James A Sharpe1, Sunil Kumar, Arun N Sundaram. 1. Division of Neurology, University Health Network, University of Toronto, Toronto, Ontario, Canada. james.sharpe@uhn.on.ca
Abstract
PURPOSE: This article considers vertical misalignment and torsion of the eyes that arise from disorders of vestibulo-ocular reflex (VOR) pathways. RECENT FINDINGS: Infarction of the nodulus is one of the causes of skew deviation, a vertical strabismus accompanied by torsion of the eyes and tilt of the subjective visual vertical. Vertical components of childhood strabismus may arise from dysgenesis of vestibular projections in the brainstem. If vertical misalignment decreases greatly in the supine position compared to the erect poison one may conclude that skew deviation rather than a fourth nerve palsy is responsible for the strabismus. Impairment of the horizontal translational VOR in patients with skew has provided further evidence that imbalance in the otolith-ocular pathway, caused by disruption of projections from the utricle to motor neurons, is the mechanism of skew deviation. Bedside examination showing a normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation is sensitive and specific for stroke. Skew deviation can identify stroke when an abnormal head impulse test falsely suggests a peripheral vestiblular lesion. Reduction in gain and failure of adaptation to vision of the torsional angular VOR in head positions away from the erect signify fundamental differences in the central organization of convergence of semicircular canal and otolith signals, when compared to the horizontal and vertical angular VORs. SUMMARY: The effects of head position and of lesions of the nodulus are assuming increasing importance in analysis and differential diagnosis of vertical misalignment and torsion of the eyes.
PURPOSE: This article considers vertical misalignment and torsion of the eyes that arise from disorders of vestibulo-ocular reflex (VOR) pathways. RECENT FINDINGS: Infarction of the nodulus is one of the causes of skew deviation, a vertical strabismus accompanied by torsion of the eyes and tilt of the subjective visual vertical. Vertical components of childhood strabismus may arise from dysgenesis of vestibular projections in the brainstem. If vertical misalignment decreases greatly in the supine position compared to the erect poison one may conclude that skew deviation rather than a fourth nerve palsy is responsible for the strabismus. Impairment of the horizontal translational VOR in patients with skew has provided further evidence that imbalance in the otolith-ocular pathway, caused by disruption of projections from the utricle to motor neurons, is the mechanism of skew deviation. Bedside examination showing a normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation is sensitive and specific for stroke. Skew deviation can identify stroke when an abnormal head impulse test falsely suggests a peripheral vestiblular lesion. Reduction in gain and failure of adaptation to vision of the torsional angular VOR in head positions away from the erect signify fundamental differences in the central organization of convergence of semicircular canal and otolith signals, when compared to the horizontal and vertical angular VORs. SUMMARY: The effects of head position and of lesions of the nodulus are assuming increasing importance in analysis and differential diagnosis of vertical misalignment and torsion of the eyes.