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Co-Development of VEP Motion Response and Binocular Vision in Normal Infants and Infantile Esotropes

¹ From the Retina Foundation SW, 9900 North Central Expressway, Suite 400, Dallas, Texas; the ² Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas; and the ³ Ophthalmology Service, Children’s Medical Center, Dallas.

PURPOSE. To determine the maturational course of nasotemporal asymmetry in infantile esotropia and to define the relationships among the symmetry of the motion visual evoked potential (MVEP), eye alignment, fusion, and stereopsis.

METHODS. Sixty healthy term infants and 34 infants with esotropia participated. Nasotemporal MVEP asymmetry was assessed by the presence of a significant F₁ response component with an inter-ocular phase difference of approximately 180° and by an amplitude "asymmetry index." Fusion was evaluated using the 4 p.d. base out prism test. Random dot stereoacuity was assessed in infants with forced-choice preferential looking (FPL) using the Infant Random Dot Stereocards. Eye alignment was assessed by the alternate prism and cover or the modified Krimsky test.

RESULTS. Normal infants 2 to 3 months of age exhibited marked nasotemporal MVEP asymmetry, which rapidly diminished by 6 to 8 months. Neonates did not exhibit MVEP asymmetry. There was good concordance between fusion and MVEP symmetry and between stereopsis and MVEP symmetry; the concordance between MVEP symmetry and orthoposition of the visual axes was significantly poorer. The same proportion of normal and young esotropic infants showed symmetrical MVEPs. Regardless of the age at surgery, most patients with infantile esotropia had asymmetrical MVEPs after surgery.

CONCLUSIONS. These data support a strong link between fusion and MVEP symmetry during both normal maturation and in infantile esotropia. Furthermore, the finding that the youngest infants with esotropia do not differ significantly from normal suggests that the nasotemporal asymmetry found in older patients with infantile esotropia does not represent an arrest of maturation but, rather, a pathologic change of the motion pathways.

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