Strabismus (Misaligned Eyes)

Strabismus, commonly called misaligned eyes, crossed eyes, or wandering eye, is a group of oculomotor disorders in which the two eyes do not point at the same object at the same time. In a healthy visual system, both eyes aim at the same target simultaneously, allowing the brain to fuse the two images into a single, three-dimensional picture with depth perception. In strabismus, one eye points in a different direction—inward, outward, upward, or downward—either constantly or intermittently.

Strabismus is not a single condition. It is an umbrella term for dozens of distinct oculomotor disorders that vary by the direction of the eye turn, what is causing it, when it developed, and how consistently the misalignment is present. About 75–95% of all strabismus cases are developmental—caused by problems in the central brain pathways that govern visual coordination—rather than by disease of the eye muscles themselves. The remainder result from neurological conditions, structural muscle problems, genetic syndromes, or mechanical restrictions inside the eye socket.

Strabismus affects approximately 2–6% of people worldwide and 2–4% of children in the United States, making it the most common reason for a pediatric ophthalmology visit. It is closely associated with amblyopia (lazy eye)—a condition in which one eye develops poorer vision than the other because the brain learns to ignore the input from the deviating eye. Amblyopia is the leading preventable cause of unilateral vision loss in children. About half of children with esotropia (inward-turning eye) and about one quarter of those with exotropia (outward-turning eye) also develop amblyopia. Strabismus is significantly more common in children with Down syndrome (affecting about 30%) and in children with cerebral palsy (affecting about 28–34%).

Doctors classify strabismus by the direction of the eye turn, whether the deviation stays constant in all gaze directions (comitant) or changes (incomitant), when it developed, how often it occurs, and what is causing it. The major types are described below.

Esotropia is a strabismus in which one or both eyes turn inward toward the nose. It is the dominant form in children under age 6, accounting for 52–76% of all strabismus in this age group.

• Infantile (congenital) esotropia: onset by 6 months of age. The inward turn is large, constant, and not caused by uncorrected farsightedness. Glasses do not help; surgical correction is required early. Associated features include a spontaneous upward drift of one eye when the other is covered (dissociated vertical deviation—DVD) and jerky eye movements (latent nystagmus).
• Fully refractive accommodative esotropia: caused entirely by uncorrected farsightedness (hyperopia). The extra focusing effort the eye makes to see clearly triggers an excessive inward convergence drive. Correcting the farsightedness with glasses eliminates the esotropia completely without surgery. Develops typically between ages 2 and 4.
• Partially refractive accommodative esotropia: Glasses reduce but do not fully correct the eye turn. Surgery is required in addition to glasses for the remaining angle.
• High accommodative convergence/accommodation (AC/A) ratio esotropia (convergence excess): The eye turns inward much more for near than for distance tasks. Bifocal glasses that reduce the near focusing effort are the primary treatment.
• Acute-onset esotropia in adults: sudden inward turn in an adult, particularly one who is very nearsighted. Brain magnetic resonance imaging (MRI) is required to exclude an intracranial cause before a benign diagnosis is assumed.
• Sensory esotropia: an inward drift in an eye that has reduced vision from another cause—cataract, corneal scar, or optic nerve damage. An eye that cannot see clearly tends to drift inward.

Exotropia is a strabismus in which one or both eyes turn outward. It becomes the dominant form by adolescence, accounting for about 76% of strabismus in teenagers.

• Intermittent exotropia (IXT): the most common type of outward eye turn, present in approximately 25% of all strabismus cases and about 1% of the general population. The eye drifts outward only intermittently—often in bright sunlight, when tired, or during daydreaming—but fuses correctly at other times. Children frequently close one eye outdoors in bright light. Treatment ranges from observation to glasses, patching, vision therapy, and surgery.
• Constant exotropia: The outward turn is present all the time at all distances. This often represents an intermittent exotropia that has lost its ability to control the deviation, or a sensory exotropia from a visually impaired eye.
• Convergence insufficiency: The eyes cannot converge adequately for near tasks like reading, causing strain and outward drift at near range. Common in teenagers and adults. It produces headaches, blurred near vision, and difficulty concentrating. Treated with convergence exercises or prism glasses.

• Hypertropia: One eye drifts upward relative to the other. The most common cause is fourth cranial nerve (trochlear nerve) palsy, which weakens the superior oblique muscle. It causes vertical and torsional double vision, and many patients tilt their head to the opposite shoulder to compensate.
• Dissociated vertical deviation (DVD): a spontaneous upward drifting of one eye when it is not actively fixating. Associated with infantile esotropia. It does not follow the usual rules of eye muscle balance and is often mild enough not to require treatment.

Congenital cranial dysinnervation disorders (CCDDs) are rare congenital strabismus syndromes caused by the failure of specific cranial nerves to develop normally before birth, producing stable abnormal eye movements from birth.

• Duane retraction syndrome: The sixth cranial nerve fails to develop, and the third cranial nerve abnormally innervates the lateral rectus muscle. When the eye turns inward, both nerve signals fire at once, causing the eye to retract into the socket and the eyelid opening to narrow. Most patients use a compensatory head turn to maintain single vision in their primary gaze direction.
• Congenital fibrosis of extraocular muscles (CFEOM): three genetic subtypes (CFEOM1: KIF21A mutation; CFEOM2: PHOX2A mutation; CFEOM3: TUBB3 mutation) in which abnormal nerve development leaves the extraocular muscles stiff and the eyes fixed in a downward or outward position from birth. All are associated with bilateral eyelid drooping (ptosis).
• Mobius syndrome: failure of the sixth and seventh cranial nerves to develop normally. Affected individuals have an expressionless face, inability to look sideways, and an inward-turning eye, associated with PLXND1 and REV3L gene mutations.

• Third cranial nerve (oculomotor) palsy: causes eyelid drooping, an eye that drifts outward and downward, and—when caused by an aneurysm compressing the nerve—a large, non-reactive (dilated) pupil. This combination of eye movement paralysis and a dilated pupil is a neurological emergency.
• Fourth cranial nerve (trochlear) palsy: the most common isolated cranial nerve palsy. Causes vertical and torsional double vision with a head tilt. May be congenital or acquired from trauma or microvascular disease.
• Sixth cranial nerve (abducens) palsy: causes an inward-turning eye with inability to look outward. Results from elevated intracranial pressure, trauma, brainstem lesions, or diabetic microvascular disease.

• Thyroid eye disease-related strabismus: the most common cause of restrictive strabismus in adults. Fibrosis of the inferior rectus muscle prevents the eye from looking upward, causing it to sit lower than normal. Surgery is performed only after the disease has been inactive for at least six months.
• Orbital blowout fracture: a fracture of the orbital floor that traps the inferior rectus muscle in the fracture gap, restricting upward gaze and causing double vision. Surgical repair of the fracture releases the muscle.
• Sagging eye syndrome: age-related degeneration of the connective tissue pulleys that direct the path of the lateral rectus muscle, causing a slowly progressive horizontal and/or vertical deviation in older adults. Diagnosed on orbital MRI.

The causes of strabismus differ substantially by type. In the majority of cases, the underlying problem lies in the brain’s systems for coordinating eye movement and binocular fusion—not in the eye muscles themselves.

The brain’s precise control of binocular alignment is a complex, learned process that develops during the first years of life. Functional magnetic resonance imaging (MRI) and structural brain imaging in people with comitant strabismus show reduced gray matter volume in the visual cortex and parietal regions responsible for spatial processing and oculomotor control—confirming that the brain is genuinely different in affected individuals. In premature infants, white matter damage around the brain’s ventricles (periventricular leukomalacia—PVL) disrupts the cortical pathways that control eye alignment, which is one of the key reasons strabismus is so much more prevalent in children with cerebral palsy.

Uncorrected farsightedness (hyperopia) is the most important refractive cause of strabismus. When a farsighted eye focuses, it triggers an accommodative convergence drive that can overwhelm the brain’s ability to keep the eyes aligned. Children with hyperopia of 5 diopters or more have approximately 122 times the esotropia risk of those with little or no farsightedness. Nearsightedness (myopia) is linearly associated with exotropia. Unequal refractive error between the two eyes (anisometropia) disrupts binocular balance and independently raises strabismus risk.

About 30% of strabismus patients have a first-degree relative with the condition. For CCDDs and congenital fibrosis syndromes, specific mutations have been identified: KIF21A for CFEOM1, PHOX2A for CFEOM2, TUBB3 for CFEOM3, and CHN1 for some cases of Duane retraction syndrome. For common esotropia and exotropia, susceptibility loci have been identified on chromosomes 4 and 7, and gene expression studies show that 25% of muscle-specific genes are abnormally expressed in the eye muscles of strabismic patients.

Maternal smoking during pregnancy disrupts fetal cortical development in oculomotor brain regions and is statistically associated with increased strabismus risk in offspring. Maternal alcohol and drug exposure during pregnancy also impairs central nervous system (CNS) oculomotor development. Premature birth creates multiple strabismus risk pathways through retinopathy of prematurity, periventricular leukomalacia, and general CNS immaturity.

Physical restrictions inside the orbit prevent normal eye alignment in several conditions. Thyroid eye disease causes glycosaminoglycan accumulation in the extraocular muscles, leading to fibrosis and restricted movement. Orbital fractures trap muscles in fracture gaps. Age-related connective tissue degeneration causes sagging eye syndrome. Cranial nerve damage from stroke, head injury, tumor, vascular disease, or elevated intracranial pressure causes paralytic strabismus in adults.

Strabismus can develop without any known risk factors, but the following characteristics are associated with significantly higher likelihood.

• Family history: About 30% of esotropia patients and 20% of exotropia patients have a first-degree relative with strabismus, indicating strong familial aggregation.
• Uncorrected farsightedness (hyperopia): About 59% of all children with esotropia have hyperopia of 3 diopters or more. Significant farsightedness in a young child should trigger ophthalmological monitoring even before strabismus appears.
• Premature birth: present in about 12.5% of esotropia cases and about 6% of exotropia cases. Prematurity affects the developing brain and retina through multiple mechanisms.
• Neonatal intensive care unit (NICU) admission: A history of NICU stay is present in about 10% of both esotropia and exotropia patients.
• Neurological conditions: Down syndrome, cerebral palsy, intellectual disability, and seizure disorders dramatically increase strabismus prevalence. Down syndrome carries approximately a 30% rate; cerebral palsy approximately 28–34%.
• Congenital cataract or other visual deprivation: When one eye cannot see clearly from birth, it tends to drift (sensory strabismus) and develop amblyopia. Prompt treatment is essential.
• Maternal smoking during pregnancy: This is statistically associated with increased strabismus risk in offspring through disruption of fetal cortical development.

• Diabetes mellitus: Diabetic microvascular disease can damage cranial nerves supplying the extraocular muscles, causing sudden-onset paralytic strabismus.
• Hypertension and cardiovascular disease: These share vascular risk factors with cranial nerve microvascular palsies.
• Thyroid disease (Graves’ disease): This is the most common cause of new-onset strabismus in adults through orbital muscle fibrosis.
• Head or orbital trauma: This can cause direct muscle injury and cranial nerve damage.
• Stroke or intracranial tumor: Damage to the brainstem or oculomotor pathways produces paralytic strabismus.
• High myopia: Very high nearsightedness (greater than 8 diopters) is associated with sagging eye syndrome and heavy eye syndrome, causing mechanical esotropia.

Early detection of strabismus and amblyopia is one of the most important goals in pediatric eye care. The window for preventing permanent vision loss from amblyopia closes during the critical period of visual development—roughly by age 7 to 9. Screening begins at birth and continues through school age.

The red reflex test is performed at every well-child visit starting in the newborn nursery. The doctor shines a light into the baby’s eyes and looks for a symmetric reddish-orange glow in both pupils. An absent, white, or asymmetric reflex requires urgent ophthalmological referral. The corneal light reflex test at the 6-month well-child visit checks whether a penlight reflection falls symmetrically on the center of each pupil—an off-center reflection indicates possible misalignment. The cover-uncover test—in which each eye is alternately covered while the examiner watches for movement of the uncovered eye—is the gold standard for detecting manifest strabismus in children old enough to cooperate.

The American Academy of Pediatrics recommends instrument-based vision screening using handheld devices (such as the Welch Allyn SPOT Vision Screener, Plusoptix, or Pediatric Vision Scanner) at well-child visits at ages 12 months, 3, 4, and 5 years. These devices can detect refractive errors, unequal focus, and fixation asymmetry before visual development is permanently compromised. Children at higher risk—those with a family history of strabismus, Down syndrome, cerebral palsy, prematurity, or history of congenital cataract—should have a comprehensive ophthalmological exam by age 6 months.

• Correct refractive errors with glasses early: Prescribing glasses for significant farsightedness in young children reduces the accommodative convergence driving esotropia and lowers amblyopia risk.
• Treat amblyopia promptly: Patching or blurring the stronger eye during the sensitive period of visual development is the most effective way to prevent permanent vision loss from amblyopia.
• Avoid smoking during pregnancy: Maternal smoking is associated with increased strabismus risk in offspring. Cessation before or during pregnancy reduces this risk.
• Maintain euthyroidism in Graves’ disease: Controlling thyroid hormone levels reduces the risk of thyroid eye disease-related restrictive strabismus in adults.
• Manage cardiovascular and diabetic risk factors: Reducing blood pressure, blood sugar, and cholesterol lowers the risk of microvascular cranial nerve palsies that cause acquired paralytic strabismus.
• Attend scheduled well-child visits: Consistent pediatric care ensures screening catches strabismus and amblyopia risk factors early, when treatment is most effective.

The most obvious sign of strabismus is an eye that appears to turn in a different direction than the other. However, not all strabismus is visible—particularly intermittent forms that only misalign in certain conditions, or small-angle deviations that are subtle even to trained observers. Symptoms depend on age, severity, and whether the brain has learned to suppress (actively ignore) the image from the deviating eye to avoid double vision.

• A visible eye turn: One eye appears to point inward, outward, upward, or downward compared to the other. In intermittent forms, this may only be apparent when the child is tired, in bright light, or daydreaming.
• Closing one eye in bright light: a hallmark behavior of intermittent exotropia. The child closes one eye outdoors to avoid the blur or double vision from the drifting eye.
• Head tilt or turn: Children with fourth nerve palsy tilt their heads to one side to align the eyes and maintain single vision. Children with Duane syndrome often turn toward the affected side.
• Squinting or frowning: The child may scrunch one eye, particularly during near tasks or in bright conditions, to suppress the deviating eye.
• Frequent eye rubbing or complaints of tired eyes: This is particularly noticeable with near work, reflecting the visual effort needed to maintain alignment.
• Difficulty with depth perception: This may present as falling more than peers, struggling with catching balls, or seeming unaware of spatial relationships.
• Reduced vision in one eye (amblyopia): usually not noticed by the child. Detected when vision screening shows the child reads the chart less well with one eye covered.
• Reading difficulties and headaches: In older children, convergence insufficiency causes eyestrain, blurred vision with reading, headaches, and difficulty sustaining attention.

• Double vision (diplopia): Adults who develop strabismus after visual maturity almost always experience double vision because the adult brain cannot suppress a second image the way a child’s brain can. Sudden-onset double vision in an adult requires urgent evaluation to exclude neurological causes.
• Eye strain and headaches: These are particularly common with convergence insufficiency; the visual system works constantly to maintain alignment, causing fatigue with sustained near tasks.
• Reduced depth perception: Even in long-standing strabismus, reduced stereopsis affects tasks requiring accurate spatial judgment.
• Psychosocial impact: Studies consistently document reduced quality of life, social difficulties, and higher rates of anxiety and depression in adults with untreated or residual strabismus, reflecting the significant interpersonal consequences of visible eye misalignment.

• In infants under 6 months: Some intermittent drifting is normal as the visual system matures. Any constant or large-angle deviation by 3 months, or any eye turn that persists past 6 months, is abnormal and should be evaluated.
• In children 6 months to 6 years: the critical period for visual development. Strabismus during this period carries the highest risk for permanent amblyopia. Children in this age range rarely complain of double vision—the brain suppresses the second image. Watch for the behavioral signs described above.
• In school-age children and adolescents: Convergence insufficiency becomes more prevalent as reading demands increase. Intermittent exotropia often worsens. Children may report words jumping, blurring during reading, or needing to re-read lines.
• In adults over 50: Acquired strabismus is often caused by microvascular cranial nerve palsy (from diabetes or hypertension), sagging eye syndrome, or thyroid eye disease. Any new-onset double vision in this age group requires neuroimaging and systemic evaluation.

Strabismus is diagnosed and managed by a pediatric ophthalmologist, a strabismologist (an ophthalmologist specializing in eye movement disorders), or an orthoptist. The diagnostic process establishes the type and size of the deviation, identifies the cause, assesses visual acuity and binocularity, and guides treatment. In adults with acquired strabismus, neuroimaging and systemic testing are essential to exclude serious underlying causes.

Measuring visual acuity in each eye separately identifies amblyopia and quantifies visual inequality between the eyes. Cycloplegic refraction—using dilating drops to temporarily relax the focusing muscle—reveals the true refractive error, particularly any hidden farsightedness that could be driving accommodative esotropia. Identifying and fully correcting the refractive error with glasses is essential before measuring the residual angle of deviation and planning surgery.

• Cover-uncover test: the gold standard for detecting manifest strabismus. The examiner covers one eye and watches whether the other eye moves to take up fixation. Any movement confirms a manifest deviation. Repeated for both eyes and at near and distance.
• Alternate prism cover test (APCT): the gold standard for measuring the total angle of deviation. Prisms are placed before the deviating eye while the examiner alternately covers each eye until no movement is seen. The prism power required to neutralize movement gives the total deviation in prism diopters, measured at near and distance.

Randot, Frisby, Lang, and TNO stereotest cards measure depth perception (stereoacuity)—how precisely the visual system detects differences in depth between the two eyes. Normal distance stereoacuity is approximately 40 arc seconds; reduced stereoacuity reflects the degree to which strabismus has disrupted binocular fusion. Distance stereo testing is particularly sensitive for detecting intermittent exotropia.

Eye movements are tested in all nine gaze positions to determine whether the angle of deviation changes with gaze direction—identifying incomitant strabismus caused by a specific muscle or cranial nerve problem. The Parks-Bielschowsky three-step test is a standardized three-question examination used specifically to confirm and identify fourth cranial nerve palsy as the cause of a vertical deviation.

Brain and orbital MRI is required for all cases of acquired adult strabismus, new-onset diplopia, and any feature suggesting a non-benign cause. Computed tomography (CT) angiography or magnetic resonance (MR) angiography is performed urgently when a third cranial nerve palsy with pupil involvement is present, due to concern for a posterior communicating artery aneurysm. In suspected thyroid eye disease, orbital CT shows the characteristic muscle belly enlargement with tendon sparing. In adults with new-onset oculomotor palsy: fasting blood glucose and HbA1c for diabetes, thyroid function tests and thyroid receptor antibodies (TRAbs) for thyroid eye disease, and erythrocyte sedimentation rate/C-reactive protein (ESR/CRP) for inflammatory causes.

Strabismus does not resolve on its own, and untreated strabismus can result in permanent amblyopia and lifelong loss of depth perception. Treatment begins as soon as the diagnosis is confirmed, at any age, and typically involves a combination of glasses, occlusion therapy, vision exercises, pharmacologic treatment, and surgery. The specific plan depends on the type and cause of the strabismus, the patient’s age, the size of the deviation, and whether amblyopia is present. For adults, treatment goals include eliminating double vision, restoring comfortable binocular vision, and improving eye alignment.

For accommodative esotropia—the form driven by uncorrected farsightedness—glasses are the primary and often the sole treatment. Providing the full hyperopic correction eliminates the accommodative convergence that is driving the inward turn. In fully accommodative esotropia, glasses alone straighten the eyes completely without surgery. Bifocal glasses are used when the deviation is significantly greater at near than at distance (convergence excess esotropia)—the added bifocal reduces near convergence demand. For convergence insufficiency, plus-power reading glasses reduce the near focusing demand. Prism lenses can neutralize double vision in small-angle adult strabismus and cranial nerve palsies while awaiting recovery or surgery.

Treating amblyopia is always the first priority when it is present, because no amount of eye alignment surgery will restore vision to an amblyopic eye after the critical period has passed. Patching (occlusion therapy) places an adhesive patch over the stronger eye for a prescribed number of hours daily, forcing the brain to use the weaker eye. Atropine penalization uses atropine eye drops in the stronger eye to blur its near vision and similarly redirect the brain’s reliance to the weaker eye. Both approaches are equally effective in moderate amblyopia. Engaging the amblyopic eye in near activities—drawing, puzzles, handheld games—during patching time accelerates improvement. Treatment can produce meaningful improvement up to age 12 to 14 in some patients, though earlier is always better.

Botulinum toxin A (Botox®) injected directly into an overacting extraocular muscle temporarily paralyzes it for approximately three to four months, allowing the opposing muscle to strengthen and the eye to shift position. In patients with acute-onset cranial nerve palsies, small-angle deviations, or very young infants, a single injection can achieve a lasting result even after the toxin effect wears off. Side effects include temporary eyelid drooping (ptosis) and temporary overcorrection. Multiple injections may be needed.

Vision therapy is a structured program of supervised exercises designed to strengthen the brain’s ability to use both eyes together—particularly to improve convergence for near tasks and improve control of intermittent exotropia. The Convergence Insufficiency Treatment Trial (CITT) demonstrated that office-based vergence and accommodative therapy significantly outperforms home pencil push-ups alone for convergence insufficiency. Vision therapy is most effective as an adjunct to optical and surgical treatment rather than as a standalone treatment for large or constant strabismus.

Surgery is the definitive treatment for most forms of strabismus not fully corrected by glasses. The goal is to change the position and pulling force of one or more extraocular muscles to align the eyes. Surgery is performed under general anesthesia in children and typically under local anesthesia with sedation in adults. It is an outpatient procedure—patients go home the same day. Three primary surgical techniques are used:

• Recession: The muscle is detached from its insertion point on the eye and reattached further back, reducing its effective pulling force. Recession of the medial rectus muscles corrects esotropia; recession of the lateral rectus corrects exotropia; recession of the inferior rectus corrects hypotropia.
• Resection: A section of the muscle is removed and the shortened muscle reattached at its original insertion, increasing its effective pulling force. Resection of the lateral rectus corrects exotropia; resection of the medial rectus corrects esotropia.
• Transposition procedures: One or more muscles are surgically moved to a different location to redirect their pulling direction. Used for paralytic strabismus, where a muscle is permanently non-functional. The Knapp procedure, for example, moves both vertical rectus muscles to provide lateral pulling force when the lateral rectus has been permanently paralyzed.

Adjustable suture surgery is a modification available for selected adult patients—temporary slip-knot sutures allow the surgeon to fine-tune eye position on the first postoperative day while the patient is awake and able to report their alignment and double vision. The sutures are then permanently tied. This technique is particularly valuable in thyroid eye disease-related strabismus, complex mechanical strabismus, and paralytic cases where the exact amount of correction is difficult to predict. Some patients require more than one surgery to achieve optimal alignment, particularly those with large or complex deviations or whose strabismus was present from infancy.

Strabismus is a highly treatable condition, and the outlook for children diagnosed and treated early is very good. With consistent glasses, successful amblyopia therapy during the sensitive period, and well-timed surgery, many children achieve normal or near-normal visual acuity and functional binocular vision. For those with more complex strabismus—infantile esotropia, CCDDs, or paralytic forms—the goal is optimal alignment and visual function, and most achieve alignment that is cosmetically and functionally satisfactory. Adults with newly acquired strabismus from cranial nerve palsy or thyroid eye disease can expect double vision to be eliminated in the majority of cases through nerve recovery, prisms, or surgery. For adults with long-standing, untreated childhood strabismus who have lost binocularity, surgery is still beneficial—research consistently shows that correcting the alignment significantly improves quality of life, social interactions, and self-confidence even when stereopsis cannot be fully restored.

To further your understanding of your diagnosis and to contribute to cutting-edge research, consider participating in a clinical trial so clinicians and scientists can learn more about causes, symptoms, treatment, and prevention of strabismus and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat, or prevent disease.

All types of volunteers are needed—those who are healthy or may have an illness or disease—of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.