Objective: To explore the mechanisms underlying the hypertropia associated with unilateral coronal synostosis. Methods: In 13 patients with unilateral coronal synostosis, we measured gaze-dependent binocular alignment before and after strabismus surgery, assessed the superior rectus muscle (SRM) pulley using computed tomography, and simulated posterior displacement of the trochlea and superolateral displacement of the SRM pulley. Results: All the patients had an ipsilateral hypertropia in primary gaze (3-30 diopters) that increased in contralateral gaze and decreased in ipsilateral gaze and that simulated an inferior oblique muscle overaction. Strabismus surgery fully or partially corrected the hypertropia in only 7 of 11 patients. High-resolution computed tomography demonstrated that the pulley of the SRM relative to the inferior rectus muscle was translated 0 to 11.0 mm laterally and up to 2.7 mm vertically. Lateral translation (up to 10 mm) alone or combined with vertical translation (up to 5 mm) of the SRM pulley in the simulated model produced a hypertropia with lateral incomitance. Posterior translation (15 mm) of the trochlea did not induce a significant hypertropia. Conclusion: Superolateral translation of the SRM pulley creates an imbalance of muscle pulling forces that better accounts for the hypertropia than posterior displacement of the trochlea. Objective: To explore the mechanisms underlying the hypertropia associated with unilateral coronal synostosis. Methods: In 13 patients with unilateral coronal synostosis, we measured gaze-dependent binocular alignment before and after strabismus surgery, assessed the superior rectus muscle (SRM) pulley using computed tomography , and simulated posterior displacement of the trochlea and superolateral displacement of the SRM pulley. Results: All the patients had an ipsilateral hypertropia in primary gaze (3-30 diopters) that increased in contralateral gaze and decreased in ipsilateral gaze and that simulated an inferior oblique Strabismus surgery fully or partially corrected the hypertropia in only 7 of 11 patients. High-resolution computed tomographyiform that the pulley of the SRM relative to the inferior rectus muscle was translated 0 to 11.0 mm laterally and up to 2.7 mm vertically. Lateral translation (up to 10 mm) alone or combined with vertical translatio (up to 5 mm) of the SRM pulley in the simulated model produced a hypertropia with lateral incomitance. Posterior translation (15 mm) of the trochlea did not induce a significant hypertropia. Conclusion: Superolateral translation of the SRM pulley creates an imbalance of muscle pulling forces that better accounts for the hypertropia than posterior displacement of the trochlea.