensatory measures for congenital fourth nerve palsy are development of large vertical fusional amplitudes and lack of subjective symptoms of , even in the presence of great ocular rotation.

Congenital fourth nerve palsy may remain undetected until adulthood, when intermittent diplopia may arise, due to decompensated ability to overcome the vertical deviation. Until this occurs, many ophthalmologists and optometrists may miss the other signs and symptoms. Reduced vertical fusional reserves result from fatigue (stress, fever, other illnesses, a lot of near work) or simply the effects of old age. Diplopia from congenital fourth nerve palsy has occasionally been reported to manifest transiently during pregnancy. Congenital fourth nerve palsy may also become evident following cataract surgery once binocular vision is restored after a long period of progressive monocular visual loss and accompanying vergence decompensation. Other adult patients complain of neck pain, after years of chronic head tilting (ocular torticollis).

Congenital fourth nerve palsy can affect reading comprehension (and concentration during other near tasks) due to the increased vertical fusional demands and head tilting required to maintain single vision and prevent vertical diplopia. Some patients find they lose their place easily while reading, and find a marker or using a finger to guide them helpful.

The head posture is right 4th nerve palsy can be easily understood by this thumb rule- The body performs the action which the paralysed muscle had to perform. Keeping this thumb rule in mind, let us decipher the head posture in right 4th nerve palsy. As SO causes intorsion, the head tilts towards the left. As SO causes depression in adduction, the head turns towards left and depressed chin. So the patient has left side deflection, tilt and a downward gaze. The left SO palsy head posture can be understood similarly as well.

In the clinical setting, the principal difficulties in differential diagnosis arise as a consequence of the very early age at which patients with this condition first present. The clinician must be persistent in examining abduction and adduction, and in looking for any associated palpebral fissure changes or head postures, when attempting to determine whether what often presents as a common childhood squint (note-"squint" is a British term for two eyes not looking in the same direction) is in fact Duane syndrome. Fissure changes, and the other associated characteristics of Duane's such as up or down shoots and globe retraction, are also vital when deciding whether any abduction limitation is the result of Duane's and not a consequence of VI or abducens cranial nerve palsy.

Acquired Duane's syndrome is a rare event occurring after peripheral nerve palsy.

Many cases are asymptomatic, however patients many have decreased vision, glare, monocular diplopia or polyopia, and noticeable iris changes [2,6]. On exam patients have normal to decreased visual acuity, and a “beaten metal appearance” of the corneal endothelium, corneal edema, increased intraocular pressure, peripheral anterior synechiae, and iris changes [1,2,6].

The characteristic features of the syndrome are:

- Limitation of abduction (outward movement) of the affected eye.

- Less marked limitation of adduction (inward movement) of the same eye.

- Retraction of the eyeball into the socket on adduction, with associated narrowing of the palpebral fissure (eye closing).

- Widening of the palpebral fissure on attempted abduction. (N. B. Mein and Trimble point out that this is "probably of no significance" as the phenomenon also occurs in other conditions in which abduction is limited.)

- Poor convergence.

- A head turn to the side of the affected eye to compensate for the movement limitations of the eye(s) and to maintain binocular vision.

While usually isolated to the eye abnormalities, Duane syndrome can be associated with other problems including cervical spine abnormalities Klippel-Feil syndrome, Goldenhar syndrome, heterochromia, and congenital deafness.

- "For acquired fourth nerve palsy, see fourth nerve palsy"

Congenital fourth nerve palsy is a condition present at birth characterized by a vertical misalignment of the eyes due to a weakness or paralysis of the superior oblique muscle.

Other names for fourth nerve palsy include superior oblique palsy and trochlear nerve palsy.

When looking to the right/left the nerve/muscle isn't strong enough or is too long and the eye drifts up.

Iridocorneal Endothelial (ICE) syndromes are a spectrum of diseases characteriezed by slowly progressive abnormalities of the corneal endothelium and features including corneal edema, iris distortion, and secondary angle-closure glaucoma. [1,2,4] ICE syndromes are predominantly unilateral and nonhereditary [1,2,4]. The condition occurs in predominantly middle-aged women [1,3,4].