Abstract
PURPOSE: Pattern strabismus describes vertically incomitant horizontal strabismus. Conventional theories emphasized the role of orbital etiologies, such as abnormal fundus torsion and misaligned orbital pulleys as a cause of the pattern strabismus. Experiments in animal models, however, suggested the role of abnormal cross-connections between the neural circuits. We quantitatively assessed eye movements in patients with pattern strabismus with a goal to delineate the role of neural circuits versus orbital etiologies. METHODS: We measured saccadic eye movements with high-precision video-oculography in 14 subjects with pattern strabismus, 5 with comitant strabismus, and 15 healthy controls. We assessed change in eye position in the direction orthogonal to that of the desired eye movement (cross-coupled responses). We used fundus photography to quantify the fundus torsion. RESULTS: We found cross-coupling of saccades in all patients with pattern strabismus. The cross-coupled responses were in the same direction in both eyes, but larger in the nonviewing eye. All patients had clinically apparent inferior oblique overaction with abnormal excylotorsion. There was no correlation between the amount of the fundus torsion or the grade of oblique overaction and the severity of cross-coupling. The disconjugacy in the saccade direction and amplitude in pattern strabismics did not have characteristics predicted by clinically apparent inferior oblique overaction. CONCLUSIONS: Our results validated primate models of pattern strabismus in human patients. We found no correlation between ocular torsion or oblique overaction and cross-coupling. Therefore, we could not ascribe cross-coupling exclusively to the orbital etiology. Patients with pattern strabismus could have abnormalities in the saccade generators.