A biomechanical model of congenital/infantile esotropia and its treatment

To evaluate the ability of a computer assisted model of ocular motility, to reproduce this syndrome using known ocular anatomic biomechanical muscular parameters, and to hypothesize pathogenetic mechanisms deduced from clinical and laboratory experiences.

The manipulation of anatomic, elastic, contractile and innervational parameters available in the computer software program Orbit 1.6, were used to model: a) anatomic ocular and orbital parameters found in the 12 months old infant; b) static (biomechanical) changes measured intraoperatively in the extraocular muscles (medial and lateral rectus muscles) of infantile esotropes; and c) dynamic components of the horizontal deviation, including crossed fixation and bilateral limitation of abduction. Bilateral medial rectus recession surgery was also simulated on the completed model by moving backwards the insertions of both medial rectus muscles.

Small, fairly comitant, esotropic deviation were simulated using real data of the mechanical status of medial and lateral rectus muscles collected intraoperatively (length-tension measurements). The more typical large esotropic deviations with bilateral limitation of abduction of the congenital/infantile esotropia syndrome were only obtained when subtle modifications of the medial and lateral rectus muscles' thresholds to innervation were added to the anatomical-mechanical model. An orthotropic primary position binocular alignment with full rotations was obtained in this model following standard bilateral medial rectus recessions, showing surgical dose/response figures close to those usually found in the treatment of real cases of congenital/infantile esotropia.

This biomechanical computer-assisted model may provide a very useful tool not only to test new or different surgical procedures and dosages but also to explore different pathogenetic mechanisms.