Mechanisms of Vertical Fusional Vergence in Patients With "Congenital Superior Oblique Paresis" Investigated With an Eye-Tracking Haploscope.

By analysis of the accompanying torsional movement of an eye during vertical movement, one can judge the relative contribution of the oblique muscles versus the vertical rectus muscles to that vertical movement. Such analyses have suggested that the oblique extraocular muscles play a predominant role in vertical fusional vergence in healthy individuals.1–4 Vertical fusional vergence induced by prism-produced vertical disparity in healthy subjects, and assessed using manual video-oculography, was associated with a cycloversion of the eyes (torsion of both eyes in the same direction), with the downward-moving eye intorting and the upward-moving eye extorting.1 This movement pattern suggested that the oblique muscles were largely responsible for disparity-induced vertical vergence movements. This movement pattern was largely confirmed in healthy subjects using scleral search coil recordings, with the caveat that part of the cycloversion response was in the form of torsional nystagmus.2 Subsequent studies using an afterimage technique3 and automated video-oculography4 further supported the above findings in healthy subjects and supported the idea that the oblique muscles were the primary mediators of normal vertical fusional vergence.3,4 The fourth cranial nerve, which innervates only the superior oblique muscle, can be damaged from blunt head trauma. This causes a characteristic ocular motility pattern, with elevation and extorsion of the higher eye and a compensatory head tilt away from the higher eye, which we call acquired fourth nerve paresis/palsy or superior oblique paresis/palsy (SOP). A very similar ocular motility pattern of misalignment, however, with no such trauma, can occur in any decade of life and is of uncertain etiology. The historically presumed cause has been an inborn weakness (“paresis”) of the superior oblique muscle not manifest until later in life (therefore historically termed “congenital” SOP). Magnetic resonance imaging studies, however, have shown that many patients with apparent congenital SOP have superior oblique muscles with normal cross-sectional area and normal contractility,5,6 suggesting other causes for “congenital” SOP in many cases.7,8 Because of different mechanisms likely involved in the genesis of the ocular motility pattern known as SOP, one should not be surprised if patients use different vertical vergence mechanisms to compensate for such deviations when small enough to allow motor fusion. The particular mechanism used may also correlate with surgical outcome, and thus may influence the best approach for surgical correction. Indeed, different mechanisms of vertical fusional vergence, not predominately relying on the oblique muscles, were found by Mudgil and colleagues9 in patients with various forms of “SOP.” Using scleral search coil eye movement recordings, they identified three different patterns of vertical fusional vergence during attempted fusion in patients with unilateral SOP. The predominant pattern, involving extorsion of the downward-moving eye and intorsion of the upward-moving eye, suggested a predominant role of the vertical rectus muscles. This was found in all of their patients with true, acquired SOP, but in only one-third of patients with “congenital” SOP.9 The purpose of this study was to investigate cyclovertical eye movement patterns during vertical fusion in patients with “congenital unilateral SOP” using our custom eye-tracking haploscope,4,10,11 and to investigate the value of classifying “congenital SOP” by the type of compensatory fusion used, in hopes of guiding the approach used for surgical correction.