Should we require evidence about the etiology of A-pattern strabismus?

Abstract

In this issue of the Journal, Donahue and Itharat 1 suggest that A-pattern strabismus with overdepression in adduction may be a bilateral skew deviation. Is this novel proposition credible? Donahue and Itharat report 13 patients with A-pattern strabismus averaging 27Δ, and at least +2 overdepression in adduction, equating this to "superior oblique overaction." In 11 of the 13 patients, vertical binocular alignment did not change during head tilt, and 12 had some unspecified degree of bilateral fundus incyclotorsion. Most strabismologists recognize such patients.The authors then speculate that central otolith-ocular reflex pathology causes the A patterns. Recall that each labyrinth has two otolith organs-the utriculus and the sacculus-that sense linear acceleration including gravity. Donahue and Itharat speculate that their patients have bilateral lesions of otolith ocular reflex connections corresponding to the anterior semicircular canal pathways. They postulate a bilateral brain lesion diminishing input from the otolith equivalent of the anterior semicircular canal, allowing dominance of analogous input from the otolith equivalent of the posterior semicircular canal. This putatively activates the inferior rectus and superior oblique muscles and inhibits the inferior oblique and superior rectus muscles. Donahue and Itharat propose that this vestibular drive for conjugate deorsumversion does not "sunset" the eyes because visual "fixation" input overrides it. Innervation to the superior oblique muscles putatively remains maximal, and the inferior oblique is putatively inhibited. The "tonus" hypothesis requires that these oblique commands generates maximum possible intorsion, rendering the obliques unresponsive to supranuclear input from "fixation" to cancel the intorsion, and from otolith input to explain the negative head tilt test. What is the