ular muscle (EOM) paths during asymmetrical convergence were evaluated by tri-planar, contrast-enhanced magnetic resonance imaging of the orbits of eight young adults during binocular fixation of a target aligned to one eye at 800 and 15 cm distance. Cross sections and paths of EOMs were determined from area centroids. In convergence, the aligned eye rotated and translated negligibly, while its inferior oblique (IO) muscle exhibited significant contractile thickening. There were no significant contractile changes in the cross sections of aligned eye rectus or superior oblique (SO) muscles in convergence. The converging eye rotated nasally 22.4°but translated negligibly. The converging eye medial (MR) and lateral rectus (LR) muscles exhibited large contractile cross-section changes, and the IO showed significant contractile thickening, while the vertical rectus muscles and the SO did not. Anterior paths of three aligned eye rectus EOMs could be determined in convergence and shifted consistent with a 1.9°extorsion of the rectus pulley array. Such extorsional reconfiguration of the rectus pulleys would move the pulleys in coordination with globe extorsion and avoid imparting torsional action to these EOMs. Extorsional rectus pulley shift in convergence is inconsistent with the reconfiguration predicted to explain the temporal tilting of Listing's planes, instead suggesting that this temporal tilting is due to variations in oblique EOM innervation. Absence of globe translation in convergence argues against overall EOM co-contraction. The reconfiguration of EOM geometry in convergence has important implications for single-unit studies of neural control.

Quantitative morphometry by MRI can demonstrate IO size and contractility. Even in cases of unequivocal SO palsy associated with ipsilesional SO atrophy and deficient contractility, the degree of elevation in adduction was not correlated with IO size. This finding suggests that the associated overelevation in adduction, commonly termed "inferior oblique overaction," actually arises from some other mechanism than IO hypertrophy or excess contractility. Revision of clinical terminology seems warranted.

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