Strabismus, commonly known as “crossed eyes,” is a condition where the eyes do not align in the same direction, causing them to point inward, outward, upward, or downward. Its development is complex, resulting from a combination of inherited susceptibility and external factors. Understanding the interplay between these two components is key to grasping the full picture of strabismus risk.
Defining Strabismus: More Than Just Misalignment
Strabismus is fundamentally a problem with the neurological control and coordination of eye movement. Six distinct muscles surround each eyeball, working in precise coordination to ensure both eyes focus on the same target simultaneously. The brain directs these muscles through intricate nerve signals, and a disruption in this system causes the eyes to drift.
The condition is classified by the direction of the eye turn, which helps specialists determine the underlying cause and appropriate treatment. An inward turn is called esotropia, and an outward deviation is known as exotropia. Vertical misalignments include hypertropia (upward turn) and hypotropia (downward turn). This failure of binocular vision means the eyes are not working together as a coordinated pair.
The Evidence for Genetic Inheritance
The role of heredity in strabismus has been recognized for centuries, and current evidence supports a significant genetic component. Strabismus is a multifactorial trait, meaning multiple genes interact with environmental factors to determine risk, rather than being caused by a single gene. The clustering of cases within families indicates this genetic link.
Studies report that 20% to 30% of individuals diagnosed with strabismus have at least one close relative who is also affected. Twin studies offer compelling evidence, showing a high concordance rate for strabismus in monozygotic (identical) twins (54% to 82%), compared to a lower rate in dizygotic (fraternal) twins (14% to 47%). This disparity confirms that shared genes are a substantial risk factor.
Researchers have identified several gene loci that appear to increase susceptibility, such as a location on chromosome 7p22.1, but no single gene is responsible for most common cases. The genetic influence is particularly notable for esotropia, the inward turning form of strabismus, which shows a higher estimated heritability than exotropia. These susceptibility genes often affect neurological development, potentially leading to issues in the brain’s ability to control the extraocular muscles and coordinate eye movements.
Non-Inherited Factors Contributing to Strabismus
While genetics provides the underlying susceptibility, several non-inherited factors can contribute to the onset of strabismus. A common acquired form is accommodative esotropia, which often develops in children with significant uncorrected farsightedness (hyperopia). To achieve clear focus, the child’s eyes naturally over-converge, causing the inward turn.
Strabismus can also be triggered by developmental issues or acquired medical conditions that affect the brain or nerves controlling the eyes. These include complications associated with premature birth, such as retinopathy of prematurity. Traumatic brain injury or neurological conditions like cerebral palsy or hydrocephalus carry an elevated risk because they impair the central nervous system’s control over eye alignment. For adults, the sudden onset of strabismus is often a sign of an underlying event like a stroke, which damages the nerve pathways responsible for eye movement coordination.
The Importance of Early Diagnosis
The primary reason for seeking prompt medical attention for strabismus is functional, focusing on the preservation of vision. When the eyes are misaligned, the brain receives two conflicting images, leading to confusion and double vision. To resolve this, the developing brain often learns to ignore or suppress the image from the misaligned eye.
If left uncorrected, this suppression results in a permanent reduction of vision in the affected eye, known as amblyopia or “lazy eye.” The visual system develops rapidly during a “critical period,” which extends through the first seven to nine years of life, with the highest plasticity occurring before age three. Intervention during this window is extremely effective, as the visual pathways are still highly adaptable. Delaying diagnosis significantly reduces the potential for achieving full visual function and binocular depth perception.