Special features of superior oblique hypofunction due to tendon abnormalities

While most cases of superior oblique (SO) hypofunction represent contractile weakness due to denervation, sometimes the lesion is exclusively in the tendon. This study sought to distinguish the pattern of incomitant strabismus caused by deficiency of SO oculorotary force caused by tendon abnormalities versus that of neurogenic palsy. Clinical and magnetic resonance imaging (MRI) findings of 7 cases of unilateral SO tendon interruption or extirpation were compared with 11 cases of age matched unilateral SO palsy having intact tendons. We compared angles of misalignment with high-resolution MRI in central gaze and deorsumversion. Muscle bellies in neurogenic palsy were markedly atrophic with maximal cross sections averaging 6.5 ± 2.7 mm², in contrast with 13.5 ± 3.0 mm² contralesionally (P < .0001). In contrast, SO muscle bellies ipsilateral to tendon interruption had maximum cross sections averaging 15.1 ± 3.0 mm² occurring more posterior than on the contralesional side whose maximum averaged 12.1 ± 2.4 mm². While cross sections of SO bellies ipsilateral to tendon interruption exhibited normal contractile increase in infraduction (P < .0005), there was nevertheless strabismus with incomitance similar to that in SO atrophy. Binocular alignment was statistically similar (P > .5) in the two groups for all diagnostic positions, including head tilt, except in deorsumversion, where cases with SO tendon abnormalities averaged 20.5 ± 6.9Δ ipsilateral hypertropia, significantly more than 8.5 ± 6.6Δ in neurogenic SO atrophy (P = .001). The average difference in hypertropia Hypertropia averaged 9D greater in deorsumversion than central gaze in tendon abnormalities, but 4.1Δ less in SO atrophy (P< .019). In contralesional version, average overelevation in adduction was 1.7 (scale of 0-4) in tendon abnormalities, and 2.6 in SO atrophy (P = .23), while average underdepression in adduction was -2.3 in cases of tendon abnormalities and -1.6 in SO atrophy (P = .82). Repair of the SO tendon in three cases was effective, while alternative procedures were performed when repair was infeasible. While both denervation and tendon interruption impair SO oculorotary function, interruption causes greater hypertropia in infraversion. Surgical tightening of interrupted SO tendons may have particularly gratifying effects. Posterior SO thickening and large hypertropia in infraversion suggest SO tendon interruption that may guide a surgical strategy of tendon repair.