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Purpose Using high-resolution magnetic resonance imaging (MRI), we investigated whether rectus pulleys are significantly displaced in superior oblique (SO) palsy and whether displacements account for strabismus patterns. Design Prospective case-control study. Participants Twenty-four patients diagnosed with SO palsy based on atrophy of the SO muscle on MRI and 19 age-matched orthotropic control subjects. Methods High-resolution, surface coil MRI scans were obtained in multiple, contiguous, quasicoronal planes during monocular central gaze fixation. Pulley locations in oculocentric coordinates in the following subgroups of patients with SO palsy were compared with normal results in subgroups of patients with SO palsy: unilateral versus bilateral, congenital versus acquired, and isotropic (round) versus anisotropic (elongated) SO atrophy. Expected effects of pulley displacements were modeled using Orbit 1.8 (Eidactics, San Francisco, CA) computational simulation. Main Outcome Measures Rectus pulley positions and ocular torsion. Results Rectus pulleys typically were displaced in SO palsy. In unilateral SO palsy, on average the medial rectus (MR) pulley was displaced 1.1 mm superiorly, the superior rectus (SR) pulley was displaced 0.8 mm temporally, and the inferior rectus (IR) pulley was displaced 0.6 mm superiorly and 0.9 mm nasally from normal. Displacements were similar in bilateral SO palsy, with the SR pulley additionally displaced 0.9 mm superiorly. However, the lateral rectus pulley was not displaced in either unilateral or bilateral SO palsy. The SR and MR pulleys were displaced in congenital SO palsy, whereas the IR and MR pulleys were displaced in acquired palsy. Pulley positions did not differ between isotropic and anisotropic palsy or between patients with cyclotropia of less than 7° versus cyclotropia of 7° or more. Simulations predicted that the observed pulley displacements alone could cause patterns of incomitant strabismus typical of SO palsy, without requiring any abnormality of SO or inferior oblique strength. Conclusions Rectus pulley displacements alone, without abnormal oblique muscle contractility, can create the clinical patterns of incomitant strabismus in SO palsy. This finding supports accumulating evidence that clinical binocular misalignment patterns are not reliable indicators of contractile function of the SO muscle. Ocular torsion does not correlate with and thus cannot account for pulley displacements in SO palsy. [ABSTRACT FROM AUTHOR]

Purpose To determine whether rectus extraocular muscle (EOM) sizes and pulley locations contribute to exotropia, we used magnetic resonance imaging (MRI) to measure these factors in normal control participants and in patients with concomitant and pattern exotropia. Design Prospective case-control study. Participants Nine patients with concomitant exotropia, 6 patients with pattern exotropia, and 21 orthotropic normal control participants. Methods High-resolution surface-coil MRI scans were obtained in contiguous, quasicoronal planes. Rectus pulley locations were determined in oculocentric coordinates for central gaze, supraduction, and infraduction. Cross sections in 4 contiguous image planes were summed and multiplied by the 2-mm slice thickness to obtain horizontal rectus posterior partial volumes (PPVs). Main Outcome Measures Rectus pulley locations and horizontal rectus PPVs. Results Rectus pulleys were located differently in patients with A-pattern, versus V- and Y-pattern, exotropia. The lateral rectus (LR) pulleys were displaced significantly superiorly, the medial rectus (MR) pulleys were displaced inferiorly, and the inferior rectus pulleys were displaced laterally in A-pattern exotropia. However, the array of all rectus pulleys was excyclorotated in V- and Y-pattern exotropia. The PPV of the medial rectus muscle was statistically subnormal by approximately 29% in concomitant, but not pattern, exotropia ( P < 0.05). The ratio of the PPV of the LR relative to the MR muscles in concomitant exotropia was significantly greater than in control participants and those with pattern exotropia ( P < 0.05). Conclusions Abnormalities of EOMs and pulleys contribute differently in pattern versus concomitant exotropia. Abnormal rectus pulley locations derange EOM pulling directions that contribute to pattern exotropia, but in concomitant exotropia, pulley locations are normal, and relatively small medial rectus size reduces relative adducting force. [ABSTRACT FROM AUTHOR]