Medication is used for strabismus in certain circumstances. In 1989, the US FDA approved Botulinum toxin therapy for strabismus in patients over 12 years old. Most commonly used in adults, the technique is also used for treating children, in particular children affected by infantile esotropia. The toxin is injected in the stronger muscle, causing temporary and partial paralysis. The treatment may need to be repeated three to four months later once the paralysis wears off. Common side effects are double vision, droopy eyelid, overcorrection, and no effect. The side effects typically resolve also within three to four months. Botulinum toxin therapy has been reported to be similarly successful as strabismus surgery for people with binocular vision and less successful than surgery for those who have no binocular vision.

When strabismus is congenital or develops in infancy, it can cause amblyopia, in which the brain ignores input from the deviated eye. Even with therapy for amblyopia, stereoblindness may occur. The appearance of strabismus may also be a cosmetic problem. One study reported 85% of adult strabismus patients "reported that they had problems with work, school, and sports because of their strabismus." The same study also reported 70% said strabismus "had a negative effect on their self-image." A second operation is sometimes required to straighten the eyes.

Suppression may treated with vision therapy, though there is a wide range of opinions on long-term effectiveness between eye care professionals, with little scientific evidence of long-term improvement of suppression, if the underlying cause is not addressed (strabismus, amblyopia, etc.).

Young children with strabismus normally suppress the visual field of one eye (or part of it), whereas adults who develop strabismus normally do not suppress and therefore suffer from double vision (diplopia). This also means that adults (and older children) have a higher risk of post-operative diplopia after undergoing strabismus surgery than young children. Patients who have undergone strabismus surgery at a young age often have monofixation syndrome (with peripheral binocular fusion and a central suppression scotoma).

The prognosis for each patient with esotropia will depend upon the origin and classification of their condition. However, in general, management will take the following course:

1. Identify and treat any underlying systemic condition.

2. Prescribe any glasses required and allow the patient time to 'settle into' them.

3. Use occlusion to treat any amblyopia present and encourage alternation.

4. Where appropriate, orthoptic exercises can be used to attempt to restore binocularity.

5. Where appropriate, prismatic correction can be used, either temporarily or permanently, to relieve symptoms of double vision.

6. In specific cases, and primarily in adult patients, botulinum toxin can be used either as a permanent therapeutic approach, or as a temporary measure to prevent contracture of muscles prior to surgery

7. Where necessary, extra-ocular muscle surgery can be undertaken to improve cosmesis and, on occasion, restore binocularity.

The appropriate treatment for binocular diplopia will depend upon the cause of the condition producing the symptoms. Efforts must first be made to identify and treat the underlying cause of the problem. Treatment options include eye exercises, wearing an eye patch on alternative eyes, prism correction, and in more extreme situations, surgery or botulinum toxin.

If diplopia turns out to be intractable, it can be managed as last resort by obscuring part of the patient's field of view. This approach is outlined in the article on diplopia occurring in association with a condition called "horror fusionis".

According to a Cochrane review of 2012, controversies remain regarding type of surgery, non-surgical intervention and age of intervention.

The aims of treatment are as follows:

The elimination of any amblyopia

A cosmetically acceptable ocular alignment

long term stability of eye position

binocular cooperation.

It is essential that a child with strabismus is presented to the ophthalmologist as early as possible for diagnosis and treatment in order to allow best possible monocular and binocular vision to develop. Initially, the patient will have a full eye examination to identify any associated pathology, and any glasses required to optimise acuity will be prescribed – although infantile esotropia is not typically associated with refractive error. Studies have found that approximately 15% of infantile esotropia patients have accommodative esotropia. For these patients, antiaccommodative therapy (with spectacles) is indicated before any surgery as antiaccommodative therapy fully corrects their esotropia in many cases and significantly decreases their deviation angle in others.

Amblyopia will be treated via occlusion treatment (using patching or atropine drops) of the non-squinting eye with the aim of achieving full alternation of fixation. Management thereafter will be surgical. As alternative to surgery, also botulinum toxin therapy has been used in children with infantile esotropia. Furthermore, as accompaniment to ophtalmologic treatment, craniosacral therapy may be performed in order to relieve tension ("see also:" Management of strabismus).

A comprehensive eye examination including an ocular motility (i.e., eye movement) evaluation and an evaluation of the internal ocular structures will allow an eye doctor to accurately diagnose the exotropia. Although glasses and/or patching therapy, exercises, or prisms may reduce or help control the outward-turning eye in some children, surgery is often required.

There is a common form of exotropia known as "convergence insufficiency" that responds well to orthoptic vision therapy including exercises. This disorder is characterized by an inability of the eyes to work together when used for near viewing, such as reading. Instead of the eyes focusing together on the near object, one deviates outward.

"Consecutive exotropia" is an exotropia that arises after an initial esotropia. Most often it results from surgical overcorrection of the initial esotropia. It can be addressed with further surgery or with vision therapy; vision therapy has shown promising results if the consecutive exotropia is intermittent, alternating and of small magnitude. (Consecutive exotropia may however also spontaneously develop from esotropia, without surgery or botulinum toxin treatment.)

Because of the risks of surgery, and because about 35% of people require at least one more surgery, many people try vision therapy first. This consists of visual exercises. Although vision therapy is generally not covered by American health insurance companies, many large insurers such as Aetna have recently begun offering full or partial coverage in response to recent studies.

Strabismus surgery is sometimes recommended if the exotropia is present for more than half of each day or if the frequency is increasing over time. It is also indicated if a child has significant exotropia when reading or viewing near objects or if there is evidence that the eyes are losing their ability to work as a single unit (binocular vision). If none of these criteria are met, surgery may be postponed pending simple observation with or without some form of eyeglass and/or patching therapy. In very mild cases, there is a chance that the exotropia will diminish with time. The long-term success of surgical treatment for conditions such as intermittent exotropia is not well proven, and surgery can often result in a worsening of symptoms due to overcorrection. Evidence from the available literature suggests that unilateral surgery was more effective than bilateral surgery for individuals affected with intermittent exotropia.

The surgical procedure for the correction of exotropia involves making a small incision in the tissue covering the eye in order to reach the eye muscles. The appropriate muscles are then repositioned in order to allow the eye to move properly. The procedure is usually done under general anesthesia. Recovery time is rapid, and most people are able to resume normal activities within a few days. Following surgery, corrective eyeglasses may be needed and, in many cases, further surgery is required later to keep the eyes straight.

When a child requires surgery, the procedure is usually performed before the child attains school age. This is easier for the child and gives the eyes a better chance to work together. As with all surgery, there are some risks. However, strabismus surgery is usually a safe and effective treatment.

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.

Refractive surgery causes only minimal size differences, similar to contact lenses. In a study performed on 53 children who had amblyopia due to anisometropia, surgical correction of the anisometropia followed by strabismus surgery if required led to improved visual acuity and even to stereopsis in many of the children ("see:" Refractive surgery#Children).

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".

Management of this condition is surgical and typically involves reducing the strength of the superior rectus muscle or anterior transposition of the inferior oblique muscle of the affected eyes.

Several different surgical procedures exist for the correction of DVD including: inferior oblique anteriorization, inferior oblique anteriorization plus resection, superior rectus recession, superior rectus recession plus posterior fixation suture, and inferior oblique myectomy, though there is insufficient evidence to determine which procedure results in the best outcomes for patients.

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.

Dissociated vertical deviation (DVD) is an eye condition which occurs in association with a squint, typically infantile esotropia. The exact cause is unknown, although it is logical to assume it is from faulty innervation of eye muscles.

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".

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.

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.

Esophoria is an eye condition involving inward deviation of the eye, usually due to extra-ocular muscle imbalance. It is a type of heterophoria.

Causes include:

- Refractive errors

- Divergence insufficiency

- Convergence excess; this can be due to nerve, muscle, congenital or mechanical anomalies.

Unlike esotropia, fusion is possible and therefore diplopia is uncommon.

Congenital fourth cranial nerve palsy can be treated with strabismus surgery, where muscle attachment sites on the globe are modified to realign the eyes. Some eye doctors prefer conservative or no management of congenital fourth nerve palsy.

Other eye doctors recommend surgery early in a patient's life to prevent the compensatory torticollis and facial asymmetry that develop with age.

Prism lenses set to make minor optical changes in the vertical alignment may be prescribed instead of or after surgery to fine-tune the correction. Prism lenses do not address torsional misalignment and this may limit their use in certain cases. An additional consideration of prism lenses is that they must be worn at all times. Prism lenses reduce vertical fusional demands by allowing the eyes to rest in their vertically misaligned state. When they are removed the patient may experience vertical diplopia they find hard to resolve due to the rested state of their eyes.

Cases of congenital fourth nerve palsy vary in magnitude and way they affect the motion of the superior oblique muscle. Therefore different surgeries are available dependent upon the type of misalignment. Sometimes surgery on more than one eye muscle is required. In some simpler, unilateral cases a single surgery may suffice. In these cases the main problem is that the inferior oblique muscle of the same eye acts unopposed by the weakened superior oblique muscle, pulling the eye up. An example of a safe and effective procedure is a disinsertion of the inferior oblique muscle to allow it to reattach itself further down the globe of the eye. This acts to 'weaken' its action and allow the eye to move back into a more neutral alignment.

In all cases of congenital fourth nerve palsy, it is important to see an experienced strabismologist about management/treatment options. A strabismologist is an ophthalmologist (eye doctor) specialising in eye movement disorders.

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).

A scotoma (Greek σκότος/"skótos", "darkness"; plural: "scotomas" or "scotomata") is an area of partial alteration in the field of vision consisting of a partially diminished or entirely degenerated visual acuity that is surrounded by a field of normal – or relatively well-preserved – vision.

Every normal mammal eye has a scotoma in its field of vision, usually termed its blind spot. This is a location with no photoreceptor cells, where the retinal ganglion cell axons that compose the optic nerve exit the retina. This location is called the optic disc. There is no direct conscious awareness of visual scotomas. They are simply regions of reduced information within the visual field. Rather than recognizing an incomplete image, patients with scotomas report that things "disappear" on them.

The presence of the blind spot scotoma can be demonstrated subjectively by covering one eye, carefully holding fixation with the open eye, and placing an object (such as one's thumb) in the lateral and horizontal visual field, about 15 degrees from fixation (see the blind spot article). The size of the monocular scotoma is 5×7 degrees of visual angle.

A scotoma can be a symptom of damage to any part of the visual system, such as retinal damage from exposure to high-powered lasers, macular degeneration and brain damage.

The term "scotoma" is also used metaphorically in several fields. The common theme of all the figurative senses is of a gap not in visual function but in the mind's perception, cognition, or world view.

The first aims of management should be to identify and treat the cause of the condition, where this is possible, and to relieve the patient's symptoms, where present. In children, who rarely appreciate diplopia, the aim will be to maintain binocular vision and, thus, promote proper visual development.

Thereafter, a period of observation of around 9 to 12 months is appropriate before any further intervention, as some palsies will recover without the need for surgery.

This is most commonly achieved through the use of fresnel prisms. These slim flexible plastic prisms can be attached to the patient's glasses, or to plano glasses if the patient has no refractive error, and serve to compensate for the inward misalignment of the affected eye. Unfortunately, the prism only correct for a fixed degree of misalignment and, because the affected individual's degree of misalignment will vary depending upon their direction of gaze, they may still experience diplopia when looking to the affected side. The prisms are available in different strengths and the most appropriate one can be selected for each patient. However, in patients with large deviations, the thickness of the prism required may reduce vision so much that binocularity is not achievable. In such cases it may be more appropriate simply to occlude one eye temporarily. Occlusion would never be used in infants though both because of the risk of inducing stimulus deprivation amblyopia and because they do not experience diplopia.

Other management options at this initial stage include the use of botulinum toxin, which is injected into the ipsilateral medial rectus (botulinum toxin therapy of strabismus). The use of BT serves a number of purposes. Firstly, it helps to prevent the contracture of the medial rectus which might result from its acting unopposed for a long period. Secondly, by reducing the size of the deviation temporarily it might allow prismatic correction to be used where this was not previously possible, and, thirdly, by removing the pull of the medial rectus it may serve to reveal whether the palsy is partial or complete by allowing any residual movement capability of the lateral rectus to operate. Thus, the toxin works both therapeutically, by helping to reduce symptoms and enhancing the prospects for fuller ocular movements post-operatively, and diagnostically, by helping to determine the type of operation most appropriate for each patient.

Monofixation syndrome (MFS) (also: microtropia or microstrabismus) is an eye condition defined by less-than-perfect binocular vision. It is defined by a small angle deviation with suppression of the deviated eye and the presence of binocular peripheral fusion. That is, MFS implies peripheral fusion without central fusion.

Aside the manifest small-angle deviation ("tropia"), subjects with MFS often also have a large-angle latent deviation ("phoria"). Their stereoacuity is often in the range of 3000 to 70 arcsecond, and a small central suppression scotoma of 2 to 5 deg.

A rare condition, MFS is estimated to affect only 1% of the general population. There are three distinguishable forms of this condition: primary constant, primary decompensating, and consecutive MFS. It is believed that primary MFS is a result of a primary sensorial defect, predisposing to anomalous retinal correspondence.

Secondary MFS is a frequent outcome of surgical treatment of congenital esotropia. A study of 1981 showed MFS to result in the vast majority of cases if surgical alignment is reached before the age of 24 months and only in a minority of cases if it is reached later.

MFS was first described by Marshall Parks.