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Chapter: Ophthalmology: Ocular Motility and Strabismus

Concomitant Strabismus

Concomitant strabismus differs from paralytic strabismus in that the angle of deviation remains the same in every direction of gaze. The deviating eye fol-lows the normal fellow eye at a constant angle.

Concomitant Strabismus


Concomitant strabismus differs from paralytic strabismus in that the angle of deviation remains the same in every direction of gaze. The deviating eye fol-lows the normal fellow eye at a constant angle.


Concomitant strabismus occurs almost exclusively inchildren. Approximately 5.3 – 7.4% of all children are affected. In 60 – 70% of all cases, the disorder initially manifests itself within the first two years of life.


Vision at birth is neither focused nor binocular, and both sen-sorimotor coordination and binocular vision are very unstable during the first few years of life. Impairments of the sensory or motor systems or central pro-cessing of visual perceptions that occur during this time can disturb thecoordination between the eyes and lead to strabismus. However, the causes of concomitant strabismus are often unclear. The following causes have been identified to date:

Genetic factors: Approximately 60% of children with strabismus have afamily history of increased incidence.

Uncorrected refractive errors are partially responsible for the occurrenceof strabismus. Children with hyperopia (farsightedness) tend to have esotropia. This is because convergence and accommodation are coupled.Children with hyperopia have to accommodate without converging when gazing into the distance to compensate for their refractive error. However, accommodation always triggers a convergence impulse that can cause esotropia.

Insufficient fusion: This can occur in conjunction withanisometropia(unequal refractive power in the two eyes) and aniseikonia (unequal reti-nal image size). It can also occur in heterophoria (latent strabismus) after one eye has been covered with a bandage for a prolonged period.

Unilateral visual impairment: Severe nearsightedness, corneal scarring,lens opacities (cataract), macular changes, and retinal disorders can cause secondary strabismus. Retinal causes include retinoblastoma, Coats’ dis-ease, retinopathy of prematurity, retinal detachment, or central retinal scarring in congenital toxoplasmosis.

Any initial examination of a patient with strabismus must invariably include examination of the fundus of both eyes under mydriasis in addi-tion to examination of the anterior segments of the eye

Other possible causes of concomitant strabismus include:

–  Perinatal lesions such as preterm birth and asphyxia.

–  Cerebral trauma and encephalitis.


Deviation of the visual axis of the deviating eye causesobjects to be projected to noncorresponding points on the retina. One would expect these patients suffer from constant double vision because the left and right eyes supply different information to the brain. However, the central nervous system utilizes two mechanisms to help avoid double vision in con-comitant strabismus:

1. Suppression: A central inhibiting mechanism suppresses the visualstimuli from the deviating eye. There are two different types of suppres-sion:

Central scotoma: This visual field defect occurs when the perceived objectis projected to the same location on the fovea in both eyes but strabismus causes the eyes to perceive it as separate objects. As this would cause con-fusion, the object projected on the fovea of the deviating eye is suppress-ed.

Fixation point scotoma: This visual field defect occurs when the image per-ceived by the leading eye is projected to a point next to the fovea in the deviating eye. This results in diplopia as the fixation point does not lie within the fovea as it would in physiologic sight. The scotoma occurs at this noncorresponding point next to the fovea to suppress the diplopia.

2. Sensory adaptation: Inbinocularvision with the gaze directed straightahead, the fixation point of the deviating eye can fall beyond the fovea. This produces anomalous retinal correspondence as the fixation point in the nondeviating eye always falls on the fovea. This means that the image created in the deviating eye is not as sharply focused as the image in the leading eye and is suppressed.

Amblyopia secondary to suppression.Constant suppression in strabismus inthe form of a central and fixation scotomas can lead to severe amblyopia, especially in children below the age of six. The prospects for successful treat-ment decrease with age, and amblyopia becomes irreversible beyond the age of six to eight. 

Amblyopia only occurs in unilateral strabismus. In alternating strabismus, fixation or deviation alternates between both eyes so that both eyes learn to see. A differential diagnosis must distinguish amblyopia in stra-bismus from other forms of amblyopia. These are listed in Table 17.2.

Strabismus occurring before the age of six will frequently lead to ambly-opia. Early examination and treatment by an ophthalmologist are crucial.


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