Superior oblique (SO) palsy is prototypic for cyclovertical strabismus. Theoretical, experimental, and much clinical evidence support the idea that acute, unilateral SO palsy produces a small ipsilateral hypertropia that increases with contralateral gaze and with head tilt to the ipsilateral shoulder.
1,2 The basis of this three-step test is traditionally believed to be related to ocular counterrolling, so that the eye ipsilateral to head tilt is normally intorted by the SO and superior rectus (SR) muscles whose vertical actions cancel.
3 However, ipsilateral to a palsied SO, unopposed SR elevating action is supposed to create hypertropia. The three-step test has been the cornerstone of diagnosis and classification of cyclovertical strabismus for generations of clinicians.
4,5 When the three-step test result is positive, clinicians infer SO weakness and attribute the large amount of interindividual alignment variability to secondary changes,
6 such as inferior oblique overaction and SR contracture. Much evidence, however, indicates that the mechanism of the three-step test is misunderstood. If traditional teaching were true, then IO weakening, the most common surgery for SO palsy, should increase the head tilt-dependent change in hypertropia; the opposite has been observed.
7 Among numerous inconsistencies with common clinical observations,
7 bilateral SO palsy should cause greater head-tilt-dependent change in hypertropia than should unilateral SO palsy; however, the opposite has been found.
8,9 Modeling and simulation of putative effects of head tilt in SO palsy suggest that SO weakness alone cannot account for typical findings in the three-step test.
10,11 Beyond actual contractile weakness of the SO muscle, additional changes in other extraocular muscles (EOMs) have been typically postulated in SO palsy.