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Squint

A squint, medically termed , is a visual disorder in which the eyes fail to align properly, with one eye deviating inward, outward, upward, or downward relative to the other when focusing on an object. This misalignment disrupts and can lead to symptoms such as (diplopia), reduced , and eye strain. Strabismus affects approximately 2% to 4% of the global population, with a higher prevalence in children—estimated at 4% in the United States—though it can manifest at any age due to congenital factors or later-onset causes. The condition arises from various etiologies, including imbalances in the controlling eye movement, uncorrected refractive errors like hyperopia (), neurological issues such as cranial palsies, genetic predispositions, or trauma to the orbit or brain. Common types include (inward deviation, or "crossed eyes"), (outward deviation), and vertical deviations like . In infants and young children, it often appears as an infantile form linked to immature visual development, while adults may develop it secondary to conditions like thyroid eye disease, , or . Untreated strabismus can result in (), where the brain suppresses input from the deviating eye to avoid confusion, potentially leading to permanent vision loss in that eye if not addressed early. typically involves a comprehensive , including cover testing to assess alignment and to identify underlying errors. Treatment is multifaceted and aims to restore alignment and binocular function: non-surgical options include corrective lenses for refractive errors, eye patching or atropine drops to treat amblyopia, and prism lenses to alleviate double vision; surgical intervention, involving adjustment of eye muscles, is common for persistent cases and boasts success rates of 70-90% in improving alignment. Early intervention, ideally before age 7, is crucial for optimal visual outcomes, though adults can also benefit from therapy to enhance and cosmetic appearance.

Definition and Classification

Definition

Squint, also known as , is a visual characterized by the misalignment of the eyes, where the visual axes do not point in the same direction when focusing on an object, resulting in one eye deviating inward, outward, upward, or downward. This condition disrupts the normal coordination between the eyes, preventing them from working together effectively. Normal requires the visual axes of both eyes to intersect at the fixation point to fuse images into a single, three-dimensional with depth. In squint, this alignment is compromised, leading to (double vision) or suppression of input from the deviating eye as the brain adapts to avoid confusion. The misalignment can affect one or both eyes and may manifest as various types based on the direction of deviation. Key terminology includes for inward deviation toward the nose, for outward deviation, for upward deviation, and hypotropia for downward deviation. Squint can be constant, occurring all the time, or intermittent, appearing only under certain conditions such as fatigue or distance viewing. Squint affects approximately 2% to 4% of the , with higher in children where it often presents before .

Types

, commonly known as squint, is classified in multiple ways to reflect its clinical variations, primarily by the direction of eye deviation, of onset, and underlying mechanisms of misalignment. These classifications help clinicians differentiate between forms that may require distinct approaches to evaluation and management. The most fundamental classification is by direction of deviation. , or convergent squint, involves inward deviation of one or both eyes toward the nose, often noticeable when focusing on near objects. , or divergent squint, features outward deviation away from the nose, which may be constant or intermittent. Vertical deviations include , where one eye drifts upward relative to the other, and hypotropia, where it drifts downward; these can occur in isolation or combined with horizontal deviations. Torsional deviations, such as incyclotorsion (inward twisting) or excyclotorsion (outward twisting), are less common but contribute to complex misalignments. Classification by onset distinguishes congenital or infantile , which manifests at birth or within the first six months of life, from acquired that develops later, typically after six months. Infantile serves as a classic example of the congenital type, presenting as a constant inward deviation in otherwise healthy infants and affecting approximately 1 in 100 to 500 individuals. In contrast, acquired forms may emerge in childhood or adulthood due to evolving factors, though specific etiologies are varied. Additional classifications address functional aspects and patterns. Accommodative squint refers to triggered by refractive errors like hyperopia, where excessive focusing effort leads to over-convergence. Paralytic squint arises from dysfunction in ocular motor s or muscles, resulting in variable misalignment. Restrictive squint stems from mechanical restrictions preventing full , such as orbital scarring. is further categorized as comitant, where the deviation angle remains consistent across all directions, or incomitant, where it varies by position, often indicating underlying or muscle issues. Subtypes include alternating squint, in which either eye can fixate while the other deviates interchangeably, and squint, where one eye consistently deviates. Intermittent exemplifies an acquired, often comitant form common in children, characterized by periodic outward drift, particularly during fatigue or distant viewing. Pattern deviations, such as A- or V-patterns, describe horizontal misalignments that intensify in specific vertical gazes, adding nuance to directional classification.

Causes and Pathophysiology

Causes

Squint, or , arises from a variety of etiological factors that disrupt normal eye alignment. Genetic influences play a significant role, with family history substantially increasing the risk of developing the condition. Studies have shown a higher prevalence of among relatives of affected individuals, indicating a hereditary component. Specific genetic mutations, such as those in the gene, are implicated in certain congenital forms, where missense mutations can lead to familial concomitant . Developmental causes often stem from issues in early visual maturation. Poor development of binocular fusion during infancy contributes to infantile , a common type of inward deviation. Uncorrected refractive errors, particularly hyperopia (farsightedness), can trigger accommodative esotropia by overstimulating eye convergence to focus on near objects. Neurological factors account for many acquired cases. Palsies of the controlling eye movements—specifically the third (oculomotor), fourth (trochlear), or sixth (abducens) nerves—impair muscle function and cause misalignment. injuries, such as those from or , and intracranial tumors can also disrupt neural pathways, leading to . Other causes include mechanical and systemic conditions. Orbital fractures may restrict eye movement, mimicking nerve palsies and resulting in deviation. Thyroid eye disease causes restrictive through extraocular muscle enlargement and inflammation. , an autoimmune disorder affecting neuromuscular transmission, can produce variable misalignment. Congenital anomalies like involve aberrant innervation of eye muscles, leading to limited abduction and retraction on adduction. Certain risk factors heighten susceptibility to specific causes. Prematurity and are strongly associated with infantile , likely due to immature development. In children, uncorrected increases the likelihood of accommodative if refractive errors go unaddressed.

Pathophysiology

Strabismus, or squint, arises from an imbalance in the coordinated action of the , which are responsible for precise eye alignment and movement. Each eye is controlled by six extraocular muscles: the superior and inferior recti, medial and lateral recti, and superior and inferior obliques. These muscles are innervated by the oculomotor (cranial nerve III), trochlear (cranial nerve IV), and abducens (cranial nerve VI) nerves, originating from nuclei. Imbalance in or innervation leads to ocular deviation, disrupting normal conjugate . Neural control of eye movements involves the brainstem's oculomotor nuclei and supranuclear pathways, which coordinate conjugate eye movements through interconnected circuits in the , , and . Disruptions in these pathways, such as of the oculomotor nuclei or abnormal signaling in the pontine , can impair conjugate and contribute to strabismic misalignment. In infantile or congenital cases, early developmental anomalies in these neural structures prevent the establishment of proper binocular coordination. Fundamental to this control are , which dictates that yoke muscles in both eyes receive equal neural input for conjugate movements, and Sherrington's law of , which ensures that muscle activation is matched by relaxation. In congenital , breakdown of these laws during infancy—due to genetic or environmental factors affecting neural maturation—results in persistent deviation, as the developing fails to calibrate equal innervation across eyes. For instance, unequal innervation to yoke muscles can exacerbate or in primary gaze positions. This misalignment disrupts by projecting non-corresponding images onto the retinas, preventing fusion and the development of . The brain responds by suppressing input from the deviating eye to avoid , which can lead to if prolonged during critical visual development periods. Suppression occurs at cortical levels, particularly in the , where interocular rivalry favors the dominant eye's input. In restrictive forms of , mechanical factors such as orbital restrictions or muscle limit passive . Conditions like congenital of the involve fibrotic replacement of muscle fibers, often due to aberrant innervation from cranial nerve misrouting or primary , leading to fixed deviations and reduced . These restrictions differ from paretic types by involving physical rather than neural deficits alone.

Signs and Symptoms

Ocular Signs

Squint, or , manifests through noticeable ocular misalignment where the eyes fail to point in the same direction simultaneously. This can present as , with one eye turning inward toward the nose; , where the eye drifts outward; or vertical deviations such as (upward) or hypotropia (downward). Additional common symptoms include headaches, , closing or covering one eye in bright light or during near tasks, and frequent or squinting. To compensate for the misalignment and minimize visual discomfort, individuals may adopt abnormal head postures, including a head tilt or face turn—for instance, turning the head away from the affected side in cases of to align the eyes better. Strabismus frequently coexists with refractive errors such as hyperopia, , or . Visual symptoms primarily involve disruptions in . Adults often experience , or double vision, due to the brain receiving conflicting images from the misaligned eyes. In children, however, the developing typically suppresses the image from the deviating eye to avoid , which can lead to reduced in that eye if prolonged. Untreated strabismus often begins intermittently, triggered by factors like fatigue or distance viewing, but can progress to a constant deviation over time, particularly in childhood-onset cases.

Associated Effects

One of the primary associated effects of squint, or , is , commonly known as , which involves reduced in the deviating eye resulting from active cortical suppression by the to avoid double vision. This suppression disrupts normal visual development, leading the brain to favor input from the non-deviating eye. In untreated cases, amblyopia develops in approximately 40-50% of children with strabismus, highlighting its high prevalence as a secondary complication. Strabismus also frequently results in the loss of , or binocular , due to the disruption of normal binocular fusion where corresponding retinal images fail to align properly. Without this fusion, individuals rely on cues for depth judgment, which are less precise and can impair tasks requiring accurate spatial awareness, such as or . This effect is particularly pronounced in early-onset strabismus, as the critical developmental window for stereopsis (typically 3-6 months to 8 years) is compromised, often leading to permanent deficits if not addressed. As a sensory to chronic misalignment, the brain may develop anomalous retinal , remapping visual inputs so that non-corresponding retinal points are perceived as aligned, thereby minimizing and promoting a single . This neural plasticity, most common in small-angle (less than 5 degrees deviation), occurs primarily in childhood through cortical reorganization in the , suppressing eccentric retinal areas to achieve pseudo-binocular vision. However, ARC can complicate treatment by maintaining the deviation even after alignment correction. Untreated during the of visual development (from birth to approximately 7-8 years) carries the risk of permanent visual loss, including irreversible and diminished , as the visual system loses plasticity beyond this window. In children, these visual impairments can extend to psychosocial consequences, such as lowered , experiences of , and due to perceived differences in appearance. Studies indicate higher rates of issues, with children showing 1.6 times greater odds of and adults exhibiting prevalence rates up to 33% for compared to 14% in non-strabismic individuals. Additionally, adults may face anxiety, avoidance of eye contact, and employment challenges stemming from negative social biases.

Diagnosis

Clinical Evaluation

The clinical evaluation of squint, or , begins with a detailed to identify potential etiologies and guide further assessment. Key elements include the age of onset, which helps differentiate congenital from acquired forms; family of strabismus or related ocular conditions; birth complications such as prematurity or low birth weight; progression of refractive errors like hypermetropia; presence of diplopia, which is more common in older children with acute deviations; and abnormal head postures that may compensate for misalignment. Visual acuity testing follows to detect or refractive contributions to the squint. In adults and cooperative children, standardized methods like the are used, while age-appropriate tools such as picture charts, Lea symbols, or preferential looking tests (e.g., Teller acuity cards) are employed for younger patients to measure monocular and binocular acuity with optimal refractive correction. Ocular motility is assessed through ductions, which evaluate monocular eye movements in cardinal directions, and versions, which test binocular pursuits to identify restrictions, overactions, or incomitancy. The cover test, performed at distance and near fixations, is essential: the cover-uncover test detects phorias by observing refixation upon uncovering, while the alternate cover test dissociates the eyes to reveal tropias through movement of the uncovered eye. Alignment is quantified using the for gross estimation, where the position of a corneal light reflex is observed; asymmetry indicates deviation, with approximately 15 to 21 prism diopters per millimeter of displacement from the pupil center, depending on corneal radius. For precise measurement, the neutralizes the deviation with prisms to determine the exact angle in prism diopters. Binocular function is evaluated to assess sensory adaptations like suppression or . The Worth 4-dot detects suppression by presenting polarized lights, where failure to report all dots from one eye indicates suppression. Stereopsis is measured using tests such as the Titmus fly, which quantifies through random dot patterns, with normal stereoacuity at 40 seconds of arc or better (≤40 seconds of arc) in non-strabismic individuals.

Diagnostic Tests

Refraction testing, including cycloplegic refraction, is essential to identify uncorrected refractive errors that may contribute to or exacerbate strabismus, particularly hyperopia leading to accommodative esotropia. Cycloplegic agents, such as cyclopentolate, temporarily paralyze accommodation to allow accurate measurement via retinoscopy or autorefraction, ensuring a precise prescription that can influence eye alignment. This exam is routinely performed in pediatric cases to rule out refractive causes before considering other etiologies. Fundoscopy and slit-lamp examination are conducted to detect underlying ocular abnormalities, such as retinal detachments, tumors, or anterior segment issues like cataracts, which could underlie or mimic symptoms. The slit-lamp provides detailed visualization of the , , and , while dilated fundoscopy assesses the posterior segment for pathologies like anomalies or macular issues that might affect alignment. These tests help exclude organic causes in the diagnostic workup. Imaging modalities, including magnetic resonance imaging (MRI) and computed tomography (CT), are indicated when neurological or structural causes are suspected, such as cranial nerve palsies from tumors or strokes. High-resolution MRI can visualize extraocular muscle atrophy, nerve involvement, or orbital masses, aiding in confirming paralytic strabismus. Orbital ultrasound serves as a non-invasive initial tool to evaluate for masses, inflammation, or post-traumatic changes contributing to restrictive strabismus. Electrophysiological tests, such as (EMG), assess extraocular muscle function in cases of suspected paralytic , detecting abnormalities in nerve conduction or muscle activity due to conditions like . Visual evoked potentials (VEP) provide an objective measure of visual pathway integrity, particularly useful in evaluating associated by identifying delays in cortical response from the amblyopic eye. For , , including TSH and free T4 levels, are recommended in adults with new-onset to screen for thyroid eye disease, which can cause restrictive patterns. Genetic screening may be pursued in congenital cases with family history or syndromic features, targeting genes like those involved in congenital syndromes via whole . Emerging diagnostic tools as of 2025 include (AI)-based systems for automated detection and classification. models analyze facial images or videos to quantify deviations, offering potential for improved screening in resource-limited settings, though they are not yet standard in clinical practice.

Management

Non-Surgical Options

Non-surgical options for managing primarily focus on correcting underlying refractive errors, treating associated , and improving eye alignment through therapeutic interventions, particularly in children where allows for better outcomes. These approaches aim to enhance and prevent long-term visual deficits without invasive procedures. Spectacle correction is a treatment, especially for accommodative , where hyperopia triggers excessive . A full cycloplegic is performed to determine the precise prescription, often involving plus lenses to relax and reduce the inward deviation; this can fully correct the misalignment in fully accommodative cases, with studies showing improved stereoacuity post-correction. Patching and occlusion therapy address , a common associated effect of where the weaker eye is suppressed. The stronger eye is covered for 2-6 hours daily, or alternating with atropine penalization drops to blur its vision, forcing use of the deviated eye; meta-analyses indicate significant reduction in deviation angles and improved in pediatric cases when initiated before age 7. Vision therapy, including orthoptic exercises, promotes fusion and through targeted activities like pencil push-ups or computer-based training to strengthen eye coordination. Prism may be incorporated temporarily to shift images and alleviate , achieving alignment in 80% of small-angle cases over time; virtual reality-enhanced programs have shown higher rates of orthophoria in follow-up trials, including post-surgical cases. Botulinum toxin injections weaken overactive extraocular muscles, offering a reversible alternative for select cases like acute esotropia or residual deviations; success rates reach 70% in maintaining alignment for up to 36 months, particularly in children avoiding general anesthesia. Regular monitoring through follow-up examinations is essential, especially for intermittent strabismus in children under 8 years, to track progression, adjust therapies, and intervene early if alignment worsens; pediatric ophthalmologists recommend visits every 3-6 months to optimize outcomes.

Surgical Options

Surgical intervention for strabismus is indicated when non-surgical treatments fail to correct persistent ocular deviation, particularly in cases involving large angles of misalignment such as greater than 15 prism diopters or greater than 20 prism diopters, as well as in restrictive or paralytic forms where cannot be adequately managed conservatively. These indications aim to improve eye alignment, enhance , and mitigate psychosocial effects from disfigurement. Timing of surgery is ideally sequenced after addressing any associated to maximize visual outcomes, though early can sometimes aid amblyopia resolution in select cases. For congenital , procedures are often performed between 6 months and 2 years of age to support critical periods of visual development and stereoacuity. The primary surgical technique is recession-resection, which weakens an overactive extraocular muscle by recessing its insertion posteriorly (typically 4-6 mm for horizontal recti) while strengthening the antagonist muscle through resection (shortening by 3-5 mm excision). Adjustable sutures are frequently incorporated to allow intraoperative or immediate postoperative adjustment of muscle tension, enabling fine-tuning of within 5-7 days under . Horizontal strabismus, such as or , is addressed by targeting the medial or lateral rectus muscles, whereas vertical deviations like involve the superior or inferior rectus and oblique muscles, often using recession of the inferior oblique or tucking of the superior oblique. Surgical approaches may be unilateral for smaller deviations or bilateral for larger angles exceeding 50 prism diopters, with bilateral methods providing more symmetric correction and reducing the risk of induced deviations in the fellow eye. Complications of strabismus surgery, though rare overall, include over- or under-correction leading to residual misalignment, postoperative infection with an incidence of approximately 0.14%, and anesthesia-related risks such as the occurring in 14-90% of cases, which is managed with agents. Reoperation rates are approximately 20%, primarily due to recurrent deviation or unsatisfactory alignment, particularly in esotropic cases.

Prognosis and Epidemiology

Prognosis

The prognosis for , also known as squint, varies based on the age of onset, timeliness of , and adherence to , with overall success rates for achieving good ocular ranging from 60% to 80% following surgical correction. Recovery from associated is most effective when initiated before age 7, as visual plasticity diminishes significantly thereafter, leading to suboptimal improvements in and binocular function. Early intervention, particularly in childhood, substantially enhances the likelihood of restoring and fusion, whereas adult-onset often yields poorer recovery of these functions due to longstanding suppression and neural adaptations. If left untreated, can result in permanent , irreversible loss of (), and psychosocial challenges such as reduced and that persist into adulthood. Recurrence of misalignment occurs in up to 25% of cases post-treatment, often necessitating additional , and patients require lifelong monitoring to detect changes influenced by age, neurological factors, or refractive shifts. Recent studies indicate improved outcomes with non-surgical approaches, such as prismatic correction achieving resolution rates up to 81% in select pediatric cases of strabismus-related ; however, significant gaps remain in support for adults, where emotional and quality-of-life burdens are often inadequately addressed.

Epidemiology

Strabismus affects approximately 2% to 5% of the global population, with a pooled of 1.93% based on a and of 56 studies encompassing over 600,000 participants across various regions. In the United States, is similarly estimated at 2% to 5% overall, but it is higher among children, reaching up to 4% in those under 6 years old according to population-based surveys. tends to be more prevalent in European populations, where studies report rates around 0.8% compared to 0.3% for , resulting in an esotropia-to- ratio of 2:1. In contrast, predominates in Asian regions, with ratios as high as 9:1 favoring over in school-aged children. Demographic patterns show no significant overall difference in prevalence, with rates nearly identical at about 2.58% for both males and females in horizontal cases from a of 42 population-based studies. However, certain subtypes exhibit variations; for instance, intermittent is nearly twice as common in females. Risk is substantially elevated in premature infants, with incidence rates reaching 15% to 20% in cohorts and up to 42% in very preterm individuals with gestational ages below 32 weeks, far exceeding the 2% to 4% seen in full-term children. Geographic variations highlight higher reported rates in developing countries, such as 17.9% in Ethiopian populations, potentially linked to delayed screening and limited access to early detection. Ethnic differences also influence subtype distribution, with being more common than in African populations, including African American children where accounts for a greater proportion of cases compared to white children. Overall trends in prevalence remain stable at 2% to 5% globally, though improved pediatric screening programs have led to increased detection rates in children, particularly in high-income settings. Data on adult-onset strabismus is incomplete due to underreporting and less routine screening in older populations, with prevalence estimates of 0.90% in U.S. adults as of a 2025 study using the database but likely underestimated due to healthcare access disparities. Historically, strabismus has been recognized since ancient times, with descriptions dating back to in medical texts attributing it to anatomical or obscure causes, while modern epidemiological data emerged from 20th-century population studies establishing its 2% to 5% incidence.

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